Bruce Jancin

EDINBURGH – Depression is common, underdiagnosed, and undertreated in patients with psoriatic arthritis.

Psychiatric evaluation of 50 consecutive patients at the University of Glasgow psoriatic arthritis clinic indicated that 15 patients, or 30%, were depressed. Three were rated as severely depressed based on their scores on the Hospital Anxiety and Depression Scale (HADS), while 12 others had moderate depression, Dr. Rajeev Krishnadas reported at the International Congress of the Royal College of Psychiatrists.

This high prevalence of depression in psoriatic arthritis patients is consistent with reports in the dermatologic literature (Br. J. Dermatol. 2008;159:704-10).

Of note, none of the depressed Scottish psoriatic arthritis patients was on a therapeutic dose of an antidepressant, added Dr. Krishnadas of the Sackler Institute of Psychobiological Research, Southern General Hospital, Glasgow.

This study is part of a larger ongoing investigation looking at the relationship between systemic inflammation and depression in patients with rheumatoid arthritis or psoriatic arthritis. In this portion of the study, a positive association was noted between HADS scores and C-reactive protein levels in the psoriatic arthritis cohort, although it must be noted that CRP scores accounted for only 7% of the overall variance in HADS scores.

Not surprisingly, higher HADS scores were associated with worse quality of life as assessed by the Dermatology Quality of Life Questionnaire as well as with higher scores on a self-rated pain scale.

Of greater interest psychodynamically, a negative correlation was found between HADS scores and emotional intelligence as measured by the Trait Emotional Intelligence Questionnaire – Short Form. High trait emotional intelligence reflects greater awareness of one’s own feelings as well as the feelings of others’. Individuals with high emotional intelligence are far better able to regulate their emotions than are those with lower trait emotional intelligence.

Patients who scored high in trait emotional intelligence had higher quality of life scores, lower CRP levels, and lower scores on the pain scale.

These findings are consistent with the hypothesis that a poor ability to be aware of and regulate one’s emotions predisposes to depression in the presence of a chronic medical condition or other major stressor, according to Dr. Krishnadas.

He declared having no conflicts of interest.

EDINBURGH – Depression is common, underdiagnosed, and undertreated in patients with psoriatic arthritis.

Psychiatric evaluation of 50 consecutive patients at the University of Glasgow psoriatic arthritis clinic indicated that 15 patients, or 30%, were depressed. Three were rated as severely depressed based on their scores on the Hospital Anxiety and Depression Scale (HADS), while 12 others had moderate depression, Dr. Rajeev Krishnadas reported at the International Congress of the Royal College of Psychiatrists.

This high prevalence of depression in psoriatic arthritis patients is consistent with reports in the dermatologic literature (Br. J. Dermatol. 2008;159:704-10).

Of note, none of the depressed Scottish psoriatic arthritis patients was on a therapeutic dose of an antidepressant, added Dr. Krishnadas of the Sackler Institute of Psychobiological Research, Southern General Hospital, Glasgow.

This study is part of a larger ongoing investigation looking at the relationship between systemic inflammation and depression in patients with rheumatoid arthritis or psoriatic arthritis. In this portion of the study, a positive association was noted between HADS scores and C-reactive protein levels in the psoriatic arthritis cohort, although it must be noted that CRP scores accounted for only 7% of the overall variance in HADS scores.

Not surprisingly, higher HADS scores were associated with worse quality of life as assessed by the Dermatology Quality of Life Questionnaire as well as with higher scores on a self-rated pain scale.

Of greater interest psychodynamically, a negative correlation was found between HADS scores and emotional intelligence as measured by the Trait Emotional Intelligence Questionnaire – Short Form. High trait emotional intelligence reflects greater awareness of one’s own feelings as well as the feelings of others’. Individuals with high emotional intelligence are far better able to regulate their emotions than are those with lower trait emotional intelligence.

Patients who scored high in trait emotional intelligence had higher quality of life scores, lower CRP levels, and lower scores on the pain scale.

These findings are consistent with the hypothesis that a poor ability to be aware of and regulate one’s emotions predisposes to depression in the presence of a chronic medical condition or other major stressor, according to Dr. Krishnadas.

He declared having no conflicts of interest.

EDINBURGH – Depression is common, underdiagnosed, and undertreated in patients with psoriatic arthritis.

Psychiatric evaluation of 50 consecutive patients at the University of Glasgow psoriatic arthritis clinic indicated that 15 patients, or 30%, were depressed. Three were rated as severely depressed based on their scores on the Hospital Anxiety and Depression Scale (HADS), while 12 others had moderate depression, Dr. Rajeev Krishnadas reported at the International Congress of the Royal College of Psychiatrists.

This high prevalence of depression in psoriatic arthritis patients is consistent with reports in the dermatologic literature (Br. J. Dermatol. 2008;159:704-10).

Of note, none of the depressed Scottish psoriatic arthritis patients was on a therapeutic dose of an antidepressant, added Dr. Krishnadas of the Sackler Institute of Psychobiological Research, Southern General Hospital, Glasgow.

This study is part of a larger ongoing investigation looking at the relationship between systemic inflammation and depression in patients with rheumatoid arthritis or psoriatic arthritis. In this portion of the study, a positive association was noted between HADS scores and C-reactive protein levels in the psoriatic arthritis cohort, although it must be noted that CRP scores accounted for only 7% of the overall variance in HADS scores.

Not surprisingly, higher HADS scores were associated with worse quality of life as assessed by the Dermatology Quality of Life Questionnaire as well as with higher scores on a self-rated pain scale.

Of greater interest psychodynamically, a negative correlation was found between HADS scores and emotional intelligence as measured by the Trait Emotional Intelligence Questionnaire – Short Form. High trait emotional intelligence reflects greater awareness of one’s own feelings as well as the feelings of others’. Individuals with high emotional intelligence are far better able to regulate their emotions than are those with lower trait emotional intelligence.

Patients who scored high in trait emotional intelligence had higher quality of life scores, lower CRP levels, and lower scores on the pain scale.

These findings are consistent with the hypothesis that a poor ability to be aware of and regulate one’s emotions predisposes to depression in the presence of a chronic medical condition or other major stressor, according to Dr. Krishnadas.

He declared having no conflicts of interest.

GOTHENBURG, Sweden – Rapid progression of cutaneous lupus erythematosus to SLE occurs considerably more often than previously recognized, a comprehensive nationwide Swedish study found.

The population-based study, which included all 1,088 patients diagnosed with CLE in Sweden from 2005 to 2007, found that the risk of being diagnosed with SLE during the first year of CLE diagnosis was 12%. The 3-year rate of progression to SLE was 18%, Dr. Carina M. Grönhagen reported at the annual congress of the European Academy of Dermatology and Venereology.

Moreover, 24% of patients already carried the diagnosis of SLE at the time they were diagnosed with CLE, added Dr. Grönhagen, a dermatology resident at the Karolinska Institutet, Danderyd Hospital, Stockholm.

Patients with the subacute form of CLE had the highest rate of early progression to SLE, with a 3-year incidence of nearly 25%. Patients with subacute CLE accounted for 15.7% of the overall Swedish CLE cohort.

Discoid CLE accounted for 79.8% of all cases of CLE diagnosed in Sweden during the study period, while lupus panniculitis and other less common forms of local LE comprised the remainder.

Women with newly diagnosed CLE had a 3-year rate of progression to SLE of 20%, twice that of men. The incidence of CLE was threefold greater in Swedish women than men.

Patients with newly diagnosed CLE should be informed of the risk of early progression to SLE, Dr. Grönhagen said. They should be made aware of the systemic signs and symptoms, such as fevers and joint pains, so appropriate treatment for SLE is not delayed.

Her study relied upon Swedish National Patient Register data, which, since 2001, has included outpatient specialist care as well as inpatient care.

The incidence of CLE in Sweden, based on these data, is 4.0 per 100,000 population per year. The peak incidence of CLE in women was in the 65- to 74-year-old group, while the peak in men was at age 55-64. This pattern was skewed in the subset of patients with subacute CLE; their peak incidence was later, and there were far fewer cases diagnosed before age 45 than for discoid and other forms of CLE.

"One theory behind this is that the subacute form is drug induced to a larger extent than previously believed. An important known trigger for subacute CLE is antihypertensive drugs, which are mostly taken by people age 45 and older," Dr. Grönhagen said.

During her presentation at the meeting of the European Society of Cutaneous Lupus Erythematosus, held in conjunction with the EADV congress, audience members noted that there has been a dearth of population-based studies reporting the incidence of isolated CLE. They also commented on the large size of the population in Dr. Grönhagen’s study and the 3-year follow-up.

Audience members noted that the Swedish national study, since it included outpatients as well as inpatients, is relatively immune to selection bias. Although it was noted that the reported CLE incidence of 4.0/100,000 is up to 10-fold lower than cited in some other studies, Dr. Grönhagen countered that prior studies have been much smaller and less comprehensive.

Still, she said, the 4.0/100,000 incidence figure is probably an underestimate. It is likely that the mildest cases of discoid LE were never referred to a dermatologist or other specialist and, hence, weren't recorded in the outpatient portion of the national registry.

Dr. Grönhagen declared having no relevant financial interests.

GOTHENBURG, Sweden – Rapid progression of cutaneous lupus erythematosus to SLE occurs considerably more often than previously recognized, a comprehensive nationwide Swedish study found.

The population-based study, which included all 1,088 patients diagnosed with CLE in Sweden from 2005 to 2007, found that the risk of being diagnosed with SLE during the first year of CLE diagnosis was 12%. The 3-year rate of progression to SLE was 18%, Dr. Carina M. Grönhagen reported at the annual congress of the European Academy of Dermatology and Venereology.

Moreover, 24% of patients already carried the diagnosis of SLE at the time they were diagnosed with CLE, added Dr. Grönhagen, a dermatology resident at the Karolinska Institutet, Danderyd Hospital, Stockholm.

Patients with the subacute form of CLE had the highest rate of early progression to SLE, with a 3-year incidence of nearly 25%. Patients with subacute CLE accounted for 15.7% of the overall Swedish CLE cohort.

Discoid CLE accounted for 79.8% of all cases of CLE diagnosed in Sweden during the study period, while lupus panniculitis and other less common forms of local LE comprised the remainder.

Women with newly diagnosed CLE had a 3-year rate of progression to SLE of 20%, twice that of men. The incidence of CLE was threefold greater in Swedish women than men.

Patients with newly diagnosed CLE should be informed of the risk of early progression to SLE, Dr. Grönhagen said. They should be made aware of the systemic signs and symptoms, such as fevers and joint pains, so appropriate treatment for SLE is not delayed.

Her study relied upon Swedish National Patient Register data, which, since 2001, has included outpatient specialist care as well as inpatient care.

The incidence of CLE in Sweden, based on these data, is 4.0 per 100,000 population per year. The peak incidence of CLE in women was in the 65- to 74-year-old group, while the peak in men was at age 55-64. This pattern was skewed in the subset of patients with subacute CLE; their peak incidence was later, and there were far fewer cases diagnosed before age 45 than for discoid and other forms of CLE.

"One theory behind this is that the subacute form is drug induced to a larger extent than previously believed. An important known trigger for subacute CLE is antihypertensive drugs, which are mostly taken by people age 45 and older," Dr. Grönhagen said.

During her presentation at the meeting of the European Society of Cutaneous Lupus Erythematosus, held in conjunction with the EADV congress, audience members noted that there has been a dearth of population-based studies reporting the incidence of isolated CLE. They also commented on the large size of the population in Dr. Grönhagen’s study and the 3-year follow-up.

Audience members noted that the Swedish national study, since it included outpatients as well as inpatients, is relatively immune to selection bias. Although it was noted that the reported CLE incidence of 4.0/100,000 is up to 10-fold lower than cited in some other studies, Dr. Grönhagen countered that prior studies have been much smaller and less comprehensive.

Still, she said, the 4.0/100,000 incidence figure is probably an underestimate. It is likely that the mildest cases of discoid LE were never referred to a dermatologist or other specialist and, hence, weren't recorded in the outpatient portion of the national registry.

Dr. Grönhagen declared having no relevant financial interests.

GOTHENBURG, Sweden – Rapid progression of cutaneous lupus erythematosus to SLE occurs considerably more often than previously recognized, a comprehensive nationwide Swedish study found.

The population-based study, which included all 1,088 patients diagnosed with CLE in Sweden from 2005 to 2007, found that the risk of being diagnosed with SLE during the first year of CLE diagnosis was 12%. The 3-year rate of progression to SLE was 18%, Dr. Carina M. Grönhagen reported at the annual congress of the European Academy of Dermatology and Venereology.

Moreover, 24% of patients already carried the diagnosis of SLE at the time they were diagnosed with CLE, added Dr. Grönhagen, a dermatology resident at the Karolinska Institutet, Danderyd Hospital, Stockholm.

Patients with the subacute form of CLE had the highest rate of early progression to SLE, with a 3-year incidence of nearly 25%. Patients with subacute CLE accounted for 15.7% of the overall Swedish CLE cohort.

Discoid CLE accounted for 79.8% of all cases of CLE diagnosed in Sweden during the study period, while lupus panniculitis and other less common forms of local LE comprised the remainder.

Women with newly diagnosed CLE had a 3-year rate of progression to SLE of 20%, twice that of men. The incidence of CLE was threefold greater in Swedish women than men.

Patients with newly diagnosed CLE should be informed of the risk of early progression to SLE, Dr. Grönhagen said. They should be made aware of the systemic signs and symptoms, such as fevers and joint pains, so appropriate treatment for SLE is not delayed.

Her study relied upon Swedish National Patient Register data, which, since 2001, has included outpatient specialist care as well as inpatient care.

The incidence of CLE in Sweden, based on these data, is 4.0 per 100,000 population per year. The peak incidence of CLE in women was in the 65- to 74-year-old group, while the peak in men was at age 55-64. This pattern was skewed in the subset of patients with subacute CLE; their peak incidence was later, and there were far fewer cases diagnosed before age 45 than for discoid and other forms of CLE.

"One theory behind this is that the subacute form is drug induced to a larger extent than previously believed. An important known trigger for subacute CLE is antihypertensive drugs, which are mostly taken by people age 45 and older," Dr. Grönhagen said.

During her presentation at the meeting of the European Society of Cutaneous Lupus Erythematosus, held in conjunction with the EADV congress, audience members noted that there has been a dearth of population-based studies reporting the incidence of isolated CLE. They also commented on the large size of the population in Dr. Grönhagen’s study and the 3-year follow-up.

Audience members noted that the Swedish national study, since it included outpatients as well as inpatients, is relatively immune to selection bias. Although it was noted that the reported CLE incidence of 4.0/100,000 is up to 10-fold lower than cited in some other studies, Dr. Grönhagen countered that prior studies have been much smaller and less comprehensive.

Still, she said, the 4.0/100,000 incidence figure is probably an underestimate. It is likely that the mildest cases of discoid LE were never referred to a dermatologist or other specialist and, hence, weren't recorded in the outpatient portion of the national registry.

Dr. Grönhagen declared having no relevant financial interests.

GOTHENBURG, Sweden – Rapid progression of cutaneous lupus erythematosus to SLE occurs considerably more often than previously recognized, a comprehensive nationwide Swedish study found.

The population-based study, which included all 1,088 patients diagnosed with CLE in Sweden from 2005 to 2007, found that the risk of being diagnosed with SLE during the first year of CLE diagnosis was 12%. The 3-year rate of progression to SLE was 18%, Dr. Carina M. Grönhagen reported at the annual congress of the European Academy of Dermatology and Venereology.

Moreover, 24% of patients already carried the diagnosis of SLE at the time they were diagnosed with CLE, added Dr. Grönhagen, a dermatology resident at the Karolinska Institutet, Danderyd Hospital, Stockholm.

Patients with the subacute form of CLE had the highest rate of early progression to SLE, with a 3-year incidence of nearly 25%. Patients with subacute CLE accounted for 15.7% of the overall Swedish CLE cohort.

Discoid CLE accounted for 79.8% of all cases of CLE diagnosed in Sweden during the study period, while lupus panniculitis and other less common forms of local LE comprised the remainder.

Women with newly diagnosed CLE had a 3-year rate of progression to SLE of 20%, twice that of men. The incidence of CLE was threefold greater in Swedish women than men.

Patients with newly diagnosed CLE should be informed of the risk of early progression to SLE, Dr. Grönhagen said. They should be made aware of the systemic signs and symptoms, such as fevers and joint pains, so appropriate treatment for SLE is not delayed.

Her study relied upon Swedish National Patient Register data, which, since 2001, has included outpatient specialist care as well as inpatient care.

The incidence of CLE in Sweden, based on these data, is 4.0 per 100,000 population per year. The peak incidence of CLE in women was in the 65- to 74-year-old group, while the peak in men was at age 55-64. This pattern was skewed in the subset of patients with subacute CLE; their peak incidence was later, and there were far fewer cases diagnosed before age 45 than for discoid and other forms of CLE.

"One theory behind this is that the subacute form is drug induced to a larger extent than previously believed. An important known trigger for subacute CLE is antihypertensive drugs, which are mostly taken by people age 45 and older," Dr. Grönhagen said.

During her presentation at the meeting of the European Society of Cutaneous Lupus Erythematosus, held in conjunction with the EADV congress, audience members noted that there has been a dearth of population-based studies reporting the incidence of isolated CLE. They also commented on the large size of the population in Dr. Grönhagen’s study and the 3-year follow-up.

Audience members noted that the Swedish national study, since it included outpatients as well as inpatients, is relatively immune to selection bias. Although it was noted that the reported CLE incidence of 4.0/100,000 is up to 10-fold lower than cited in some other studies, Dr. Grönhagen countered that prior studies have been much smaller and less comprehensive.

Still, she said, the 4.0/100,000 incidence figure is probably an underestimate. It is likely that the mildest cases of discoid LE were never referred to a dermatologist or other specialist and, hence, weren't recorded in the outpatient portion of the national registry.

Dr. Grönhagen declared having no relevant financial interests.

GOTHENBURG, Sweden – Rapid progression of cutaneous lupus erythematosus to SLE occurs considerably more often than previously recognized, a comprehensive nationwide Swedish study found.

The population-based study, which included all 1,088 patients diagnosed with CLE in Sweden from 2005 to 2007, found that the risk of being diagnosed with SLE during the first year of CLE diagnosis was 12%. The 3-year rate of progression to SLE was 18%, Dr. Carina M. Grönhagen reported at the annual congress of the European Academy of Dermatology and Venereology.

Moreover, 24% of patients already carried the diagnosis of SLE at the time they were diagnosed with CLE, added Dr. Grönhagen, a dermatology resident at the Karolinska Institutet, Danderyd Hospital, Stockholm.

Patients with the subacute form of CLE had the highest rate of early progression to SLE, with a 3-year incidence of nearly 25%. Patients with subacute CLE accounted for 15.7% of the overall Swedish CLE cohort.

Discoid CLE accounted for 79.8% of all cases of CLE diagnosed in Sweden during the study period, while lupus panniculitis and other less common forms of local LE comprised the remainder.

Women with newly diagnosed CLE had a 3-year rate of progression to SLE of 20%, twice that of men. The incidence of CLE was threefold greater in Swedish women than men.

Patients with newly diagnosed CLE should be informed of the risk of early progression to SLE, Dr. Grönhagen said. They should be made aware of the systemic signs and symptoms, such as fevers and joint pains, so appropriate treatment for SLE is not delayed.

Her study relied upon Swedish National Patient Register data, which, since 2001, has included outpatient specialist care as well as inpatient care.

The incidence of CLE in Sweden, based on these data, is 4.0 per 100,000 population per year. The peak incidence of CLE in women was in the 65- to 74-year-old group, while the peak in men was at age 55-64. This pattern was skewed in the subset of patients with subacute CLE; their peak incidence was later, and there were far fewer cases diagnosed before age 45 than for discoid and other forms of CLE.

"One theory behind this is that the subacute form is drug induced to a larger extent than previously believed. An important known trigger for subacute CLE is antihypertensive drugs, which are mostly taken by people age 45 and older," Dr. Grönhagen said.

During her presentation at the meeting of the European Society of Cutaneous Lupus Erythematosus, held in conjunction with the EADV congress, audience members noted that there has been a dearth of population-based studies reporting the incidence of isolated CLE. They also commented on the large size of the population in Dr. Grönhagen’s study and the 3-year follow-up.

Audience members noted that the Swedish national study, since it included outpatients as well as inpatients, is relatively immune to selection bias. Although it was noted that the reported CLE incidence of 4.0/100,000 is up to 10-fold lower than cited in some other studies, Dr. Grönhagen countered that prior studies have been much smaller and less comprehensive.

Still, she said, the 4.0/100,000 incidence figure is probably an underestimate. It is likely that the mildest cases of discoid LE were never referred to a dermatologist or other specialist and, hence, weren't recorded in the outpatient portion of the national registry.

Dr. Grönhagen declared having no relevant financial interests.

GOTHENBURG, Sweden – Rapid progression of cutaneous lupus erythematosus to SLE occurs considerably more often than previously recognized, a comprehensive nationwide Swedish study found.

The population-based study, which included all 1,088 patients diagnosed with CLE in Sweden from 2005 to 2007, found that the risk of being diagnosed with SLE during the first year of CLE diagnosis was 12%. The 3-year rate of progression to SLE was 18%, Dr. Carina M. Grönhagen reported at the annual congress of the European Academy of Dermatology and Venereology.

Moreover, 24% of patients already carried the diagnosis of SLE at the time they were diagnosed with CLE, added Dr. Grönhagen, a dermatology resident at the Karolinska Institutet, Danderyd Hospital, Stockholm.

Patients with the subacute form of CLE had the highest rate of early progression to SLE, with a 3-year incidence of nearly 25%. Patients with subacute CLE accounted for 15.7% of the overall Swedish CLE cohort.

Discoid CLE accounted for 79.8% of all cases of CLE diagnosed in Sweden during the study period, while lupus panniculitis and other less common forms of local LE comprised the remainder.

Women with newly diagnosed CLE had a 3-year rate of progression to SLE of 20%, twice that of men. The incidence of CLE was threefold greater in Swedish women than men.

Patients with newly diagnosed CLE should be informed of the risk of early progression to SLE, Dr. Grönhagen said. They should be made aware of the systemic signs and symptoms, such as fevers and joint pains, so appropriate treatment for SLE is not delayed.

Her study relied upon Swedish National Patient Register data, which, since 2001, has included outpatient specialist care as well as inpatient care.

The incidence of CLE in Sweden, based on these data, is 4.0 per 100,000 population per year. The peak incidence of CLE in women was in the 65- to 74-year-old group, while the peak in men was at age 55-64. This pattern was skewed in the subset of patients with subacute CLE; their peak incidence was later, and there were far fewer cases diagnosed before age 45 than for discoid and other forms of CLE.

"One theory behind this is that the subacute form is drug induced to a larger extent than previously believed. An important known trigger for subacute CLE is antihypertensive drugs, which are mostly taken by people age 45 and older," Dr. Grönhagen said.

During her presentation at the meeting of the European Society of Cutaneous Lupus Erythematosus, held in conjunction with the EADV congress, audience members noted that there has been a dearth of population-based studies reporting the incidence of isolated CLE. They also commented on the large size of the population in Dr. Grönhagen’s study and the 3-year follow-up.

Audience members noted that the Swedish national study, since it included outpatients as well as inpatients, is relatively immune to selection bias. Although it was noted that the reported CLE incidence of 4.0/100,000 is up to 10-fold lower than cited in some other studies, Dr. Grönhagen countered that prior studies have been much smaller and less comprehensive.

Still, she said, the 4.0/100,000 incidence figure is probably an underestimate. It is likely that the mildest cases of discoid LE were never referred to a dermatologist or other specialist and, hence, weren't recorded in the outpatient portion of the national registry.

Dr. Grönhagen declared having no relevant financial interests.

STOCKHOLM – A single bolus dose of 100 U/kg of unfractionated heparin in patients who undergo elective percutaneous coronary intervention is superior to the long-standard 140-U/kg regimen, according to a large prospective study.

Photo credit: European Society of Cardiology

“This reduced dose of heparin represents a simple and safe method of lowering the bleeding risk after PCI without increasing the risk of ischemic complications,” Dr. Stefanie Schulz concluded in presenting the findings of the ISAR-REACT 3A (Intracoronary Stenting and Antithrombotic Regimen: Rapid Early Action for Coronary Treatment) trial at the annual congress of the European Society of Cardiology.

ISAR-REACT 3A was a single-center study that included 2,505 cardiac biomarker–negative patients who underwent elective PCI after being premedicated with clopidogrel. All patients received a single bolus of unfractionated heparin (UFH) at 100 U/kg

The study featured two control arms, both comprising historical controls that were obtained from the previously published ISAR-REACT 3 trial (N. Engl. J. Med. 2008;359:688-96). One control group consisted of 2,281 patients randomized to a single 140-U/kg bolus of UFH, the regimen that was followed in elective PCI for decades by many interventional cardiologists. The other comparison group was made up of 2,289 patients randomized to bivalirudin in the same trial.

The ISAR-REACT 3A study was carried out because in the earlier ISAR-REACT 3, the 140-U/kg dose of UFH proved to be comparable with bivalirudin in terms of net clinical outcome, but was associated with a significantly greater bleeding rate. The main hypothesis tested in ISAR-REACT 3A was that a lower dose of heparin would be as effective as 140 U/kg in preventing ischemic events, and would have less bleeding.

This proved to be the case. The primary study quadruple end point – the 30-day combined rate of death, MI, urgent target vessel revascularization, and in-hospital major bleeding – occurred in 7.3% of the lower-dose UFH group, compared with 8.7% of those on 140 U/kg. The resultant highly significant 25% relative risk reduction that emerged from a multivariate propensity analysis was driven largely by the reduced risk of major bleeding in the 100-U/kg UFH group (3.6% vs 4.6%), reported Dr. Schulz of the German Heart Center at the Technical University of Munich.

The comparison between the lower-dose UFH and the bivalirudin study arms was designed as a noninferiority analysis. The 30-day, combined end point occurred in 7.3% of the UFH group and 8.3% of those on bivalirudin, indicating that the net clinical outcome with 100 U/kg of UFH was noninferior to the direct thrombin inhibitor. The major bleeding rate was 3.6% with UFH and 3.1% with bivalirudin.

Discussant Dr. Christian Hamm hailed ISAR-REACT 3A as “an important contribution to interventional cardiology” because the use of UFH has for decades been guided mainly by expert opinion, with very little in the way of randomized, controlled data.

He wished, however, that the Munich researchers had tested an even lower dose of UFH – say, 70 U/kg.

“I think it’s reasonable to even further reduce our anticoagulation in elective PCI because we have fewer thrombogenic guidewires and other materials today, we have shorter procedures because the materials are better, we have less thrombogenic contrast media, and we have in most patients premedication with clopidogrel. So in my view, the take-home message from ISAR-REACT 3A is that in elective PCI, don’t use more than 100 U/kg of UFH; you probably can use even less,” declared Dr. Hamm of the Kerckhoff Clinic, Bad Nauheim, Germany.

Disclosures: Dr. Schulz and Dr. Hamm declared having no financial conflicts.

STOCKHOLM – A single bolus dose of 100 U/kg of unfractionated heparin in patients who undergo elective percutaneous coronary intervention is superior to the long-standard 140-U/kg regimen, according to a large prospective study.

Photo credit: European Society of Cardiology

“This reduced dose of heparin represents a simple and safe method of lowering the bleeding risk after PCI without increasing the risk of ischemic complications,” Dr. Stefanie Schulz concluded in presenting the findings of the ISAR-REACT 3A (Intracoronary Stenting and Antithrombotic Regimen: Rapid Early Action for Coronary Treatment) trial at the annual congress of the European Society of Cardiology.

ISAR-REACT 3A was a single-center study that included 2,505 cardiac biomarker–negative patients who underwent elective PCI after being premedicated with clopidogrel. All patients received a single bolus of unfractionated heparin (UFH) at 100 U/kg

The study featured two control arms, both comprising historical controls that were obtained from the previously published ISAR-REACT 3 trial (N. Engl. J. Med. 2008;359:688-96). One control group consisted of 2,281 patients randomized to a single 140-U/kg bolus of UFH, the regimen that was followed in elective PCI for decades by many interventional cardiologists. The other comparison group was made up of 2,289 patients randomized to bivalirudin in the same trial.

The ISAR-REACT 3A study was carried out because in the earlier ISAR-REACT 3, the 140-U/kg dose of UFH proved to be comparable with bivalirudin in terms of net clinical outcome, but was associated with a significantly greater bleeding rate. The main hypothesis tested in ISAR-REACT 3A was that a lower dose of heparin would be as effective as 140 U/kg in preventing ischemic events, and would have less bleeding.

This proved to be the case. The primary study quadruple end point – the 30-day combined rate of death, MI, urgent target vessel revascularization, and in-hospital major bleeding – occurred in 7.3% of the lower-dose UFH group, compared with 8.7% of those on 140 U/kg. The resultant highly significant 25% relative risk reduction that emerged from a multivariate propensity analysis was driven largely by the reduced risk of major bleeding in the 100-U/kg UFH group (3.6% vs 4.6%), reported Dr. Schulz of the German Heart Center at the Technical University of Munich.

The comparison between the lower-dose UFH and the bivalirudin study arms was designed as a noninferiority analysis. The 30-day, combined end point occurred in 7.3% of the UFH group and 8.3% of those on bivalirudin, indicating that the net clinical outcome with 100 U/kg of UFH was noninferior to the direct thrombin inhibitor. The major bleeding rate was 3.6% with UFH and 3.1% with bivalirudin.

Discussant Dr. Christian Hamm hailed ISAR-REACT 3A as “an important contribution to interventional cardiology” because the use of UFH has for decades been guided mainly by expert opinion, with very little in the way of randomized, controlled data.

He wished, however, that the Munich researchers had tested an even lower dose of UFH – say, 70 U/kg.

“I think it’s reasonable to even further reduce our anticoagulation in elective PCI because we have fewer thrombogenic guidewires and other materials today, we have shorter procedures because the materials are better, we have less thrombogenic contrast media, and we have in most patients premedication with clopidogrel. So in my view, the take-home message from ISAR-REACT 3A is that in elective PCI, don’t use more than 100 U/kg of UFH; you probably can use even less,” declared Dr. Hamm of the Kerckhoff Clinic, Bad Nauheim, Germany.

Disclosures: Dr. Schulz and Dr. Hamm declared having no financial conflicts.

STOCKHOLM – A single bolus dose of 100 U/kg of unfractionated heparin in patients who undergo elective percutaneous coronary intervention is superior to the long-standard 140-U/kg regimen, according to a large prospective study.

Photo credit: European Society of Cardiology

“This reduced dose of heparin represents a simple and safe method of lowering the bleeding risk after PCI without increasing the risk of ischemic complications,” Dr. Stefanie Schulz concluded in presenting the findings of the ISAR-REACT 3A (Intracoronary Stenting and Antithrombotic Regimen: Rapid Early Action for Coronary Treatment) trial at the annual congress of the European Society of Cardiology.

ISAR-REACT 3A was a single-center study that included 2,505 cardiac biomarker–negative patients who underwent elective PCI after being premedicated with clopidogrel. All patients received a single bolus of unfractionated heparin (UFH) at 100 U/kg

The study featured two control arms, both comprising historical controls that were obtained from the previously published ISAR-REACT 3 trial (N. Engl. J. Med. 2008;359:688-96). One control group consisted of 2,281 patients randomized to a single 140-U/kg bolus of UFH, the regimen that was followed in elective PCI for decades by many interventional cardiologists. The other comparison group was made up of 2,289 patients randomized to bivalirudin in the same trial.

The ISAR-REACT 3A study was carried out because in the earlier ISAR-REACT 3, the 140-U/kg dose of UFH proved to be comparable with bivalirudin in terms of net clinical outcome, but was associated with a significantly greater bleeding rate. The main hypothesis tested in ISAR-REACT 3A was that a lower dose of heparin would be as effective as 140 U/kg in preventing ischemic events, and would have less bleeding.

This proved to be the case. The primary study quadruple end point – the 30-day combined rate of death, MI, urgent target vessel revascularization, and in-hospital major bleeding – occurred in 7.3% of the lower-dose UFH group, compared with 8.7% of those on 140 U/kg. The resultant highly significant 25% relative risk reduction that emerged from a multivariate propensity analysis was driven largely by the reduced risk of major bleeding in the 100-U/kg UFH group (3.6% vs 4.6%), reported Dr. Schulz of the German Heart Center at the Technical University of Munich.

The comparison between the lower-dose UFH and the bivalirudin study arms was designed as a noninferiority analysis. The 30-day, combined end point occurred in 7.3% of the UFH group and 8.3% of those on bivalirudin, indicating that the net clinical outcome with 100 U/kg of UFH was noninferior to the direct thrombin inhibitor. The major bleeding rate was 3.6% with UFH and 3.1% with bivalirudin.

Discussant Dr. Christian Hamm hailed ISAR-REACT 3A as “an important contribution to interventional cardiology” because the use of UFH has for decades been guided mainly by expert opinion, with very little in the way of randomized, controlled data.

He wished, however, that the Munich researchers had tested an even lower dose of UFH – say, 70 U/kg.

“I think it’s reasonable to even further reduce our anticoagulation in elective PCI because we have fewer thrombogenic guidewires and other materials today, we have shorter procedures because the materials are better, we have less thrombogenic contrast media, and we have in most patients premedication with clopidogrel. So in my view, the take-home message from ISAR-REACT 3A is that in elective PCI, don’t use more than 100 U/kg of UFH; you probably can use even less,” declared Dr. Hamm of the Kerckhoff Clinic, Bad Nauheim, Germany.

Disclosures: Dr. Schulz and Dr. Hamm declared having no financial conflicts.

STOCKHOLM – A single bolus dose of 100 U/kg of unfractionated heparin in patients who undergo elective percutaneous coronary intervention is superior to the long-standard 140-U/kg regimen, according to a large prospective study.

Photo credit: European Society of Cardiology 

“This reduced dose of heparin represents a simple and safe method of lowering the bleeding risk after PCI without increasing the risk of ischemic complications,” Dr. Stefanie Schulz concluded in presenting the findings of the ISAR-REACT 3A (Intracoronary Stenting and Antithrombotic Regimen: Rapid Early Action for Coronary Treatment) trial at the annual congress of the European Society of Cardiology.

ISAR-REACT 3A was a single-center study that included 2,505 cardiac biomarker–negative patients who underwent elective PCI after being premedicated with clopidogrel. All patients received a single bolus of unfractionated heparin (UFH) at 100 U/kg

The study featured two control arms, both comprising historical controls that were obtained from the previously published ISAR-REACT 3 trial (N. Engl. J. Med. 2008;359:688-96). One control group consisted of 2,281 patients randomized to a single 140-U/kg bolus of UFH, the regimen that was followed in elective PCI for decades by many interventional cardiologists. The other comparison group was made up of 2,289 patients randomized to bivalirudin in the same trial.

The ISAR-REACT 3A study was carried out because in the earlier ISAR-REACT 3, the 140-U/kg dose of UFH proved to be comparable with bivalirudin in terms of net clinical outcome, but was associated with a significantly greater bleeding rate. The main hypothesis tested in ISAR-REACT 3A was that a lower dose of heparin would be as effective as 140 U/kg in preventing ischemic events, and would have less bleeding.

This proved to be the case. The primary study quadruple end point – the 30-day combined rate of death, MI, urgent target vessel revascularization, and in-hospital major bleeding – occurred in 7.3% of the lower-dose UFH group, compared with 8.7% of those on 140 U/kg. The resultant highly significant 25% relative risk reduction that emerged from a multivariate propensity analysis was driven largely by the reduced risk of major bleeding in the 100-U/kg UFH group (3.6% vs 4.6%), reported Dr. Schulz of the German Heart Center at the Technical University of Munich.

The comparison between the lower-dose UFH and the bivalirudin study arms was designed as a noninferiority analysis. The 30-day, combined end point occurred in 7.3% of the UFH group and 8.3% of those on bivalirudin, indicating that the net clinical outcome with 100 U/kg of UFH was noninferior to the direct thrombin inhibitor. The major bleeding rate was 3.6% with UFH and 3.1% with bivalirudin.

Discussant Dr. Christian Hamm hailed ISAR-REACT 3A as “an important contribution to interventional cardiology” because the use of UFH has for decades been guided mainly by expert opinion, with very little in the way of randomized, controlled data.

He wished, however, that the Munich researchers had tested an even lower dose of UFH – say, 70 U/kg.

“I think it’s reasonable to even further reduce our anticoagulation in elective PCI because we have fewer thrombogenic guidewires and other materials today, we have shorter procedures because the materials are better, we have less thrombogenic contrast media, and we have in most patients premedication with clopidogrel. So in my view, the take-home message from ISAR-REACT 3A is that in elective PCI, don’t use more than 100 U/kg of UFH; you probably can use even less,” declared Dr. Hamm of the Kerckhoff Clinic, Bad Nauheim, Germany.

Disclosures: Dr. Schulz and Dr. Hamm declared having no financial conflicts.

STOCKHOLM – A single bolus dose of 100 U/kg of unfractionated heparin in patients who undergo elective percutaneous coronary intervention is superior to the long-standard 140-U/kg regimen, according to a large prospective study.

Photo credit: European Society of Cardiology 

“This reduced dose of heparin represents a simple and safe method of lowering the bleeding risk after PCI without increasing the risk of ischemic complications,” Dr. Stefanie Schulz concluded in presenting the findings of the ISAR-REACT 3A (Intracoronary Stenting and Antithrombotic Regimen: Rapid Early Action for Coronary Treatment) trial at the annual congress of the European Society of Cardiology.

ISAR-REACT 3A was a single-center study that included 2,505 cardiac biomarker–negative patients who underwent elective PCI after being premedicated with clopidogrel. All patients received a single bolus of unfractionated heparin (UFH) at 100 U/kg

The study featured two control arms, both comprising historical controls that were obtained from the previously published ISAR-REACT 3 trial (N. Engl. J. Med. 2008;359:688-96). One control group consisted of 2,281 patients randomized to a single 140-U/kg bolus of UFH, the regimen that was followed in elective PCI for decades by many interventional cardiologists. The other comparison group was made up of 2,289 patients randomized to bivalirudin in the same trial.

The ISAR-REACT 3A study was carried out because in the earlier ISAR-REACT 3, the 140-U/kg dose of UFH proved to be comparable with bivalirudin in terms of net clinical outcome, but was associated with a significantly greater bleeding rate. The main hypothesis tested in ISAR-REACT 3A was that a lower dose of heparin would be as effective as 140 U/kg in preventing ischemic events, and would have less bleeding.

This proved to be the case. The primary study quadruple end point – the 30-day combined rate of death, MI, urgent target vessel revascularization, and in-hospital major bleeding – occurred in 7.3% of the lower-dose UFH group, compared with 8.7% of those on 140 U/kg. The resultant highly significant 25% relative risk reduction that emerged from a multivariate propensity analysis was driven largely by the reduced risk of major bleeding in the 100-U/kg UFH group (3.6% vs 4.6%), reported Dr. Schulz of the German Heart Center at the Technical University of Munich.

The comparison between the lower-dose UFH and the bivalirudin study arms was designed as a noninferiority analysis. The 30-day, combined end point occurred in 7.3% of the UFH group and 8.3% of those on bivalirudin, indicating that the net clinical outcome with 100 U/kg of UFH was noninferior to the direct thrombin inhibitor. The major bleeding rate was 3.6% with UFH and 3.1% with bivalirudin.

Discussant Dr. Christian Hamm hailed ISAR-REACT 3A as “an important contribution to interventional cardiology” because the use of UFH has for decades been guided mainly by expert opinion, with very little in the way of randomized, controlled data.

He wished, however, that the Munich researchers had tested an even lower dose of UFH – say, 70 U/kg.

“I think it’s reasonable to even further reduce our anticoagulation in elective PCI because we have fewer thrombogenic guidewires and other materials today, we have shorter procedures because the materials are better, we have less thrombogenic contrast media, and we have in most patients premedication with clopidogrel. So in my view, the take-home message from ISAR-REACT 3A is that in elective PCI, don’t use more than 100 U/kg of UFH; you probably can use even less,” declared Dr. Hamm of the Kerckhoff Clinic, Bad Nauheim, Germany.

Disclosures: Dr. Schulz and Dr. Hamm declared having no financial conflicts.

STOCKHOLM – A single bolus dose of 100 U/kg of unfractionated heparin in patients who undergo elective percutaneous coronary intervention is superior to the long-standard 140-U/kg regimen, according to a large prospective study.

Photo credit: European Society of Cardiology 

“This reduced dose of heparin represents a simple and safe method of lowering the bleeding risk after PCI without increasing the risk of ischemic complications,” Dr. Stefanie Schulz concluded in presenting the findings of the ISAR-REACT 3A (Intracoronary Stenting and Antithrombotic Regimen: Rapid Early Action for Coronary Treatment) trial at the annual congress of the European Society of Cardiology.

ISAR-REACT 3A was a single-center study that included 2,505 cardiac biomarker–negative patients who underwent elective PCI after being premedicated with clopidogrel. All patients received a single bolus of unfractionated heparin (UFH) at 100 U/kg

The study featured two control arms, both comprising historical controls that were obtained from the previously published ISAR-REACT 3 trial (N. Engl. J. Med. 2008;359:688-96). One control group consisted of 2,281 patients randomized to a single 140-U/kg bolus of UFH, the regimen that was followed in elective PCI for decades by many interventional cardiologists. The other comparison group was made up of 2,289 patients randomized to bivalirudin in the same trial.

The ISAR-REACT 3A study was carried out because in the earlier ISAR-REACT 3, the 140-U/kg dose of UFH proved to be comparable with bivalirudin in terms of net clinical outcome, but was associated with a significantly greater bleeding rate. The main hypothesis tested in ISAR-REACT 3A was that a lower dose of heparin would be as effective as 140 U/kg in preventing ischemic events, and would have less bleeding.

This proved to be the case. The primary study quadruple end point – the 30-day combined rate of death, MI, urgent target vessel revascularization, and in-hospital major bleeding – occurred in 7.3% of the lower-dose UFH group, compared with 8.7% of those on 140 U/kg. The resultant highly significant 25% relative risk reduction that emerged from a multivariate propensity analysis was driven largely by the reduced risk of major bleeding in the 100-U/kg UFH group (3.6% vs 4.6%), reported Dr. Schulz of the German Heart Center at the Technical University of Munich.

The comparison between the lower-dose UFH and the bivalirudin study arms was designed as a noninferiority analysis. The 30-day, combined end point occurred in 7.3% of the UFH group and 8.3% of those on bivalirudin, indicating that the net clinical outcome with 100 U/kg of UFH was noninferior to the direct thrombin inhibitor. The major bleeding rate was 3.6% with UFH and 3.1% with bivalirudin.

Discussant Dr. Christian Hamm hailed ISAR-REACT 3A as “an important contribution to interventional cardiology” because the use of UFH has for decades been guided mainly by expert opinion, with very little in the way of randomized, controlled data.

He wished, however, that the Munich researchers had tested an even lower dose of UFH – say, 70 U/kg.

“I think it’s reasonable to even further reduce our anticoagulation in elective PCI because we have fewer thrombogenic guidewires and other materials today, we have shorter procedures because the materials are better, we have less thrombogenic contrast media, and we have in most patients premedication with clopidogrel. So in my view, the take-home message from ISAR-REACT 3A is that in elective PCI, don’t use more than 100 U/kg of UFH; you probably can use even less,” declared Dr. Hamm of the Kerckhoff Clinic, Bad Nauheim, Germany.

Disclosures: Dr. Schulz and Dr. Hamm declared having no financial conflicts.

STOCKHOLM – The initial report from the world’s largest atrial fibrillation registry demonstrates that in everyday clinical practice, the arrhythmia is frequently not controlled – and even when it is, most patients remain symptomatic.

The RealiseAF registry data also underscore that real-world patients with atrial fibrillation (AF) have a disturbingly highly cardiovascular event rate, with 29% of the more than 10,000 enrollees having experienced an unplanned hospital admission for a serious cardiovascular event within the past 12 months. The most frequent reasons for admission were acute decompensated heart failure, acute coronary syndromes, stroke, and transient ischemic attack, Dr. P. Gabriel Steg said at the annual congress of the European Society of Cardiology.

The RealiseAF registry provides an unprecedented look at contemporary management of AF in 26 countries. Unlike the highly selected and frequently nonrepresentative patients chosen for clinical trials, the 10,523 enrollees in RealiseAF were consecutive outpatients with all types of AF who were seen in 2010 by cardiologists or primary care physicians at 768 sites, explained Dr. Steg, professor of cardiology at the University of Paris–VII.

One of the registry’s big surprises was how common permanent AF turns out to be in routine clinical practice. Fully 46% of registry participants had permanent AF, a far higher figure than in previous, less comprehensive surveys.

In all, 25% of patients had paroxysmal AF, 22% had persistent AF, and 5% had lone AF. The rest could not be classified because their index AF episode was their first ever.

Among other highlights of RealiseAF were the following findings:

• Control of AF is achieved in just 59% of patients. Only 26.5% of RealiseAF participants were in sinus rhythm, whereas 32.5% achieved rate control (defined as a heart rate of 80 beats per minute or fewer).

• AF control is not synonymous with symptom control. In all, 56% of patients whose AF was controlled experienced at least one symptom – most often dyspnea, palpitations, fatigue, or chest pain – within the past 7 days. Symptoms were even more common in those with uncontrolled AF.

• Rate control is the most popular and least effective AF management strategy. At the end of the office visit on the day of enrollment, rate control was the strategy selected for 56% of patients, whereas rhythm control was chosen for 37%. However, 71% of patients in the rate control group ultimately failed to achieve rate control.

• The AF population is rife with cardiovascular risk factors. Hypertension was present in 72% of RealiseAF participants, and 46% had dyslipidemia; 61% were physically inactive. Furthermore, 77% of AF patients had at least one cardiovascular morbidity: One-third of the population had coronary artery disease, one-quarter had valvular heart disease, and 14% had cerebrovascular disease.

• Adherence to guidelines is far from optimal. Of the 25.6% of RealiseAF patients on amiodarone as first-line antiarrhythmic therapy, one-half did not qualify according to the 2006 joint American College of Cardiology/American Heart Association/European Society of Cardiology AF guidelines. Of the 12% of patients on class Ic antiarrhythmic agents, 20% did not qualify, according to the guidelines.

Moreover, of the more than 6,000 RealiseAF participants who had a CHADS2 score of 2 or more and therefore were supposed to be on warfarin, according to the guidelines, only 53% actually were. At the other end of the risk spectrum, 46% of patients with a CHADS2 score of 0 were on warfarin – contrary to the guidelines – and only 25% were on an antiplatelet drug only, as recommended in the guidelines.

“These results suggest a continuing need for medical education and information,” Dr. Steg noted.

Another key message from the RealiseAF registry is that new antiarrhythmic agents and antithrombotic drugs are sorely needed in order to better manage AF with a view toward improved cardiovascular outcomes, he added.

Disclosures: The registry is sponsored by Sanofi-Aventis. Dr. Steg declared that he serves as a consultant to that pharmaceutical company as well as more than a dozen others.

STOCKHOLM – The initial report from the world’s largest atrial fibrillation registry demonstrates that in everyday clinical practice, the arrhythmia is frequently not controlled – and even when it is, most patients remain symptomatic.

The RealiseAF registry data also underscore that real-world patients with atrial fibrillation (AF) have a disturbingly highly cardiovascular event rate, with 29% of the more than 10,000 enrollees having experienced an unplanned hospital admission for a serious cardiovascular event within the past 12 months. The most frequent reasons for admission were acute decompensated heart failure, acute coronary syndromes, stroke, and transient ischemic attack, Dr. P. Gabriel Steg said at the annual congress of the European Society of Cardiology.

The RealiseAF registry provides an unprecedented look at contemporary management of AF in 26 countries. Unlike the highly selected and frequently nonrepresentative patients chosen for clinical trials, the 10,523 enrollees in RealiseAF were consecutive outpatients with all types of AF who were seen in 2010 by cardiologists or primary care physicians at 768 sites, explained Dr. Steg, professor of cardiology at the University of Paris–VII.

One of the registry’s big surprises was how common permanent AF turns out to be in routine clinical practice. Fully 46% of registry participants had permanent AF, a far higher figure than in previous, less comprehensive surveys.

In all, 25% of patients had paroxysmal AF, 22% had persistent AF, and 5% had lone AF. The rest could not be classified because their index AF episode was their first ever.

Among other highlights of RealiseAF were the following findings:

• Control of AF is achieved in just 59% of patients. Only 26.5% of RealiseAF participants were in sinus rhythm, whereas 32.5% achieved rate control (defined as a heart rate of 80 beats per minute or fewer).

• AF control is not synonymous with symptom control. In all, 56% of patients whose AF was controlled experienced at least one symptom – most often dyspnea, palpitations, fatigue, or chest pain – within the past 7 days. Symptoms were even more common in those with uncontrolled AF.

• Rate control is the most popular and least effective AF management strategy. At the end of the office visit on the day of enrollment, rate control was the strategy selected for 56% of patients, whereas rhythm control was chosen for 37%. However, 71% of patients in the rate control group ultimately failed to achieve rate control.

• The AF population is rife with cardiovascular risk factors. Hypertension was present in 72% of RealiseAF participants, and 46% had dyslipidemia; 61% were physically inactive. Furthermore, 77% of AF patients had at least one cardiovascular morbidity: One-third of the population had coronary artery disease, one-quarter had valvular heart disease, and 14% had cerebrovascular disease.

• Adherence to guidelines is far from optimal. Of the 25.6% of RealiseAF patients on amiodarone as first-line antiarrhythmic therapy, one-half did not qualify according to the 2006 joint American College of Cardiology/American Heart Association/European Society of Cardiology AF guidelines. Of the 12% of patients on class Ic antiarrhythmic agents, 20% did not qualify, according to the guidelines.

Moreover, of the more than 6,000 RealiseAF participants who had a CHADS2 score of 2 or more and therefore were supposed to be on warfarin, according to the guidelines, only 53% actually were. At the other end of the risk spectrum, 46% of patients with a CHADS2 score of 0 were on warfarin – contrary to the guidelines – and only 25% were on an antiplatelet drug only, as recommended in the guidelines.

“These results suggest a continuing need for medical education and information,” Dr. Steg noted.

Another key message from the RealiseAF registry is that new antiarrhythmic agents and antithrombotic drugs are sorely needed in order to better manage AF with a view toward improved cardiovascular outcomes, he added.

Disclosures: The registry is sponsored by Sanofi-Aventis. Dr. Steg declared that he serves as a consultant to that pharmaceutical company as well as more than a dozen others.

STOCKHOLM – The initial report from the world’s largest atrial fibrillation registry demonstrates that in everyday clinical practice, the arrhythmia is frequently not controlled – and even when it is, most patients remain symptomatic.

The RealiseAF registry data also underscore that real-world patients with atrial fibrillation (AF) have a disturbingly highly cardiovascular event rate, with 29% of the more than 10,000 enrollees having experienced an unplanned hospital admission for a serious cardiovascular event within the past 12 months. The most frequent reasons for admission were acute decompensated heart failure, acute coronary syndromes, stroke, and transient ischemic attack, Dr. P. Gabriel Steg said at the annual congress of the European Society of Cardiology.

The RealiseAF registry provides an unprecedented look at contemporary management of AF in 26 countries. Unlike the highly selected and frequently nonrepresentative patients chosen for clinical trials, the 10,523 enrollees in RealiseAF were consecutive outpatients with all types of AF who were seen in 2010 by cardiologists or primary care physicians at 768 sites, explained Dr. Steg, professor of cardiology at the University of Paris–VII.

One of the registry’s big surprises was how common permanent AF turns out to be in routine clinical practice. Fully 46% of registry participants had permanent AF, a far higher figure than in previous, less comprehensive surveys.

In all, 25% of patients had paroxysmal AF, 22% had persistent AF, and 5% had lone AF. The rest could not be classified because their index AF episode was their first ever.

Among other highlights of RealiseAF were the following findings:

• Control of AF is achieved in just 59% of patients. Only 26.5% of RealiseAF participants were in sinus rhythm, whereas 32.5% achieved rate control (defined as a heart rate of 80 beats per minute or fewer).

• AF control is not synonymous with symptom control. In all, 56% of patients whose AF was controlled experienced at least one symptom – most often dyspnea, palpitations, fatigue, or chest pain – within the past 7 days. Symptoms were even more common in those with uncontrolled AF.

• Rate control is the most popular and least effective AF management strategy. At the end of the office visit on the day of enrollment, rate control was the strategy selected for 56% of patients, whereas rhythm control was chosen for 37%. However, 71% of patients in the rate control group ultimately failed to achieve rate control.

• The AF population is rife with cardiovascular risk factors. Hypertension was present in 72% of RealiseAF participants, and 46% had dyslipidemia; 61% were physically inactive. Furthermore, 77% of AF patients had at least one cardiovascular morbidity: One-third of the population had coronary artery disease, one-quarter had valvular heart disease, and 14% had cerebrovascular disease.

• Adherence to guidelines is far from optimal. Of the 25.6% of RealiseAF patients on amiodarone as first-line antiarrhythmic therapy, one-half did not qualify according to the 2006 joint American College of Cardiology/American Heart Association/European Society of Cardiology AF guidelines. Of the 12% of patients on class Ic antiarrhythmic agents, 20% did not qualify, according to the guidelines.

Moreover, of the more than 6,000 RealiseAF participants who had a CHADS2 score of 2 or more and therefore were supposed to be on warfarin, according to the guidelines, only 53% actually were. At the other end of the risk spectrum, 46% of patients with a CHADS2 score of 0 were on warfarin – contrary to the guidelines – and only 25% were on an antiplatelet drug only, as recommended in the guidelines.

“These results suggest a continuing need for medical education and information,” Dr. Steg noted.

Another key message from the RealiseAF registry is that new antiarrhythmic agents and antithrombotic drugs are sorely needed in order to better manage AF with a view toward improved cardiovascular outcomes, he added.

Disclosures: The registry is sponsored by Sanofi-Aventis. Dr. Steg declared that he serves as a consultant to that pharmaceutical company as well as more than a dozen others.

STOCKHOLM – The initial report from the world’s largest atrial fibrillation registry demonstrates that in everyday clinical practice, the arrhythmia is frequently not controlled – and even when it is, most patients remain symptomatic.

The RealiseAF registry data also underscore that real-world patients with atrial fibrillation (AF) have a disturbingly highly cardiovascular event rate, with 29% of the more than 10,000 enrollees having experienced an unplanned hospital admission for a serious cardiovascular event within the past 12 months. The most frequent reasons for admission were acute decompensated heart failure, acute coronary syndromes, stroke, and transient ischemic attack, Dr. P. Gabriel Steg said at the annual congress of the European Society of Cardiology.

The RealiseAF registry provides an unprecedented look at contemporary management of AF in 26 countries. Unlike the highly selected and frequently nonrepresentative patients chosen for clinical trials, the 10,523 enrollees in RealiseAF were consecutive outpatients with all types of AF who were seen in 2010 by cardiologists or primary care physicians at 768 sites, explained Dr. Steg, professor of cardiology at the University of Paris–VII.

One of the registry’s big surprises was how common permanent AF turns out to be in routine clinical practice. Fully 46% of registry participants had permanent AF, a far higher figure than in previous, less comprehensive surveys.

In all, 25% of patients had paroxysmal AF, 22% had persistent AF, and 5% had lone AF. The rest could not be classified because their index AF episode was their first ever.

Among other highlights of RealiseAF were the following findings:

• Control of AF is achieved in just 59% of patients. Only 26.5% of RealiseAF participants were in sinus rhythm, whereas 32.5% achieved rate control (defined as a heart rate of 80 beats per minute or fewer).

• AF control is not synonymous with symptom control. In all, 56% of patients whose AF was controlled experienced at least one symptom – most often dyspnea, palpitations, fatigue, or chest pain – within the past 7 days. Symptoms were even more common in those with uncontrolled AF.

• Rate control is the most popular and least effective AF management strategy. At the end of the office visit on the day of enrollment, rate control was the strategy selected for 56% of patients, whereas rhythm control was chosen for 37%. However, 71% of patients in the rate control group ultimately failed to achieve rate control.

• The AF population is rife with cardiovascular risk factors. Hypertension was present in 72% of RealiseAF participants, and 46% had dyslipidemia; 61% were physically inactive. Furthermore, 77% of AF patients had at least one cardiovascular morbidity: One-third of the population had coronary artery disease, one-quarter had valvular heart disease, and 14% had cerebrovascular disease.

• Adherence to guidelines is far from optimal. Of the 25.6% of RealiseAF patients on amiodarone as first-line antiarrhythmic therapy, one-half did not qualify according to the 2006 joint American College of Cardiology/American Heart Association/European Society of Cardiology AF guidelines. Of the 12% of patients on class Ic antiarrhythmic agents, 20% did not qualify, according to the guidelines.

Moreover, of the more than 6,000 RealiseAF participants who had a CHADS2 score of 2 or more and therefore were supposed to be on warfarin, according to the guidelines, only 53% actually were. At the other end of the risk spectrum, 46% of patients with a CHADS2 score of 0 were on warfarin – contrary to the guidelines – and only 25% were on an antiplatelet drug only, as recommended in the guidelines.

“These results suggest a continuing need for medical education and information,” Dr. Steg noted.

Another key message from the RealiseAF registry is that new antiarrhythmic agents and antithrombotic drugs are sorely needed in order to better manage AF with a view toward improved cardiovascular outcomes, he added.

Disclosures: The registry is sponsored by Sanofi-Aventis. Dr. Steg declared that he serves as a consultant to that pharmaceutical company as well as more than a dozen others.

STOCKHOLM – The initial report from the world’s largest atrial fibrillation registry demonstrates that in everyday clinical practice, the arrhythmia is frequently not controlled – and even when it is, most patients remain symptomatic.

The RealiseAF registry data also underscore that real-world patients with atrial fibrillation (AF) have a disturbingly highly cardiovascular event rate, with 29% of the more than 10,000 enrollees having experienced an unplanned hospital admission for a serious cardiovascular event within the past 12 months. The most frequent reasons for admission were acute decompensated heart failure, acute coronary syndromes, stroke, and transient ischemic attack, Dr. P. Gabriel Steg said at the annual congress of the European Society of Cardiology.

The RealiseAF registry provides an unprecedented look at contemporary management of AF in 26 countries. Unlike the highly selected and frequently nonrepresentative patients chosen for clinical trials, the 10,523 enrollees in RealiseAF were consecutive outpatients with all types of AF who were seen in 2010 by cardiologists or primary care physicians at 768 sites, explained Dr. Steg, professor of cardiology at the University of Paris–VII.

One of the registry’s big surprises was how common permanent AF turns out to be in routine clinical practice. Fully 46% of registry participants had permanent AF, a far higher figure than in previous, less comprehensive surveys.

In all, 25% of patients had paroxysmal AF, 22% had persistent AF, and 5% had lone AF. The rest could not be classified because their index AF episode was their first ever.

Among other highlights of RealiseAF were the following findings:

• Control of AF is achieved in just 59% of patients. Only 26.5% of RealiseAF participants were in sinus rhythm, whereas 32.5% achieved rate control (defined as a heart rate of 80 beats per minute or fewer).

• AF control is not synonymous with symptom control. In all, 56% of patients whose AF was controlled experienced at least one symptom – most often dyspnea, palpitations, fatigue, or chest pain – within the past 7 days. Symptoms were even more common in those with uncontrolled AF.

• Rate control is the most popular and least effective AF management strategy. At the end of the office visit on the day of enrollment, rate control was the strategy selected for 56% of patients, whereas rhythm control was chosen for 37%. However, 71% of patients in the rate control group ultimately failed to achieve rate control.

• The AF population is rife with cardiovascular risk factors. Hypertension was present in 72% of RealiseAF participants, and 46% had dyslipidemia; 61% were physically inactive. Furthermore, 77% of AF patients had at least one cardiovascular morbidity: One-third of the population had coronary artery disease, one-quarter had valvular heart disease, and 14% had cerebrovascular disease.

• Adherence to guidelines is far from optimal. Of the 25.6% of RealiseAF patients on amiodarone as first-line antiarrhythmic therapy, one-half did not qualify according to the 2006 joint American College of Cardiology/American Heart Association/European Society of Cardiology AF guidelines. Of the 12% of patients on class Ic antiarrhythmic agents, 20% did not qualify, according to the guidelines.

Moreover, of the more than 6,000 RealiseAF participants who had a CHADS2 score of 2 or more and therefore were supposed to be on warfarin, according to the guidelines, only 53% actually were. At the other end of the risk spectrum, 46% of patients with a CHADS2 score of 0 were on warfarin – contrary to the guidelines – and only 25% were on an antiplatelet drug only, as recommended in the guidelines.

“These results suggest a continuing need for medical education and information,” Dr. Steg noted.

Another key message from the RealiseAF registry is that new antiarrhythmic agents and antithrombotic drugs are sorely needed in order to better manage AF with a view toward improved cardiovascular outcomes, he added.

Disclosures: The registry is sponsored by Sanofi-Aventis. Dr. Steg declared that he serves as a consultant to that pharmaceutical company as well as more than a dozen others.

STOCKHOLM – The initial report from the world’s largest atrial fibrillation registry demonstrates that in everyday clinical practice, the arrhythmia is frequently not controlled – and even when it is, most patients remain symptomatic.

The RealiseAF registry data also underscore that real-world patients with atrial fibrillation (AF) have a disturbingly highly cardiovascular event rate, with 29% of the more than 10,000 enrollees having experienced an unplanned hospital admission for a serious cardiovascular event within the past 12 months. The most frequent reasons for admission were acute decompensated heart failure, acute coronary syndromes, stroke, and transient ischemic attack, Dr. P. Gabriel Steg said at the annual congress of the European Society of Cardiology.

The RealiseAF registry provides an unprecedented look at contemporary management of AF in 26 countries. Unlike the highly selected and frequently nonrepresentative patients chosen for clinical trials, the 10,523 enrollees in RealiseAF were consecutive outpatients with all types of AF who were seen in 2010 by cardiologists or primary care physicians at 768 sites, explained Dr. Steg, professor of cardiology at the University of Paris–VII.

One of the registry’s big surprises was how common permanent AF turns out to be in routine clinical practice. Fully 46% of registry participants had permanent AF, a far higher figure than in previous, less comprehensive surveys.

In all, 25% of patients had paroxysmal AF, 22% had persistent AF, and 5% had lone AF. The rest could not be classified because their index AF episode was their first ever.

Among other highlights of RealiseAF were the following findings:

• Control of AF is achieved in just 59% of patients. Only 26.5% of RealiseAF participants were in sinus rhythm, whereas 32.5% achieved rate control (defined as a heart rate of 80 beats per minute or fewer).

• AF control is not synonymous with symptom control. In all, 56% of patients whose AF was controlled experienced at least one symptom – most often dyspnea, palpitations, fatigue, or chest pain – within the past 7 days. Symptoms were even more common in those with uncontrolled AF.

• Rate control is the most popular and least effective AF management strategy. At the end of the office visit on the day of enrollment, rate control was the strategy selected for 56% of patients, whereas rhythm control was chosen for 37%. However, 71% of patients in the rate control group ultimately failed to achieve rate control.

• The AF population is rife with cardiovascular risk factors. Hypertension was present in 72% of RealiseAF participants, and 46% had dyslipidemia; 61% were physically inactive. Furthermore, 77% of AF patients had at least one cardiovascular morbidity: One-third of the population had coronary artery disease, one-quarter had valvular heart disease, and 14% had cerebrovascular disease.

• Adherence to guidelines is far from optimal. Of the 25.6% of RealiseAF patients on amiodarone as first-line antiarrhythmic therapy, one-half did not qualify according to the 2006 joint American College of Cardiology/American Heart Association/European Society of Cardiology AF guidelines. Of the 12% of patients on class Ic antiarrhythmic agents, 20% did not qualify, according to the guidelines.

Moreover, of the more than 6,000 RealiseAF participants who had a CHADS2 score of 2 or more and therefore were supposed to be on warfarin, according to the guidelines, only 53% actually were. At the other end of the risk spectrum, 46% of patients with a CHADS2 score of 0 were on warfarin – contrary to the guidelines – and only 25% were on an antiplatelet drug only, as recommended in the guidelines.

“These results suggest a continuing need for medical education and information,” Dr. Steg noted.

Another key message from the RealiseAF registry is that new antiarrhythmic agents and antithrombotic drugs are sorely needed in order to better manage AF with a view toward improved cardiovascular outcomes, he added.

Disclosures: The registry is sponsored by Sanofi-Aventis. Dr. Steg declared that he serves as a consultant to that pharmaceutical company as well as more than a dozen others.

STOCKHOLM – Stand-alone angiotensin II receptor blocker therapy proved of no benefit in preventing recurrences of paroxysmal atrial fibrillation in patients without structural heart disease in a large German randomized double-blind trial.

“ARB therapy may not be recommended as first-line treatment for paroxysmal atrial fibrillation if not indicated for other reasons,” Dr. Andreas Goette concluded, in presenting the results of the ANTIPAF trial at the annual congress of the European Society of Cardiology.

The ANTIPAF (Angiotensin II Antagonist in Paroxysmal Atrial Fibrillation) trial involved 425 patients at 37 participating German centers. All participants had documented paroxysmal atrial fibrillation (PAF) and no or minimal structural heart disease. They were randomized in double-blind fashion to receive olmesartan at 40 mg/day or placebo and followed for 12 months, during which they were not permitted to be on concomitant antiarrhythmic agents, other ARBs, or ACE inhibitors. If they were on a beta-blocker before enrollment, they could stay on it, but starting a beta-blocker after randomization was not allowed.

The primary study end point was total atrial fibrillation burden during 1 year of follow-up, as assessed using a novel tele-ECG technology employed on a daily basis. Based on an analysis of nearly 88,000 tele-ECGs, it was clear that olmesartan had no impact on total atrial fibrillation burden. Patients on olmesartan had a mean 0.151% of days of atrial fibrillation during follow-up, while those on placebo had 0.147%, reported Dr. Goette of St. Vincenz Hospital in Paderborn, Germany.

The two groups did not differ in terms of numerous prespecified secondary end points either, including time to first recurrence of atrial fibrillation, quality of life measures, time to development of persistent atrial fibrillation, and number of hospitalizations.

Atrial fibrillation affects roughly 4% of people in their 60s and up to 20% of those in their 80s. Good-quality animal and cellular data suggest angiotensin II is a major player in atrial fibrillation, figuring prominently in the vicious cycle in which atrial fibrillation begets more frequent and severe atrial fibrillation by promoting atrial remodeling and left ventricular dysfunction, and vice versa.

“From experimental work, it appears very appealing to inhibit the action of angiotensin II to treat atrial fibrillation,” the cardiologist observed.

Early clinical trials suggested PAF could be suppressed by ARB therapy, particularly when combined with an antiarrhythmic agent, but these studies had various weaknesses that left open the question of whether stand-alone ARB therapy is effective in PAF. This was the question ANTIPAF addressed.

Dr. Goette said he sees the tele-ECG monitoring as one of the trial’s unique strengths. Patients carried the credit card–sized tele-ECG device around with them during the day and were asked to press a button and hold it to their chest to record an ECG at least once daily. They phoned in the data for storage and analysis.

Unlike Dr. Goette, discussant Dr. A. John Camm took a dim view of the tele-ECG–based primary end point.

“The intermittent and noncontinuous monitoring of the heart rhythm is important. Although we heard of the tens of thousands of ECGs that were involved, there are on the order of a thousandfold that number of heart beats, and continuous monitoring might have been much better,” said Dr. Camm of St. George’s University of London.

He also took issue with the duration of follow-up in ANTIPAF: “The length of the follow-up is intermediate. For an effect to reverse fibrosis we might need far longer than 1 year.”

Although there are reasonably persuasive clinical trials data indicating ARBs are effective for the primary prevention of atrial fibrillation, ANTIPAF joins several earlier studies in failing to show any benefit for various ARBs in preventing recurrences of PAF, he said.

Disclosures: The ANTIPAF trial was funded by the German Ministry of Research and Education and carried out by the German Competence Network on Atrial Fibrillation. Dr. Goette said he had no financial conflicts.

STOCKHOLM – Stand-alone angiotensin II receptor blocker therapy proved of no benefit in preventing recurrences of paroxysmal atrial fibrillation in patients without structural heart disease in a large German randomized double-blind trial.

“ARB therapy may not be recommended as first-line treatment for paroxysmal atrial fibrillation if not indicated for other reasons,” Dr. Andreas Goette concluded, in presenting the results of the ANTIPAF trial at the annual congress of the European Society of Cardiology.

The ANTIPAF (Angiotensin II Antagonist in Paroxysmal Atrial Fibrillation) trial involved 425 patients at 37 participating German centers. All participants had documented paroxysmal atrial fibrillation (PAF) and no or minimal structural heart disease. They were randomized in double-blind fashion to receive olmesartan at 40 mg/day or placebo and followed for 12 months, during which they were not permitted to be on concomitant antiarrhythmic agents, other ARBs, or ACE inhibitors. If they were on a beta-blocker before enrollment, they could stay on it, but starting a beta-blocker after randomization was not allowed.

The primary study end point was total atrial fibrillation burden during 1 year of follow-up, as assessed using a novel tele-ECG technology employed on a daily basis. Based on an analysis of nearly 88,000 tele-ECGs, it was clear that olmesartan had no impact on total atrial fibrillation burden. Patients on olmesartan had a mean 0.151% of days of atrial fibrillation during follow-up, while those on placebo had 0.147%, reported Dr. Goette of St. Vincenz Hospital in Paderborn, Germany.

The two groups did not differ in terms of numerous prespecified secondary end points either, including time to first recurrence of atrial fibrillation, quality of life measures, time to development of persistent atrial fibrillation, and number of hospitalizations.

Atrial fibrillation affects roughly 4% of people in their 60s and up to 20% of those in their 80s. Good-quality animal and cellular data suggest angiotensin II is a major player in atrial fibrillation, figuring prominently in the vicious cycle in which atrial fibrillation begets more frequent and severe atrial fibrillation by promoting atrial remodeling and left ventricular dysfunction, and vice versa.

“From experimental work, it appears very appealing to inhibit the action of angiotensin II to treat atrial fibrillation,” the cardiologist observed.

Early clinical trials suggested PAF could be suppressed by ARB therapy, particularly when combined with an antiarrhythmic agent, but these studies had various weaknesses that left open the question of whether stand-alone ARB therapy is effective in PAF. This was the question ANTIPAF addressed.

Dr. Goette said he sees the tele-ECG monitoring as one of the trial’s unique strengths. Patients carried the credit card–sized tele-ECG device around with them during the day and were asked to press a button and hold it to their chest to record an ECG at least once daily. They phoned in the data for storage and analysis.

Unlike Dr. Goette, discussant Dr. A. John Camm took a dim view of the tele-ECG–based primary end point.

“The intermittent and noncontinuous monitoring of the heart rhythm is important. Although we heard of the tens of thousands of ECGs that were involved, there are on the order of a thousandfold that number of heart beats, and continuous monitoring might have been much better,” said Dr. Camm of St. George’s University of London.

He also took issue with the duration of follow-up in ANTIPAF: “The length of the follow-up is intermediate. For an effect to reverse fibrosis we might need far longer than 1 year.”

Although there are reasonably persuasive clinical trials data indicating ARBs are effective for the primary prevention of atrial fibrillation, ANTIPAF joins several earlier studies in failing to show any benefit for various ARBs in preventing recurrences of PAF, he said.

Disclosures: The ANTIPAF trial was funded by the German Ministry of Research and Education and carried out by the German Competence Network on Atrial Fibrillation. Dr. Goette said he had no financial conflicts.

STOCKHOLM – Stand-alone angiotensin II receptor blocker therapy proved of no benefit in preventing recurrences of paroxysmal atrial fibrillation in patients without structural heart disease in a large German randomized double-blind trial.

“ARB therapy may not be recommended as first-line treatment for paroxysmal atrial fibrillation if not indicated for other reasons,” Dr. Andreas Goette concluded, in presenting the results of the ANTIPAF trial at the annual congress of the European Society of Cardiology.

The ANTIPAF (Angiotensin II Antagonist in Paroxysmal Atrial Fibrillation) trial involved 425 patients at 37 participating German centers. All participants had documented paroxysmal atrial fibrillation (PAF) and no or minimal structural heart disease. They were randomized in double-blind fashion to receive olmesartan at 40 mg/day or placebo and followed for 12 months, during which they were not permitted to be on concomitant antiarrhythmic agents, other ARBs, or ACE inhibitors. If they were on a beta-blocker before enrollment, they could stay on it, but starting a beta-blocker after randomization was not allowed.

The primary study end point was total atrial fibrillation burden during 1 year of follow-up, as assessed using a novel tele-ECG technology employed on a daily basis. Based on an analysis of nearly 88,000 tele-ECGs, it was clear that olmesartan had no impact on total atrial fibrillation burden. Patients on olmesartan had a mean 0.151% of days of atrial fibrillation during follow-up, while those on placebo had 0.147%, reported Dr. Goette of St. Vincenz Hospital in Paderborn, Germany.

The two groups did not differ in terms of numerous prespecified secondary end points either, including time to first recurrence of atrial fibrillation, quality of life measures, time to development of persistent atrial fibrillation, and number of hospitalizations.

Atrial fibrillation affects roughly 4% of people in their 60s and up to 20% of those in their 80s. Good-quality animal and cellular data suggest angiotensin II is a major player in atrial fibrillation, figuring prominently in the vicious cycle in which atrial fibrillation begets more frequent and severe atrial fibrillation by promoting atrial remodeling and left ventricular dysfunction, and vice versa.

“From experimental work, it appears very appealing to inhibit the action of angiotensin II to treat atrial fibrillation,” the cardiologist observed.

Early clinical trials suggested PAF could be suppressed by ARB therapy, particularly when combined with an antiarrhythmic agent, but these studies had various weaknesses that left open the question of whether stand-alone ARB therapy is effective in PAF. This was the question ANTIPAF addressed.

Dr. Goette said he sees the tele-ECG monitoring as one of the trial’s unique strengths. Patients carried the credit card–sized tele-ECG device around with them during the day and were asked to press a button and hold it to their chest to record an ECG at least once daily. They phoned in the data for storage and analysis.

Unlike Dr. Goette, discussant Dr. A. John Camm took a dim view of the tele-ECG–based primary end point.

“The intermittent and noncontinuous monitoring of the heart rhythm is important. Although we heard of the tens of thousands of ECGs that were involved, there are on the order of a thousandfold that number of heart beats, and continuous monitoring might have been much better,” said Dr. Camm of St. George’s University of London.

He also took issue with the duration of follow-up in ANTIPAF: “The length of the follow-up is intermediate. For an effect to reverse fibrosis we might need far longer than 1 year.”

Although there are reasonably persuasive clinical trials data indicating ARBs are effective for the primary prevention of atrial fibrillation, ANTIPAF joins several earlier studies in failing to show any benefit for various ARBs in preventing recurrences of PAF, he said.

Disclosures: The ANTIPAF trial was funded by the German Ministry of Research and Education and carried out by the German Competence Network on Atrial Fibrillation. Dr. Goette said he had no financial conflicts.

STOCKHOLM — Higher blood levels of the bone hormone osteoprotegerin are linked with a higher long-term risk of death in patients with chronic heart failure, reported Dr. Ragnhild R. Roysland.

The relationship between osteoprotegerin (OPG) and mortality in heart failure is independent of the conventional cardiovascular risk factors, based on a secondary analysis of results of the Italian GISSI-Heart Failure trial.

Osteoprotegerin, a cytokine that's a member of the tumor necrosis factor superfamily, is drawing increasing attention among cardiovascular researchers as a likely key player in what's known as “the calcification paradox.” In animal studies, low levels of OPG are associated with decreased skeletal calcification, osteoporosis, and increased calcification of the major arteries. But in recent human studies, increased OPG levels have been linked to a greater atherosclerotic burden; an increased risk of death following acute MI; and now, in GISSI-HF, to increased mortality in the setting of chronic HF, Dr. Roysland said at the congress.

The GISSI-HF study was a randomized clinical trial in which 6,975 Italian patients with chronic heart failure were assigned to rosuvastatin, fish oil, or placebo and followed up for a median of 3.9 years (Lancet 2008;372:1223–30;1231–9). Dr. Roysland presented a new substudy involving 1,229 GISSI-HF participants for whom baseline OPG levels were available.

The aim was to see if baseline OPG was predictive of all-cause mortality. This indeed proved to be the case. During follow-up 332 patients died. The mortality rate was 20% in those in the bottom tertile for baseline OPG with a value less than 1,210 ng/L, and more than twice as great at 45% in patients in the highest tertile, with an OPG of at least 1,923 ng/L. Patients with an intermediate-tertile baseline OPG of 1,210–1,922 ng/L split the difference in terms of mortality, said Dr. Roysland of Akershus University Hospital, Lørenskog, Norway.

Treatment assignment in GISSI-HF did not affect OPG levels. However, if a medication could be identified that reduces OPG levels and attenuates the risk associated with high OPG, then OPG could become an important marker to use in managing chronic HF in clinical practice. There is early evidence that treatments for osteoporosis reduce OPG levels in a non-HF population, but no studies have been done in patients with chronic HF, she said.

Dr. Marco Metra, a member of the ESC congress scientific program committee, said he'd reviewed all the HF studies being presented at the meeting. Two studies in addition to Dr. Roysland's consistently showed that HF patients with high levels of OPG have a poor prognosis. “We know that patients with heart failure have low levels of vitamin D and increased rates of osteoporosis and bone fractures. So the bone is in some way a target of heart failure,” said Dr. Metra of the University of Brescia (Italy).

Mortality for patients with high OPG levels, at 45%, was more than twice that in patients with low levels, at 20%.

Source DR. ROYSLAND

Disclosures: Dr. Roysland said she had no financial conflicts.

STOCKHOLM — Higher blood levels of the bone hormone osteoprotegerin are linked with a higher long-term risk of death in patients with chronic heart failure, reported Dr. Ragnhild R. Roysland.

The relationship between osteoprotegerin (OPG) and mortality in heart failure is independent of the conventional cardiovascular risk factors, based on a secondary analysis of results of the Italian GISSI-Heart Failure trial.

Osteoprotegerin, a cytokine that's a member of the tumor necrosis factor superfamily, is drawing increasing attention among cardiovascular researchers as a likely key player in what's known as “the calcification paradox.” In animal studies, low levels of OPG are associated with decreased skeletal calcification, osteoporosis, and increased calcification of the major arteries. But in recent human studies, increased OPG levels have been linked to a greater atherosclerotic burden; an increased risk of death following acute MI; and now, in GISSI-HF, to increased mortality in the setting of chronic HF, Dr. Roysland said at the congress.

The GISSI-HF study was a randomized clinical trial in which 6,975 Italian patients with chronic heart failure were assigned to rosuvastatin, fish oil, or placebo and followed up for a median of 3.9 years (Lancet 2008;372:1223–30;1231–9). Dr. Roysland presented a new substudy involving 1,229 GISSI-HF participants for whom baseline OPG levels were available.

The aim was to see if baseline OPG was predictive of all-cause mortality. This indeed proved to be the case. During follow-up 332 patients died. The mortality rate was 20% in those in the bottom tertile for baseline OPG with a value less than 1,210 ng/L, and more than twice as great at 45% in patients in the highest tertile, with an OPG of at least 1,923 ng/L. Patients with an intermediate-tertile baseline OPG of 1,210–1,922 ng/L split the difference in terms of mortality, said Dr. Roysland of Akershus University Hospital, Lørenskog, Norway.

Treatment assignment in GISSI-HF did not affect OPG levels. However, if a medication could be identified that reduces OPG levels and attenuates the risk associated with high OPG, then OPG could become an important marker to use in managing chronic HF in clinical practice. There is early evidence that treatments for osteoporosis reduce OPG levels in a non-HF population, but no studies have been done in patients with chronic HF, she said.

Dr. Marco Metra, a member of the ESC congress scientific program committee, said he'd reviewed all the HF studies being presented at the meeting. Two studies in addition to Dr. Roysland's consistently showed that HF patients with high levels of OPG have a poor prognosis. “We know that patients with heart failure have low levels of vitamin D and increased rates of osteoporosis and bone fractures. So the bone is in some way a target of heart failure,” said Dr. Metra of the University of Brescia (Italy).

Mortality for patients with high OPG levels, at 45%, was more than twice that in patients with low levels, at 20%.

Source DR. ROYSLAND

Disclosures: Dr. Roysland said she had no financial conflicts.

STOCKHOLM — Higher blood levels of the bone hormone osteoprotegerin are linked with a higher long-term risk of death in patients with chronic heart failure, reported Dr. Ragnhild R. Roysland.

The relationship between osteoprotegerin (OPG) and mortality in heart failure is independent of the conventional cardiovascular risk factors, based on a secondary analysis of results of the Italian GISSI-Heart Failure trial.

Osteoprotegerin, a cytokine that's a member of the tumor necrosis factor superfamily, is drawing increasing attention among cardiovascular researchers as a likely key player in what's known as “the calcification paradox.” In animal studies, low levels of OPG are associated with decreased skeletal calcification, osteoporosis, and increased calcification of the major arteries. But in recent human studies, increased OPG levels have been linked to a greater atherosclerotic burden; an increased risk of death following acute MI; and now, in GISSI-HF, to increased mortality in the setting of chronic HF, Dr. Roysland said at the congress.

The GISSI-HF study was a randomized clinical trial in which 6,975 Italian patients with chronic heart failure were assigned to rosuvastatin, fish oil, or placebo and followed up for a median of 3.9 years (Lancet 2008;372:1223–30;1231–9). Dr. Roysland presented a new substudy involving 1,229 GISSI-HF participants for whom baseline OPG levels were available.

The aim was to see if baseline OPG was predictive of all-cause mortality. This indeed proved to be the case. During follow-up 332 patients died. The mortality rate was 20% in those in the bottom tertile for baseline OPG with a value less than 1,210 ng/L, and more than twice as great at 45% in patients in the highest tertile, with an OPG of at least 1,923 ng/L. Patients with an intermediate-tertile baseline OPG of 1,210–1,922 ng/L split the difference in terms of mortality, said Dr. Roysland of Akershus University Hospital, Lørenskog, Norway.

Treatment assignment in GISSI-HF did not affect OPG levels. However, if a medication could be identified that reduces OPG levels and attenuates the risk associated with high OPG, then OPG could become an important marker to use in managing chronic HF in clinical practice. There is early evidence that treatments for osteoporosis reduce OPG levels in a non-HF population, but no studies have been done in patients with chronic HF, she said.

Dr. Marco Metra, a member of the ESC congress scientific program committee, said he'd reviewed all the HF studies being presented at the meeting. Two studies in addition to Dr. Roysland's consistently showed that HF patients with high levels of OPG have a poor prognosis. “We know that patients with heart failure have low levels of vitamin D and increased rates of osteoporosis and bone fractures. So the bone is in some way a target of heart failure,” said Dr. Metra of the University of Brescia (Italy).

Mortality for patients with high OPG levels, at 45%, was more than twice that in patients with low levels, at 20%.

Source DR. ROYSLAND

Disclosures: Dr. Roysland said she had no financial conflicts.

KEYSTONE, COLO. — Serum cystatin C isn't ready for prime-time use in clinical practice as an alternative to urinary albumin excretion and serum creatinine in screening for diabetic nephropathy, but the unfolding research on this novel biomarker is definitely worth keeping an eye on.

“From a pediatric diabetes perspective, were we to have more data on cystatin C, it would sure be appealing to be able to collect it from a blood sample and not have to try to get overnight urines or even spot urines. This is a biomarker that may pan out as something useful in the future,” Dr. David M. Maahs said at the conference, sponsored by the Children's Diabetes Foundation at Denver.

A growing body of evidence suggests serum cystatin C provides a more accurate estimate of glomerular filtration rate (GFR) than do predictive equations based upon serum creatinine, such as the widely used Cockroft-Gault or Modification of Diet in Renal Disease equations.

“Cystatin C has been described as like an HbA_1c for renal function,” observed Dr. Maahs of the Barbara Davis Center for Childhood Diabetes and the University of Colorado, Denver.

Cystatin C also appears to be superior to serum creatinine as a predictor of the risk of death and cardiovascular events in the elderly in general (N. Engl. J. Med. 2005;352:2049–60). Furthermore, in an analysis restricted to 691 elderly diabetic participants in the Cardiovascular Health Study, cystatin C–based estimated GFR predicted mortality more strongly than did serum creatinine–based estimated GFR (Diabetes Care 2009;32:1833–8).

Moreover, in a study of 509 adults with type 1 diabetes followed for 2.5 years, Dr. Maahs and coworkers showed that serum cystatin C predicted progression of subclinical coronary atherosclerosis as reflected by coronary artery calcification better than serum creatinine, estimated glomerular filtration rate, or albumin excretion rate (Diabetes 2007;56:2774–9).

That being said, data on cystatin C's performance in pediatric populations with diabetes remain lacking, he noted.

Serum cystatin C goes up as the GFR goes down. Cystatin C is thought to better reflect GFR than does serum creatinine because it is independent of age, sex, and muscle mass. Cystatin C is a stable protein produced by nucleated cells at a constant rate. Furthermore, freely filtered at the glomerulus because of its small molecular mass, it is not reabsorbed, and it is eliminated by the kidneys.

Putting aside for the future the question of cystatin C as potential tool for following GFR in diabetic patients, Dr. Maahs stressed the importance of following guidelines for screening for diabetic nephropathy in young patients. About 20%–40% of patients with diabetes develop nephropathy. Indeed, diabetic nephropathy has become the number-one cause of end-stage renal disease in the United States, accounting for 40% of all new cases, he said.

The earliest clinical evidence of nephropathy is persistent microalbuminuria. Among 3,259 participants in the SEARCH for Diabetes in Youth study, Dr. Maahs and coworkers found that the prevalence of an elevated albumin-to-creatinine ratio indicative of microalbuminuria was 9.2% among type 1 and 22.2% in type 2 diabetic individuals under age 20 (Diabetes Care 2007;30:2593–8).

Because persistent microalbuminuria is the reversible stage of diabetic nephropathy if treated with an ACE inhibitor or angiotensin receptor blocker along with intensified glycemic control, smoking cessation, and treatment of hypertension if present, the American Diabetes Association recommends performing an annual test to assess urine albumin excretion in all patients who've had type 1 diabetes for at least 5 years and in all type 2 diabetes patients starting at the time of diagnosis.

The screening for microalbuminuria can be performed by one of three methods: measurement of the albumin to creatinine ratio in a random spot urine; a 24-hour urine collection; or a timed urine collection, often done overnight. A diagnosis of persistent microalbuminuria requires a positive result on two of three tests conducted within a 3–6 month period.

The American Diabetes Association guidelines also call for measurement of serum creatinine at least annually in all adults with diabetes regardless of their degree of urine albumin excretion. The serum creatinine is to be used to estimate GFR.

Because it's important to identify progression to microalbuminuria in a timely way in patients with type 1 diabetes, Dr. Maahs and his coworkers have developed and validated a prediction rule that identifies a subset of patients at high risk. The idea is that a few relatively easily obtainable patient characteristics can be used to help physicians identify a patient subgroup likely to benefit from screening for microalbuminuria more frequently than once yearly.

The prediction rule was developed using data from 1,115 patients in the European Diabetes Prospective Complications Study, then validated in the Finnish Diabetic Nephropathy Study, the Coronary Artery Calcification in Type 1 Diabetes Study, and the Pittsburgh Epidemiology of Diabetes Complication Study. The key variables used in the prediction rule are the albumin excretion rate, body mass index, waist:hip ratio, and a history of ever having smoked.

Thirteen percent of patients progressed to microalbuminuria during 7 years of follow-up. A high-risk subgroup consisting of 8% of the patient population was identified as having a risk of progression of 32% (Diabetologia 2010;53:254–62).

Disclosure: Dr. Maahs disclosed receiving research support from Merck & Co. Inc. and Eli Lilly.

KEYSTONE, COLO. — Serum cystatin C isn't ready for prime-time use in clinical practice as an alternative to urinary albumin excretion and serum creatinine in screening for diabetic nephropathy, but the unfolding research on this novel biomarker is definitely worth keeping an eye on.

“From a pediatric diabetes perspective, were we to have more data on cystatin C, it would sure be appealing to be able to collect it from a blood sample and not have to try to get overnight urines or even spot urines. This is a biomarker that may pan out as something useful in the future,” Dr. David M. Maahs said at the conference, sponsored by the Children's Diabetes Foundation at Denver.

A growing body of evidence suggests serum cystatin C provides a more accurate estimate of glomerular filtration rate (GFR) than do predictive equations based upon serum creatinine, such as the widely used Cockroft-Gault or Modification of Diet in Renal Disease equations.

“Cystatin C has been described as like an HbA_1c for renal function,” observed Dr. Maahs of the Barbara Davis Center for Childhood Diabetes and the University of Colorado, Denver.

Cystatin C also appears to be superior to serum creatinine as a predictor of the risk of death and cardiovascular events in the elderly in general (N. Engl. J. Med. 2005;352:2049–60). Furthermore, in an analysis restricted to 691 elderly diabetic participants in the Cardiovascular Health Study, cystatin C–based estimated GFR predicted mortality more strongly than did serum creatinine–based estimated GFR (Diabetes Care 2009;32:1833–8).

Moreover, in a study of 509 adults with type 1 diabetes followed for 2.5 years, Dr. Maahs and coworkers showed that serum cystatin C predicted progression of subclinical coronary atherosclerosis as reflected by coronary artery calcification better than serum creatinine, estimated glomerular filtration rate, or albumin excretion rate (Diabetes 2007;56:2774–9).

That being said, data on cystatin C's performance in pediatric populations with diabetes remain lacking, he noted.

Serum cystatin C goes up as the GFR goes down. Cystatin C is thought to better reflect GFR than does serum creatinine because it is independent of age, sex, and muscle mass. Cystatin C is a stable protein produced by nucleated cells at a constant rate. Furthermore, freely filtered at the glomerulus because of its small molecular mass, it is not reabsorbed, and it is eliminated by the kidneys.

Putting aside for the future the question of cystatin C as potential tool for following GFR in diabetic patients, Dr. Maahs stressed the importance of following guidelines for screening for diabetic nephropathy in young patients. About 20%–40% of patients with diabetes develop nephropathy. Indeed, diabetic nephropathy has become the number-one cause of end-stage renal disease in the United States, accounting for 40% of all new cases, he said.

The earliest clinical evidence of nephropathy is persistent microalbuminuria. Among 3,259 participants in the SEARCH for Diabetes in Youth study, Dr. Maahs and coworkers found that the prevalence of an elevated albumin-to-creatinine ratio indicative of microalbuminuria was 9.2% among type 1 and 22.2% in type 2 diabetic individuals under age 20 (Diabetes Care 2007;30:2593–8).

Because persistent microalbuminuria is the reversible stage of diabetic nephropathy if treated with an ACE inhibitor or angiotensin receptor blocker along with intensified glycemic control, smoking cessation, and treatment of hypertension if present, the American Diabetes Association recommends performing an annual test to assess urine albumin excretion in all patients who've had type 1 diabetes for at least 5 years and in all type 2 diabetes patients starting at the time of diagnosis.

The screening for microalbuminuria can be performed by one of three methods: measurement of the albumin to creatinine ratio in a random spot urine; a 24-hour urine collection; or a timed urine collection, often done overnight. A diagnosis of persistent microalbuminuria requires a positive result on two of three tests conducted within a 3–6 month period.

The American Diabetes Association guidelines also call for measurement of serum creatinine at least annually in all adults with diabetes regardless of their degree of urine albumin excretion. The serum creatinine is to be used to estimate GFR.

Because it's important to identify progression to microalbuminuria in a timely way in patients with type 1 diabetes, Dr. Maahs and his coworkers have developed and validated a prediction rule that identifies a subset of patients at high risk. The idea is that a few relatively easily obtainable patient characteristics can be used to help physicians identify a patient subgroup likely to benefit from screening for microalbuminuria more frequently than once yearly.

The prediction rule was developed using data from 1,115 patients in the European Diabetes Prospective Complications Study, then validated in the Finnish Diabetic Nephropathy Study, the Coronary Artery Calcification in Type 1 Diabetes Study, and the Pittsburgh Epidemiology of Diabetes Complication Study. The key variables used in the prediction rule are the albumin excretion rate, body mass index, waist:hip ratio, and a history of ever having smoked.

Thirteen percent of patients progressed to microalbuminuria during 7 years of follow-up. A high-risk subgroup consisting of 8% of the patient population was identified as having a risk of progression of 32% (Diabetologia 2010;53:254–62).

Disclosure: Dr. Maahs disclosed receiving research support from Merck & Co. Inc. and Eli Lilly.

KEYSTONE, COLO. — Serum cystatin C isn't ready for prime-time use in clinical practice as an alternative to urinary albumin excretion and serum creatinine in screening for diabetic nephropathy, but the unfolding research on this novel biomarker is definitely worth keeping an eye on.

“From a pediatric diabetes perspective, were we to have more data on cystatin C, it would sure be appealing to be able to collect it from a blood sample and not have to try to get overnight urines or even spot urines. This is a biomarker that may pan out as something useful in the future,” Dr. David M. Maahs said at the conference, sponsored by the Children's Diabetes Foundation at Denver.

A growing body of evidence suggests serum cystatin C provides a more accurate estimate of glomerular filtration rate (GFR) than do predictive equations based upon serum creatinine, such as the widely used Cockroft-Gault or Modification of Diet in Renal Disease equations.

“Cystatin C has been described as like an HbA_1c for renal function,” observed Dr. Maahs of the Barbara Davis Center for Childhood Diabetes and the University of Colorado, Denver.

Cystatin C also appears to be superior to serum creatinine as a predictor of the risk of death and cardiovascular events in the elderly in general (N. Engl. J. Med. 2005;352:2049–60). Furthermore, in an analysis restricted to 691 elderly diabetic participants in the Cardiovascular Health Study, cystatin C–based estimated GFR predicted mortality more strongly than did serum creatinine–based estimated GFR (Diabetes Care 2009;32:1833–8).

Moreover, in a study of 509 adults with type 1 diabetes followed for 2.5 years, Dr. Maahs and coworkers showed that serum cystatin C predicted progression of subclinical coronary atherosclerosis as reflected by coronary artery calcification better than serum creatinine, estimated glomerular filtration rate, or albumin excretion rate (Diabetes 2007;56:2774–9).

That being said, data on cystatin C's performance in pediatric populations with diabetes remain lacking, he noted.

Serum cystatin C goes up as the GFR goes down. Cystatin C is thought to better reflect GFR than does serum creatinine because it is independent of age, sex, and muscle mass. Cystatin C is a stable protein produced by nucleated cells at a constant rate. Furthermore, freely filtered at the glomerulus because of its small molecular mass, it is not reabsorbed, and it is eliminated by the kidneys.

Putting aside for the future the question of cystatin C as potential tool for following GFR in diabetic patients, Dr. Maahs stressed the importance of following guidelines for screening for diabetic nephropathy in young patients. About 20%–40% of patients with diabetes develop nephropathy. Indeed, diabetic nephropathy has become the number-one cause of end-stage renal disease in the United States, accounting for 40% of all new cases, he said.

The earliest clinical evidence of nephropathy is persistent microalbuminuria. Among 3,259 participants in the SEARCH for Diabetes in Youth study, Dr. Maahs and coworkers found that the prevalence of an elevated albumin-to-creatinine ratio indicative of microalbuminuria was 9.2% among type 1 and 22.2% in type 2 diabetic individuals under age 20 (Diabetes Care 2007;30:2593–8).

Because persistent microalbuminuria is the reversible stage of diabetic nephropathy if treated with an ACE inhibitor or angiotensin receptor blocker along with intensified glycemic control, smoking cessation, and treatment of hypertension if present, the American Diabetes Association recommends performing an annual test to assess urine albumin excretion in all patients who've had type 1 diabetes for at least 5 years and in all type 2 diabetes patients starting at the time of diagnosis.

The screening for microalbuminuria can be performed by one of three methods: measurement of the albumin to creatinine ratio in a random spot urine; a 24-hour urine collection; or a timed urine collection, often done overnight. A diagnosis of persistent microalbuminuria requires a positive result on two of three tests conducted within a 3–6 month period.

The American Diabetes Association guidelines also call for measurement of serum creatinine at least annually in all adults with diabetes regardless of their degree of urine albumin excretion. The serum creatinine is to be used to estimate GFR.

Because it's important to identify progression to microalbuminuria in a timely way in patients with type 1 diabetes, Dr. Maahs and his coworkers have developed and validated a prediction rule that identifies a subset of patients at high risk. The idea is that a few relatively easily obtainable patient characteristics can be used to help physicians identify a patient subgroup likely to benefit from screening for microalbuminuria more frequently than once yearly.

The prediction rule was developed using data from 1,115 patients in the European Diabetes Prospective Complications Study, then validated in the Finnish Diabetic Nephropathy Study, the Coronary Artery Calcification in Type 1 Diabetes Study, and the Pittsburgh Epidemiology of Diabetes Complication Study. The key variables used in the prediction rule are the albumin excretion rate, body mass index, waist:hip ratio, and a history of ever having smoked.

Thirteen percent of patients progressed to microalbuminuria during 7 years of follow-up. A high-risk subgroup consisting of 8% of the patient population was identified as having a risk of progression of 32% (Diabetologia 2010;53:254–62).

Disclosure: Dr. Maahs disclosed receiving research support from Merck & Co. Inc. and Eli Lilly.