Neil Osterweil

BOSTON — Taller men appear to have a twofold greater risk for venous thromboembolic events than do men of more modest height, Norwegian investigators reported.

Men taller than 181 cm (about 5 feet 11 inches) had double the risk of either provoked or unprovoked venous thromboembolic events (VTEs), compared with men 173 cm (about 5 feet 8 inches) or shorter, reported Dr. Knut H. Borch of the Center for Atherothrombotic Research in Tromsø, Norway, and his colleagues.

In men, each 10-cm increase in height was associated with a significant hazard ratio of 1.34. In women, height was not a significant risk factor for VTE (HR 1.13), he said at a meeting of the International Society on Thrombosis and Haemostasis.

“We suggest that body height should be considered in risk stratification of VTE,” Dr. Borch said. More research is needed to determine how height interacts with other risk factors for VTE.

A 2005 analysis of data from the Physicians' Health Study (Am. J. Epidemiol. 2005;162:975-82) found that every 10 cm of height was associated with about a 36% increase in risk in men. In a separate study, Swedish researchers also found a positive association between body height and VTE risk in men (J. Thromb. Haemost. 2008;6:558-64).

Dr. Borch and his colleagues drew data from the Tromsø Study, a prospective population-based study of men and women aged 25 years and older in the town of Tromsø, in northern Norway. The study included 26,727 residents. The researchers recorded all first lifetime VTEs from the date of study enrollment (1994-1995) through Sept. 1, 2007. Cases were identified by discharge diagnosis, autopsy registry, and radiology procedure registry. VTE was confirmed by diagnostic procedure or autopsy, and the data collected included diagnosis of deep vein thromboembolism (DVT) or pulmonary embolism, signs and symptoms consistent with VTE, and VTE treatment.

During the median follow-up of 12.5 years, there were 462 VTEs, 193 (41.8%) of which were classified as provoked (associated with major surgery or an acute medical condition within 8 weeks of the event, cancer at the time of the event, prolonged immobilization, or other known risk factors). Of the provoked VTEs, 64.3% were DVTs. Overall, the incidence of VTE was 1.6 per 1,000 person-years.

Among men, there were 219 VTEs. Men in the tallest quartile (181 cm and taller) had a significantly increased risk for VTE, vs. men in the lowest height quartile (less than 173 cm). In a multivariate analysis that adjusted for other risk factors, the hazard ratio for the tallest men was 1.99. The hazard ratio for each 10 cm of height was 1.34. Height had no effect on total VTE risk among women. In both men and women, the risks for provoked vs. unprovoked VTE were similar.

Possible explanations for the sex difference in the VTE-height relationship include unidentified sex-specific differences in venous architecture, or differences in pressure dynamics or stasis, Dr. Borch said.

The funding source for the study was not disclosed. Dr. Borch declared that neither he nor his coauthors had relevant financial disclosures.

BOSTON — Taller men appear to have a twofold greater risk for venous thromboembolic events than do men of more modest height, Norwegian investigators reported.

Men taller than 181 cm (about 5 feet 11 inches) had double the risk of either provoked or unprovoked venous thromboembolic events (VTEs), compared with men 173 cm (about 5 feet 8 inches) or shorter, reported Dr. Knut H. Borch of the Center for Atherothrombotic Research in Tromsø, Norway, and his colleagues.

In men, each 10-cm increase in height was associated with a significant hazard ratio of 1.34. In women, height was not a significant risk factor for VTE (HR 1.13), he said at a meeting of the International Society on Thrombosis and Haemostasis.

“We suggest that body height should be considered in risk stratification of VTE,” Dr. Borch said. More research is needed to determine how height interacts with other risk factors for VTE.

A 2005 analysis of data from the Physicians' Health Study (Am. J. Epidemiol. 2005;162:975-82) found that every 10 cm of height was associated with about a 36% increase in risk in men. In a separate study, Swedish researchers also found a positive association between body height and VTE risk in men (J. Thromb. Haemost. 2008;6:558-64).

Dr. Borch and his colleagues drew data from the Tromsø Study, a prospective population-based study of men and women aged 25 years and older in the town of Tromsø, in northern Norway. The study included 26,727 residents. The researchers recorded all first lifetime VTEs from the date of study enrollment (1994-1995) through Sept. 1, 2007. Cases were identified by discharge diagnosis, autopsy registry, and radiology procedure registry. VTE was confirmed by diagnostic procedure or autopsy, and the data collected included diagnosis of deep vein thromboembolism (DVT) or pulmonary embolism, signs and symptoms consistent with VTE, and VTE treatment.

During the median follow-up of 12.5 years, there were 462 VTEs, 193 (41.8%) of which were classified as provoked (associated with major surgery or an acute medical condition within 8 weeks of the event, cancer at the time of the event, prolonged immobilization, or other known risk factors). Of the provoked VTEs, 64.3% were DVTs. Overall, the incidence of VTE was 1.6 per 1,000 person-years.

Among men, there were 219 VTEs. Men in the tallest quartile (181 cm and taller) had a significantly increased risk for VTE, vs. men in the lowest height quartile (less than 173 cm). In a multivariate analysis that adjusted for other risk factors, the hazard ratio for the tallest men was 1.99. The hazard ratio for each 10 cm of height was 1.34. Height had no effect on total VTE risk among women. In both men and women, the risks for provoked vs. unprovoked VTE were similar.

Possible explanations for the sex difference in the VTE-height relationship include unidentified sex-specific differences in venous architecture, or differences in pressure dynamics or stasis, Dr. Borch said.

The funding source for the study was not disclosed. Dr. Borch declared that neither he nor his coauthors had relevant financial disclosures.

BOSTON — Taller men appear to have a twofold greater risk for venous thromboembolic events than do men of more modest height, Norwegian investigators reported.

Men taller than 181 cm (about 5 feet 11 inches) had double the risk of either provoked or unprovoked venous thromboembolic events (VTEs), compared with men 173 cm (about 5 feet 8 inches) or shorter, reported Dr. Knut H. Borch of the Center for Atherothrombotic Research in Tromsø, Norway, and his colleagues.

In men, each 10-cm increase in height was associated with a significant hazard ratio of 1.34. In women, height was not a significant risk factor for VTE (HR 1.13), he said at a meeting of the International Society on Thrombosis and Haemostasis.

“We suggest that body height should be considered in risk stratification of VTE,” Dr. Borch said. More research is needed to determine how height interacts with other risk factors for VTE.

A 2005 analysis of data from the Physicians' Health Study (Am. J. Epidemiol. 2005;162:975-82) found that every 10 cm of height was associated with about a 36% increase in risk in men. In a separate study, Swedish researchers also found a positive association between body height and VTE risk in men (J. Thromb. Haemost. 2008;6:558-64).

Dr. Borch and his colleagues drew data from the Tromsø Study, a prospective population-based study of men and women aged 25 years and older in the town of Tromsø, in northern Norway. The study included 26,727 residents. The researchers recorded all first lifetime VTEs from the date of study enrollment (1994-1995) through Sept. 1, 2007. Cases were identified by discharge diagnosis, autopsy registry, and radiology procedure registry. VTE was confirmed by diagnostic procedure or autopsy, and the data collected included diagnosis of deep vein thromboembolism (DVT) or pulmonary embolism, signs and symptoms consistent with VTE, and VTE treatment.

During the median follow-up of 12.5 years, there were 462 VTEs, 193 (41.8%) of which were classified as provoked (associated with major surgery or an acute medical condition within 8 weeks of the event, cancer at the time of the event, prolonged immobilization, or other known risk factors). Of the provoked VTEs, 64.3% were DVTs. Overall, the incidence of VTE was 1.6 per 1,000 person-years.

Among men, there were 219 VTEs. Men in the tallest quartile (181 cm and taller) had a significantly increased risk for VTE, vs. men in the lowest height quartile (less than 173 cm). In a multivariate analysis that adjusted for other risk factors, the hazard ratio for the tallest men was 1.99. The hazard ratio for each 10 cm of height was 1.34. Height had no effect on total VTE risk among women. In both men and women, the risks for provoked vs. unprovoked VTE were similar.

Possible explanations for the sex difference in the VTE-height relationship include unidentified sex-specific differences in venous architecture, or differences in pressure dynamics or stasis, Dr. Borch said.

The funding source for the study was not disclosed. Dr. Borch declared that neither he nor his coauthors had relevant financial disclosures.

BOSTON — A genomewide scan of sibling pairs from families with a genetic susceptibility to developing venous thromboembolism has identified mutations in four genes on chromosome 7 as likely genetic markers for familial thrombophilia.

Single nucleotide polymorphisms (SNPs) in the four genes were linked to familial thrombophilia syndromes. The genes, which don't overlap with genes previously linked to venous thromboembolism (VTE), may account for a large proportion of missing VTE risk factors, Dr. Marieke de Visser said at a meeting of the International Society on Thrombosis and Haemostasis.

The findings could “greatly expand our repertoire of VTE candidate genes,” commented Dr. Edwin Bovill, chairman of the department of pathology and laboratory medicine at the University of Vermont in Burlington.

VTE is a multicausal disease in which both environmental and genetic factors are known to be involved, said Dr. de Visser of the department of thrombosis and hemostasis at Leiden (the Netherlands) University Medical Center.

“So-called familial thrombophilia is thought to be an oligogenetic disease in which at least two genetic risk factors are present,” she said. About 30% of families with familial thrombophilia have known genetic risk factors, suggesting that a significant proportion of risk factors has yet to be identified. “The idea that genetic risk factors are missing is further supported by the observation that many hemostasis-related proteins both correlate with thrombosis risk and show high hereditability.”

Investigators from the Genetics in Familial Thrombosis (GIFT) collaborative collected data on families seen at 29 Dutch anticoagulation clinics. They recruited 211 families consisting of 213 sibships, with 287 sibling pairs that included 460 siblings (87% of sibships consisted of two siblings, 19% had three siblings, and 3% had four siblings). Affected family members had confirmed VTE at or before the age of 45 years. The authors looked at data on both an index sample (two generations, 211 participants) and a nonindex sample (249 participants).

In both the index and nonindex samples, the mean age at first VTE was about 33.5 years, and 46% had more than one event. In about two-thirds of each group, the first VTE was a deep vein thromboembolism (DVT) in the leg or arm. Pulmonary embolism (PE) was the first presentation in about 20% of patients, DVT and PE occurred in about 9%, and thrombophlebitis occurred in about 9%. In nearly half of the families, at least one parent also had a VTE.

The index group had a high prevalence of genetic risk factors, including factor V Leiden in 36.5%, ABO blood group non-O (82.9%), protein S deficiency type III (10.5%), and protein S deficiency type I (7.6%).

The researchers narrowed their search down to SNPs in four candidate genes on chromosome 7: RAC1, COL28A1, NXPH1, and, most robustly, THSD7A. These candidate genes may account for many of the missing genetic factors associated with VTE risk, Dr. de Visser said.

The study was supported by grants from the Netherlands Heart Foundation and the Netherlands Organization for Scientific Research. Dr. de Visser said that neither she nor her coauthors had relevant conflicts of interest.

BOSTON — A genomewide scan of sibling pairs from families with a genetic susceptibility to developing venous thromboembolism has identified mutations in four genes on chromosome 7 as likely genetic markers for familial thrombophilia.

Single nucleotide polymorphisms (SNPs) in the four genes were linked to familial thrombophilia syndromes. The genes, which don't overlap with genes previously linked to venous thromboembolism (VTE), may account for a large proportion of missing VTE risk factors, Dr. Marieke de Visser said at a meeting of the International Society on Thrombosis and Haemostasis.

The findings could “greatly expand our repertoire of VTE candidate genes,” commented Dr. Edwin Bovill, chairman of the department of pathology and laboratory medicine at the University of Vermont in Burlington.

VTE is a multicausal disease in which both environmental and genetic factors are known to be involved, said Dr. de Visser of the department of thrombosis and hemostasis at Leiden (the Netherlands) University Medical Center.

“So-called familial thrombophilia is thought to be an oligogenetic disease in which at least two genetic risk factors are present,” she said. About 30% of families with familial thrombophilia have known genetic risk factors, suggesting that a significant proportion of risk factors has yet to be identified. “The idea that genetic risk factors are missing is further supported by the observation that many hemostasis-related proteins both correlate with thrombosis risk and show high hereditability.”

Investigators from the Genetics in Familial Thrombosis (GIFT) collaborative collected data on families seen at 29 Dutch anticoagulation clinics. They recruited 211 families consisting of 213 sibships, with 287 sibling pairs that included 460 siblings (87% of sibships consisted of two siblings, 19% had three siblings, and 3% had four siblings). Affected family members had confirmed VTE at or before the age of 45 years. The authors looked at data on both an index sample (two generations, 211 participants) and a nonindex sample (249 participants).

In both the index and nonindex samples, the mean age at first VTE was about 33.5 years, and 46% had more than one event. In about two-thirds of each group, the first VTE was a deep vein thromboembolism (DVT) in the leg or arm. Pulmonary embolism (PE) was the first presentation in about 20% of patients, DVT and PE occurred in about 9%, and thrombophlebitis occurred in about 9%. In nearly half of the families, at least one parent also had a VTE.

The index group had a high prevalence of genetic risk factors, including factor V Leiden in 36.5%, ABO blood group non-O (82.9%), protein S deficiency type III (10.5%), and protein S deficiency type I (7.6%).

The researchers narrowed their search down to SNPs in four candidate genes on chromosome 7: RAC1, COL28A1, NXPH1, and, most robustly, THSD7A. These candidate genes may account for many of the missing genetic factors associated with VTE risk, Dr. de Visser said.

The study was supported by grants from the Netherlands Heart Foundation and the Netherlands Organization for Scientific Research. Dr. de Visser said that neither she nor her coauthors had relevant conflicts of interest.

BOSTON — A genomewide scan of sibling pairs from families with a genetic susceptibility to developing venous thromboembolism has identified mutations in four genes on chromosome 7 as likely genetic markers for familial thrombophilia.

Single nucleotide polymorphisms (SNPs) in the four genes were linked to familial thrombophilia syndromes. The genes, which don't overlap with genes previously linked to venous thromboembolism (VTE), may account for a large proportion of missing VTE risk factors, Dr. Marieke de Visser said at a meeting of the International Society on Thrombosis and Haemostasis.

The findings could “greatly expand our repertoire of VTE candidate genes,” commented Dr. Edwin Bovill, chairman of the department of pathology and laboratory medicine at the University of Vermont in Burlington.

VTE is a multicausal disease in which both environmental and genetic factors are known to be involved, said Dr. de Visser of the department of thrombosis and hemostasis at Leiden (the Netherlands) University Medical Center.

“So-called familial thrombophilia is thought to be an oligogenetic disease in which at least two genetic risk factors are present,” she said. About 30% of families with familial thrombophilia have known genetic risk factors, suggesting that a significant proportion of risk factors has yet to be identified. “The idea that genetic risk factors are missing is further supported by the observation that many hemostasis-related proteins both correlate with thrombosis risk and show high hereditability.”

Investigators from the Genetics in Familial Thrombosis (GIFT) collaborative collected data on families seen at 29 Dutch anticoagulation clinics. They recruited 211 families consisting of 213 sibships, with 287 sibling pairs that included 460 siblings (87% of sibships consisted of two siblings, 19% had three siblings, and 3% had four siblings). Affected family members had confirmed VTE at or before the age of 45 years. The authors looked at data on both an index sample (two generations, 211 participants) and a nonindex sample (249 participants).

In both the index and nonindex samples, the mean age at first VTE was about 33.5 years, and 46% had more than one event. In about two-thirds of each group, the first VTE was a deep vein thromboembolism (DVT) in the leg or arm. Pulmonary embolism (PE) was the first presentation in about 20% of patients, DVT and PE occurred in about 9%, and thrombophlebitis occurred in about 9%. In nearly half of the families, at least one parent also had a VTE.

The index group had a high prevalence of genetic risk factors, including factor V Leiden in 36.5%, ABO blood group non-O (82.9%), protein S deficiency type III (10.5%), and protein S deficiency type I (7.6%).

The researchers narrowed their search down to SNPs in four candidate genes on chromosome 7: RAC1, COL28A1, NXPH1, and, most robustly, THSD7A. These candidate genes may account for many of the missing genetic factors associated with VTE risk, Dr. de Visser said.

The study was supported by grants from the Netherlands Heart Foundation and the Netherlands Organization for Scientific Research. Dr. de Visser said that neither she nor her coauthors had relevant conflicts of interest.

BOSTON — Air travel can put frequent or casual flyers at significantly increased risk for a venous thromboembolic event for up to a month after the end of a trip, British researchers reported at a meeting of the International Society on Thrombosis and Haemostasis.

Flying for more than 4 hours at a stretch—or a total flying time of more than 12 hours in the past 4 weeks—was associated with a two- to nearly threefold greater risk for venous thromboembolism (VTE), compared with nontraveling controls, reported Dr. Peter K. MacCallum of Barts and The London at the University of London.

“In this community-based case-control study, we found that air travel was a mild risk factor for venous thrombosis in the subsequent 4 weeks. The risk seen at 4 weeks was no longer apparent at the 12-week time-frame, so the dose response and the declining risk with the passage of time tend to support a causal relationship between air travel and subsequent thrombosis,” Dr. MacCallum said.

The size of the air-travel effect on VTE risk was comparable to that of low-risk surgery. Other factors associated with increased VTE risk were body mass index from 25 to 30 kg/m

Case series linking air travel to VTE risk date to the 1950s, and by 1977 the phenomenon had been dubbed “economy class syndrome.” Case-control, observational, follow-up, intervention, and laboratory studies have been conducted in the past decade, Dr. MacCallum said.

The current study findings echo those of a recent meta-analysis, which suggested that air travel was associated with about a threefold risk for VTE (Ann. Intern. Med. 2009;151:180-90).

Dr. MacCallum and his colleagues studied patients in 123 general practices in the United Kingdom. They identified patients who had received a prescription for warfarin over the previous 12 months, performed a record search to identify patients with confirmed deep vein thromboembolism/pulmonary embolism (DVT/PE), and assigned six age- and sex-matched controls for each case.

The researchers contacted cases and controls by mail, and received replies from 638 cases (55%) and 3,162 controls (58%). After exclusions for various reasons, they arrived at 550 cases and 1,971 controls for the final sample (1:36 ratio).

In a univariate analysis, the only significant flight-associated risk factor for short-term VTE was total flight time longer than 12 hours (odds ratio 1.91; 95% confidence interval 1.08-3.39). In a multivariate analysis adjusted for BMI, surgery, and past history of VTE, the only significant risk factors for VTE within 4 weeks of flying were any flight leg longer than 4 hours (OR 2.20; 95% CI 1.29-3.73) and total flying time greater than 12 hours (OR 2.75; 95% CI 1.44-5.28). By week 12, neither flight leg duration nor total flight time was significantly associated with increased risk for VTE.

The authors plan to conduct additional analyses to explore the relationship between air travel and other risk factors, although they are working with fairly small samples, Dr. MacCallum acknowledged.

The funding source for the study was not disclosed. Dr. MacCallum said that he had no relevant conflict-of-interest disclosures.

BOSTON — Air travel can put frequent or casual flyers at significantly increased risk for a venous thromboembolic event for up to a month after the end of a trip, British researchers reported at a meeting of the International Society on Thrombosis and Haemostasis.

Flying for more than 4 hours at a stretch—or a total flying time of more than 12 hours in the past 4 weeks—was associated with a two- to nearly threefold greater risk for venous thromboembolism (VTE), compared with nontraveling controls, reported Dr. Peter K. MacCallum of Barts and The London at the University of London.

“In this community-based case-control study, we found that air travel was a mild risk factor for venous thrombosis in the subsequent 4 weeks. The risk seen at 4 weeks was no longer apparent at the 12-week time-frame, so the dose response and the declining risk with the passage of time tend to support a causal relationship between air travel and subsequent thrombosis,” Dr. MacCallum said.

The size of the air-travel effect on VTE risk was comparable to that of low-risk surgery. Other factors associated with increased VTE risk were body mass index from 25 to 30 kg/m

Case series linking air travel to VTE risk date to the 1950s, and by 1977 the phenomenon had been dubbed “economy class syndrome.” Case-control, observational, follow-up, intervention, and laboratory studies have been conducted in the past decade, Dr. MacCallum said.

The current study findings echo those of a recent meta-analysis, which suggested that air travel was associated with about a threefold risk for VTE (Ann. Intern. Med. 2009;151:180-90).

Dr. MacCallum and his colleagues studied patients in 123 general practices in the United Kingdom. They identified patients who had received a prescription for warfarin over the previous 12 months, performed a record search to identify patients with confirmed deep vein thromboembolism/pulmonary embolism (DVT/PE), and assigned six age- and sex-matched controls for each case.

The researchers contacted cases and controls by mail, and received replies from 638 cases (55%) and 3,162 controls (58%). After exclusions for various reasons, they arrived at 550 cases and 1,971 controls for the final sample (1:36 ratio).

In a univariate analysis, the only significant flight-associated risk factor for short-term VTE was total flight time longer than 12 hours (odds ratio 1.91; 95% confidence interval 1.08-3.39). In a multivariate analysis adjusted for BMI, surgery, and past history of VTE, the only significant risk factors for VTE within 4 weeks of flying were any flight leg longer than 4 hours (OR 2.20; 95% CI 1.29-3.73) and total flying time greater than 12 hours (OR 2.75; 95% CI 1.44-5.28). By week 12, neither flight leg duration nor total flight time was significantly associated with increased risk for VTE.

The authors plan to conduct additional analyses to explore the relationship between air travel and other risk factors, although they are working with fairly small samples, Dr. MacCallum acknowledged.

The funding source for the study was not disclosed. Dr. MacCallum said that he had no relevant conflict-of-interest disclosures.

BOSTON — Air travel can put frequent or casual flyers at significantly increased risk for a venous thromboembolic event for up to a month after the end of a trip, British researchers reported at a meeting of the International Society on Thrombosis and Haemostasis.

Flying for more than 4 hours at a stretch—or a total flying time of more than 12 hours in the past 4 weeks—was associated with a two- to nearly threefold greater risk for venous thromboembolism (VTE), compared with nontraveling controls, reported Dr. Peter K. MacCallum of Barts and The London at the University of London.

“In this community-based case-control study, we found that air travel was a mild risk factor for venous thrombosis in the subsequent 4 weeks. The risk seen at 4 weeks was no longer apparent at the 12-week time-frame, so the dose response and the declining risk with the passage of time tend to support a causal relationship between air travel and subsequent thrombosis,” Dr. MacCallum said.

The size of the air-travel effect on VTE risk was comparable to that of low-risk surgery. Other factors associated with increased VTE risk were body mass index from 25 to 30 kg/m

Case series linking air travel to VTE risk date to the 1950s, and by 1977 the phenomenon had been dubbed “economy class syndrome.” Case-control, observational, follow-up, intervention, and laboratory studies have been conducted in the past decade, Dr. MacCallum said.

The current study findings echo those of a recent meta-analysis, which suggested that air travel was associated with about a threefold risk for VTE (Ann. Intern. Med. 2009;151:180-90).

Dr. MacCallum and his colleagues studied patients in 123 general practices in the United Kingdom. They identified patients who had received a prescription for warfarin over the previous 12 months, performed a record search to identify patients with confirmed deep vein thromboembolism/pulmonary embolism (DVT/PE), and assigned six age- and sex-matched controls for each case.

The researchers contacted cases and controls by mail, and received replies from 638 cases (55%) and 3,162 controls (58%). After exclusions for various reasons, they arrived at 550 cases and 1,971 controls for the final sample (1:36 ratio).

In a univariate analysis, the only significant flight-associated risk factor for short-term VTE was total flight time longer than 12 hours (odds ratio 1.91; 95% confidence interval 1.08-3.39). In a multivariate analysis adjusted for BMI, surgery, and past history of VTE, the only significant risk factors for VTE within 4 weeks of flying were any flight leg longer than 4 hours (OR 2.20; 95% CI 1.29-3.73) and total flying time greater than 12 hours (OR 2.75; 95% CI 1.44-5.28). By week 12, neither flight leg duration nor total flight time was significantly associated with increased risk for VTE.

The authors plan to conduct additional analyses to explore the relationship between air travel and other risk factors, although they are working with fairly small samples, Dr. MacCallum acknowledged.

The funding source for the study was not disclosed. Dr. MacCallum said that he had no relevant conflict-of-interest disclosures.

BOSTON — The more women weigh, the greater their risk for incident pulmonary embolism, according to an analysis of prospective data from more than 85,000 women enrolled in the Nurses' Health Study.

The investigators found a relative risk for pulmonary embolism (PE) of 1.08 for every 1-kg/m

“We found that there is a strong, independent, positive, linear association between BMI and incident PE, and that this effect seems to impact not only obese subjects, but [also] subjects with relatively modest increases in their BMI,” reported Dr. Kabrhel of Harvard Medical School and Massachusetts General Hospital, Boston, and his colleagues.

Cross-sectional and case-control studies have shown that patients who experience deep vein thrombosis and pulmonary embolism tend to have higher BMIs, and prospective studies have shown an association between severe overweight or obesity and pulmonary embolism, he noted.

The investigators examined the association between weight and thromboembolic events using data from 87,226 women enrolled in the prospective, longitudinal Nurses' Health Study, which has collected data on PE since its inception in 1976 and on diet, physical activity, and other risk factors for PE since 1984.

Participants enrolled in the Nurses' Health Study during 1984-2002, and were excluded from the current analysis if they had a PE diagnosis before 1984 or if their records were missing data necessary to calculate BMI.

The investigators divided participants into six BMI categories: less than 22.5 kg/m

The primary outcome was idiopathic PE, defined as cases of PE that were confirmed in the medical record and not associated with prior surgery, trauma, or malignancy. The authors also performed a secondary analysis of nonidiopathic PE.

During the period studied, there were 157 incident cases of idiopathic PE and 338 cases of nonidiopathic PE, and these correlated strongly with BMI. For both idiopathic and nonidiopathic PE, the relative risk for every 1-kg/m

Associations between BMI and nonidiopathic PE were similar, ranging from a relative risk of 1.48 for patients in the 22.5-24.9 range compared with those in the lowest BMI category, to a relative risk of 5.42 for patients in the highest vs. lowest BMI categories.

“There is a significant increase with the combined idiopathic PE and nonidiopathic PE. In other words, for our total PE, there is a significant increase in the risk of PE even with relatively modest increases in BMI—that is to say, subjects that would not be considered either overweight or obese, but within the normal range,” Dr. Kabrhel said.

A potential mechanism for the association between BMI and PE is the regulatory hormone leptin, which has been shown to induce tissue-factor activity in vitro and to be elevated in obese individuals, he said.

Alternatively, estrogen and progesterone, which have been linked to obesity and the risk of PE in women, may play a role, although there was no evidence of a hormone-PE interaction in their study, he said.

Dr. Kabrhel acknowledged that the study was limited by its inclusion of only women, and by the racial and ethnic imbalance of the Nurses' Health Study cohort, which represents a demographic sample of nurses in the United States. The study may also be subject to measurement bias because it relied on subject-reported weights.

The authors received grant and research support for the study from the National Institutes of Health. No other conflicts of interest were reported.

BOSTON — The more women weigh, the greater their risk for incident pulmonary embolism, according to an analysis of prospective data from more than 85,000 women enrolled in the Nurses' Health Study.

The investigators found a relative risk for pulmonary embolism (PE) of 1.08 for every 1-kg/m

“We found that there is a strong, independent, positive, linear association between BMI and incident PE, and that this effect seems to impact not only obese subjects, but [also] subjects with relatively modest increases in their BMI,” reported Dr. Kabrhel of Harvard Medical School and Massachusetts General Hospital, Boston, and his colleagues.

Cross-sectional and case-control studies have shown that patients who experience deep vein thrombosis and pulmonary embolism tend to have higher BMIs, and prospective studies have shown an association between severe overweight or obesity and pulmonary embolism, he noted.

The investigators examined the association between weight and thromboembolic events using data from 87,226 women enrolled in the prospective, longitudinal Nurses' Health Study, which has collected data on PE since its inception in 1976 and on diet, physical activity, and other risk factors for PE since 1984.

Participants enrolled in the Nurses' Health Study during 1984-2002, and were excluded from the current analysis if they had a PE diagnosis before 1984 or if their records were missing data necessary to calculate BMI.

The investigators divided participants into six BMI categories: less than 22.5 kg/m

The primary outcome was idiopathic PE, defined as cases of PE that were confirmed in the medical record and not associated with prior surgery, trauma, or malignancy. The authors also performed a secondary analysis of nonidiopathic PE.

During the period studied, there were 157 incident cases of idiopathic PE and 338 cases of nonidiopathic PE, and these correlated strongly with BMI. For both idiopathic and nonidiopathic PE, the relative risk for every 1-kg/m

Associations between BMI and nonidiopathic PE were similar, ranging from a relative risk of 1.48 for patients in the 22.5-24.9 range compared with those in the lowest BMI category, to a relative risk of 5.42 for patients in the highest vs. lowest BMI categories.

“There is a significant increase with the combined idiopathic PE and nonidiopathic PE. In other words, for our total PE, there is a significant increase in the risk of PE even with relatively modest increases in BMI—that is to say, subjects that would not be considered either overweight or obese, but within the normal range,” Dr. Kabrhel said.

A potential mechanism for the association between BMI and PE is the regulatory hormone leptin, which has been shown to induce tissue-factor activity in vitro and to be elevated in obese individuals, he said.

Alternatively, estrogen and progesterone, which have been linked to obesity and the risk of PE in women, may play a role, although there was no evidence of a hormone-PE interaction in their study, he said.

Dr. Kabrhel acknowledged that the study was limited by its inclusion of only women, and by the racial and ethnic imbalance of the Nurses' Health Study cohort, which represents a demographic sample of nurses in the United States. The study may also be subject to measurement bias because it relied on subject-reported weights.

The authors received grant and research support for the study from the National Institutes of Health. No other conflicts of interest were reported.

BOSTON — The more women weigh, the greater their risk for incident pulmonary embolism, according to an analysis of prospective data from more than 85,000 women enrolled in the Nurses' Health Study.

The investigators found a relative risk for pulmonary embolism (PE) of 1.08 for every 1-kg/m

“We found that there is a strong, independent, positive, linear association between BMI and incident PE, and that this effect seems to impact not only obese subjects, but [also] subjects with relatively modest increases in their BMI,” reported Dr. Kabrhel of Harvard Medical School and Massachusetts General Hospital, Boston, and his colleagues.

Cross-sectional and case-control studies have shown that patients who experience deep vein thrombosis and pulmonary embolism tend to have higher BMIs, and prospective studies have shown an association between severe overweight or obesity and pulmonary embolism, he noted.

The investigators examined the association between weight and thromboembolic events using data from 87,226 women enrolled in the prospective, longitudinal Nurses' Health Study, which has collected data on PE since its inception in 1976 and on diet, physical activity, and other risk factors for PE since 1984.

Participants enrolled in the Nurses' Health Study during 1984-2002, and were excluded from the current analysis if they had a PE diagnosis before 1984 or if their records were missing data necessary to calculate BMI.

The investigators divided participants into six BMI categories: less than 22.5 kg/m

The primary outcome was idiopathic PE, defined as cases of PE that were confirmed in the medical record and not associated with prior surgery, trauma, or malignancy. The authors also performed a secondary analysis of nonidiopathic PE.

During the period studied, there were 157 incident cases of idiopathic PE and 338 cases of nonidiopathic PE, and these correlated strongly with BMI. For both idiopathic and nonidiopathic PE, the relative risk for every 1-kg/m

Associations between BMI and nonidiopathic PE were similar, ranging from a relative risk of 1.48 for patients in the 22.5-24.9 range compared with those in the lowest BMI category, to a relative risk of 5.42 for patients in the highest vs. lowest BMI categories.

“There is a significant increase with the combined idiopathic PE and nonidiopathic PE. In other words, for our total PE, there is a significant increase in the risk of PE even with relatively modest increases in BMI—that is to say, subjects that would not be considered either overweight or obese, but within the normal range,” Dr. Kabrhel said.

A potential mechanism for the association between BMI and PE is the regulatory hormone leptin, which has been shown to induce tissue-factor activity in vitro and to be elevated in obese individuals, he said.

Alternatively, estrogen and progesterone, which have been linked to obesity and the risk of PE in women, may play a role, although there was no evidence of a hormone-PE interaction in their study, he said.

Dr. Kabrhel acknowledged that the study was limited by its inclusion of only women, and by the racial and ethnic imbalance of the Nurses' Health Study cohort, which represents a demographic sample of nurses in the United States. The study may also be subject to measurement bias because it relied on subject-reported weights.

The authors received grant and research support for the study from the National Institutes of Health. No other conflicts of interest were reported.

BOSTON — Bariatric surgery can lead to sustained remission of type 2 diabetes and improvements in cardiovascular health that lower the risk for diabetes-specific mortality, according to Dr. Ted D. Adams, a cardiovascular researcher at the University of Utah, Salt Lake City.

In published studies, 64%-100% of patients experienced remission of type 2 diabetes, 62%-69% had resolution of hypertension at 1 or 2 years after surgery, and up to 85% had resolution of sleep apnea, Dr. Adams noted at a symposium sponsored by the International Atherosclerosis Society.

“Observational studies reporting mortality of obese subjects who have lost weight without bariatric surgery are inconclusive, with studies reporting no change, increased, or reduced mortality,” Dr. Adams said. To date, 11 published studies have examined mortality following bariatric surgery. The studies varied considerably by type of surgery, length of follow-up, selection of control groups, and body mass index; however, the eight studies with severely obese control groups reported increases in longevity among bariatric surgery patients. The reductions ranged from a mean of 29% in one study to 89% in a different study, Dr. Adams said.

A study of 232 morbidly obese patients with type 2 diabetes showed mortality rates of 9% for the 154 Roux-en-Y gastric bypass patients compared with 28% for 78 patients who did not undergo surgery. For each year of follow-up, surgical patients had a 1% chance of dying, compared with a 4.5% per year chance for controls. The investigators found that the improved mortality rate among the gastric bypass recipients was attributable primarily to a decrease in the number of cardiovascular deaths (J. Gastrointest. Surg. 1997;1:213-20).

In a case-control study, Dr. Adams and his colleagues compared 7,925 patients who underwent gastric bypass with age- weight-, and gender-matched controls from Utah driver license data. The patients' median age was 39.5 years, and their median body mass index was 45.3. The investigators found that over an 18-year follow-up period (mean 7.1 years), 2.7% of patients had died, compared with 4.1% of controls. The adjusted reduction in death associated with gastric bypass surgery was 40% (N. Engl. J. Med. 2007;357:753-61).

There were 55 cardiovascular disease deaths among cases, compared with 104 among controls, and there were fewer deaths from coronary artery disease among cases compared with controls (15 vs. 33, respectively).

There were only two deaths attributed to diabetes among cases, compared with 19 among controls, Dr. Adams noted.

In an analysis of cause-specific mortality, the authors saw a decrease of 56% in coronary artery disease for cases vs. controls (2.6 vs. 5.9 per 10,000 person-years, P = .006), a 92% reduction for cases in diabetes deaths (0.4 vs. 3.4 per 10,000 p-y, P = .005), and a 60% decrease in cancer deaths (5.5 vs. 13.3 per 10,000 p-y, respectively, P less than .001). Nondisease causes of death, such as accidents and suicide, were higher among cases compared with controls (11.1 vs. 6.4 per 10,000).

In another study, Dr. Adams and colleagues compared severely obese patients who underwent Roux-en-Y gastric bypass with patients who qualified for such surgery but were denied insurance coverage, and with matched controls not seeking surgery (Obesity 2009 June 4 [doi: 10.1038/oby.2009.178

In studies, 64%-100% of patients experienced remission of type 2 diabetes at 1 or 2 years after surgery.

Source DR. ADAMS

BOSTON — Bariatric surgery can lead to sustained remission of type 2 diabetes and improvements in cardiovascular health that lower the risk for diabetes-specific mortality, according to Dr. Ted D. Adams, a cardiovascular researcher at the University of Utah, Salt Lake City.

In published studies, 64%-100% of patients experienced remission of type 2 diabetes, 62%-69% had resolution of hypertension at 1 or 2 years after surgery, and up to 85% had resolution of sleep apnea, Dr. Adams noted at a symposium sponsored by the International Atherosclerosis Society.

“Observational studies reporting mortality of obese subjects who have lost weight without bariatric surgery are inconclusive, with studies reporting no change, increased, or reduced mortality,” Dr. Adams said. To date, 11 published studies have examined mortality following bariatric surgery. The studies varied considerably by type of surgery, length of follow-up, selection of control groups, and body mass index; however, the eight studies with severely obese control groups reported increases in longevity among bariatric surgery patients. The reductions ranged from a mean of 29% in one study to 89% in a different study, Dr. Adams said.

A study of 232 morbidly obese patients with type 2 diabetes showed mortality rates of 9% for the 154 Roux-en-Y gastric bypass patients compared with 28% for 78 patients who did not undergo surgery. For each year of follow-up, surgical patients had a 1% chance of dying, compared with a 4.5% per year chance for controls. The investigators found that the improved mortality rate among the gastric bypass recipients was attributable primarily to a decrease in the number of cardiovascular deaths (J. Gastrointest. Surg. 1997;1:213-20).

In a case-control study, Dr. Adams and his colleagues compared 7,925 patients who underwent gastric bypass with age- weight-, and gender-matched controls from Utah driver license data. The patients' median age was 39.5 years, and their median body mass index was 45.3. The investigators found that over an 18-year follow-up period (mean 7.1 years), 2.7% of patients had died, compared with 4.1% of controls. The adjusted reduction in death associated with gastric bypass surgery was 40% (N. Engl. J. Med. 2007;357:753-61).

There were 55 cardiovascular disease deaths among cases, compared with 104 among controls, and there were fewer deaths from coronary artery disease among cases compared with controls (15 vs. 33, respectively).

There were only two deaths attributed to diabetes among cases, compared with 19 among controls, Dr. Adams noted.

In an analysis of cause-specific mortality, the authors saw a decrease of 56% in coronary artery disease for cases vs. controls (2.6 vs. 5.9 per 10,000 person-years, P = .006), a 92% reduction for cases in diabetes deaths (0.4 vs. 3.4 per 10,000 p-y, P = .005), and a 60% decrease in cancer deaths (5.5 vs. 13.3 per 10,000 p-y, respectively, P less than .001). Nondisease causes of death, such as accidents and suicide, were higher among cases compared with controls (11.1 vs. 6.4 per 10,000).

In another study, Dr. Adams and colleagues compared severely obese patients who underwent Roux-en-Y gastric bypass with patients who qualified for such surgery but were denied insurance coverage, and with matched controls not seeking surgery (Obesity 2009 June 4 [doi: 10.1038/oby.2009.178

In studies, 64%-100% of patients experienced remission of type 2 diabetes at 1 or 2 years after surgery.

Source DR. ADAMS

BOSTON — Bariatric surgery can lead to sustained remission of type 2 diabetes and improvements in cardiovascular health that lower the risk for diabetes-specific mortality, according to Dr. Ted D. Adams, a cardiovascular researcher at the University of Utah, Salt Lake City.

In published studies, 64%-100% of patients experienced remission of type 2 diabetes, 62%-69% had resolution of hypertension at 1 or 2 years after surgery, and up to 85% had resolution of sleep apnea, Dr. Adams noted at a symposium sponsored by the International Atherosclerosis Society.

“Observational studies reporting mortality of obese subjects who have lost weight without bariatric surgery are inconclusive, with studies reporting no change, increased, or reduced mortality,” Dr. Adams said. To date, 11 published studies have examined mortality following bariatric surgery. The studies varied considerably by type of surgery, length of follow-up, selection of control groups, and body mass index; however, the eight studies with severely obese control groups reported increases in longevity among bariatric surgery patients. The reductions ranged from a mean of 29% in one study to 89% in a different study, Dr. Adams said.

A study of 232 morbidly obese patients with type 2 diabetes showed mortality rates of 9% for the 154 Roux-en-Y gastric bypass patients compared with 28% for 78 patients who did not undergo surgery. For each year of follow-up, surgical patients had a 1% chance of dying, compared with a 4.5% per year chance for controls. The investigators found that the improved mortality rate among the gastric bypass recipients was attributable primarily to a decrease in the number of cardiovascular deaths (J. Gastrointest. Surg. 1997;1:213-20).

In a case-control study, Dr. Adams and his colleagues compared 7,925 patients who underwent gastric bypass with age- weight-, and gender-matched controls from Utah driver license data. The patients' median age was 39.5 years, and their median body mass index was 45.3. The investigators found that over an 18-year follow-up period (mean 7.1 years), 2.7% of patients had died, compared with 4.1% of controls. The adjusted reduction in death associated with gastric bypass surgery was 40% (N. Engl. J. Med. 2007;357:753-61).

There were 55 cardiovascular disease deaths among cases, compared with 104 among controls, and there were fewer deaths from coronary artery disease among cases compared with controls (15 vs. 33, respectively).

There were only two deaths attributed to diabetes among cases, compared with 19 among controls, Dr. Adams noted.

In an analysis of cause-specific mortality, the authors saw a decrease of 56% in coronary artery disease for cases vs. controls (2.6 vs. 5.9 per 10,000 person-years, P = .006), a 92% reduction for cases in diabetes deaths (0.4 vs. 3.4 per 10,000 p-y, P = .005), and a 60% decrease in cancer deaths (5.5 vs. 13.3 per 10,000 p-y, respectively, P less than .001). Nondisease causes of death, such as accidents and suicide, were higher among cases compared with controls (11.1 vs. 6.4 per 10,000).

In another study, Dr. Adams and colleagues compared severely obese patients who underwent Roux-en-Y gastric bypass with patients who qualified for such surgery but were denied insurance coverage, and with matched controls not seeking surgery (Obesity 2009 June 4 [doi: 10.1038/oby.2009.178

In studies, 64%-100% of patients experienced remission of type 2 diabetes at 1 or 2 years after surgery.

Source DR. ADAMS

BOSTON — Air travel can put frequent or casual flyers at significantly increased risk for a venous thromboembolic event for up to a month after the end of a trip, British investigators reported at a meeting of the International Society on Thrombosis and Haemostasis.

Flying for more than 4 hours at a stretch—or a total flying time of more than 12 hours in the past 4 weeks—was associated with a two- to nearly threefold greater risk for VTE, compared with nontraveling controls, reported Dr. Peter K. MacCallum of Barts and The London at the University of London.

“In this community-based case-control study, we found that air travel was a mild risk factor for venous thrombosis in the subsequent 4 weeks. The risk seen at 4 weeks was no longer apparent at the 12-week time-frame, so the dose response and the declining risk with the passage of time tend to support a causal relationship between air travel and subsequent thrombosis,” Dr. MacCallum said.

The size of the air-travel effect on VTE risk was comparable to that of low-risk surgery. Other factors associated with increased risk for VTE were body mass index from 25 kg/m

Cases series linking air travel to VTE risk date to the 1950s, and by 1977 the phenomenon had earned the nickname “Economy class syndrome.” Over the last decade, researchers have taken a more systematic approach, with case-control, observational, follow-up, intervention, and laboratory studies.

The findings echo those of a recently published meta-analysis, which suggested that air travel was associated with about a threefold risk for VTE (Ann. Intern. Med. 2009 Aug. 4 [Epub ahead of print]).

Dr. MacCallum and his colleagues conducted a community-based, case-control study looking at venous thromboembolic events among patients in 123 general practices in the United Kingdom. They identified patients who had received a prescription for warfarin over the previous 12 months, performed a record search to identify those patients who had confirmed deep vein thromboembolism/pulmonary embolism (DVT/PE), and assigned six age- and sex-matched controls for each case.

All cases and controls were contacted by mail with consent forms and questionnaires. A total of 550 cases and 1,971 controls were studied.

In univariate analysis, the only significant flight-associated risk factor for short-term VTE was total flight time longer than 12 hours (OR, 1.91; 95% confidence interval, 1.08-3.39). In multivariate analysis adjusted for BMI, surgery, and past history of VTE, the only significant risk factors for VTE within 4 weeks of flying were any flight leg longer than 4 hours (OR, 2.20; 95% CI, 1.29-3.73) and total flying time greater than 12 hours (OR, 2.75; 95% CI, 1.44-5.28). By week 12, however, neither flight leg duration nor total flight time was significantly associated with increased risk for VTE.

The funding source for the study was not disclosed. Dr. MacCallum said that he had no relevant conflict-of-interest disclosures.

BOSTON — Air travel can put frequent or casual flyers at significantly increased risk for a venous thromboembolic event for up to a month after the end of a trip, British investigators reported at a meeting of the International Society on Thrombosis and Haemostasis.

Flying for more than 4 hours at a stretch—or a total flying time of more than 12 hours in the past 4 weeks—was associated with a two- to nearly threefold greater risk for VTE, compared with nontraveling controls, reported Dr. Peter K. MacCallum of Barts and The London at the University of London.

“In this community-based case-control study, we found that air travel was a mild risk factor for venous thrombosis in the subsequent 4 weeks. The risk seen at 4 weeks was no longer apparent at the 12-week time-frame, so the dose response and the declining risk with the passage of time tend to support a causal relationship between air travel and subsequent thrombosis,” Dr. MacCallum said.

The size of the air-travel effect on VTE risk was comparable to that of low-risk surgery. Other factors associated with increased risk for VTE were body mass index from 25 kg/m

Cases series linking air travel to VTE risk date to the 1950s, and by 1977 the phenomenon had earned the nickname “Economy class syndrome.” Over the last decade, researchers have taken a more systematic approach, with case-control, observational, follow-up, intervention, and laboratory studies.

The findings echo those of a recently published meta-analysis, which suggested that air travel was associated with about a threefold risk for VTE (Ann. Intern. Med. 2009 Aug. 4 [Epub ahead of print]).

Dr. MacCallum and his colleagues conducted a community-based, case-control study looking at venous thromboembolic events among patients in 123 general practices in the United Kingdom. They identified patients who had received a prescription for warfarin over the previous 12 months, performed a record search to identify those patients who had confirmed deep vein thromboembolism/pulmonary embolism (DVT/PE), and assigned six age- and sex-matched controls for each case.

All cases and controls were contacted by mail with consent forms and questionnaires. A total of 550 cases and 1,971 controls were studied.

In univariate analysis, the only significant flight-associated risk factor for short-term VTE was total flight time longer than 12 hours (OR, 1.91; 95% confidence interval, 1.08-3.39). In multivariate analysis adjusted for BMI, surgery, and past history of VTE, the only significant risk factors for VTE within 4 weeks of flying were any flight leg longer than 4 hours (OR, 2.20; 95% CI, 1.29-3.73) and total flying time greater than 12 hours (OR, 2.75; 95% CI, 1.44-5.28). By week 12, however, neither flight leg duration nor total flight time was significantly associated with increased risk for VTE.

The funding source for the study was not disclosed. Dr. MacCallum said that he had no relevant conflict-of-interest disclosures.

BOSTON — Air travel can put frequent or casual flyers at significantly increased risk for a venous thromboembolic event for up to a month after the end of a trip, British investigators reported at a meeting of the International Society on Thrombosis and Haemostasis.

Flying for more than 4 hours at a stretch—or a total flying time of more than 12 hours in the past 4 weeks—was associated with a two- to nearly threefold greater risk for VTE, compared with nontraveling controls, reported Dr. Peter K. MacCallum of Barts and The London at the University of London.

“In this community-based case-control study, we found that air travel was a mild risk factor for venous thrombosis in the subsequent 4 weeks. The risk seen at 4 weeks was no longer apparent at the 12-week time-frame, so the dose response and the declining risk with the passage of time tend to support a causal relationship between air travel and subsequent thrombosis,” Dr. MacCallum said.

The size of the air-travel effect on VTE risk was comparable to that of low-risk surgery. Other factors associated with increased risk for VTE were body mass index from 25 kg/m

Cases series linking air travel to VTE risk date to the 1950s, and by 1977 the phenomenon had earned the nickname “Economy class syndrome.” Over the last decade, researchers have taken a more systematic approach, with case-control, observational, follow-up, intervention, and laboratory studies.

The findings echo those of a recently published meta-analysis, which suggested that air travel was associated with about a threefold risk for VTE (Ann. Intern. Med. 2009 Aug. 4 [Epub ahead of print]).

Dr. MacCallum and his colleagues conducted a community-based, case-control study looking at venous thromboembolic events among patients in 123 general practices in the United Kingdom. They identified patients who had received a prescription for warfarin over the previous 12 months, performed a record search to identify those patients who had confirmed deep vein thromboembolism/pulmonary embolism (DVT/PE), and assigned six age- and sex-matched controls for each case.

All cases and controls were contacted by mail with consent forms and questionnaires. A total of 550 cases and 1,971 controls were studied.

In univariate analysis, the only significant flight-associated risk factor for short-term VTE was total flight time longer than 12 hours (OR, 1.91; 95% confidence interval, 1.08-3.39). In multivariate analysis adjusted for BMI, surgery, and past history of VTE, the only significant risk factors for VTE within 4 weeks of flying were any flight leg longer than 4 hours (OR, 2.20; 95% CI, 1.29-3.73) and total flying time greater than 12 hours (OR, 2.75; 95% CI, 1.44-5.28). By week 12, however, neither flight leg duration nor total flight time was significantly associated with increased risk for VTE.

The funding source for the study was not disclosed. Dr. MacCallum said that he had no relevant conflict-of-interest disclosures.

BOSTON — High-density lipoprotein cholesterol may not be as beneficial as once believed, according to the results of a large data analysis.

Among women, high levels of HDL cholesterol were associated with a near 40% increased risk for unprovoked venous thromboembolic events (VTE), compared with women with lower levels of the so-called “good cholesterol,” according to Dr. Knut H. Borch from the Center for Atherothrombotic Research, University of Trosmø in Norway.

“We found no association between HDL cholesterol levels and risk of provoked VTE in men or in women. However, high HDL cholesterol was associated with increased risk of unprovoked VTE in women, but not in men,” Dr. Borch explained at a meeting of the International Society on Thrombosis and Haemostasis.

The investigators looked for a potential protective effect of HDL on VTE by examining data from a prospective population-based study on all men and women age 25 and older in the town of Tromsø.

A total of 26,676 adult men and women were included in the study, after exclusion of some participants for missing HDL data, or for other reasons. The investigators looked for all first lifetime events of VTE during follow-up from the date of enrollment (1994-1995) through Sept. 1, 2007.

Cases were identified by a computerized index of discharge diagnoses, autopsy registry, and radiology procedure registry. VTE was confirmed either by diagnostic procedure or autopsy, and the data collected included diagnosis of deep vein thromboembolism or pulmonary embolism, signs and symptoms consistent with VTE and VTE treatment.

The investigators further classified VTE as being provoked or unprovoked. Provoked VTEs were those associated with major surgery or an acute medical condition within 8 weeks of the event, cancer at the time of the event, prolonged immobilization, or other known risk factors. Unprovoked VTEs were those occurring in the absence of any of the known provoking factors.

The median follow-up was 12.5 years, and a total of 288,572 person-years.

During that time, there were 458 VTEs in the cohort, 191 (42%) of which were identified as provoked, and of this group, 64% were DVT. This translated into an incidence of 1.6 VTEs per 1,000 person-years. There were no between-gender differences in provoking factors or type of VTE.

In a multivariate analysis, the researchers found no significant differences between the lowest and highest HDL quartiles for either women (hazard ratio .90, .73-1.11) or men (HR 1.06, .83-1.35).

In terms of unprovoked VTE events, however, there was a significantly increased risk for VTE among women with the highest versus the lowest HDL quartiles (HR 1.39, 1.10-1.75). There was no significant difference in unprovoked VTE events among men in the highest versus lowest HDL quartiles (HR 1.15, .87-1.53).

Dr. Borch said that the strengths of the study include its prospective design, large number of participants, high compliance rate (77%), and exclusive hospital care by the University Hospital of Northern Norway. Limitations included HDL blood draws performed at different times of day with patients in a nonfasting state.

“However, HDL is not known to have a substantial diurnal variation or to be severely affected by meals,” Dr. Borch said.

He also noted that a common problem of cohort studies is that risk factors for individual patients may change over time, especially when there is a long follow-up period. Additionally, the researchers had no information about treatment during follow-up, and, therefore, could not control for it.

The findings are consistent with those of two previous cohort studies examining a possible link between HDL cholesterol levels and VTE, and raise doubts about potential antithrombotic properties of HDL particles (Blood 2008;112:2675-80; J. Thromb. Haemost. 2009;7:588-96).

Dr. Borch said that further studies are needed to determine whether the increased risk of unprovoked VTE in women is a direct result of HDL particles or of some unrecognized confounder.

Dr. Borch reported that neither he nor his colleagues had any financial disclosures relevant to the study.

BOSTON — High-density lipoprotein cholesterol may not be as beneficial as once believed, according to the results of a large data analysis.

Among women, high levels of HDL cholesterol were associated with a near 40% increased risk for unprovoked venous thromboembolic events (VTE), compared with women with lower levels of the so-called “good cholesterol,” according to Dr. Knut H. Borch from the Center for Atherothrombotic Research, University of Trosmø in Norway.

“We found no association between HDL cholesterol levels and risk of provoked VTE in men or in women. However, high HDL cholesterol was associated with increased risk of unprovoked VTE in women, but not in men,” Dr. Borch explained at a meeting of the International Society on Thrombosis and Haemostasis.

The investigators looked for a potential protective effect of HDL on VTE by examining data from a prospective population-based study on all men and women age 25 and older in the town of Tromsø.

A total of 26,676 adult men and women were included in the study, after exclusion of some participants for missing HDL data, or for other reasons. The investigators looked for all first lifetime events of VTE during follow-up from the date of enrollment (1994-1995) through Sept. 1, 2007.

Cases were identified by a computerized index of discharge diagnoses, autopsy registry, and radiology procedure registry. VTE was confirmed either by diagnostic procedure or autopsy, and the data collected included diagnosis of deep vein thromboembolism or pulmonary embolism, signs and symptoms consistent with VTE and VTE treatment.

The investigators further classified VTE as being provoked or unprovoked. Provoked VTEs were those associated with major surgery or an acute medical condition within 8 weeks of the event, cancer at the time of the event, prolonged immobilization, or other known risk factors. Unprovoked VTEs were those occurring in the absence of any of the known provoking factors.

The median follow-up was 12.5 years, and a total of 288,572 person-years.

During that time, there were 458 VTEs in the cohort, 191 (42%) of which were identified as provoked, and of this group, 64% were DVT. This translated into an incidence of 1.6 VTEs per 1,000 person-years. There were no between-gender differences in provoking factors or type of VTE.

In a multivariate analysis, the researchers found no significant differences between the lowest and highest HDL quartiles for either women (hazard ratio .90, .73-1.11) or men (HR 1.06, .83-1.35).

In terms of unprovoked VTE events, however, there was a significantly increased risk for VTE among women with the highest versus the lowest HDL quartiles (HR 1.39, 1.10-1.75). There was no significant difference in unprovoked VTE events among men in the highest versus lowest HDL quartiles (HR 1.15, .87-1.53).

Dr. Borch said that the strengths of the study include its prospective design, large number of participants, high compliance rate (77%), and exclusive hospital care by the University Hospital of Northern Norway. Limitations included HDL blood draws performed at different times of day with patients in a nonfasting state.

“However, HDL is not known to have a substantial diurnal variation or to be severely affected by meals,” Dr. Borch said.

He also noted that a common problem of cohort studies is that risk factors for individual patients may change over time, especially when there is a long follow-up period. Additionally, the researchers had no information about treatment during follow-up, and, therefore, could not control for it.

The findings are consistent with those of two previous cohort studies examining a possible link between HDL cholesterol levels and VTE, and raise doubts about potential antithrombotic properties of HDL particles (Blood 2008;112:2675-80; J. Thromb. Haemost. 2009;7:588-96).

Dr. Borch said that further studies are needed to determine whether the increased risk of unprovoked VTE in women is a direct result of HDL particles or of some unrecognized confounder.

Dr. Borch reported that neither he nor his colleagues had any financial disclosures relevant to the study.

BOSTON — High-density lipoprotein cholesterol may not be as beneficial as once believed, according to the results of a large data analysis.

Among women, high levels of HDL cholesterol were associated with a near 40% increased risk for unprovoked venous thromboembolic events (VTE), compared with women with lower levels of the so-called “good cholesterol,” according to Dr. Knut H. Borch from the Center for Atherothrombotic Research, University of Trosmø in Norway.

“We found no association between HDL cholesterol levels and risk of provoked VTE in men or in women. However, high HDL cholesterol was associated with increased risk of unprovoked VTE in women, but not in men,” Dr. Borch explained at a meeting of the International Society on Thrombosis and Haemostasis.

The investigators looked for a potential protective effect of HDL on VTE by examining data from a prospective population-based study on all men and women age 25 and older in the town of Tromsø.

A total of 26,676 adult men and women were included in the study, after exclusion of some participants for missing HDL data, or for other reasons. The investigators looked for all first lifetime events of VTE during follow-up from the date of enrollment (1994-1995) through Sept. 1, 2007.

Cases were identified by a computerized index of discharge diagnoses, autopsy registry, and radiology procedure registry. VTE was confirmed either by diagnostic procedure or autopsy, and the data collected included diagnosis of deep vein thromboembolism or pulmonary embolism, signs and symptoms consistent with VTE and VTE treatment.

The investigators further classified VTE as being provoked or unprovoked. Provoked VTEs were those associated with major surgery or an acute medical condition within 8 weeks of the event, cancer at the time of the event, prolonged immobilization, or other known risk factors. Unprovoked VTEs were those occurring in the absence of any of the known provoking factors.

The median follow-up was 12.5 years, and a total of 288,572 person-years.

During that time, there were 458 VTEs in the cohort, 191 (42%) of which were identified as provoked, and of this group, 64% were DVT. This translated into an incidence of 1.6 VTEs per 1,000 person-years. There were no between-gender differences in provoking factors or type of VTE.

In a multivariate analysis, the researchers found no significant differences between the lowest and highest HDL quartiles for either women (hazard ratio .90, .73-1.11) or men (HR 1.06, .83-1.35).

In terms of unprovoked VTE events, however, there was a significantly increased risk for VTE among women with the highest versus the lowest HDL quartiles (HR 1.39, 1.10-1.75). There was no significant difference in unprovoked VTE events among men in the highest versus lowest HDL quartiles (HR 1.15, .87-1.53).

Dr. Borch said that the strengths of the study include its prospective design, large number of participants, high compliance rate (77%), and exclusive hospital care by the University Hospital of Northern Norway. Limitations included HDL blood draws performed at different times of day with patients in a nonfasting state.

“However, HDL is not known to have a substantial diurnal variation or to be severely affected by meals,” Dr. Borch said.

He also noted that a common problem of cohort studies is that risk factors for individual patients may change over time, especially when there is a long follow-up period. Additionally, the researchers had no information about treatment during follow-up, and, therefore, could not control for it.

The findings are consistent with those of two previous cohort studies examining a possible link between HDL cholesterol levels and VTE, and raise doubts about potential antithrombotic properties of HDL particles (Blood 2008;112:2675-80; J. Thromb. Haemost. 2009;7:588-96).

Dr. Borch said that further studies are needed to determine whether the increased risk of unprovoked VTE in women is a direct result of HDL particles or of some unrecognized confounder.

Dr. Borch reported that neither he nor his colleagues had any financial disclosures relevant to the study.

BOSTON — The more women weigh, the greater their risk for incident pulmonary embolism, according to an analysis of prospective data from more than 85,000 women enrolled in the Nurses' Health Study.

The investigators found a relative risk for pulmonary embolism (PE) of 1.08 for every 1 kg/m

“We found that there is a strong, independent, positive, linear association between BMI and incident PE, and that this effect seems to impact not only obese subjects, but [also] subjects with relatively modest increases in their BMI,” reported Dr. Kabrhel, of Harvard Medical School and Massachusetts General Hospital in Boston, and his colleagues.

Cross-sectional and case-control studies have shown that patients who experience deep vein thrombosis and pulmonary embolism tend to have higher BMIs, and prospective studies have shown an association between severe overweight or obesity and pulmonary embolism, he noted.

The investigators examined the association between weight and thromboembolic events using data from 87,226 women enrolled in the prospective, longitudinal Nurses' Health Study, which has collected data on PE since its inception in 1976 and on diet, physical activity, and other risk factors for PE since 1984.

Participants enrolled in the Nurses' Health Study during 1984-2002, and were excluded from the current analysis if they had a PE diagnosis before 1984 or if their records were missing data necessary to calculate BMI.

The investigators divided participants into six BMI categories: less than 22.5 kg/m

The primary outcome was idiopathic PE, defined as cases of PE that were confirmed in the medical record and not associated with prior surgery, trauma, or malignancy. The authors also performed a secondary analysis of nonidiopathic PE. They used a multivariate Cox proportional hazards model to control for age, physical activity, caloric intake, smoking and pack-years, race, spouse's educational attainment, parity, menopausal status, NSAID use, warfarin use, multivitamin supplement use, hypertension, coronary heart disease, and rheumatologic disease.

During the period studied, there were 157 incident cases of idiopathic PE and 338 cases of nonidiopathic PE, and these correlated strongly with BMI. For both idiopathic and nonidiopathic PE, the relative risk for every 1 kg/m

Associations between BMI and nonidiopathic PE were similar, ranging from a relative risk of 1.48 for patients in the 22.5-24.9 range compared with those in the lowest BMI category, to a relative risk of 5.42 for patients in the highest vs. lowest BMI categories.

“There is a significant increase with the combined idiopathic PE and nonidiopathic PE. In other words, for our total PE, there is a significant increase in the risk of PE even with relatively modest increases in BMI—that is to say, subjects that would not be considered either overweight or obese, but within the normal range,” Dr. Kabrhel said.

In secondary analyses adjusted for all of the variables, neither waist-to-hip ratio nor weight change since age 18 were significantly associated with risk for PE.

A potential mechanism for the association between BMI and PE is the regulatory hormone leptin, which has been shown to induce tissue-factor activity in vitro and to be elevated in obese individuals, he said.

Alternatively, estrogen and progesterone, which have been linked to obesity and the risk of PE in women, may play a role, although there was no evidence of a hormone-PE interaction in their study, he said.

Dr. Kabrhel acknowledged that the study was limited by its inclusion of only women, and by the racial and ethnic imbalance of the Nurses' Health Study cohort, which represents a demographic sample of nurses in the United States. The study may also be subject to measurement bias because it relied on subject-reported weights.

The authors received grant and research support for the study from the National Institutes of Health. No other conflicts of interest were reported.

BOSTON — The more women weigh, the greater their risk for incident pulmonary embolism, according to an analysis of prospective data from more than 85,000 women enrolled in the Nurses' Health Study.

The investigators found a relative risk for pulmonary embolism (PE) of 1.08 for every 1 kg/m

“We found that there is a strong, independent, positive, linear association between BMI and incident PE, and that this effect seems to impact not only obese subjects, but [also] subjects with relatively modest increases in their BMI,” reported Dr. Kabrhel, of Harvard Medical School and Massachusetts General Hospital in Boston, and his colleagues.

Cross-sectional and case-control studies have shown that patients who experience deep vein thrombosis and pulmonary embolism tend to have higher BMIs, and prospective studies have shown an association between severe overweight or obesity and pulmonary embolism, he noted.

The investigators examined the association between weight and thromboembolic events using data from 87,226 women enrolled in the prospective, longitudinal Nurses' Health Study, which has collected data on PE since its inception in 1976 and on diet, physical activity, and other risk factors for PE since 1984.

Participants enrolled in the Nurses' Health Study during 1984-2002, and were excluded from the current analysis if they had a PE diagnosis before 1984 or if their records were missing data necessary to calculate BMI.

The investigators divided participants into six BMI categories: less than 22.5 kg/m

The primary outcome was idiopathic PE, defined as cases of PE that were confirmed in the medical record and not associated with prior surgery, trauma, or malignancy. The authors also performed a secondary analysis of nonidiopathic PE. They used a multivariate Cox proportional hazards model to control for age, physical activity, caloric intake, smoking and pack-years, race, spouse's educational attainment, parity, menopausal status, NSAID use, warfarin use, multivitamin supplement use, hypertension, coronary heart disease, and rheumatologic disease.

During the period studied, there were 157 incident cases of idiopathic PE and 338 cases of nonidiopathic PE, and these correlated strongly with BMI. For both idiopathic and nonidiopathic PE, the relative risk for every 1 kg/m

Associations between BMI and nonidiopathic PE were similar, ranging from a relative risk of 1.48 for patients in the 22.5-24.9 range compared with those in the lowest BMI category, to a relative risk of 5.42 for patients in the highest vs. lowest BMI categories.

“There is a significant increase with the combined idiopathic PE and nonidiopathic PE. In other words, for our total PE, there is a significant increase in the risk of PE even with relatively modest increases in BMI—that is to say, subjects that would not be considered either overweight or obese, but within the normal range,” Dr. Kabrhel said.

In secondary analyses adjusted for all of the variables, neither waist-to-hip ratio nor weight change since age 18 were significantly associated with risk for PE.

A potential mechanism for the association between BMI and PE is the regulatory hormone leptin, which has been shown to induce tissue-factor activity in vitro and to be elevated in obese individuals, he said.

Alternatively, estrogen and progesterone, which have been linked to obesity and the risk of PE in women, may play a role, although there was no evidence of a hormone-PE interaction in their study, he said.

Dr. Kabrhel acknowledged that the study was limited by its inclusion of only women, and by the racial and ethnic imbalance of the Nurses' Health Study cohort, which represents a demographic sample of nurses in the United States. The study may also be subject to measurement bias because it relied on subject-reported weights.

The authors received grant and research support for the study from the National Institutes of Health. No other conflicts of interest were reported.

BOSTON — The more women weigh, the greater their risk for incident pulmonary embolism, according to an analysis of prospective data from more than 85,000 women enrolled in the Nurses' Health Study.

The investigators found a relative risk for pulmonary embolism (PE) of 1.08 for every 1 kg/m

“We found that there is a strong, independent, positive, linear association between BMI and incident PE, and that this effect seems to impact not only obese subjects, but [also] subjects with relatively modest increases in their BMI,” reported Dr. Kabrhel, of Harvard Medical School and Massachusetts General Hospital in Boston, and his colleagues.

Cross-sectional and case-control studies have shown that patients who experience deep vein thrombosis and pulmonary embolism tend to have higher BMIs, and prospective studies have shown an association between severe overweight or obesity and pulmonary embolism, he noted.

The investigators examined the association between weight and thromboembolic events using data from 87,226 women enrolled in the prospective, longitudinal Nurses' Health Study, which has collected data on PE since its inception in 1976 and on diet, physical activity, and other risk factors for PE since 1984.

Participants enrolled in the Nurses' Health Study during 1984-2002, and were excluded from the current analysis if they had a PE diagnosis before 1984 or if their records were missing data necessary to calculate BMI.

The investigators divided participants into six BMI categories: less than 22.5 kg/m

The primary outcome was idiopathic PE, defined as cases of PE that were confirmed in the medical record and not associated with prior surgery, trauma, or malignancy. The authors also performed a secondary analysis of nonidiopathic PE. They used a multivariate Cox proportional hazards model to control for age, physical activity, caloric intake, smoking and pack-years, race, spouse's educational attainment, parity, menopausal status, NSAID use, warfarin use, multivitamin supplement use, hypertension, coronary heart disease, and rheumatologic disease.

During the period studied, there were 157 incident cases of idiopathic PE and 338 cases of nonidiopathic PE, and these correlated strongly with BMI. For both idiopathic and nonidiopathic PE, the relative risk for every 1 kg/m

Associations between BMI and nonidiopathic PE were similar, ranging from a relative risk of 1.48 for patients in the 22.5-24.9 range compared with those in the lowest BMI category, to a relative risk of 5.42 for patients in the highest vs. lowest BMI categories.

“There is a significant increase with the combined idiopathic PE and nonidiopathic PE. In other words, for our total PE, there is a significant increase in the risk of PE even with relatively modest increases in BMI—that is to say, subjects that would not be considered either overweight or obese, but within the normal range,” Dr. Kabrhel said.

In secondary analyses adjusted for all of the variables, neither waist-to-hip ratio nor weight change since age 18 were significantly associated with risk for PE.

A potential mechanism for the association between BMI and PE is the regulatory hormone leptin, which has been shown to induce tissue-factor activity in vitro and to be elevated in obese individuals, he said.

Alternatively, estrogen and progesterone, which have been linked to obesity and the risk of PE in women, may play a role, although there was no evidence of a hormone-PE interaction in their study, he said.

Dr. Kabrhel acknowledged that the study was limited by its inclusion of only women, and by the racial and ethnic imbalance of the Nurses' Health Study cohort, which represents a demographic sample of nurses in the United States. The study may also be subject to measurement bias because it relied on subject-reported weights.

The authors received grant and research support for the study from the National Institutes of Health. No other conflicts of interest were reported.

BOSTON — Proponents of the Atkins low-carbohydrate/high saturated fat diet say that you can have your steak and eat it, too, and still lose weight.

But the adverse metabolic consequences are too heavy a price to pay, Australian investigators reported at a symposium sponsored by the International Atherosclerosis Society.

After 1 year, overweight and obese patients randomly assigned to the Atkins diet or to a low-saturated-fat, high-carbohydrate diet lost similar amounts of weight. But patients on the Atkins diet had a deterioration in flow-mediated arterial dilatation, a marker for cardiovascular disease, and higher levels of LDL cholesterol than at baseline, reported Dr. Peter Clifton of the Commonwealth Scientific and Industrial Research Organization in Adelaide, South Australia.

“What I really want to know is, does the early elevation of HDL, which has been shown convincingly [with the Atkins diet], and lowering of triglycerides plus the lowering of blood pressure and glucose, outweigh the rise in LDL cholesterol that you see in some individuals in some studies?” said Dr. Clifton.

He and colleagues analyzed the effects of two diets on flow-mediated dilatation (FMD), a measurement of the ability of blood vessels to dilate in response to increases in blood flow. FMD is reduced in both cardiovascular disease and diabetes, but whether it improves with significant weight loss is unclear; if so, it might be related to either decreases in glucose or in LDL, Dr. Clifton said.

The study's aim was to evaluate the effects on markers of endothelial dysfunction and cardiovascular disease risk of a very-low-carbohydrate/high-saturated-fat diet, and an isocaloric high-carbohydrate/low-saturated-fat diet.

The outcomes were FMD and markers of endothelial dysfunction, including cellular adhesion molecules, inhibitors and promoters of fibrinolysis, adiponectin, glucose, insulin, C-reactive protein (CRP), lipids, and apolipoprotein B.

The study involved 70 men and women aged 16-60 years with body mass index between 27 and 40 kg/m

After 1 year, the 33 patients on the Atkins diet lost slightly more weight on average (14.5 kg), than did the 36 patients on the low-fat diet (11.5 kg), but this difference was not significant.

There was no diet-specific effect on blood pressure, glucose, insulin or CRP, but the Atkins diet was superior to the low-fat diet at decreasing triglycerides and increasing HDL. The Atkins diet also was associated with increases in LDL levels.

Overall, 49 patients (26 on the Atkins diet, 23 on the low-fat diet) underwent FMD assessment. Endothelial function decreased by almost half from baseline among patients in the Atkins diet, compared with no change among patients on the low-fat diet. “Overall, FMD deteriorated after 12 months on a high-saturated-fat Atkins diet, despite their fantastic weight loss and improvement in all those other things,” Dr. Clifton said. “Solely because the LDL increased, it outweighed all the other measures of weight loss. The other measures of endothelial function that we took actually improved except ICAM-1 on the Atkins diet, so there seems to be a separation of endothelial functions as expressed by nitric oxide and these other endothelial markers.

“This really calls into question that fantastic elevation of HDL [with the Atkins diet] as being a good thing or having anything much to do with cardiovascular health,” he added.

Dr. Clifton disclosed that he has coauthored diet books, but they do not include the information he presented.

The meat-heavy Atkins diet increased both HDL and LDL cholesterol.

Source ©Graça Victoria/Fotolia.com

BOSTON — Proponents of the Atkins low-carbohydrate/high saturated fat diet say that you can have your steak and eat it, too, and still lose weight.

But the adverse metabolic consequences are too heavy a price to pay, Australian investigators reported at a symposium sponsored by the International Atherosclerosis Society.

After 1 year, overweight and obese patients randomly assigned to the Atkins diet or to a low-saturated-fat, high-carbohydrate diet lost similar amounts of weight. But patients on the Atkins diet had a deterioration in flow-mediated arterial dilatation, a marker for cardiovascular disease, and higher levels of LDL cholesterol than at baseline, reported Dr. Peter Clifton of the Commonwealth Scientific and Industrial Research Organization in Adelaide, South Australia.

“What I really want to know is, does the early elevation of HDL, which has been shown convincingly [with the Atkins diet], and lowering of triglycerides plus the lowering of blood pressure and glucose, outweigh the rise in LDL cholesterol that you see in some individuals in some studies?” said Dr. Clifton.

He and colleagues analyzed the effects of two diets on flow-mediated dilatation (FMD), a measurement of the ability of blood vessels to dilate in response to increases in blood flow. FMD is reduced in both cardiovascular disease and diabetes, but whether it improves with significant weight loss is unclear; if so, it might be related to either decreases in glucose or in LDL, Dr. Clifton said.

The study's aim was to evaluate the effects on markers of endothelial dysfunction and cardiovascular disease risk of a very-low-carbohydrate/high-saturated-fat diet, and an isocaloric high-carbohydrate/low-saturated-fat diet.

The outcomes were FMD and markers of endothelial dysfunction, including cellular adhesion molecules, inhibitors and promoters of fibrinolysis, adiponectin, glucose, insulin, C-reactive protein (CRP), lipids, and apolipoprotein B.

The study involved 70 men and women aged 16-60 years with body mass index between 27 and 40 kg/m

After 1 year, the 33 patients on the Atkins diet lost slightly more weight on average (14.5 kg), than did the 36 patients on the low-fat diet (11.5 kg), but this difference was not significant.

There was no diet-specific effect on blood pressure, glucose, insulin or CRP, but the Atkins diet was superior to the low-fat diet at decreasing triglycerides and increasing HDL. The Atkins diet also was associated with increases in LDL levels.

Overall, 49 patients (26 on the Atkins diet, 23 on the low-fat diet) underwent FMD assessment. Endothelial function decreased by almost half from baseline among patients in the Atkins diet, compared with no change among patients on the low-fat diet. “Overall, FMD deteriorated after 12 months on a high-saturated-fat Atkins diet, despite their fantastic weight loss and improvement in all those other things,” Dr. Clifton said. “Solely because the LDL increased, it outweighed all the other measures of weight loss. The other measures of endothelial function that we took actually improved except ICAM-1 on the Atkins diet, so there seems to be a separation of endothelial functions as expressed by nitric oxide and these other endothelial markers.

“This really calls into question that fantastic elevation of HDL [with the Atkins diet] as being a good thing or having anything much to do with cardiovascular health,” he added.

Dr. Clifton disclosed that he has coauthored diet books, but they do not include the information he presented.

The meat-heavy Atkins diet increased both HDL and LDL cholesterol.

Source ©Graça Victoria/Fotolia.com

BOSTON — Proponents of the Atkins low-carbohydrate/high saturated fat diet say that you can have your steak and eat it, too, and still lose weight.

But the adverse metabolic consequences are too heavy a price to pay, Australian investigators reported at a symposium sponsored by the International Atherosclerosis Society.

After 1 year, overweight and obese patients randomly assigned to the Atkins diet or to a low-saturated-fat, high-carbohydrate diet lost similar amounts of weight. But patients on the Atkins diet had a deterioration in flow-mediated arterial dilatation, a marker for cardiovascular disease, and higher levels of LDL cholesterol than at baseline, reported Dr. Peter Clifton of the Commonwealth Scientific and Industrial Research Organization in Adelaide, South Australia.

“What I really want to know is, does the early elevation of HDL, which has been shown convincingly [with the Atkins diet], and lowering of triglycerides plus the lowering of blood pressure and glucose, outweigh the rise in LDL cholesterol that you see in some individuals in some studies?” said Dr. Clifton.

He and colleagues analyzed the effects of two diets on flow-mediated dilatation (FMD), a measurement of the ability of blood vessels to dilate in response to increases in blood flow. FMD is reduced in both cardiovascular disease and diabetes, but whether it improves with significant weight loss is unclear; if so, it might be related to either decreases in glucose or in LDL, Dr. Clifton said.

The study's aim was to evaluate the effects on markers of endothelial dysfunction and cardiovascular disease risk of a very-low-carbohydrate/high-saturated-fat diet, and an isocaloric high-carbohydrate/low-saturated-fat diet.

The outcomes were FMD and markers of endothelial dysfunction, including cellular adhesion molecules, inhibitors and promoters of fibrinolysis, adiponectin, glucose, insulin, C-reactive protein (CRP), lipids, and apolipoprotein B.

The study involved 70 men and women aged 16-60 years with body mass index between 27 and 40 kg/m

After 1 year, the 33 patients on the Atkins diet lost slightly more weight on average (14.5 kg), than did the 36 patients on the low-fat diet (11.5 kg), but this difference was not significant.

There was no diet-specific effect on blood pressure, glucose, insulin or CRP, but the Atkins diet was superior to the low-fat diet at decreasing triglycerides and increasing HDL. The Atkins diet also was associated with increases in LDL levels.

Overall, 49 patients (26 on the Atkins diet, 23 on the low-fat diet) underwent FMD assessment. Endothelial function decreased by almost half from baseline among patients in the Atkins diet, compared with no change among patients on the low-fat diet. “Overall, FMD deteriorated after 12 months on a high-saturated-fat Atkins diet, despite their fantastic weight loss and improvement in all those other things,” Dr. Clifton said. “Solely because the LDL increased, it outweighed all the other measures of weight loss. The other measures of endothelial function that we took actually improved except ICAM-1 on the Atkins diet, so there seems to be a separation of endothelial functions as expressed by nitric oxide and these other endothelial markers.

“This really calls into question that fantastic elevation of HDL [with the Atkins diet] as being a good thing or having anything much to do with cardiovascular health,” he added.

Dr. Clifton disclosed that he has coauthored diet books, but they do not include the information he presented.

The meat-heavy Atkins diet increased both HDL and LDL cholesterol.

Source ©Graça Victoria/Fotolia.com

BOSTON — Nonfasting lipid status may be a better marker for impaired lipid metabolism than fasting lipids, according to a prospective study.

The findings suggest that patients need not deny themselves a good breakfast or lunch before having their blood drawn for plasma lipid testing.

Dr. István Reiber and Dr. Izabella Mezõ from the Szent György Hospital in Székesfehérvár, Hungary, compared fasting and postprandial lipid levels among 102 nondiabetic patients (44 men), and found that the only significant differences in any lipid parameters were between fasting and nonfasting triglycerides.

It is well known that there are no significant changes in total cholesterol and HDL cholesterol levels between the fasting and postprandial state.

In addition, recent study findings suggest that nonfasting triglyceride concentrations in plasma are more predictive of cardiovascular events than are conventional measures of fasting triglycerides, the investigators wrote in a scientific poster presented at a symposium sponsored by the International Atherosclerosis Society.

The study participants had never received lipid-lowering drugs. They underwent separate venous blood draws following an overnight fast, 3 hours after eating their usual breakfasts, and 3 hours after their usual lunches.

Overall, the total cholesterol in the fasting state was 5.51 mmol/L, compared with 5.48 mmol/L after breakfast, and 5.69 mmol/L after lunch, a difference that was not significant.

HDL levels also were comparable between the fasting and postprandial states, at 1.12 mmol/L, 1.14 mmol/L (breakfast), and 1.20 mmol/L (lunch), respectively. Triglyceride levels, however, were significantly higher after eating, rising from 2.21 mmol/L in the fasting state, to 2.31 mmol/L after breakfast, and 2.94 mmol/L after lunch.

The researchers also found that both postprandial triglyceride measures correlated significantly with fasting triglycerides. All volunteers who had fasting triglyceride levels below 1.5 mmol/L had postprandial triglyceride levels below 2.0 mmol/L.

Neither of the investigators disclosed relevant conflicts of interest.

BOSTON — Nonfasting lipid status may be a better marker for impaired lipid metabolism than fasting lipids, according to a prospective study.

The findings suggest that patients need not deny themselves a good breakfast or lunch before having their blood drawn for plasma lipid testing.

Dr. István Reiber and Dr. Izabella Mezõ from the Szent György Hospital in Székesfehérvár, Hungary, compared fasting and postprandial lipid levels among 102 nondiabetic patients (44 men), and found that the only significant differences in any lipid parameters were between fasting and nonfasting triglycerides.

It is well known that there are no significant changes in total cholesterol and HDL cholesterol levels between the fasting and postprandial state.

In addition, recent study findings suggest that nonfasting triglyceride concentrations in plasma are more predictive of cardiovascular events than are conventional measures of fasting triglycerides, the investigators wrote in a scientific poster presented at a symposium sponsored by the International Atherosclerosis Society.

The study participants had never received lipid-lowering drugs. They underwent separate venous blood draws following an overnight fast, 3 hours after eating their usual breakfasts, and 3 hours after their usual lunches.

Overall, the total cholesterol in the fasting state was 5.51 mmol/L, compared with 5.48 mmol/L after breakfast, and 5.69 mmol/L after lunch, a difference that was not significant.

HDL levels also were comparable between the fasting and postprandial states, at 1.12 mmol/L, 1.14 mmol/L (breakfast), and 1.20 mmol/L (lunch), respectively. Triglyceride levels, however, were significantly higher after eating, rising from 2.21 mmol/L in the fasting state, to 2.31 mmol/L after breakfast, and 2.94 mmol/L after lunch.

The researchers also found that both postprandial triglyceride measures correlated significantly with fasting triglycerides. All volunteers who had fasting triglyceride levels below 1.5 mmol/L had postprandial triglyceride levels below 2.0 mmol/L.

Neither of the investigators disclosed relevant conflicts of interest.

BOSTON — Nonfasting lipid status may be a better marker for impaired lipid metabolism than fasting lipids, according to a prospective study.

The findings suggest that patients need not deny themselves a good breakfast or lunch before having their blood drawn for plasma lipid testing.

Dr. István Reiber and Dr. Izabella Mezõ from the Szent György Hospital in Székesfehérvár, Hungary, compared fasting and postprandial lipid levels among 102 nondiabetic patients (44 men), and found that the only significant differences in any lipid parameters were between fasting and nonfasting triglycerides.

It is well known that there are no significant changes in total cholesterol and HDL cholesterol levels between the fasting and postprandial state.

In addition, recent study findings suggest that nonfasting triglyceride concentrations in plasma are more predictive of cardiovascular events than are conventional measures of fasting triglycerides, the investigators wrote in a scientific poster presented at a symposium sponsored by the International Atherosclerosis Society.

The study participants had never received lipid-lowering drugs. They underwent separate venous blood draws following an overnight fast, 3 hours after eating their usual breakfasts, and 3 hours after their usual lunches.

Overall, the total cholesterol in the fasting state was 5.51 mmol/L, compared with 5.48 mmol/L after breakfast, and 5.69 mmol/L after lunch, a difference that was not significant.

HDL levels also were comparable between the fasting and postprandial states, at 1.12 mmol/L, 1.14 mmol/L (breakfast), and 1.20 mmol/L (lunch), respectively. Triglyceride levels, however, were significantly higher after eating, rising from 2.21 mmol/L in the fasting state, to 2.31 mmol/L after breakfast, and 2.94 mmol/L after lunch.

The researchers also found that both postprandial triglyceride measures correlated significantly with fasting triglycerides. All volunteers who had fasting triglyceride levels below 1.5 mmol/L had postprandial triglyceride levels below 2.0 mmol/L.

Neither of the investigators disclosed relevant conflicts of interest.