Anticoagulation Hub

Hormone therapy in postmenopausal women does not prevent heart disease but does increase the risk of stroke and blood clots, according to a recently updated Cochrane review.

“Our review findings provide strong evidence that treatment with hormone therapy in postmenopausal women for either primary or secondary prevention of cardiovascular disease events has little if any benefit overall, and causes an increase in the risk of stroke, or venous thromboembolic events,” reported Dr. Henry Boardman of the University of Oxford John Radcliffe Hospital, and his associates.

The researchers updated a review published in 2013 with data from an additional six randomized controlled trials. The total of 19 trials, involving 40,410 postmenopausal women, all compared orally-administered estrogen, with or without progestogen, to a placebo or no treatment for a minimum of 6 months (Cochrane Database Syst. Rev. 2015 March 10 [doi:10.1002/14651858.CD002229.pub4]).

The average age of the women in the studies, mostly from the United States, was older than 60 years, and the women received hormone therapy anywhere from 7 months to 10 years across the studies. The overall quality of the studies was “good” with a low risk of bias.

The sharp rise in cardiovascular disease rates in women after menopause had been hypothesized to be related to a decline in hormone levels that causes a higher androgen-to-estradiol ratio, and observational studies starting in the 1980s showed lower mortality rates and cardiovascular events in women receiving hormone therapy – previously called hormone replacement therapy – compared to those not receiving hormone therapy.

Two subsequent randomized controlled trials contradicted these observational findings, though, leading to further study. In this review, hormone therapy showed no risk reduction for all-cause mortality, cardiovascular death, nonfatal myocardial infarction, angina, or revascularization.

However, the overall risk of stroke for those receiving hormone therapy for both primary and secondary prevention was 24% higher than that of women receiving placebo treatment (relative risk 1.24), with an absolute risk of 6 additional strokes per 1,000 women.

Venous thromboembolic events occurred 92% more and pulmonary emboli occurred 81% more in the hormone treatment groups (RR 1.92 and 1.81, respectively), with increased absolute risks of 8 per 1,000 women and 4 per 1,000 women, respectively.

The researchers calculated the number needed to treat for an additional harm (NNTH) at 165 women for stroke, 118 for venous thromboembolism, and 242 for pulmonary embolism.

Further analysis revealed that the relative risks or protection hormone therapy conferred depended on how long after menopause women started treatment.

Mortality was reduced 30% and coronary heart disease was reduced 48% in women who began hormone therapy less than 10 years after menopause (RR 0.70 and RR 0.52, respectively); these women still faced a 74% increased risk of venous thromboembolism, but no increased risk of stroke.

Meanwhile, women who started hormone therapy more than 10 years after menopause had a 21% increased risk of stroke and a 96% increased risk of venous thromboembolism, but no reduced risk on overall death or coronary heart disease.

“It is worth noting that the benefit seen in survival and coronary heart disease for the group starting treatment less than 10 years after the menopause is from combining five trials all performed in primary prevention populations and all with quite long follow-up, ranging from 3.4 to 10.1 years,” the authors wrote.

These results may reflect the possibility of a time interaction, with coronary heart disease events occurring earlier in predisposed women, making it impossible to say whether short duration therapy is beneficial in this population or not, the researchers wrote .

Eighteen of the 19 trials included in the analysis reported the funding source. One study was exclusively funded by Wyeth-Ayerst. Two studies received partial funding from Novo-Nordisk Pharmaceutical, and one study was funded by the National Institutes of Health with support from Wyeth-Ayerst, Hoffman-LaRoche, Pharmacia, and Upjohn. Eight other studies used medication provided by various pharmaceutical companies.

Hormone therapy in postmenopausal women does not prevent heart disease but does increase the risk of stroke and blood clots, according to a recently updated Cochrane review.

“Our review findings provide strong evidence that treatment with hormone therapy in postmenopausal women for either primary or secondary prevention of cardiovascular disease events has little if any benefit overall, and causes an increase in the risk of stroke, or venous thromboembolic events,” reported Dr. Henry Boardman of the University of Oxford John Radcliffe Hospital, and his associates.

The researchers updated a review published in 2013 with data from an additional six randomized controlled trials. The total of 19 trials, involving 40,410 postmenopausal women, all compared orally-administered estrogen, with or without progestogen, to a placebo or no treatment for a minimum of 6 months (Cochrane Database Syst. Rev. 2015 March 10 [doi:10.1002/14651858.CD002229.pub4]).

The average age of the women in the studies, mostly from the United States, was older than 60 years, and the women received hormone therapy anywhere from 7 months to 10 years across the studies. The overall quality of the studies was “good” with a low risk of bias.

The sharp rise in cardiovascular disease rates in women after menopause had been hypothesized to be related to a decline in hormone levels that causes a higher androgen-to-estradiol ratio, and observational studies starting in the 1980s showed lower mortality rates and cardiovascular events in women receiving hormone therapy – previously called hormone replacement therapy – compared to those not receiving hormone therapy.

Two subsequent randomized controlled trials contradicted these observational findings, though, leading to further study. In this review, hormone therapy showed no risk reduction for all-cause mortality, cardiovascular death, nonfatal myocardial infarction, angina, or revascularization.

However, the overall risk of stroke for those receiving hormone therapy for both primary and secondary prevention was 24% higher than that of women receiving placebo treatment (relative risk 1.24), with an absolute risk of 6 additional strokes per 1,000 women.

Venous thromboembolic events occurred 92% more and pulmonary emboli occurred 81% more in the hormone treatment groups (RR 1.92 and 1.81, respectively), with increased absolute risks of 8 per 1,000 women and 4 per 1,000 women, respectively.

The researchers calculated the number needed to treat for an additional harm (NNTH) at 165 women for stroke, 118 for venous thromboembolism, and 242 for pulmonary embolism.

Further analysis revealed that the relative risks or protection hormone therapy conferred depended on how long after menopause women started treatment.

Mortality was reduced 30% and coronary heart disease was reduced 48% in women who began hormone therapy less than 10 years after menopause (RR 0.70 and RR 0.52, respectively); these women still faced a 74% increased risk of venous thromboembolism, but no increased risk of stroke.

Meanwhile, women who started hormone therapy more than 10 years after menopause had a 21% increased risk of stroke and a 96% increased risk of venous thromboembolism, but no reduced risk on overall death or coronary heart disease.

“It is worth noting that the benefit seen in survival and coronary heart disease for the group starting treatment less than 10 years after the menopause is from combining five trials all performed in primary prevention populations and all with quite long follow-up, ranging from 3.4 to 10.1 years,” the authors wrote.

These results may reflect the possibility of a time interaction, with coronary heart disease events occurring earlier in predisposed women, making it impossible to say whether short duration therapy is beneficial in this population or not, the researchers wrote .

Eighteen of the 19 trials included in the analysis reported the funding source. One study was exclusively funded by Wyeth-Ayerst. Two studies received partial funding from Novo-Nordisk Pharmaceutical, and one study was funded by the National Institutes of Health with support from Wyeth-Ayerst, Hoffman-LaRoche, Pharmacia, and Upjohn. Eight other studies used medication provided by various pharmaceutical companies.

Hormone therapy in postmenopausal women does not prevent heart disease but does increase the risk of stroke and blood clots, according to a recently updated Cochrane review.

“Our review findings provide strong evidence that treatment with hormone therapy in postmenopausal women for either primary or secondary prevention of cardiovascular disease events has little if any benefit overall, and causes an increase in the risk of stroke, or venous thromboembolic events,” reported Dr. Henry Boardman of the University of Oxford John Radcliffe Hospital, and his associates.

The researchers updated a review published in 2013 with data from an additional six randomized controlled trials. The total of 19 trials, involving 40,410 postmenopausal women, all compared orally-administered estrogen, with or without progestogen, to a placebo or no treatment for a minimum of 6 months (Cochrane Database Syst. Rev. 2015 March 10 [doi:10.1002/14651858.CD002229.pub4]).

The average age of the women in the studies, mostly from the United States, was older than 60 years, and the women received hormone therapy anywhere from 7 months to 10 years across the studies. The overall quality of the studies was “good” with a low risk of bias.

The sharp rise in cardiovascular disease rates in women after menopause had been hypothesized to be related to a decline in hormone levels that causes a higher androgen-to-estradiol ratio, and observational studies starting in the 1980s showed lower mortality rates and cardiovascular events in women receiving hormone therapy – previously called hormone replacement therapy – compared to those not receiving hormone therapy.

Two subsequent randomized controlled trials contradicted these observational findings, though, leading to further study. In this review, hormone therapy showed no risk reduction for all-cause mortality, cardiovascular death, nonfatal myocardial infarction, angina, or revascularization.

However, the overall risk of stroke for those receiving hormone therapy for both primary and secondary prevention was 24% higher than that of women receiving placebo treatment (relative risk 1.24), with an absolute risk of 6 additional strokes per 1,000 women.

Venous thromboembolic events occurred 92% more and pulmonary emboli occurred 81% more in the hormone treatment groups (RR 1.92 and 1.81, respectively), with increased absolute risks of 8 per 1,000 women and 4 per 1,000 women, respectively.

The researchers calculated the number needed to treat for an additional harm (NNTH) at 165 women for stroke, 118 for venous thromboembolism, and 242 for pulmonary embolism.

Further analysis revealed that the relative risks or protection hormone therapy conferred depended on how long after menopause women started treatment.

Mortality was reduced 30% and coronary heart disease was reduced 48% in women who began hormone therapy less than 10 years after menopause (RR 0.70 and RR 0.52, respectively); these women still faced a 74% increased risk of venous thromboembolism, but no increased risk of stroke.

Meanwhile, women who started hormone therapy more than 10 years after menopause had a 21% increased risk of stroke and a 96% increased risk of venous thromboembolism, but no reduced risk on overall death or coronary heart disease.

“It is worth noting that the benefit seen in survival and coronary heart disease for the group starting treatment less than 10 years after the menopause is from combining five trials all performed in primary prevention populations and all with quite long follow-up, ranging from 3.4 to 10.1 years,” the authors wrote.

These results may reflect the possibility of a time interaction, with coronary heart disease events occurring earlier in predisposed women, making it impossible to say whether short duration therapy is beneficial in this population or not, the researchers wrote .

Eighteen of the 19 trials included in the analysis reported the funding source. One study was exclusively funded by Wyeth-Ayerst. Two studies received partial funding from Novo-Nordisk Pharmaceutical, and one study was funded by the National Institutes of Health with support from Wyeth-Ayerst, Hoffman-LaRoche, Pharmacia, and Upjohn. Eight other studies used medication provided by various pharmaceutical companies.

Venous thromboembolisms affected 6.4% of patients who underwent radical cystectomy, even though all patients received heparin in the hospital as recommended by the American Urological Association, researchers reported.

“Using an in-house, heparin-based anticoagulation protocol consistent with current AUA guidelines has not decreased the rate of venous thromboembolism compared to historical warfarin use,” wrote Dr. Andrew Sun and his colleagues at the University of Southern California Institute of Urology in Los Angeles. Most episodes of VTE occurred after patients were discharged home, and “future studies are needed to establish the benefits of extended-duration [VTE] prophylaxis regimens that cover the critical posthospitalization period,” the researchers added (J. UroL 2015;193:565-9).

Previous studies have reported venous thromboembolism rates of 3%-6% in cystectomy patients, a rate that is more than double that reported for nephrectomy or prostatectomy patients. For their study, the investigators retrospectively assessed 2,316 patients who underwent open radical cystectomy and extended pelvic lymph node dissection for urothelial bladder cancer between 1971 and 2012. Symptomatic VTE developed among 109 patients overall (4.7%), compared with 6.4% of those who received the modern, heparin-based protocol implemented in 2009 (P = .089).

Furthermore, 58% of all cases occurred after patients stopped anticoagulation therapy and were discharged home. The median time of onset was 20 days after surgery (range, 2-91 days), and VTE was significantly more common among patients with a higher body mass index, prolonged hospital stays, positive surgical margins and orthotopic diversion procedures, compared with other patients. Surgical techniques remained consistent throughout the study.

The study was retrospective, and thus “could not prove any cause and effect relationships. This underscores the need for additional prospective data in this area of research,” said the investigators. “We focused only on open radical cystectomy, and thus, findings may not be generalizable to minimally invasive modalities, on which there is even a greater paucity of data.”

Senior author Dr. Siamak Daneshmand reported financial or other relationships with Endo and Cubist. The authors reported no funding sources or other relevant conflicts of interest.

Venous thromboembolisms affected 6.4% of patients who underwent radical cystectomy, even though all patients received heparin in the hospital as recommended by the American Urological Association, researchers reported.

“Using an in-house, heparin-based anticoagulation protocol consistent with current AUA guidelines has not decreased the rate of venous thromboembolism compared to historical warfarin use,” wrote Dr. Andrew Sun and his colleagues at the University of Southern California Institute of Urology in Los Angeles. Most episodes of VTE occurred after patients were discharged home, and “future studies are needed to establish the benefits of extended-duration [VTE] prophylaxis regimens that cover the critical posthospitalization period,” the researchers added (J. UroL 2015;193:565-9).

Previous studies have reported venous thromboembolism rates of 3%-6% in cystectomy patients, a rate that is more than double that reported for nephrectomy or prostatectomy patients. For their study, the investigators retrospectively assessed 2,316 patients who underwent open radical cystectomy and extended pelvic lymph node dissection for urothelial bladder cancer between 1971 and 2012. Symptomatic VTE developed among 109 patients overall (4.7%), compared with 6.4% of those who received the modern, heparin-based protocol implemented in 2009 (P = .089).

Furthermore, 58% of all cases occurred after patients stopped anticoagulation therapy and were discharged home. The median time of onset was 20 days after surgery (range, 2-91 days), and VTE was significantly more common among patients with a higher body mass index, prolonged hospital stays, positive surgical margins and orthotopic diversion procedures, compared with other patients. Surgical techniques remained consistent throughout the study.

The study was retrospective, and thus “could not prove any cause and effect relationships. This underscores the need for additional prospective data in this area of research,” said the investigators. “We focused only on open radical cystectomy, and thus, findings may not be generalizable to minimally invasive modalities, on which there is even a greater paucity of data.”

Senior author Dr. Siamak Daneshmand reported financial or other relationships with Endo and Cubist. The authors reported no funding sources or other relevant conflicts of interest.

Venous thromboembolisms affected 6.4% of patients who underwent radical cystectomy, even though all patients received heparin in the hospital as recommended by the American Urological Association, researchers reported.

“Using an in-house, heparin-based anticoagulation protocol consistent with current AUA guidelines has not decreased the rate of venous thromboembolism compared to historical warfarin use,” wrote Dr. Andrew Sun and his colleagues at the University of Southern California Institute of Urology in Los Angeles. Most episodes of VTE occurred after patients were discharged home, and “future studies are needed to establish the benefits of extended-duration [VTE] prophylaxis regimens that cover the critical posthospitalization period,” the researchers added (J. UroL 2015;193:565-9).

Previous studies have reported venous thromboembolism rates of 3%-6% in cystectomy patients, a rate that is more than double that reported for nephrectomy or prostatectomy patients. For their study, the investigators retrospectively assessed 2,316 patients who underwent open radical cystectomy and extended pelvic lymph node dissection for urothelial bladder cancer between 1971 and 2012. Symptomatic VTE developed among 109 patients overall (4.7%), compared with 6.4% of those who received the modern, heparin-based protocol implemented in 2009 (P = .089).

Furthermore, 58% of all cases occurred after patients stopped anticoagulation therapy and were discharged home. The median time of onset was 20 days after surgery (range, 2-91 days), and VTE was significantly more common among patients with a higher body mass index, prolonged hospital stays, positive surgical margins and orthotopic diversion procedures, compared with other patients. Surgical techniques remained consistent throughout the study.

The study was retrospective, and thus “could not prove any cause and effect relationships. This underscores the need for additional prospective data in this area of research,” said the investigators. “We focused only on open radical cystectomy, and thus, findings may not be generalizable to minimally invasive modalities, on which there is even a greater paucity of data.”

Senior author Dr. Siamak Daneshmand reported financial or other relationships with Endo and Cubist. The authors reported no funding sources or other relevant conflicts of interest.

Patients with coronary heart disease who have both depression and stress are at increased risk of myocardial infarction and death, according to findings from a large, prospective, cohort study.

Of 4,487 adults with CHD who were part of the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, 1,337 experienced MI or death during a median of nearly 6 years of follow-up. Those with both high depressive symptoms and high stress at baseline – about 6% of the study population – were at significantly increased risk of such events (adjusted hazard ratio, 1.48) during the first 2.5 years of follow-up, compared with those with low stress and low depressive symptoms. However, the association was not significant beyond the initial 2.5 years (HR, 0.89), Carmela Alcántara, Ph.D., of Columbia University, New York, and her colleagues reported.

Those with low stress and high depressive symptoms, and those with high stress and low depressive symptoms, were not at increased risk (HR, 0.92 and 0.86, respectively) at any point during follow-up (Circ. Cardiovasc. Qual. Outcomes 2015 March 10 [doi:10.1161/IRCOUTCOMES.114.001180]).

The findings provide initial empirical evidence to support a “psychosocial perfect storm conceptual model” based on the idea that it takes an underlying chronic psychosocial vulnerability such as depression along with a more transient state such as psychological stress to precipitate a clinical event. The confluence of these factors may be particularly destructive in the short term, the investigators concluded, noting that the findings could have implications for the development of preventive treatments that focus on depression and stress during this vulnerable period in CHD patients.

The National Institute of Neurological Disorders and Stroke and the National Heart, Lung, and Blood Institute supported the study. Dr. Alcantara reported having no disclosures, but two other authors received salary support from Amgen for research, and one served as a consultant for DiaDexus.

Patients with coronary heart disease who have both depression and stress are at increased risk of myocardial infarction and death, according to findings from a large, prospective, cohort study.

Of 4,487 adults with CHD who were part of the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, 1,337 experienced MI or death during a median of nearly 6 years of follow-up. Those with both high depressive symptoms and high stress at baseline – about 6% of the study population – were at significantly increased risk of such events (adjusted hazard ratio, 1.48) during the first 2.5 years of follow-up, compared with those with low stress and low depressive symptoms. However, the association was not significant beyond the initial 2.5 years (HR, 0.89), Carmela Alcántara, Ph.D., of Columbia University, New York, and her colleagues reported.

Those with low stress and high depressive symptoms, and those with high stress and low depressive symptoms, were not at increased risk (HR, 0.92 and 0.86, respectively) at any point during follow-up (Circ. Cardiovasc. Qual. Outcomes 2015 March 10 [doi:10.1161/IRCOUTCOMES.114.001180]).

The findings provide initial empirical evidence to support a “psychosocial perfect storm conceptual model” based on the idea that it takes an underlying chronic psychosocial vulnerability such as depression along with a more transient state such as psychological stress to precipitate a clinical event. The confluence of these factors may be particularly destructive in the short term, the investigators concluded, noting that the findings could have implications for the development of preventive treatments that focus on depression and stress during this vulnerable period in CHD patients.

The National Institute of Neurological Disorders and Stroke and the National Heart, Lung, and Blood Institute supported the study. Dr. Alcantara reported having no disclosures, but two other authors received salary support from Amgen for research, and one served as a consultant for DiaDexus.

Patients with coronary heart disease who have both depression and stress are at increased risk of myocardial infarction and death, according to findings from a large, prospective, cohort study.

Of 4,487 adults with CHD who were part of the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, 1,337 experienced MI or death during a median of nearly 6 years of follow-up. Those with both high depressive symptoms and high stress at baseline – about 6% of the study population – were at significantly increased risk of such events (adjusted hazard ratio, 1.48) during the first 2.5 years of follow-up, compared with those with low stress and low depressive symptoms. However, the association was not significant beyond the initial 2.5 years (HR, 0.89), Carmela Alcántara, Ph.D., of Columbia University, New York, and her colleagues reported.

Those with low stress and high depressive symptoms, and those with high stress and low depressive symptoms, were not at increased risk (HR, 0.92 and 0.86, respectively) at any point during follow-up (Circ. Cardiovasc. Qual. Outcomes 2015 March 10 [doi:10.1161/IRCOUTCOMES.114.001180]).

The findings provide initial empirical evidence to support a “psychosocial perfect storm conceptual model” based on the idea that it takes an underlying chronic psychosocial vulnerability such as depression along with a more transient state such as psychological stress to precipitate a clinical event. The confluence of these factors may be particularly destructive in the short term, the investigators concluded, noting that the findings could have implications for the development of preventive treatments that focus on depression and stress during this vulnerable period in CHD patients.

The National Institute of Neurological Disorders and Stroke and the National Heart, Lung, and Blood Institute supported the study. Dr. Alcantara reported having no disclosures, but two other authors received salary support from Amgen for research, and one served as a consultant for DiaDexus.

For every 1,000 patients who underwent heart transplantation, about 45 had an episode of venous thromboembolism within a year after surgery, according to a retrospective study reported in the February issue of the Journal of Heart and Lung Transplantation.

Furthermore, patients who had a single VTE episode after transplant had a “high” risk of recurrent VTE, said Dr. Rolando Alvarez, a cardiologist at Complejo Hospitalario Universitario A Coruna in A Coruna, Spain, and his associates.

“Our opinion is that long-term oral anticoagulation should be maintained in these patients, especially if other risk factors are present and provided that the bleeding risk is not excessive,” said the researchers.

Venous thromboembolism is a common complication of lung, kidney, and liver transplantation, but less is known about VTE after heart transplant. The researchers found that “classic” risk factors for VTE, such as being older, obese, or having renal dysfunction, also increased the risk of VTE after heart transplant (J. Heart Lung Transplant. 2015;34:167-74).

The study included data from 635 consecutive patients who underwent heart transplantation at a single hospital between 1991 and 2013. During a median of 8.4 years of follow-up, the cumulative incidence of VTE was 8.5%, for an annual incidence rate of 12.7 episodes per year for every 1,000 patients, the researchers reported. The risk of VTE was far higher during the first year after transplant (45.1 episodes per 1,000 patients), but even after excluding these episodes, VTE was six times more common among heart transplant recipients than among the general population. Furthermore, VTE recurred an estimated 30.5 times/1,000 patient-years, and 50.8 times/1,000 patients-years among patients who had stopped anticoagulants.

The cumulative incidence rate of DVT and PE were 8.4 and 8.7 episodes per 1,000 patient-years.

In the multivariate analysis, significant risk factors for VTE at less than 1 year after transplantation included age, obesity, chronic kidney disease, and emergency transplantation, the investigators said. More than a year after transplantation, only use of the mammalian target of rapamycin (mTOR) inhibitors sirolimus and everolimus significantly increased VTE risk.

“The evidence that supports a potential association between mTOR inhibitors and an increased risk of VTE events is still weak, and might be confounded by a high prevalence of comorbid conditions such as chronic renal failure, dyslipidemia, or malignancy in patients taking these kinds of drugs,” the investigators cautioned.

The authors suggested that in view of the high recurrence rate, long-term anticoagulation should be considered in heart transplant patients after their first VTE episode.

The Fundacion BBVA-Carolina funded the study. Four coauthors reported receiving travel support from Novartis Pharma and Astellas Pharma. The other authors reported no relevant conflicts of interest.

For every 1,000 patients who underwent heart transplantation, about 45 had an episode of venous thromboembolism within a year after surgery, according to a retrospective study reported in the February issue of the Journal of Heart and Lung Transplantation.

Furthermore, patients who had a single VTE episode after transplant had a “high” risk of recurrent VTE, said Dr. Rolando Alvarez, a cardiologist at Complejo Hospitalario Universitario A Coruna in A Coruna, Spain, and his associates.

“Our opinion is that long-term oral anticoagulation should be maintained in these patients, especially if other risk factors are present and provided that the bleeding risk is not excessive,” said the researchers.

Venous thromboembolism is a common complication of lung, kidney, and liver transplantation, but less is known about VTE after heart transplant. The researchers found that “classic” risk factors for VTE, such as being older, obese, or having renal dysfunction, also increased the risk of VTE after heart transplant (J. Heart Lung Transplant. 2015;34:167-74).

The study included data from 635 consecutive patients who underwent heart transplantation at a single hospital between 1991 and 2013. During a median of 8.4 years of follow-up, the cumulative incidence of VTE was 8.5%, for an annual incidence rate of 12.7 episodes per year for every 1,000 patients, the researchers reported. The risk of VTE was far higher during the first year after transplant (45.1 episodes per 1,000 patients), but even after excluding these episodes, VTE was six times more common among heart transplant recipients than among the general population. Furthermore, VTE recurred an estimated 30.5 times/1,000 patient-years, and 50.8 times/1,000 patients-years among patients who had stopped anticoagulants.

The cumulative incidence rate of DVT and PE were 8.4 and 8.7 episodes per 1,000 patient-years.

In the multivariate analysis, significant risk factors for VTE at less than 1 year after transplantation included age, obesity, chronic kidney disease, and emergency transplantation, the investigators said. More than a year after transplantation, only use of the mammalian target of rapamycin (mTOR) inhibitors sirolimus and everolimus significantly increased VTE risk.

“The evidence that supports a potential association between mTOR inhibitors and an increased risk of VTE events is still weak, and might be confounded by a high prevalence of comorbid conditions such as chronic renal failure, dyslipidemia, or malignancy in patients taking these kinds of drugs,” the investigators cautioned.

The authors suggested that in view of the high recurrence rate, long-term anticoagulation should be considered in heart transplant patients after their first VTE episode.

The Fundacion BBVA-Carolina funded the study. Four coauthors reported receiving travel support from Novartis Pharma and Astellas Pharma. The other authors reported no relevant conflicts of interest.

For every 1,000 patients who underwent heart transplantation, about 45 had an episode of venous thromboembolism within a year after surgery, according to a retrospective study reported in the February issue of the Journal of Heart and Lung Transplantation.

Furthermore, patients who had a single VTE episode after transplant had a “high” risk of recurrent VTE, said Dr. Rolando Alvarez, a cardiologist at Complejo Hospitalario Universitario A Coruna in A Coruna, Spain, and his associates.

“Our opinion is that long-term oral anticoagulation should be maintained in these patients, especially if other risk factors are present and provided that the bleeding risk is not excessive,” said the researchers.

Venous thromboembolism is a common complication of lung, kidney, and liver transplantation, but less is known about VTE after heart transplant. The researchers found that “classic” risk factors for VTE, such as being older, obese, or having renal dysfunction, also increased the risk of VTE after heart transplant (J. Heart Lung Transplant. 2015;34:167-74).

The study included data from 635 consecutive patients who underwent heart transplantation at a single hospital between 1991 and 2013. During a median of 8.4 years of follow-up, the cumulative incidence of VTE was 8.5%, for an annual incidence rate of 12.7 episodes per year for every 1,000 patients, the researchers reported. The risk of VTE was far higher during the first year after transplant (45.1 episodes per 1,000 patients), but even after excluding these episodes, VTE was six times more common among heart transplant recipients than among the general population. Furthermore, VTE recurred an estimated 30.5 times/1,000 patient-years, and 50.8 times/1,000 patients-years among patients who had stopped anticoagulants.

The cumulative incidence rate of DVT and PE were 8.4 and 8.7 episodes per 1,000 patient-years.

In the multivariate analysis, significant risk factors for VTE at less than 1 year after transplantation included age, obesity, chronic kidney disease, and emergency transplantation, the investigators said. More than a year after transplantation, only use of the mammalian target of rapamycin (mTOR) inhibitors sirolimus and everolimus significantly increased VTE risk.

“The evidence that supports a potential association between mTOR inhibitors and an increased risk of VTE events is still weak, and might be confounded by a high prevalence of comorbid conditions such as chronic renal failure, dyslipidemia, or malignancy in patients taking these kinds of drugs,” the investigators cautioned.

The authors suggested that in view of the high recurrence rate, long-term anticoagulation should be considered in heart transplant patients after their first VTE episode.

The Fundacion BBVA-Carolina funded the study. Four coauthors reported receiving travel support from Novartis Pharma and Astellas Pharma. The other authors reported no relevant conflicts of interest.

NASHVILLE, TENN. – Bringing a CT scanner and thrombolytic treatment directly to stroke patients in the field sped the time to thrombolysis, compared with waiting for the patient to arrive at the hospital.

Some U.S. stroke centers now send out a team that can immediately assess and start treating stroke patients in the community. In 2014, the first two U.S. mobile stroke-treatment units began operating, one in Houston and the second in Cleveland.

Mitchel L. Zoler/Frontline Medical News

Initial reports show both programs were successful in cutting the time to deliver thrombolytic treatment with intravenous tissue plasminogen activator (TPA) to appropriate patients.

In Houston, the active phase of the program started in May 2014, and by October 2014, 47 acute ischemic stroke patients had been treated with TPA. The mobile-unit crews started 43% of eligible patients on thrombolysis within 60 minutes of their symptom onset and another 31% were treated starting 61-80 minutes after symptom onset, said Stephanie A. Parker at the International Stroke Conference.

Courtesy American Heart Association

The unit also treats patients diagnosed with hemorrhagic stroke with intravenous nicardipine for rapid blood pressure reduction, said Ms. Parker, a critical care and emergency medicine–trained registered nurse who is project manager for the Houston mobile unit.

The Cleveland program began in July 2014; of the first 100 stroke patients seen by the mobile unit 16 of 19 eligible patients received tPA, with an average time of 56 minutes from symptom onset to treatment. This compared with an average 94 minutes to tPA onset in patients brought conventionally last year to a Cleveland-area hospital, Dr. M. Shazam Hussain said in a report at the meeting, sponsored by the American Heart Association.

Courtesy Amercian Heart Association

The clinical impact and cost effectiveness of the pilot programs using the mobile units have not yet been assessed from the data, Dr. Hussain and Ms. Parker emphasized. Funding for the Cleveland and Houston vehicles came from local donors; the Houston program also received equipment donations from manufacturers.

The two mobile units are standard 12-foot, box-shaped ambulances outfitted with a CT scanner, a point-of-care lab, and telemedicine components as well as more standard emergency-vehicle equipment. The Houston vehicle contains “all the diagnostic equipment that is in our emergency room,” Ms. Parker said.

The concept behind both the Cleveland unit, operated by the Cleveland Clinic, and the Houston unit, operated by the University of Texas, Houston, is that the mobile stroke unit arrives to a patient with a suspected stroke, the unit is stationary while a CT scan and other diagnostic tests are run, diagnosis occurs with telemedicine assistance. If the patient is cleared for TPA treatment, the infusion starts and the vehicle carries the patient to an appropriate stroke center.

Mitchel L. Zoler/Frontline Medical News

Currently, the Houston unit goes out with a vascular neurologist and a telemedicine physician on board, but plans are in place to test the feasibility of relying entirely on telemedicine when making diagnostic and treatment decisions. The Cleveland mobile unit already operates in this fashion, with no physician on board, and was the first mobile stroke unit in the world to depend completely on telemedicine, according to Dr. Hussain, a neurologist and head of the stroke program at the Cleveland Clinic.

The world’s first mobile stroke unit began operating in Saarland, Germany, in 2008 (Lancet Neurology 2012;11:397-404), and a second unit began running in Berlin after that, Dr. Hussain noted. Because of limited funding, the service he directs in Cleveland has been operating from 8 a.m.-8 p.m., 7 days a week. The program plans to expand to 24-hour coverage. The Houston mobile unit operates 24/7; it averages two runs per day and administers TPA on 1 of every 10 runs, Ms. Parker said. Both the Houston and Cleveland units tie into the local 911 emergency activation systems for their respective regions. 

[email protected]

On Twitter @mitchelzoler

NASHVILLE, TENN. – Bringing a CT scanner and thrombolytic treatment directly to stroke patients in the field sped the time to thrombolysis, compared with waiting for the patient to arrive at the hospital.

Some U.S. stroke centers now send out a team that can immediately assess and start treating stroke patients in the community. In 2014, the first two U.S. mobile stroke-treatment units began operating, one in Houston and the second in Cleveland.

Mitchel L. Zoler/Frontline Medical News

Initial reports show both programs were successful in cutting the time to deliver thrombolytic treatment with intravenous tissue plasminogen activator (TPA) to appropriate patients.

In Houston, the active phase of the program started in May 2014, and by October 2014, 47 acute ischemic stroke patients had been treated with TPA. The mobile-unit crews started 43% of eligible patients on thrombolysis within 60 minutes of their symptom onset and another 31% were treated starting 61-80 minutes after symptom onset, said Stephanie A. Parker at the International Stroke Conference.

Courtesy American Heart Association

The unit also treats patients diagnosed with hemorrhagic stroke with intravenous nicardipine for rapid blood pressure reduction, said Ms. Parker, a critical care and emergency medicine–trained registered nurse who is project manager for the Houston mobile unit.

The Cleveland program began in July 2014; of the first 100 stroke patients seen by the mobile unit 16 of 19 eligible patients received tPA, with an average time of 56 minutes from symptom onset to treatment. This compared with an average 94 minutes to tPA onset in patients brought conventionally last year to a Cleveland-area hospital, Dr. M. Shazam Hussain said in a report at the meeting, sponsored by the American Heart Association.

Courtesy Amercian Heart Association

The clinical impact and cost effectiveness of the pilot programs using the mobile units have not yet been assessed from the data, Dr. Hussain and Ms. Parker emphasized. Funding for the Cleveland and Houston vehicles came from local donors; the Houston program also received equipment donations from manufacturers.

The two mobile units are standard 12-foot, box-shaped ambulances outfitted with a CT scanner, a point-of-care lab, and telemedicine components as well as more standard emergency-vehicle equipment. The Houston vehicle contains “all the diagnostic equipment that is in our emergency room,” Ms. Parker said.

The concept behind both the Cleveland unit, operated by the Cleveland Clinic, and the Houston unit, operated by the University of Texas, Houston, is that the mobile stroke unit arrives to a patient with a suspected stroke, the unit is stationary while a CT scan and other diagnostic tests are run, diagnosis occurs with telemedicine assistance. If the patient is cleared for TPA treatment, the infusion starts and the vehicle carries the patient to an appropriate stroke center.

Mitchel L. Zoler/Frontline Medical News

Currently, the Houston unit goes out with a vascular neurologist and a telemedicine physician on board, but plans are in place to test the feasibility of relying entirely on telemedicine when making diagnostic and treatment decisions. The Cleveland mobile unit already operates in this fashion, with no physician on board, and was the first mobile stroke unit in the world to depend completely on telemedicine, according to Dr. Hussain, a neurologist and head of the stroke program at the Cleveland Clinic.

The world’s first mobile stroke unit began operating in Saarland, Germany, in 2008 (Lancet Neurology 2012;11:397-404), and a second unit began running in Berlin after that, Dr. Hussain noted. Because of limited funding, the service he directs in Cleveland has been operating from 8 a.m.-8 p.m., 7 days a week. The program plans to expand to 24-hour coverage. The Houston mobile unit operates 24/7; it averages two runs per day and administers TPA on 1 of every 10 runs, Ms. Parker said. Both the Houston and Cleveland units tie into the local 911 emergency activation systems for their respective regions. 

[email protected]

On Twitter @mitchelzoler

NASHVILLE, TENN. – Bringing a CT scanner and thrombolytic treatment directly to stroke patients in the field sped the time to thrombolysis, compared with waiting for the patient to arrive at the hospital.

Some U.S. stroke centers now send out a team that can immediately assess and start treating stroke patients in the community. In 2014, the first two U.S. mobile stroke-treatment units began operating, one in Houston and the second in Cleveland.

Mitchel L. Zoler/Frontline Medical News

Initial reports show both programs were successful in cutting the time to deliver thrombolytic treatment with intravenous tissue plasminogen activator (TPA) to appropriate patients.

In Houston, the active phase of the program started in May 2014, and by October 2014, 47 acute ischemic stroke patients had been treated with TPA. The mobile-unit crews started 43% of eligible patients on thrombolysis within 60 minutes of their symptom onset and another 31% were treated starting 61-80 minutes after symptom onset, said Stephanie A. Parker at the International Stroke Conference.

Courtesy American Heart Association

The unit also treats patients diagnosed with hemorrhagic stroke with intravenous nicardipine for rapid blood pressure reduction, said Ms. Parker, a critical care and emergency medicine–trained registered nurse who is project manager for the Houston mobile unit.

The Cleveland program began in July 2014; of the first 100 stroke patients seen by the mobile unit 16 of 19 eligible patients received tPA, with an average time of 56 minutes from symptom onset to treatment. This compared with an average 94 minutes to tPA onset in patients brought conventionally last year to a Cleveland-area hospital, Dr. M. Shazam Hussain said in a report at the meeting, sponsored by the American Heart Association.

Courtesy Amercian Heart Association

The clinical impact and cost effectiveness of the pilot programs using the mobile units have not yet been assessed from the data, Dr. Hussain and Ms. Parker emphasized. Funding for the Cleveland and Houston vehicles came from local donors; the Houston program also received equipment donations from manufacturers.

The two mobile units are standard 12-foot, box-shaped ambulances outfitted with a CT scanner, a point-of-care lab, and telemedicine components as well as more standard emergency-vehicle equipment. The Houston vehicle contains “all the diagnostic equipment that is in our emergency room,” Ms. Parker said.

The concept behind both the Cleveland unit, operated by the Cleveland Clinic, and the Houston unit, operated by the University of Texas, Houston, is that the mobile stroke unit arrives to a patient with a suspected stroke, the unit is stationary while a CT scan and other diagnostic tests are run, diagnosis occurs with telemedicine assistance. If the patient is cleared for TPA treatment, the infusion starts and the vehicle carries the patient to an appropriate stroke center.

Mitchel L. Zoler/Frontline Medical News

Currently, the Houston unit goes out with a vascular neurologist and a telemedicine physician on board, but plans are in place to test the feasibility of relying entirely on telemedicine when making diagnostic and treatment decisions. The Cleveland mobile unit already operates in this fashion, with no physician on board, and was the first mobile stroke unit in the world to depend completely on telemedicine, according to Dr. Hussain, a neurologist and head of the stroke program at the Cleveland Clinic.

The world’s first mobile stroke unit began operating in Saarland, Germany, in 2008 (Lancet Neurology 2012;11:397-404), and a second unit began running in Berlin after that, Dr. Hussain noted. Because of limited funding, the service he directs in Cleveland has been operating from 8 a.m.-8 p.m., 7 days a week. The program plans to expand to 24-hour coverage. The Houston mobile unit operates 24/7; it averages two runs per day and administers TPA on 1 of every 10 runs, Ms. Parker said. Both the Houston and Cleveland units tie into the local 911 emergency activation systems for their respective regions. 

[email protected]

On Twitter @mitchelzoler

When heart attack symptoms begin, women wait longer than do men to call for help, and it takes longer for them to arrive at a hospital that can care for them appropriately.

Further, statistical analysis suggests that this prehospital delay is a chief contributor to the higher in-hospital mortality rate for women who have sustained myocardial infarctions. Dr. Raffaele Bugiardini of the University of Bologna and his associates in the ISACS-TC study group examined data from a large international study to clarify gender disparities in heart attacks, and to identify more precisely where time is lost in caring for women.

They examined data from 2,282 women and 5,175 men who experienced ST-segment–elevation myocardial infarction (STEMI). Overall, female participants were older than males and were more likely to have diabetes, to be treated for hypertension, and to have experienced atypical chest pain – or no chest pain at all – during their heart attacks. The men were more likely to be smokers, to have chronic renal failure, and to have a prior history of angina.

The results were released in advance of the researchers’ presentation on March 14 at the annual meeting of the American College of Cardiology in San Diego.

Once symptoms began, women tended to wait significantly longer to call for help, a median 60.0 minutes, compared with 45.5 for men. Time to hospital admission was just a bit longer for women (60 minutes) compared to men (55 minutes). On admission, time to angioplasty or fibrinolysis did not vary significantly between the sexes. The likelihood of receiving appropriate medical treatment (aspirin, clopidogrel, heparin use) was also similar.

In outcome measures, 30% of women achieved hospital admission in 60 minutes or less from leaving home, compared with 70% of men. Dr. Bugiardini explained that the 60-minute admission marker is an important quality standard in the European framework. The odds ratio (OR) for a greater-than 60-minute time from home to hospital admission for women was 2.90 (95% CI, 1.52-5.82).

In-hospital mortality for women was nearly double that for men, at 11.8% compared to 6.3% for men (OR 1.34, 95% CI 1.01-1.77). However, after logistic regression analysis adjusted for the differences in time from home to hospital admission, the disparity in mortality disappeared (OR 0.90, 95% CI 0.31-2.56). Dr. Bugiardini emphasized that his analysis makes clear that delay in treatment is an important contributor to greater in-hospital mortality for women suffering heart attacks.

Though these finding were drawn from a large international study, American College of Cardiology Vice President Richard Chazal affirmed during a media briefing that the results are definitely applicable to the United States and other developed nations. “They are confirmatory,” said Dr. Chazal, “of other studies that have suggested this but have not shown this in such a complete and comprehensive way. This is very important information in this population.”

Heart disease kills more women than do all forms of cancer combined, but the varied presentation of heart attack symptoms in women is still underrecognized, noted Dr. Chazal of Lee Memorial Health System, Fort Myers, Fla. Raising awareness about heart disease risk and heart attack symptoms is critical to addressing the disparities identified in this study. “The delays in getting the patient to the hospital are really crucial in determining what the outcomes are,” he said.

“Time is still lost between contact with the system and arrival to the hospital” for women, he added. “There is less awareness not just by women, but in doctors in underestimating what’s going on with women. We are confused, so we stop and do one more EKG. We are losing time.”

Dr. Marija Vavlukis is on the speakers bureau for KRKA Macedonia. The other authors have no disclosures.

When heart attack symptoms begin, women wait longer than do men to call for help, and it takes longer for them to arrive at a hospital that can care for them appropriately.

Further, statistical analysis suggests that this prehospital delay is a chief contributor to the higher in-hospital mortality rate for women who have sustained myocardial infarctions. Dr. Raffaele Bugiardini of the University of Bologna and his associates in the ISACS-TC study group examined data from a large international study to clarify gender disparities in heart attacks, and to identify more precisely where time is lost in caring for women.

They examined data from 2,282 women and 5,175 men who experienced ST-segment–elevation myocardial infarction (STEMI). Overall, female participants were older than males and were more likely to have diabetes, to be treated for hypertension, and to have experienced atypical chest pain – or no chest pain at all – during their heart attacks. The men were more likely to be smokers, to have chronic renal failure, and to have a prior history of angina.

The results were released in advance of the researchers’ presentation on March 14 at the annual meeting of the American College of Cardiology in San Diego.

Once symptoms began, women tended to wait significantly longer to call for help, a median 60.0 minutes, compared with 45.5 for men. Time to hospital admission was just a bit longer for women (60 minutes) compared to men (55 minutes). On admission, time to angioplasty or fibrinolysis did not vary significantly between the sexes. The likelihood of receiving appropriate medical treatment (aspirin, clopidogrel, heparin use) was also similar.

In outcome measures, 30% of women achieved hospital admission in 60 minutes or less from leaving home, compared with 70% of men. Dr. Bugiardini explained that the 60-minute admission marker is an important quality standard in the European framework. The odds ratio (OR) for a greater-than 60-minute time from home to hospital admission for women was 2.90 (95% CI, 1.52-5.82).

In-hospital mortality for women was nearly double that for men, at 11.8% compared to 6.3% for men (OR 1.34, 95% CI 1.01-1.77). However, after logistic regression analysis adjusted for the differences in time from home to hospital admission, the disparity in mortality disappeared (OR 0.90, 95% CI 0.31-2.56). Dr. Bugiardini emphasized that his analysis makes clear that delay in treatment is an important contributor to greater in-hospital mortality for women suffering heart attacks.

Though these finding were drawn from a large international study, American College of Cardiology Vice President Richard Chazal affirmed during a media briefing that the results are definitely applicable to the United States and other developed nations. “They are confirmatory,” said Dr. Chazal, “of other studies that have suggested this but have not shown this in such a complete and comprehensive way. This is very important information in this population.”

Heart disease kills more women than do all forms of cancer combined, but the varied presentation of heart attack symptoms in women is still underrecognized, noted Dr. Chazal of Lee Memorial Health System, Fort Myers, Fla. Raising awareness about heart disease risk and heart attack symptoms is critical to addressing the disparities identified in this study. “The delays in getting the patient to the hospital are really crucial in determining what the outcomes are,” he said.

“Time is still lost between contact with the system and arrival to the hospital” for women, he added. “There is less awareness not just by women, but in doctors in underestimating what’s going on with women. We are confused, so we stop and do one more EKG. We are losing time.”

Dr. Marija Vavlukis is on the speakers bureau for KRKA Macedonia. The other authors have no disclosures.

When heart attack symptoms begin, women wait longer than do men to call for help, and it takes longer for them to arrive at a hospital that can care for them appropriately.

Further, statistical analysis suggests that this prehospital delay is a chief contributor to the higher in-hospital mortality rate for women who have sustained myocardial infarctions. Dr. Raffaele Bugiardini of the University of Bologna and his associates in the ISACS-TC study group examined data from a large international study to clarify gender disparities in heart attacks, and to identify more precisely where time is lost in caring for women.

They examined data from 2,282 women and 5,175 men who experienced ST-segment–elevation myocardial infarction (STEMI). Overall, female participants were older than males and were more likely to have diabetes, to be treated for hypertension, and to have experienced atypical chest pain – or no chest pain at all – during their heart attacks. The men were more likely to be smokers, to have chronic renal failure, and to have a prior history of angina.

The results were released in advance of the researchers’ presentation on March 14 at the annual meeting of the American College of Cardiology in San Diego.

Once symptoms began, women tended to wait significantly longer to call for help, a median 60.0 minutes, compared with 45.5 for men. Time to hospital admission was just a bit longer for women (60 minutes) compared to men (55 minutes). On admission, time to angioplasty or fibrinolysis did not vary significantly between the sexes. The likelihood of receiving appropriate medical treatment (aspirin, clopidogrel, heparin use) was also similar.

In outcome measures, 30% of women achieved hospital admission in 60 minutes or less from leaving home, compared with 70% of men. Dr. Bugiardini explained that the 60-minute admission marker is an important quality standard in the European framework. The odds ratio (OR) for a greater-than 60-minute time from home to hospital admission for women was 2.90 (95% CI, 1.52-5.82).

In-hospital mortality for women was nearly double that for men, at 11.8% compared to 6.3% for men (OR 1.34, 95% CI 1.01-1.77). However, after logistic regression analysis adjusted for the differences in time from home to hospital admission, the disparity in mortality disappeared (OR 0.90, 95% CI 0.31-2.56). Dr. Bugiardini emphasized that his analysis makes clear that delay in treatment is an important contributor to greater in-hospital mortality for women suffering heart attacks.

Though these finding were drawn from a large international study, American College of Cardiology Vice President Richard Chazal affirmed during a media briefing that the results are definitely applicable to the United States and other developed nations. “They are confirmatory,” said Dr. Chazal, “of other studies that have suggested this but have not shown this in such a complete and comprehensive way. This is very important information in this population.”

Heart disease kills more women than do all forms of cancer combined, but the varied presentation of heart attack symptoms in women is still underrecognized, noted Dr. Chazal of Lee Memorial Health System, Fort Myers, Fla. Raising awareness about heart disease risk and heart attack symptoms is critical to addressing the disparities identified in this study. “The delays in getting the patient to the hospital are really crucial in determining what the outcomes are,” he said.

“Time is still lost between contact with the system and arrival to the hospital” for women, he added. “There is less awareness not just by women, but in doctors in underestimating what’s going on with women. We are confused, so we stop and do one more EKG. We are losing time.”

Dr. Marija Vavlukis is on the speakers bureau for KRKA Macedonia. The other authors have no disclosures.

One year after transcatheter aortic valve replacement in the United States, the overall mortality was 23.7%, the stroke rate was 4.1%, and the composite outcome of death and stroke was 26.0%, according to a report published online March 10 in JAMA.

Long-term outcomes for TAVR haven’t been well studied until now, yet the procedure is being performed with increasing frequency for aortic stenosis in patients who are too high risk to undergo conventional surgical aortic valve replacement, said Dr. David R. Holmes Jr. of the Mayo Clinic, Rochester, Minn., and his associates.

They assessed 1-year outcomes by analyzing administrative data from the Centers for Medicare & Medicaid Services and clinical data from the Transcatheter Valve Therapies Registry, an initiative of the Society of Thoracic Surgeons and the American College of Cardiology. The study involved 12,182 patients who underwent TAVR at 299 medical centers across the country during a 19-month period. The patients’ median age was 84 years; 95% were white and 52% were women. The transfemoral approach was used in most patients, but alternative approaches were used in roughly 44%. As expected for an elderly, high-risk study population, baseline functional status was poor and comorbidities were common. They included reduced left ventricular ejection fraction (26% of patients), prior stroke (12%), moderate or severe lung disease (28%), renal failure (16%), peripheral vascular disease (32%), and atrial fibrillation (42%), Dr. Holmes and his associates reported (JAMA 2015 March 10 [doi:10.1001/jama.2015.1474]).

In addition to the mortality and stroke rates listed above, the 1-year rate of one rehospitalization was 24.4%, that of two rehospitalizations was 12.5%, and that of three or more rehospitalizations was 11.6%. The 1-year readmission rate specifically for stroke, heart failure, or repeat aortic valve intervention was 18.6%. These are important considerations for elderly, fragile patients because rehospitalizations indicate “an unacceptable quality-of-life outcome” and are very costly, the investigators noted.

Several baseline characteristics, including male sex, severe chronic obstructive pulmonary disease, dialysis-dependent end-stage renal disease, older age, higher STS Predicted Risk of Operative Mortality (PROM) score, a history of atrial fibrillation/flutter, and use of an access route (other than transfemoral), were found to be independently associated with higher 1-year mortality. Thus, “It may be possible to identify patients who may not benefit from this procedure and who should be counseled accordingly.” For example, in this study there was a small (77 patients) very high-risk subset of patients – aged 85-94 years, dependent on dialysis, and having an STS PROM score greater than 15% – whose 1-year mortality was 53.5%.

The STS and the ACC supported this study, and support the Transcatheter Valve Therapies Registry. Dr. Holmes reported having no relevant financial disclosures; his associates reported ties to Boston Scientific, Edwards Lifesciences, Janssen, Eli Lilly, Boehringer Ingelheim, Bayer, and AstraZeneca.

One year after transcatheter aortic valve replacement in the United States, the overall mortality was 23.7%, the stroke rate was 4.1%, and the composite outcome of death and stroke was 26.0%, according to a report published online March 10 in JAMA.

Long-term outcomes for TAVR haven’t been well studied until now, yet the procedure is being performed with increasing frequency for aortic stenosis in patients who are too high risk to undergo conventional surgical aortic valve replacement, said Dr. David R. Holmes Jr. of the Mayo Clinic, Rochester, Minn., and his associates.

They assessed 1-year outcomes by analyzing administrative data from the Centers for Medicare & Medicaid Services and clinical data from the Transcatheter Valve Therapies Registry, an initiative of the Society of Thoracic Surgeons and the American College of Cardiology. The study involved 12,182 patients who underwent TAVR at 299 medical centers across the country during a 19-month period. The patients’ median age was 84 years; 95% were white and 52% were women. The transfemoral approach was used in most patients, but alternative approaches were used in roughly 44%. As expected for an elderly, high-risk study population, baseline functional status was poor and comorbidities were common. They included reduced left ventricular ejection fraction (26% of patients), prior stroke (12%), moderate or severe lung disease (28%), renal failure (16%), peripheral vascular disease (32%), and atrial fibrillation (42%), Dr. Holmes and his associates reported (JAMA 2015 March 10 [doi:10.1001/jama.2015.1474]).

In addition to the mortality and stroke rates listed above, the 1-year rate of one rehospitalization was 24.4%, that of two rehospitalizations was 12.5%, and that of three or more rehospitalizations was 11.6%. The 1-year readmission rate specifically for stroke, heart failure, or repeat aortic valve intervention was 18.6%. These are important considerations for elderly, fragile patients because rehospitalizations indicate “an unacceptable quality-of-life outcome” and are very costly, the investigators noted.

Several baseline characteristics, including male sex, severe chronic obstructive pulmonary disease, dialysis-dependent end-stage renal disease, older age, higher STS Predicted Risk of Operative Mortality (PROM) score, a history of atrial fibrillation/flutter, and use of an access route (other than transfemoral), were found to be independently associated with higher 1-year mortality. Thus, “It may be possible to identify patients who may not benefit from this procedure and who should be counseled accordingly.” For example, in this study there was a small (77 patients) very high-risk subset of patients – aged 85-94 years, dependent on dialysis, and having an STS PROM score greater than 15% – whose 1-year mortality was 53.5%.

The STS and the ACC supported this study, and support the Transcatheter Valve Therapies Registry. Dr. Holmes reported having no relevant financial disclosures; his associates reported ties to Boston Scientific, Edwards Lifesciences, Janssen, Eli Lilly, Boehringer Ingelheim, Bayer, and AstraZeneca.

One year after transcatheter aortic valve replacement in the United States, the overall mortality was 23.7%, the stroke rate was 4.1%, and the composite outcome of death and stroke was 26.0%, according to a report published online March 10 in JAMA.

Long-term outcomes for TAVR haven’t been well studied until now, yet the procedure is being performed with increasing frequency for aortic stenosis in patients who are too high risk to undergo conventional surgical aortic valve replacement, said Dr. David R. Holmes Jr. of the Mayo Clinic, Rochester, Minn., and his associates.

They assessed 1-year outcomes by analyzing administrative data from the Centers for Medicare & Medicaid Services and clinical data from the Transcatheter Valve Therapies Registry, an initiative of the Society of Thoracic Surgeons and the American College of Cardiology. The study involved 12,182 patients who underwent TAVR at 299 medical centers across the country during a 19-month period. The patients’ median age was 84 years; 95% were white and 52% were women. The transfemoral approach was used in most patients, but alternative approaches were used in roughly 44%. As expected for an elderly, high-risk study population, baseline functional status was poor and comorbidities were common. They included reduced left ventricular ejection fraction (26% of patients), prior stroke (12%), moderate or severe lung disease (28%), renal failure (16%), peripheral vascular disease (32%), and atrial fibrillation (42%), Dr. Holmes and his associates reported (JAMA 2015 March 10 [doi:10.1001/jama.2015.1474]).

In addition to the mortality and stroke rates listed above, the 1-year rate of one rehospitalization was 24.4%, that of two rehospitalizations was 12.5%, and that of three or more rehospitalizations was 11.6%. The 1-year readmission rate specifically for stroke, heart failure, or repeat aortic valve intervention was 18.6%. These are important considerations for elderly, fragile patients because rehospitalizations indicate “an unacceptable quality-of-life outcome” and are very costly, the investigators noted.

Several baseline characteristics, including male sex, severe chronic obstructive pulmonary disease, dialysis-dependent end-stage renal disease, older age, higher STS Predicted Risk of Operative Mortality (PROM) score, a history of atrial fibrillation/flutter, and use of an access route (other than transfemoral), were found to be independently associated with higher 1-year mortality. Thus, “It may be possible to identify patients who may not benefit from this procedure and who should be counseled accordingly.” For example, in this study there was a small (77 patients) very high-risk subset of patients – aged 85-94 years, dependent on dialysis, and having an STS PROM score greater than 15% – whose 1-year mortality was 53.5%.

The STS and the ACC supported this study, and support the Transcatheter Valve Therapies Registry. Dr. Holmes reported having no relevant financial disclosures; his associates reported ties to Boston Scientific, Edwards Lifesciences, Janssen, Eli Lilly, Boehringer Ingelheim, Bayer, and AstraZeneca.

PHOENIX – Twice-daily ranolazine following adult cardiac surgery seemed to protect against atrial fibrillation, based on a retrospective cohort study at the University of Florida Jacksonville Medical Center.

Ranolazine (Ranexa) was dosed orally at 1,000 mg the morning of surgery, and then resumed after extubation, generally the night of surgery. The goal was 1,000 mg orally twice a day, for a maximum of 7 hospital days; patients usually went home before then, so they received an average of nine doses. The drug was discontinued at discharge.

Six (10.5%) of 57 patients in the ranolazine group developed postoperative atrial fibrillation (POAF) versus 26 (45.6%) of 57 matched controls (P < .0001). The first case came at postop day 3 in the ranolazine group, but within 24 hours in the control group. One person in the ranolazine group and one in the control group had a history of AF.

There was no statistical difference in ICU length of stay, 30-day readmission for cardiac causes, or 30-day cardiovascular mortality; the one cardiovascular death was in the control group.

Two-thirds of the patients had coronary artery bypass grafts, and the rest had either valve surgery or a combination of both surgeries. Patients were 60 years old on average, and two-thirds were men, Drayton Hammond, Pharm.D., said at the Critical Care Congress, sponsored by the Society for Critical Care Medicine.

Ranolazine is indicated for chronic angina, not POAF prevention, but some previous investigations have suggested a possible benefit. A randomized, controlled clinical trial is currently looking into the matter.

At least retrospectively, the drug was “beneficial, definitely. There is about a 35% absolute-risk reduction,” said Dr. Hammond, who conducted the study while at the Jacksonville hospital.

Doctors there continue to use ranolazine for postop AF prophylaxis, as they see fit, said Dr. Hammond, now an assistant professor of pharmacy practice at the University of Arkansas for Medical Sciences, in Little Rock.

Gilead, the maker of the Ranexa, is also working on a ranolazine-dronedarone combination for paroxysmal AF.

More than half of the ranolazine patients in the study developed symptomatic hypotension within 72 hours of surgery, versus about a third in the control group (P = .0004). The drug was discontinued in one ranolazine patient because of hypotension. The problem resolved after 72 hours.

“We don’t have a good explanation” for the side effect. Perhaps there were differences in myocardial stunning or vasopressor use between the groups, but “we had the same three surgeons” for all the cases, Dr. Hammond said.

Ranolazine labeling notes the risk of hypotension and orthostatic hypotension. Labeling also warns of QT interval prolongation and renal failure in susceptible patients. The investigators found no between-group differences in bradycardia, new renal failure, or neurological events.

Overall, 53 (93%) patients in the ranolazine group were on postoperative beta-blockers, and 54 (94.7%) on postop statins; 48 (84.2%) in the control group were on beta-blockers postop and 47 (82.5%) on statins. Beta-blockers are first-line treatment to prevent postop AF; patients on any other antiarrhythmic were excluded from the trial, as were those who died during surgery.

[email protected]

PHOENIX – Twice-daily ranolazine following adult cardiac surgery seemed to protect against atrial fibrillation, based on a retrospective cohort study at the University of Florida Jacksonville Medical Center.

Ranolazine (Ranexa) was dosed orally at 1,000 mg the morning of surgery, and then resumed after extubation, generally the night of surgery. The goal was 1,000 mg orally twice a day, for a maximum of 7 hospital days; patients usually went home before then, so they received an average of nine doses. The drug was discontinued at discharge.

Six (10.5%) of 57 patients in the ranolazine group developed postoperative atrial fibrillation (POAF) versus 26 (45.6%) of 57 matched controls (P < .0001). The first case came at postop day 3 in the ranolazine group, but within 24 hours in the control group. One person in the ranolazine group and one in the control group had a history of AF.

There was no statistical difference in ICU length of stay, 30-day readmission for cardiac causes, or 30-day cardiovascular mortality; the one cardiovascular death was in the control group.

Two-thirds of the patients had coronary artery bypass grafts, and the rest had either valve surgery or a combination of both surgeries. Patients were 60 years old on average, and two-thirds were men, Drayton Hammond, Pharm.D., said at the Critical Care Congress, sponsored by the Society for Critical Care Medicine.

Ranolazine is indicated for chronic angina, not POAF prevention, but some previous investigations have suggested a possible benefit. A randomized, controlled clinical trial is currently looking into the matter.

At least retrospectively, the drug was “beneficial, definitely. There is about a 35% absolute-risk reduction,” said Dr. Hammond, who conducted the study while at the Jacksonville hospital.

Doctors there continue to use ranolazine for postop AF prophylaxis, as they see fit, said Dr. Hammond, now an assistant professor of pharmacy practice at the University of Arkansas for Medical Sciences, in Little Rock.

Gilead, the maker of the Ranexa, is also working on a ranolazine-dronedarone combination for paroxysmal AF.

More than half of the ranolazine patients in the study developed symptomatic hypotension within 72 hours of surgery, versus about a third in the control group (P = .0004). The drug was discontinued in one ranolazine patient because of hypotension. The problem resolved after 72 hours.

“We don’t have a good explanation” for the side effect. Perhaps there were differences in myocardial stunning or vasopressor use between the groups, but “we had the same three surgeons” for all the cases, Dr. Hammond said.

Ranolazine labeling notes the risk of hypotension and orthostatic hypotension. Labeling also warns of QT interval prolongation and renal failure in susceptible patients. The investigators found no between-group differences in bradycardia, new renal failure, or neurological events.

Overall, 53 (93%) patients in the ranolazine group were on postoperative beta-blockers, and 54 (94.7%) on postop statins; 48 (84.2%) in the control group were on beta-blockers postop and 47 (82.5%) on statins. Beta-blockers are first-line treatment to prevent postop AF; patients on any other antiarrhythmic were excluded from the trial, as were those who died during surgery.

[email protected]

PHOENIX – Twice-daily ranolazine following adult cardiac surgery seemed to protect against atrial fibrillation, based on a retrospective cohort study at the University of Florida Jacksonville Medical Center.

Ranolazine (Ranexa) was dosed orally at 1,000 mg the morning of surgery, and then resumed after extubation, generally the night of surgery. The goal was 1,000 mg orally twice a day, for a maximum of 7 hospital days; patients usually went home before then, so they received an average of nine doses. The drug was discontinued at discharge.

Six (10.5%) of 57 patients in the ranolazine group developed postoperative atrial fibrillation (POAF) versus 26 (45.6%) of 57 matched controls (P < .0001). The first case came at postop day 3 in the ranolazine group, but within 24 hours in the control group. One person in the ranolazine group and one in the control group had a history of AF.

There was no statistical difference in ICU length of stay, 30-day readmission for cardiac causes, or 30-day cardiovascular mortality; the one cardiovascular death was in the control group.

Two-thirds of the patients had coronary artery bypass grafts, and the rest had either valve surgery or a combination of both surgeries. Patients were 60 years old on average, and two-thirds were men, Drayton Hammond, Pharm.D., said at the Critical Care Congress, sponsored by the Society for Critical Care Medicine.

Ranolazine is indicated for chronic angina, not POAF prevention, but some previous investigations have suggested a possible benefit. A randomized, controlled clinical trial is currently looking into the matter.

At least retrospectively, the drug was “beneficial, definitely. There is about a 35% absolute-risk reduction,” said Dr. Hammond, who conducted the study while at the Jacksonville hospital.

Doctors there continue to use ranolazine for postop AF prophylaxis, as they see fit, said Dr. Hammond, now an assistant professor of pharmacy practice at the University of Arkansas for Medical Sciences, in Little Rock.

Gilead, the maker of the Ranexa, is also working on a ranolazine-dronedarone combination for paroxysmal AF.

More than half of the ranolazine patients in the study developed symptomatic hypotension within 72 hours of surgery, versus about a third in the control group (P = .0004). The drug was discontinued in one ranolazine patient because of hypotension. The problem resolved after 72 hours.

“We don’t have a good explanation” for the side effect. Perhaps there were differences in myocardial stunning or vasopressor use between the groups, but “we had the same three surgeons” for all the cases, Dr. Hammond said.

Ranolazine labeling notes the risk of hypotension and orthostatic hypotension. Labeling also warns of QT interval prolongation and renal failure in susceptible patients. The investigators found no between-group differences in bradycardia, new renal failure, or neurological events.

Overall, 53 (93%) patients in the ranolazine group were on postoperative beta-blockers, and 54 (94.7%) on postop statins; 48 (84.2%) in the control group were on beta-blockers postop and 47 (82.5%) on statins. Beta-blockers are first-line treatment to prevent postop AF; patients on any other antiarrhythmic were excluded from the trial, as were those who died during surgery.

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PHOENIX – For every unit increase in baseline CHADS₂ score, the risk of postop atrial fibrillation increases by 17%, according to a retrospective chart review of 1,550 adults who had major vascular or thoracic surgery at the Mayo Clinic in Rochester, Minn.

On multivariate analysis, postop day 1 Sequential Organ Failure Assessment score (HR 1.08, 95% CI 1.03-1.12, per unit increase) and cumulative fluid balance (HR 1.03, 95% CI 1.01-1.06, per 1,000 mL) also correlated with the risk for new-onset atrial fibrillation (AF).

Baseline calcium channel blockers protected against new-onset AF (HR 0.52, 95% CI 0.37-0.73), but, paradoxically, the risk increased with baseline (HR 1.78, 95% CI 1.24-2.56) and postop (HR 1.44, 95% CI 1.05-1.99) beta-blocker use.

The relationship of CHADS₂ to new-onset AF (HR 1.17, 95% CI 1.04-1.31) could prove handy in the surgical ICU because “everyone is familiar with it, and it’s easy to calculate.” CHADS₂ (heart failure, hypertension, age, diabetes, prior stroke) has also recently been shown to predict AF after cardiac surgery, said lead investigator Kirstin Kooda, Pharm.D., a critical care pharmacist at Mayo.

The beta-blocker finding was a surprise, since beta-blockers are a standard AF treatment, Dr. Kooda said at the Critical Care Congress, sponsored by the Society for Critical Care Medicine. About 80% (175) of new-onset AF patients were on baseline beta-blockers, versus about 68% (892) who did not develop AF. Patients using beta-blockers received them the morning of surgery, and resumed them a median of 7 hours afterward. There were no significant differences in heart rates during surgery.

The team excluded patients with any history of AF and censored patients if they developed it, so the drugs’ use probably wasn’t related to a concern about the condition. Just under 70% of patients in both groups had baseline hypertension, another indication for the drugs.

Even so, the finding is probably real given the number of patients in the study. Most likely, the drugs were markers for additional risk factors not captured in the study, Dr. Kooda said.

Overall, 112 (20.7%) of the 540 thoracic patients and 107 (11%) of the 1,010 vascular patients developed new-onset AF a median of 55 hours after surgery. The incidence difference and timing are in line with previous reports.

The mean age in the AF group was 70 years, and in the non-AF group it was 66 years. In both, 65% were men, 5% had heart failure, 30% had diabetes, and 10% had prior strokes. Patients with pacemakers and recent myocardial infarctions – also possible settings for beta-blockers – were excluded from the trial.

The majority of the vascular cases were open aortic aneurysms, aortic bypasses, and thrombectomies or endarterectomies of central arteries. Most of the thoracic surgeries were lobectomies, pneumonectomies, and wedge or chest wall resections.

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PHOENIX – For every unit increase in baseline CHADS₂ score, the risk of postop atrial fibrillation increases by 17%, according to a retrospective chart review of 1,550 adults who had major vascular or thoracic surgery at the Mayo Clinic in Rochester, Minn.

On multivariate analysis, postop day 1 Sequential Organ Failure Assessment score (HR 1.08, 95% CI 1.03-1.12, per unit increase) and cumulative fluid balance (HR 1.03, 95% CI 1.01-1.06, per 1,000 mL) also correlated with the risk for new-onset atrial fibrillation (AF).

Baseline calcium channel blockers protected against new-onset AF (HR 0.52, 95% CI 0.37-0.73), but, paradoxically, the risk increased with baseline (HR 1.78, 95% CI 1.24-2.56) and postop (HR 1.44, 95% CI 1.05-1.99) beta-blocker use.

The relationship of CHADS₂ to new-onset AF (HR 1.17, 95% CI 1.04-1.31) could prove handy in the surgical ICU because “everyone is familiar with it, and it’s easy to calculate.” CHADS₂ (heart failure, hypertension, age, diabetes, prior stroke) has also recently been shown to predict AF after cardiac surgery, said lead investigator Kirstin Kooda, Pharm.D., a critical care pharmacist at Mayo.

The beta-blocker finding was a surprise, since beta-blockers are a standard AF treatment, Dr. Kooda said at the Critical Care Congress, sponsored by the Society for Critical Care Medicine. About 80% (175) of new-onset AF patients were on baseline beta-blockers, versus about 68% (892) who did not develop AF. Patients using beta-blockers received them the morning of surgery, and resumed them a median of 7 hours afterward. There were no significant differences in heart rates during surgery.

The team excluded patients with any history of AF and censored patients if they developed it, so the drugs’ use probably wasn’t related to a concern about the condition. Just under 70% of patients in both groups had baseline hypertension, another indication for the drugs.

Even so, the finding is probably real given the number of patients in the study. Most likely, the drugs were markers for additional risk factors not captured in the study, Dr. Kooda said.

Overall, 112 (20.7%) of the 540 thoracic patients and 107 (11%) of the 1,010 vascular patients developed new-onset AF a median of 55 hours after surgery. The incidence difference and timing are in line with previous reports.

The mean age in the AF group was 70 years, and in the non-AF group it was 66 years. In both, 65% were men, 5% had heart failure, 30% had diabetes, and 10% had prior strokes. Patients with pacemakers and recent myocardial infarctions – also possible settings for beta-blockers – were excluded from the trial.

The majority of the vascular cases were open aortic aneurysms, aortic bypasses, and thrombectomies or endarterectomies of central arteries. Most of the thoracic surgeries were lobectomies, pneumonectomies, and wedge or chest wall resections.

[email protected]

PHOENIX – For every unit increase in baseline CHADS₂ score, the risk of postop atrial fibrillation increases by 17%, according to a retrospective chart review of 1,550 adults who had major vascular or thoracic surgery at the Mayo Clinic in Rochester, Minn.

On multivariate analysis, postop day 1 Sequential Organ Failure Assessment score (HR 1.08, 95% CI 1.03-1.12, per unit increase) and cumulative fluid balance (HR 1.03, 95% CI 1.01-1.06, per 1,000 mL) also correlated with the risk for new-onset atrial fibrillation (AF).

Baseline calcium channel blockers protected against new-onset AF (HR 0.52, 95% CI 0.37-0.73), but, paradoxically, the risk increased with baseline (HR 1.78, 95% CI 1.24-2.56) and postop (HR 1.44, 95% CI 1.05-1.99) beta-blocker use.

The relationship of CHADS₂ to new-onset AF (HR 1.17, 95% CI 1.04-1.31) could prove handy in the surgical ICU because “everyone is familiar with it, and it’s easy to calculate.” CHADS₂ (heart failure, hypertension, age, diabetes, prior stroke) has also recently been shown to predict AF after cardiac surgery, said lead investigator Kirstin Kooda, Pharm.D., a critical care pharmacist at Mayo.

The beta-blocker finding was a surprise, since beta-blockers are a standard AF treatment, Dr. Kooda said at the Critical Care Congress, sponsored by the Society for Critical Care Medicine. About 80% (175) of new-onset AF patients were on baseline beta-blockers, versus about 68% (892) who did not develop AF. Patients using beta-blockers received them the morning of surgery, and resumed them a median of 7 hours afterward. There were no significant differences in heart rates during surgery.

The team excluded patients with any history of AF and censored patients if they developed it, so the drugs’ use probably wasn’t related to a concern about the condition. Just under 70% of patients in both groups had baseline hypertension, another indication for the drugs.

Even so, the finding is probably real given the number of patients in the study. Most likely, the drugs were markers for additional risk factors not captured in the study, Dr. Kooda said.

Overall, 112 (20.7%) of the 540 thoracic patients and 107 (11%) of the 1,010 vascular patients developed new-onset AF a median of 55 hours after surgery. The incidence difference and timing are in line with previous reports.

The mean age in the AF group was 70 years, and in the non-AF group it was 66 years. In both, 65% were men, 5% had heart failure, 30% had diabetes, and 10% had prior strokes. Patients with pacemakers and recent myocardial infarctions – also possible settings for beta-blockers – were excluded from the trial.

The majority of the vascular cases were open aortic aneurysms, aortic bypasses, and thrombectomies or endarterectomies of central arteries. Most of the thoracic surgeries were lobectomies, pneumonectomies, and wedge or chest wall resections.

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Through genetic analysis, researchers used gene expression profiles to differentiate between several clinical phenotypes of VTE and distinguish high-risk patients from both low-risk patients and healthy controls, in a study published in Thrombosis Research.

Dr. Deborah A. Lewis of Duke University Medical Center and her associates used differential expression analysis to find several genes previously identified as potentially having a role in the development of thrombotic disorders, including SELP, KLKB1, ANXA5, andCD46. They then compared the genetic profiles of 107 patients, separated into low-, moderate-, or high-risk groups based on their clinical presentations of VTE, as well as 25 controls.

The most accurate comparisons were between the high-risk and low-risk groups, the high-risk group and the healthy controls, and the low-risk group and healthy controls, where the AUC levels were 0.81, 0.84 and 0.80 respectively.

“The profiles obtained … provide insights into approaches that might be useful in the identification of individuals with a single thrombotic event who are at highest risk for a recurrent VTE after completing a standard course of therapy,” the investigators wrote.

For the full article, click here (Thromb. Res. 2015 [doi:10.1016/j.thromres.2015.02.003]).

Through genetic analysis, researchers used gene expression profiles to differentiate between several clinical phenotypes of VTE and distinguish high-risk patients from both low-risk patients and healthy controls, in a study published in Thrombosis Research.

Dr. Deborah A. Lewis of Duke University Medical Center and her associates used differential expression analysis to find several genes previously identified as potentially having a role in the development of thrombotic disorders, including SELP, KLKB1, ANXA5, andCD46. They then compared the genetic profiles of 107 patients, separated into low-, moderate-, or high-risk groups based on their clinical presentations of VTE, as well as 25 controls.

The most accurate comparisons were between the high-risk and low-risk groups, the high-risk group and the healthy controls, and the low-risk group and healthy controls, where the AUC levels were 0.81, 0.84 and 0.80 respectively.

“The profiles obtained … provide insights into approaches that might be useful in the identification of individuals with a single thrombotic event who are at highest risk for a recurrent VTE after completing a standard course of therapy,” the investigators wrote.

For the full article, click here (Thromb. Res. 2015 [doi:10.1016/j.thromres.2015.02.003]).

Through genetic analysis, researchers used gene expression profiles to differentiate between several clinical phenotypes of VTE and distinguish high-risk patients from both low-risk patients and healthy controls, in a study published in Thrombosis Research.

Dr. Deborah A. Lewis of Duke University Medical Center and her associates used differential expression analysis to find several genes previously identified as potentially having a role in the development of thrombotic disorders, including SELP, KLKB1, ANXA5, andCD46. They then compared the genetic profiles of 107 patients, separated into low-, moderate-, or high-risk groups based on their clinical presentations of VTE, as well as 25 controls.

The most accurate comparisons were between the high-risk and low-risk groups, the high-risk group and the healthy controls, and the low-risk group and healthy controls, where the AUC levels were 0.81, 0.84 and 0.80 respectively.

“The profiles obtained … provide insights into approaches that might be useful in the identification of individuals with a single thrombotic event who are at highest risk for a recurrent VTE after completing a standard course of therapy,” the investigators wrote.

For the full article, click here (Thromb. Res. 2015 [doi:10.1016/j.thromres.2015.02.003]).