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MI risk prediction after noncardiac surgery simplified
ORLANDO – The risk of perioperative MI or death associated with noncardiac surgery is vanishingly low in patients free of diabetes, hypertension, and smoking, Tanya Wilcox, MD, reported at the annual meeting of the American College of Cardiology.
How small is the risk? A mere 1 in 1,000, according to her analysis of more than 3.8 million major noncardiac surgeries in the American College of Surgeons National Surgical Quality Improvement Program database for 2009-2015, according to Dr. Wilcox of New York University.
Physicians are frequently asked by surgeons to clear patients for noncardiac surgery in terms of cardiovascular risk. Because current risk scores are complex, aren’t amenable to rapid bedside calculations, and may entail cardiac stress testing, Dr. Wilcox decided it was worth assessing the impact of three straightforward cardiovascular risk factors – current smoking and treatment for hypertension or diabetes – on 30-day postoperative MI-free survival. For this purpose she turned to the National Surgical Quality Improvement Program database, a validated, risk-adjusted, outcomes-based program to measure and improve the quality of surgical care utilizing data from 250 U.S. surgical centers.
Of the 3,817,113 patients who underwent major noncardiac surgery, 1,586,020 (42%) of them had none of the three cardiovascular risk factors of interest, 1,541,846 (40%) had one, 643,424 (17%) had two, and 45,823, or 1.2%, had all three. The patients’ mean age was 57, 75% were white, and 57% were women. About half of all patients underwent various operations within the realm of general surgery; next most frequent were orthopedic procedures, accounting for 18% of total noncardiac surgery. Of note, only 23% of patients with zero risk factors were American Society of Anesthesiologists Class 3-5, compared with 51% of those with one cardiovascular risk factor, 76% with two, and 71% with all three.
The incidence of acute MI or death within 30 days of noncardiac surgery climbed in stepwise fashion according to a patient’s risk factor burden. In a multivariate analysis adjusted for age, race, and gender, patients with any one of the cardiovascular risk factors had a 30-day risk of acute MI or death that was 1.52 times greater than those with no risk factors, patients with two risk factors were at 2.4-fold increased risk, and those with all three were at 3.63-fold greater risk than those with none. The degree of increased risk associated with any single risk factor ranged from 1.47-fold for hypertension to 1.94-fold for smoking.
“Further study is needed to determine whether aggressive risk factor modifications in the form of blood pressure control, glycemic control, and smoking cessation could reduce the incidence of postoperative MI,” Dr. Wilcox observed.
She reported having no financial conflicts regarding her study.
ORLANDO – The risk of perioperative MI or death associated with noncardiac surgery is vanishingly low in patients free of diabetes, hypertension, and smoking, Tanya Wilcox, MD, reported at the annual meeting of the American College of Cardiology.
How small is the risk? A mere 1 in 1,000, according to her analysis of more than 3.8 million major noncardiac surgeries in the American College of Surgeons National Surgical Quality Improvement Program database for 2009-2015, according to Dr. Wilcox of New York University.
Physicians are frequently asked by surgeons to clear patients for noncardiac surgery in terms of cardiovascular risk. Because current risk scores are complex, aren’t amenable to rapid bedside calculations, and may entail cardiac stress testing, Dr. Wilcox decided it was worth assessing the impact of three straightforward cardiovascular risk factors – current smoking and treatment for hypertension or diabetes – on 30-day postoperative MI-free survival. For this purpose she turned to the National Surgical Quality Improvement Program database, a validated, risk-adjusted, outcomes-based program to measure and improve the quality of surgical care utilizing data from 250 U.S. surgical centers.
Of the 3,817,113 patients who underwent major noncardiac surgery, 1,586,020 (42%) of them had none of the three cardiovascular risk factors of interest, 1,541,846 (40%) had one, 643,424 (17%) had two, and 45,823, or 1.2%, had all three. The patients’ mean age was 57, 75% were white, and 57% were women. About half of all patients underwent various operations within the realm of general surgery; next most frequent were orthopedic procedures, accounting for 18% of total noncardiac surgery. Of note, only 23% of patients with zero risk factors were American Society of Anesthesiologists Class 3-5, compared with 51% of those with one cardiovascular risk factor, 76% with two, and 71% with all three.
The incidence of acute MI or death within 30 days of noncardiac surgery climbed in stepwise fashion according to a patient’s risk factor burden. In a multivariate analysis adjusted for age, race, and gender, patients with any one of the cardiovascular risk factors had a 30-day risk of acute MI or death that was 1.52 times greater than those with no risk factors, patients with two risk factors were at 2.4-fold increased risk, and those with all three were at 3.63-fold greater risk than those with none. The degree of increased risk associated with any single risk factor ranged from 1.47-fold for hypertension to 1.94-fold for smoking.
“Further study is needed to determine whether aggressive risk factor modifications in the form of blood pressure control, glycemic control, and smoking cessation could reduce the incidence of postoperative MI,” Dr. Wilcox observed.
She reported having no financial conflicts regarding her study.
ORLANDO – The risk of perioperative MI or death associated with noncardiac surgery is vanishingly low in patients free of diabetes, hypertension, and smoking, Tanya Wilcox, MD, reported at the annual meeting of the American College of Cardiology.
How small is the risk? A mere 1 in 1,000, according to her analysis of more than 3.8 million major noncardiac surgeries in the American College of Surgeons National Surgical Quality Improvement Program database for 2009-2015, according to Dr. Wilcox of New York University.
Physicians are frequently asked by surgeons to clear patients for noncardiac surgery in terms of cardiovascular risk. Because current risk scores are complex, aren’t amenable to rapid bedside calculations, and may entail cardiac stress testing, Dr. Wilcox decided it was worth assessing the impact of three straightforward cardiovascular risk factors – current smoking and treatment for hypertension or diabetes – on 30-day postoperative MI-free survival. For this purpose she turned to the National Surgical Quality Improvement Program database, a validated, risk-adjusted, outcomes-based program to measure and improve the quality of surgical care utilizing data from 250 U.S. surgical centers.
Of the 3,817,113 patients who underwent major noncardiac surgery, 1,586,020 (42%) of them had none of the three cardiovascular risk factors of interest, 1,541,846 (40%) had one, 643,424 (17%) had two, and 45,823, or 1.2%, had all three. The patients’ mean age was 57, 75% were white, and 57% were women. About half of all patients underwent various operations within the realm of general surgery; next most frequent were orthopedic procedures, accounting for 18% of total noncardiac surgery. Of note, only 23% of patients with zero risk factors were American Society of Anesthesiologists Class 3-5, compared with 51% of those with one cardiovascular risk factor, 76% with two, and 71% with all three.
The incidence of acute MI or death within 30 days of noncardiac surgery climbed in stepwise fashion according to a patient’s risk factor burden. In a multivariate analysis adjusted for age, race, and gender, patients with any one of the cardiovascular risk factors had a 30-day risk of acute MI or death that was 1.52 times greater than those with no risk factors, patients with two risk factors were at 2.4-fold increased risk, and those with all three were at 3.63-fold greater risk than those with none. The degree of increased risk associated with any single risk factor ranged from 1.47-fold for hypertension to 1.94-fold for smoking.
“Further study is needed to determine whether aggressive risk factor modifications in the form of blood pressure control, glycemic control, and smoking cessation could reduce the incidence of postoperative MI,” Dr. Wilcox observed.
She reported having no financial conflicts regarding her study.
REPORTING FROM ACC 2018
Key clinical point: Noncardiac surgery patients can breathe easier regarding perioperative cardiovascular risk provided they don’t smoke and aren’t hypertensive or diabetic.
Major finding: .
Study details: This was a retrospective analysis of more than 3.8 million noncardiac surgeries contained in the American College of Surgeons National Surgical Quality Improvement Program database for 2009-2015.
Disclosures: The study presenter reported having no financial conflicts.
Galectin-3: A new post-MI prognostic biomarker?
ORLANDO – An elevated circulating galactin-3 level after an acute MI is a potent long-term predictor of both heart failure and mortality, independent of known prognostic markers, Rabea Asleh, MD, PhD, reported at the annual meeting of the American College of Cardiology.
“These findings suggest that galectin-3 measurement may have a role in the risk stratification of patients presenting with MI,” according to Dr. Asleh, an Israeli cardiologist doing a fellowship in advanced heart failure and transplant cardiology at the Mayo Clinic in Rochester, Minn.
“The changing clinical presentation of MI necessitates evolution in our approach to risk stratification,” he explained. “Over the last 2 decades we’ve observed a change in the epidemiology of MI, with more patients developing non-ST-elevation MI compared to STEMI. They present at an older age and develop heart failure with preserved ejection fraction more than heart failure with reduced ejection fraction.”
He presented a prospective population-based community cohort study of 1,401 Olmsted County, Minn., residents who had a validated MI during 2002-2012. Their mean age was 67 years, 61% were men, and 79% presented with non-STEMI. During a mean follow-up of 5.3 years, 389 of the participants developed heart failure and 512 patients died.
Galectin-3 was measured a median of 2 days post MI. The median level was 18.4 ng/mL. Patients were divided into tertiles based upon their galactin-3 measurement: Tertile 1 required a post-MI galectin-3 level below 15.2 ng/mL; tertile 2 had a level of 15.2-22.6 ng/mL; and the top tertile was for individuals with a galectin-3 above 22.6 ng/mL.
Of note, patients with a higher galectin-3 level were older, had a higher prevalence of diabetes, hypertension, hyperlipidemia, anterior MI, a higher Killip class, a higher Charlson comorbidity score, and a lower peak troponin T level. They also had a lower estimated glomerular filtration rate; indeed, the median eGFR in the top tertile for galactin-3 was 48 mL/min per 1.73 m2, compared with 68 mL/min in the lowest galectin-3 tertile. Women accounted for 27% of patients in tertile 1, 41% in tertile 2, and fully half of those in tertile 3.
In an unadjusted analysis, the risk of mortality during follow-up was sixfold greater for patients in galectin-3 tertile 3 than in tertile 1; the risk of heart failure was increased 5.5-fold.
More meaningfully, in a Cox multivariate analysis extensively adjusted for age, gender, comorbidities, malignancy, standard cardiovascular risk factors, MI characteristics, eGFR, Killip class, cardiac troponin T, and other potential confounders, patients in galectin-3 tertile 2 had a 1.6-fold increased risk of death and a 1.62-fold increased likelihood of heart failure during follow-up, compared with subjects in tertile 1, Dr. Asleh noted.
Patients in tertile 3 had a 2.4-fold increased risk of death and were at 2.1 times greater risk of heart failure than those in tertile 1. The degree of risk for heart failure associated with elevated galactin-3 was virtually identical for heart failure with preserved as compared with reduced ejection fraction, he added.
Session cochair L. Kristin Newby, MD, of Duke University, Durham, N.C., noted that the Mayo study did not adjust for brain natriuretic peptide (BNP) or N-terminal pro hormone BNP (NT-proBNP), both of which are known to be strong predictors of both heart failure and mortality after acute MI. Doesn’t their absence weaken the strength of galactin-3’s prognostic power as demonstrated in the study? she asked.
Dr. Asleh replied that those biomarkers weren’t collected in this study, which began in 2002.
“What I can tell you is, other studies show there is only a weak correlation between galactin-3 and NT-proBNP post MI. Some studies have even shown an inverse correlation,” he said. “The pathophysiological explanation is that galactin-3 is more implicated in fibrosis before the stage of development of left ventricular loading and stretching of the myocardium. So galactin-3 may be implicated in LV fibrosis leading to heart failure before the NT-proBNP comes into play.”
Also, he cited a study by other investigators conducted in patients with a left ventricular assist device for advanced heart failure. Upon device-induced left ventricular unloading the patients’ NT-proBNP levels dropped significantly while their galactin-3 remained high and unchanged. This suggests the two biomarkers are implicated in different disease pathways.
Both animal and human studies indicate galactin-3 is involved specifically in fibrosis, as opposed to, say, C-reactive protein, a well established marker of systemic inflammation, the cardiologist added.
Dr. Asleh reported having no financial conflicts of interest regarding his study, which was supported by the National Institutes of Health.
ORLANDO – An elevated circulating galactin-3 level after an acute MI is a potent long-term predictor of both heart failure and mortality, independent of known prognostic markers, Rabea Asleh, MD, PhD, reported at the annual meeting of the American College of Cardiology.
“These findings suggest that galectin-3 measurement may have a role in the risk stratification of patients presenting with MI,” according to Dr. Asleh, an Israeli cardiologist doing a fellowship in advanced heart failure and transplant cardiology at the Mayo Clinic in Rochester, Minn.
“The changing clinical presentation of MI necessitates evolution in our approach to risk stratification,” he explained. “Over the last 2 decades we’ve observed a change in the epidemiology of MI, with more patients developing non-ST-elevation MI compared to STEMI. They present at an older age and develop heart failure with preserved ejection fraction more than heart failure with reduced ejection fraction.”
He presented a prospective population-based community cohort study of 1,401 Olmsted County, Minn., residents who had a validated MI during 2002-2012. Their mean age was 67 years, 61% were men, and 79% presented with non-STEMI. During a mean follow-up of 5.3 years, 389 of the participants developed heart failure and 512 patients died.
Galectin-3 was measured a median of 2 days post MI. The median level was 18.4 ng/mL. Patients were divided into tertiles based upon their galactin-3 measurement: Tertile 1 required a post-MI galectin-3 level below 15.2 ng/mL; tertile 2 had a level of 15.2-22.6 ng/mL; and the top tertile was for individuals with a galectin-3 above 22.6 ng/mL.
Of note, patients with a higher galectin-3 level were older, had a higher prevalence of diabetes, hypertension, hyperlipidemia, anterior MI, a higher Killip class, a higher Charlson comorbidity score, and a lower peak troponin T level. They also had a lower estimated glomerular filtration rate; indeed, the median eGFR in the top tertile for galactin-3 was 48 mL/min per 1.73 m2, compared with 68 mL/min in the lowest galectin-3 tertile. Women accounted for 27% of patients in tertile 1, 41% in tertile 2, and fully half of those in tertile 3.
In an unadjusted analysis, the risk of mortality during follow-up was sixfold greater for patients in galectin-3 tertile 3 than in tertile 1; the risk of heart failure was increased 5.5-fold.
More meaningfully, in a Cox multivariate analysis extensively adjusted for age, gender, comorbidities, malignancy, standard cardiovascular risk factors, MI characteristics, eGFR, Killip class, cardiac troponin T, and other potential confounders, patients in galectin-3 tertile 2 had a 1.6-fold increased risk of death and a 1.62-fold increased likelihood of heart failure during follow-up, compared with subjects in tertile 1, Dr. Asleh noted.
Patients in tertile 3 had a 2.4-fold increased risk of death and were at 2.1 times greater risk of heart failure than those in tertile 1. The degree of risk for heart failure associated with elevated galactin-3 was virtually identical for heart failure with preserved as compared with reduced ejection fraction, he added.
Session cochair L. Kristin Newby, MD, of Duke University, Durham, N.C., noted that the Mayo study did not adjust for brain natriuretic peptide (BNP) or N-terminal pro hormone BNP (NT-proBNP), both of which are known to be strong predictors of both heart failure and mortality after acute MI. Doesn’t their absence weaken the strength of galactin-3’s prognostic power as demonstrated in the study? she asked.
Dr. Asleh replied that those biomarkers weren’t collected in this study, which began in 2002.
“What I can tell you is, other studies show there is only a weak correlation between galactin-3 and NT-proBNP post MI. Some studies have even shown an inverse correlation,” he said. “The pathophysiological explanation is that galactin-3 is more implicated in fibrosis before the stage of development of left ventricular loading and stretching of the myocardium. So galactin-3 may be implicated in LV fibrosis leading to heart failure before the NT-proBNP comes into play.”
Also, he cited a study by other investigators conducted in patients with a left ventricular assist device for advanced heart failure. Upon device-induced left ventricular unloading the patients’ NT-proBNP levels dropped significantly while their galactin-3 remained high and unchanged. This suggests the two biomarkers are implicated in different disease pathways.
Both animal and human studies indicate galactin-3 is involved specifically in fibrosis, as opposed to, say, C-reactive protein, a well established marker of systemic inflammation, the cardiologist added.
Dr. Asleh reported having no financial conflicts of interest regarding his study, which was supported by the National Institutes of Health.
ORLANDO – An elevated circulating galactin-3 level after an acute MI is a potent long-term predictor of both heart failure and mortality, independent of known prognostic markers, Rabea Asleh, MD, PhD, reported at the annual meeting of the American College of Cardiology.
“These findings suggest that galectin-3 measurement may have a role in the risk stratification of patients presenting with MI,” according to Dr. Asleh, an Israeli cardiologist doing a fellowship in advanced heart failure and transplant cardiology at the Mayo Clinic in Rochester, Minn.
“The changing clinical presentation of MI necessitates evolution in our approach to risk stratification,” he explained. “Over the last 2 decades we’ve observed a change in the epidemiology of MI, with more patients developing non-ST-elevation MI compared to STEMI. They present at an older age and develop heart failure with preserved ejection fraction more than heart failure with reduced ejection fraction.”
He presented a prospective population-based community cohort study of 1,401 Olmsted County, Minn., residents who had a validated MI during 2002-2012. Their mean age was 67 years, 61% were men, and 79% presented with non-STEMI. During a mean follow-up of 5.3 years, 389 of the participants developed heart failure and 512 patients died.
Galectin-3 was measured a median of 2 days post MI. The median level was 18.4 ng/mL. Patients were divided into tertiles based upon their galactin-3 measurement: Tertile 1 required a post-MI galectin-3 level below 15.2 ng/mL; tertile 2 had a level of 15.2-22.6 ng/mL; and the top tertile was for individuals with a galectin-3 above 22.6 ng/mL.
Of note, patients with a higher galectin-3 level were older, had a higher prevalence of diabetes, hypertension, hyperlipidemia, anterior MI, a higher Killip class, a higher Charlson comorbidity score, and a lower peak troponin T level. They also had a lower estimated glomerular filtration rate; indeed, the median eGFR in the top tertile for galactin-3 was 48 mL/min per 1.73 m2, compared with 68 mL/min in the lowest galectin-3 tertile. Women accounted for 27% of patients in tertile 1, 41% in tertile 2, and fully half of those in tertile 3.
In an unadjusted analysis, the risk of mortality during follow-up was sixfold greater for patients in galectin-3 tertile 3 than in tertile 1; the risk of heart failure was increased 5.5-fold.
More meaningfully, in a Cox multivariate analysis extensively adjusted for age, gender, comorbidities, malignancy, standard cardiovascular risk factors, MI characteristics, eGFR, Killip class, cardiac troponin T, and other potential confounders, patients in galectin-3 tertile 2 had a 1.6-fold increased risk of death and a 1.62-fold increased likelihood of heart failure during follow-up, compared with subjects in tertile 1, Dr. Asleh noted.
Patients in tertile 3 had a 2.4-fold increased risk of death and were at 2.1 times greater risk of heart failure than those in tertile 1. The degree of risk for heart failure associated with elevated galactin-3 was virtually identical for heart failure with preserved as compared with reduced ejection fraction, he added.
Session cochair L. Kristin Newby, MD, of Duke University, Durham, N.C., noted that the Mayo study did not adjust for brain natriuretic peptide (BNP) or N-terminal pro hormone BNP (NT-proBNP), both of which are known to be strong predictors of both heart failure and mortality after acute MI. Doesn’t their absence weaken the strength of galactin-3’s prognostic power as demonstrated in the study? she asked.
Dr. Asleh replied that those biomarkers weren’t collected in this study, which began in 2002.
“What I can tell you is, other studies show there is only a weak correlation between galactin-3 and NT-proBNP post MI. Some studies have even shown an inverse correlation,” he said. “The pathophysiological explanation is that galactin-3 is more implicated in fibrosis before the stage of development of left ventricular loading and stretching of the myocardium. So galactin-3 may be implicated in LV fibrosis leading to heart failure before the NT-proBNP comes into play.”
Also, he cited a study by other investigators conducted in patients with a left ventricular assist device for advanced heart failure. Upon device-induced left ventricular unloading the patients’ NT-proBNP levels dropped significantly while their galactin-3 remained high and unchanged. This suggests the two biomarkers are implicated in different disease pathways.
Both animal and human studies indicate galactin-3 is involved specifically in fibrosis, as opposed to, say, C-reactive protein, a well established marker of systemic inflammation, the cardiologist added.
Dr. Asleh reported having no financial conflicts of interest regarding his study, which was supported by the National Institutes of Health.
REPORTING FROM ACC 18
Key clinical point: Galectin-3 level post-MI is a potent long-term predictor of both heart failure and mortality independent of known prognostic markers.
Major finding: Post-MI patients in the top tertile of circulating galectin-3 were at an adjusted 2.4-fold increased mortality risk and a 2.05-fold greater risk of developing heart failure compared with those in the lowest tertile.
Study details: This prospective population-based cohort study included 1,401 MI patients followed for a mean of 5.3 years.
Disclosures: The National Institutes of Health supported the study. The presenter reported having no financial conflicts of interest.
Serum uromodulin independently predicts mortality in CAD
ORLANDO – Low serum uromodulin proved to be an independent predictor of all-cause mortality in a prospective study of 529 patients with stable coronary artery disease followed for up to 8 years, according to Christoph Saely, MD, vice president of the Vorarlberg Institute for Vascular Investigation and Treatment in Feldkirch, Austria.
“Baseline serum uromodulin is a valuable biomarker to predict overall mortality in coronary patients independent from kidney disease and the presence of type 2 diabetes. The lower the serum uromodulin, the higher the mortality,” he noted in an interview at the annual meeting of the American College of Cardiology.
In addition to presenting new evidence at ACC 2018 of serum uromodulin’s merits as a predictor of increased mortality risk in patients with CAD, Dr. Saely and his coinvestigators also showed that low serum uromodulin is associated with chronic kidney disease, type 2 diabetes, and prediabetes. Moreover, those with normal glucose metabolism and kidney function but a low serum uromodulin at baseline were at increased risk of developing abnormal glucose metabolism and impaired renal function during 4 years of follow-up.
Of the 529 patients with stable CAD, 95 died during follow-up. Among those with a low baseline serum uromodulin, defined bimodally as a level below 123.3 ng/mL, the mortality rate was 27.6%, roughly twice the 13.7% figure in patients with a baseline uromodulin above that threshold.
In a multivariate analysis adjusted extensively for age, sex, smoking, LDL cholesterol, HDL cholesterol, C-reactive protein, diabetes, estimated glomerular filtration rate, and N-terminal pro b-type natriuretic peptide level, a high baseline serum uromodulin was independently associated with a 43% reduction in the risk of mortality, according to Dr. Saely, who is both a cardiologist and an endocrinologist.
The overall mortality rate was 41% in patients with diabetes and a low baseline uromodulin, 20% in those with low uromodulin but not diabetes, 18% in diabetic patients with high uromodulin, and less than 13% with high uromodulin and no diabetes.
Enzyme-linked immunosorbent assay tests for uromodulin are marketed in Europe but remain investigational for now in the United States.
Dr. Saely reported having no financial conflicts of interest; the study was conducted without commercial support.
SOURCE: Saely C. ACC 2018, Abstract 1212-418/418.
ORLANDO – Low serum uromodulin proved to be an independent predictor of all-cause mortality in a prospective study of 529 patients with stable coronary artery disease followed for up to 8 years, according to Christoph Saely, MD, vice president of the Vorarlberg Institute for Vascular Investigation and Treatment in Feldkirch, Austria.
“Baseline serum uromodulin is a valuable biomarker to predict overall mortality in coronary patients independent from kidney disease and the presence of type 2 diabetes. The lower the serum uromodulin, the higher the mortality,” he noted in an interview at the annual meeting of the American College of Cardiology.
In addition to presenting new evidence at ACC 2018 of serum uromodulin’s merits as a predictor of increased mortality risk in patients with CAD, Dr. Saely and his coinvestigators also showed that low serum uromodulin is associated with chronic kidney disease, type 2 diabetes, and prediabetes. Moreover, those with normal glucose metabolism and kidney function but a low serum uromodulin at baseline were at increased risk of developing abnormal glucose metabolism and impaired renal function during 4 years of follow-up.
Of the 529 patients with stable CAD, 95 died during follow-up. Among those with a low baseline serum uromodulin, defined bimodally as a level below 123.3 ng/mL, the mortality rate was 27.6%, roughly twice the 13.7% figure in patients with a baseline uromodulin above that threshold.
In a multivariate analysis adjusted extensively for age, sex, smoking, LDL cholesterol, HDL cholesterol, C-reactive protein, diabetes, estimated glomerular filtration rate, and N-terminal pro b-type natriuretic peptide level, a high baseline serum uromodulin was independently associated with a 43% reduction in the risk of mortality, according to Dr. Saely, who is both a cardiologist and an endocrinologist.
The overall mortality rate was 41% in patients with diabetes and a low baseline uromodulin, 20% in those with low uromodulin but not diabetes, 18% in diabetic patients with high uromodulin, and less than 13% with high uromodulin and no diabetes.
Enzyme-linked immunosorbent assay tests for uromodulin are marketed in Europe but remain investigational for now in the United States.
Dr. Saely reported having no financial conflicts of interest; the study was conducted without commercial support.
SOURCE: Saely C. ACC 2018, Abstract 1212-418/418.
ORLANDO – Low serum uromodulin proved to be an independent predictor of all-cause mortality in a prospective study of 529 patients with stable coronary artery disease followed for up to 8 years, according to Christoph Saely, MD, vice president of the Vorarlberg Institute for Vascular Investigation and Treatment in Feldkirch, Austria.
“Baseline serum uromodulin is a valuable biomarker to predict overall mortality in coronary patients independent from kidney disease and the presence of type 2 diabetes. The lower the serum uromodulin, the higher the mortality,” he noted in an interview at the annual meeting of the American College of Cardiology.
In addition to presenting new evidence at ACC 2018 of serum uromodulin’s merits as a predictor of increased mortality risk in patients with CAD, Dr. Saely and his coinvestigators also showed that low serum uromodulin is associated with chronic kidney disease, type 2 diabetes, and prediabetes. Moreover, those with normal glucose metabolism and kidney function but a low serum uromodulin at baseline were at increased risk of developing abnormal glucose metabolism and impaired renal function during 4 years of follow-up.
Of the 529 patients with stable CAD, 95 died during follow-up. Among those with a low baseline serum uromodulin, defined bimodally as a level below 123.3 ng/mL, the mortality rate was 27.6%, roughly twice the 13.7% figure in patients with a baseline uromodulin above that threshold.
In a multivariate analysis adjusted extensively for age, sex, smoking, LDL cholesterol, HDL cholesterol, C-reactive protein, diabetes, estimated glomerular filtration rate, and N-terminal pro b-type natriuretic peptide level, a high baseline serum uromodulin was independently associated with a 43% reduction in the risk of mortality, according to Dr. Saely, who is both a cardiologist and an endocrinologist.
The overall mortality rate was 41% in patients with diabetes and a low baseline uromodulin, 20% in those with low uromodulin but not diabetes, 18% in diabetic patients with high uromodulin, and less than 13% with high uromodulin and no diabetes.
Enzyme-linked immunosorbent assay tests for uromodulin are marketed in Europe but remain investigational for now in the United States.
Dr. Saely reported having no financial conflicts of interest; the study was conducted without commercial support.
SOURCE: Saely C. ACC 2018, Abstract 1212-418/418.
REPORTING FROM ACC 2018
Key clinical point: The lower the baseline serum uromodulin in patients with CAD, the higher the subsequent mortality.
Major finding: A high baseline serum uromodulin was independently associated with a 43% reduction in all-cause mortality in patients with stable coronary artery disease.
Study details: This was a prospective study of 529 patients with stable CAD followed for up to 8 years.
Disclosures: The presenter reported having no financial conflicts regarding the study, which was conducted without commercial support.
Source: Saely C. ACC 2018, Abstract 1212-418/418.
Antidepressant therapy after MI, stroke cut CVD events
ORLANDO – Although cardiologists and neurologists aren’t typically the physicians who diagnose and treat major depressive disorder that’s newly identified in patients after MI or stroke, they’re the ones who’ll deal with the cardiovascular consequences if the mood disorder isn’t adequately treated.
That was a key message of a study presented by interventional cardiologist Sripal Bangalore, MD, at the annual meeting of the American College of Cardiology.
In his retrospective cohort study of 1,568 patients diagnosed with and treated for major depressive disorder (MDD) following an initial acute MI or stroke, antidepressant therapy deemed inadequate by either of two prespecified measures was associated during a mean follow-up of 2 years with a 20% higher risk of the primary endpoint – a composite of recurrent MI, stroke, angina, or heart failure – than the risk in patients who received what was judged to be adequate antidepressant pharmacotherapy. A precondition for study inclusion was that a patient could not have been taking any antidepressant during the year prior to the index MI or stroke.
The study utilized nationwide claims data from the Truven Health MarketScan Claims Database for 2010-2015. Depression therapy was considered adequate if during the first 90 days following diagnosis of MDD two conditions were met: a patient aged 65 or younger had to be on the equivalent of at least 20 mg of fluoxetine per day, or if older then on a fluoxetine-equivalent dose of at least 10 mg/day, and pharmacy records had to indicate the patient was covered by the antidepressant prescription for at least 72 of those 90 days.
The prevalence of inadequate antidepressant therapy for MDD by these criteria among these patients with known cardiovascular disease was eyebrow-raisingly high: fully 60%, noted Dr. Bangalore of New York University.
In a multivariate logistic regression analysis adjusted for baseline factors that could affect the propensity to receive adequate antidepressant care, Dr. Bangalore and his coinvestigators broke down the risks of insufficient antidepressant therapy associated with each of the individual components of the composite primary endpoint. The 1.2- and 1.95-fold increased risks of stroke and angina, respectively, were statistically significant. However, the 1.37-fold higher risk of MI and 1.14-fold greater risk of heart failure than in adequately treated patients with MDD, while trending in the same direction, didn’t achieve significance.
Dr. Bangalore reported serving as a consultant to Pfizer, which funded the study, as well as to Abbott, Gilead Sciences, and Merck.
ORLANDO – Although cardiologists and neurologists aren’t typically the physicians who diagnose and treat major depressive disorder that’s newly identified in patients after MI or stroke, they’re the ones who’ll deal with the cardiovascular consequences if the mood disorder isn’t adequately treated.
That was a key message of a study presented by interventional cardiologist Sripal Bangalore, MD, at the annual meeting of the American College of Cardiology.
In his retrospective cohort study of 1,568 patients diagnosed with and treated for major depressive disorder (MDD) following an initial acute MI or stroke, antidepressant therapy deemed inadequate by either of two prespecified measures was associated during a mean follow-up of 2 years with a 20% higher risk of the primary endpoint – a composite of recurrent MI, stroke, angina, or heart failure – than the risk in patients who received what was judged to be adequate antidepressant pharmacotherapy. A precondition for study inclusion was that a patient could not have been taking any antidepressant during the year prior to the index MI or stroke.
The study utilized nationwide claims data from the Truven Health MarketScan Claims Database for 2010-2015. Depression therapy was considered adequate if during the first 90 days following diagnosis of MDD two conditions were met: a patient aged 65 or younger had to be on the equivalent of at least 20 mg of fluoxetine per day, or if older then on a fluoxetine-equivalent dose of at least 10 mg/day, and pharmacy records had to indicate the patient was covered by the antidepressant prescription for at least 72 of those 90 days.
The prevalence of inadequate antidepressant therapy for MDD by these criteria among these patients with known cardiovascular disease was eyebrow-raisingly high: fully 60%, noted Dr. Bangalore of New York University.
In a multivariate logistic regression analysis adjusted for baseline factors that could affect the propensity to receive adequate antidepressant care, Dr. Bangalore and his coinvestigators broke down the risks of insufficient antidepressant therapy associated with each of the individual components of the composite primary endpoint. The 1.2- and 1.95-fold increased risks of stroke and angina, respectively, were statistically significant. However, the 1.37-fold higher risk of MI and 1.14-fold greater risk of heart failure than in adequately treated patients with MDD, while trending in the same direction, didn’t achieve significance.
Dr. Bangalore reported serving as a consultant to Pfizer, which funded the study, as well as to Abbott, Gilead Sciences, and Merck.
ORLANDO – Although cardiologists and neurologists aren’t typically the physicians who diagnose and treat major depressive disorder that’s newly identified in patients after MI or stroke, they’re the ones who’ll deal with the cardiovascular consequences if the mood disorder isn’t adequately treated.
That was a key message of a study presented by interventional cardiologist Sripal Bangalore, MD, at the annual meeting of the American College of Cardiology.
In his retrospective cohort study of 1,568 patients diagnosed with and treated for major depressive disorder (MDD) following an initial acute MI or stroke, antidepressant therapy deemed inadequate by either of two prespecified measures was associated during a mean follow-up of 2 years with a 20% higher risk of the primary endpoint – a composite of recurrent MI, stroke, angina, or heart failure – than the risk in patients who received what was judged to be adequate antidepressant pharmacotherapy. A precondition for study inclusion was that a patient could not have been taking any antidepressant during the year prior to the index MI or stroke.
The study utilized nationwide claims data from the Truven Health MarketScan Claims Database for 2010-2015. Depression therapy was considered adequate if during the first 90 days following diagnosis of MDD two conditions were met: a patient aged 65 or younger had to be on the equivalent of at least 20 mg of fluoxetine per day, or if older then on a fluoxetine-equivalent dose of at least 10 mg/day, and pharmacy records had to indicate the patient was covered by the antidepressant prescription for at least 72 of those 90 days.
The prevalence of inadequate antidepressant therapy for MDD by these criteria among these patients with known cardiovascular disease was eyebrow-raisingly high: fully 60%, noted Dr. Bangalore of New York University.
In a multivariate logistic regression analysis adjusted for baseline factors that could affect the propensity to receive adequate antidepressant care, Dr. Bangalore and his coinvestigators broke down the risks of insufficient antidepressant therapy associated with each of the individual components of the composite primary endpoint. The 1.2- and 1.95-fold increased risks of stroke and angina, respectively, were statistically significant. However, the 1.37-fold higher risk of MI and 1.14-fold greater risk of heart failure than in adequately treated patients with MDD, while trending in the same direction, didn’t achieve significance.
Dr. Bangalore reported serving as a consultant to Pfizer, which funded the study, as well as to Abbott, Gilead Sciences, and Merck.
REPORTING FROM ACC 2018
Key clinical point: Make sure patients with newly diagnosed depression post-MI or stroke are getting adequate antidepressant therapy from their primary care physician or psychiatrist.
Major finding: Patients with a first MI or stroke subsequently diagnosed with major depressive disorder were 20% more likely to experience a recurrent cardiovascular event if their antidepressant therapy was judged insufficient than if adequate.
Study details: This was a retrospective cohort study of health insurance claims data for 1,568 patients with an initial diagnosis of MI or stroke who were subsequently diagnosed with and treated for major depressive disorder.
Disclosures: The presenter reported serving as a consultant to Pfizer, which funded the study.
Ad hoc PCI dominates in elderly
ORLANDO – Ad hoc percutaneous coronary intervention is performed nearly six times more frequently than planned PCI in older patients undergoing elective PCI for stable coronary artery disease, according to a national study of Medicare claims data for 2009-2014.
The data showed no evident downside to ad hoc PCI in patients over age 65. Indeed, the ad hoc PCI strategy was associated with a significantly lower adjusted risk of in-hospital bleeding, compared with non–ad hoc PCI. The two approaches didn’t differ significantly in terms of in-hospital acute kidney injury or mortality, Kamil F. Faridi, MD, reported at the annual meeting of the American College of Cardiology.
In the past, concern had been voiced that ad hoc PCI – that is, PCI performed during the same session as diagnostic coronary angiography – doesn’t allow time for optimization of medical therapy prior to intervention, which might in theory result in worse outcomes. But such was not the case in a study of 169,434 patients age 65 years and up who underwent PCI for stable CAD with no evidence of acute coronary syndrome.
Moreover, ad hoc PCI offers several distinct advantages: a single vascular access, shorter net time in hospital, and lower cost, noted Dr. Faridi, of Beth Israel Deaconess Medical Center in Boston.
The proportion of elective PCIs that were performed on an ad hoc basis rose during the study years, from 77% in 2009 to 85% in 2014.
Patients who underwent ad hoc PCI were more likely to have angina symptoms before intervention. They were less likely to have peripheral vascular disease, heart failure, chronic kidney disease, complex lesion anatomy, or multivessel PCI than were patients who had planned PCI. Non–ad hoc PCI was more likely to occur at high-volume centers.
The in-hospital bleeding rate was 2.9% in the ad hoc PCI group, significantly lower than the 3.8% rate in the planned PCI patients. In an analysis adjusted for potential confounders, this translated to a 14% relative risk reduction. In-hospital acute kidney injury occurred in 8.0% of the ad hoc PCI group and 9.2% of the planned PCI group. The in-hospital mortality rate was 0.4% with ad hoc and 0.5% with planned PCI.
Dr. Faridi’s study was supported by the ACC National Cardiovascular Data Registry. He reported having no financial conflicts.
SOURCE: Faridi KF. ACC 2018, Abstract 1306-468/468
ORLANDO – Ad hoc percutaneous coronary intervention is performed nearly six times more frequently than planned PCI in older patients undergoing elective PCI for stable coronary artery disease, according to a national study of Medicare claims data for 2009-2014.
The data showed no evident downside to ad hoc PCI in patients over age 65. Indeed, the ad hoc PCI strategy was associated with a significantly lower adjusted risk of in-hospital bleeding, compared with non–ad hoc PCI. The two approaches didn’t differ significantly in terms of in-hospital acute kidney injury or mortality, Kamil F. Faridi, MD, reported at the annual meeting of the American College of Cardiology.
In the past, concern had been voiced that ad hoc PCI – that is, PCI performed during the same session as diagnostic coronary angiography – doesn’t allow time for optimization of medical therapy prior to intervention, which might in theory result in worse outcomes. But such was not the case in a study of 169,434 patients age 65 years and up who underwent PCI for stable CAD with no evidence of acute coronary syndrome.
Moreover, ad hoc PCI offers several distinct advantages: a single vascular access, shorter net time in hospital, and lower cost, noted Dr. Faridi, of Beth Israel Deaconess Medical Center in Boston.
The proportion of elective PCIs that were performed on an ad hoc basis rose during the study years, from 77% in 2009 to 85% in 2014.
Patients who underwent ad hoc PCI were more likely to have angina symptoms before intervention. They were less likely to have peripheral vascular disease, heart failure, chronic kidney disease, complex lesion anatomy, or multivessel PCI than were patients who had planned PCI. Non–ad hoc PCI was more likely to occur at high-volume centers.
The in-hospital bleeding rate was 2.9% in the ad hoc PCI group, significantly lower than the 3.8% rate in the planned PCI patients. In an analysis adjusted for potential confounders, this translated to a 14% relative risk reduction. In-hospital acute kidney injury occurred in 8.0% of the ad hoc PCI group and 9.2% of the planned PCI group. The in-hospital mortality rate was 0.4% with ad hoc and 0.5% with planned PCI.
Dr. Faridi’s study was supported by the ACC National Cardiovascular Data Registry. He reported having no financial conflicts.
SOURCE: Faridi KF. ACC 2018, Abstract 1306-468/468
ORLANDO – Ad hoc percutaneous coronary intervention is performed nearly six times more frequently than planned PCI in older patients undergoing elective PCI for stable coronary artery disease, according to a national study of Medicare claims data for 2009-2014.
The data showed no evident downside to ad hoc PCI in patients over age 65. Indeed, the ad hoc PCI strategy was associated with a significantly lower adjusted risk of in-hospital bleeding, compared with non–ad hoc PCI. The two approaches didn’t differ significantly in terms of in-hospital acute kidney injury or mortality, Kamil F. Faridi, MD, reported at the annual meeting of the American College of Cardiology.
In the past, concern had been voiced that ad hoc PCI – that is, PCI performed during the same session as diagnostic coronary angiography – doesn’t allow time for optimization of medical therapy prior to intervention, which might in theory result in worse outcomes. But such was not the case in a study of 169,434 patients age 65 years and up who underwent PCI for stable CAD with no evidence of acute coronary syndrome.
Moreover, ad hoc PCI offers several distinct advantages: a single vascular access, shorter net time in hospital, and lower cost, noted Dr. Faridi, of Beth Israel Deaconess Medical Center in Boston.
The proportion of elective PCIs that were performed on an ad hoc basis rose during the study years, from 77% in 2009 to 85% in 2014.
Patients who underwent ad hoc PCI were more likely to have angina symptoms before intervention. They were less likely to have peripheral vascular disease, heart failure, chronic kidney disease, complex lesion anatomy, or multivessel PCI than were patients who had planned PCI. Non–ad hoc PCI was more likely to occur at high-volume centers.
The in-hospital bleeding rate was 2.9% in the ad hoc PCI group, significantly lower than the 3.8% rate in the planned PCI patients. In an analysis adjusted for potential confounders, this translated to a 14% relative risk reduction. In-hospital acute kidney injury occurred in 8.0% of the ad hoc PCI group and 9.2% of the planned PCI group. The in-hospital mortality rate was 0.4% with ad hoc and 0.5% with planned PCI.
Dr. Faridi’s study was supported by the ACC National Cardiovascular Data Registry. He reported having no financial conflicts.
SOURCE: Faridi KF. ACC 2018, Abstract 1306-468/468
REPORTING FROM ACC 2018
Key clinical point: Ad hoc PCI in older patients has a lower bleeding risk than non–ad hoc PCI.
Major finding: Older patients undergoing ad hoc PCI for stable CAD were 14% less likely to experience significant in-hospital bleeding than were those undergoing planned PCI.
Study details: This was a retrospective study of nearly 170,000 patients age 65 years or older who underwent elective PCI for stable CAD.
Disclosures: The study was supported by the ACC National Cardiovascular Data Registry. The presenter reported having no financial conflicts.
Source: Faridi KF. ACC 2018, Abstract 1306-468/468
To detect subclinical AF, insertable monitor is unequaled
ORLANDO – with other intermittent ambulatory monitoring strategies, in a secondary analysis from the REVEAL AF study.
“If you really want to look for atrial fibrillation because your concern is that the patient has a high-risk profile, and if you saw it you would anticoagulate it and maybe prophylactically use rate control, nothing beats the implanted monitor,” James A. Reiffel, MD, said at the annual meeting of the American College of Cardiology.
As previously reported (JAMA Cardiol. 2017 Oct 1;2[10]:1120-7), the primary outcome – an AF episode lasting for at least 6 minutes – occurred during the first 18 months of the study in 29% of participants. By 30 months, it was 40%. At ACC 2018, Dr. Reiffel presented a new analysis looking at how the insertable cardiac monitor (ICM) would have stacked up against other device-based strategies aimed at detecting silent AF, including a 30-day implantable memory loop, daily transtelephonic ECG monitoring, and one-time or periodic 24- or 48-hour Holter monitoring.
To accomplish this, he and his coinvestigators conducted modeling studies harnessing the REVEAL AF continuous monitoring data. They looked at how many of the real-world patients found to have AF in the study would have been identified had they instead undergone a one-time recording period lasting 1, 2, 7, 14, or 30 days beginning at the time they would have received their ICM. They also looked at the yield of repeated monitoring strategies, including monthly or quarterly 24- or 48-hour Holter monitoring sessions. They repeated the various simulated monitoring strategies 10,000 times each in order to beef up the sample size and stability of the results.
It was no contest, according to Dr. Reiffel, professor of clinical medicine at Columbia University in New York.
That’s because the median time to AF detection in REVEAL AF was 123 days. Thus, any monitoring strategy of 30 days duration or less was doomed to be of comparatively low yield. Indeed, the 12-month AF incidence rate as detected by ICM in REVEAL AF was 27.1%, compared with 1.1%-13.5% for the various modeled monitoring strategies.
Among patients who met the primary endpoint in REVEAL AF, 10.2% had one or more AF episodes lasting 24 hours or more. So a significant proportion of the asymptomatic episodes of AF were not brief.
The take-home lesson of this analysis is straightforward, he said. “While the incidence of screen-detected atrial fibrillation is dependent upon the population screened, it is also strongly dependent upon the duration and intensity of monitoring.”
Session cochair Jeanne E. Poole, MD, observed that while the new REVEAL AF analysis is informative, it leaves unanswered the big questions regarding the clinical importance of these silent episodes of subclinical device-detected AF. That is, are these episodes associated with significantly increased stroke risk, and if so are they just another nonmodifiable risk marker, or are they a risk factor that can be dampened via oral anticoagulation, like symptomatic AF? said Dr. Poole, professor of medicine and director of the clinical cardiac electrophysiology program at the University of Washington, Seattle.
“My own belief is that they are both a risk marker and a risk factor that contributes to stroke,” Dr. Reiffel replied.
He noted that there are two major ongoing clinical trials evaluating the impact of oral anticoagulation in patients with ICM-detected AF. The 3,400-patient German multicenter Non–vitamin K Antagonist Oral Anticoagulants in Patients With Atrial High Rate Episodes (NOAH–AFNET 6 ) trial is testing whether oral anticoagulation with edoxaban (Savaysa) is superior to aspirin or no antithrombotic therapy for prevention of stroke or cardiovascular death. And the 4,000-patient Apixaban for the Reduction of Thrombo-Embolism in Patients With Device-Detected Sub-Clinical Atrial Fibrillation (ARTESIA) trial is randomizing patients to apixaban (Eliquis) or aspirin.
“We’ll know within the next 3-4 years whether patients with high-risk profiles for atrial fibrillation but no clinically manifest atrial fibrillation should in fact be detected and should in fact be anticoagulated if atrial fibrillation is detected. Putting on my ‘Carnac The Magnificent’ hat [made famous by Johnny Carson on the ‘Tonight Show’], I predict the answer to both of those questions is likely to be yes,” the cardiologist added.
He noted that the Medtronic ICM, which is one-third the size of a AAA battery, is implanted via a small incision, which is then covered by a adhesive bandage.
“There’s no major surgical technique involved in putting [int ICM] in,” he said.
The REVEAL AF study was sponsored by Medtronic. Dr. Reiffel reported serving as a consultant to the company.
SOURCE: Reiffel JA et al. ACC 2018, Abstract 900-08.
ORLANDO – with other intermittent ambulatory monitoring strategies, in a secondary analysis from the REVEAL AF study.
“If you really want to look for atrial fibrillation because your concern is that the patient has a high-risk profile, and if you saw it you would anticoagulate it and maybe prophylactically use rate control, nothing beats the implanted monitor,” James A. Reiffel, MD, said at the annual meeting of the American College of Cardiology.
As previously reported (JAMA Cardiol. 2017 Oct 1;2[10]:1120-7), the primary outcome – an AF episode lasting for at least 6 minutes – occurred during the first 18 months of the study in 29% of participants. By 30 months, it was 40%. At ACC 2018, Dr. Reiffel presented a new analysis looking at how the insertable cardiac monitor (ICM) would have stacked up against other device-based strategies aimed at detecting silent AF, including a 30-day implantable memory loop, daily transtelephonic ECG monitoring, and one-time or periodic 24- or 48-hour Holter monitoring.
To accomplish this, he and his coinvestigators conducted modeling studies harnessing the REVEAL AF continuous monitoring data. They looked at how many of the real-world patients found to have AF in the study would have been identified had they instead undergone a one-time recording period lasting 1, 2, 7, 14, or 30 days beginning at the time they would have received their ICM. They also looked at the yield of repeated monitoring strategies, including monthly or quarterly 24- or 48-hour Holter monitoring sessions. They repeated the various simulated monitoring strategies 10,000 times each in order to beef up the sample size and stability of the results.
It was no contest, according to Dr. Reiffel, professor of clinical medicine at Columbia University in New York.
That’s because the median time to AF detection in REVEAL AF was 123 days. Thus, any monitoring strategy of 30 days duration or less was doomed to be of comparatively low yield. Indeed, the 12-month AF incidence rate as detected by ICM in REVEAL AF was 27.1%, compared with 1.1%-13.5% for the various modeled monitoring strategies.
Among patients who met the primary endpoint in REVEAL AF, 10.2% had one or more AF episodes lasting 24 hours or more. So a significant proportion of the asymptomatic episodes of AF were not brief.
The take-home lesson of this analysis is straightforward, he said. “While the incidence of screen-detected atrial fibrillation is dependent upon the population screened, it is also strongly dependent upon the duration and intensity of monitoring.”
Session cochair Jeanne E. Poole, MD, observed that while the new REVEAL AF analysis is informative, it leaves unanswered the big questions regarding the clinical importance of these silent episodes of subclinical device-detected AF. That is, are these episodes associated with significantly increased stroke risk, and if so are they just another nonmodifiable risk marker, or are they a risk factor that can be dampened via oral anticoagulation, like symptomatic AF? said Dr. Poole, professor of medicine and director of the clinical cardiac electrophysiology program at the University of Washington, Seattle.
“My own belief is that they are both a risk marker and a risk factor that contributes to stroke,” Dr. Reiffel replied.
He noted that there are two major ongoing clinical trials evaluating the impact of oral anticoagulation in patients with ICM-detected AF. The 3,400-patient German multicenter Non–vitamin K Antagonist Oral Anticoagulants in Patients With Atrial High Rate Episodes (NOAH–AFNET 6 ) trial is testing whether oral anticoagulation with edoxaban (Savaysa) is superior to aspirin or no antithrombotic therapy for prevention of stroke or cardiovascular death. And the 4,000-patient Apixaban for the Reduction of Thrombo-Embolism in Patients With Device-Detected Sub-Clinical Atrial Fibrillation (ARTESIA) trial is randomizing patients to apixaban (Eliquis) or aspirin.
“We’ll know within the next 3-4 years whether patients with high-risk profiles for atrial fibrillation but no clinically manifest atrial fibrillation should in fact be detected and should in fact be anticoagulated if atrial fibrillation is detected. Putting on my ‘Carnac The Magnificent’ hat [made famous by Johnny Carson on the ‘Tonight Show’], I predict the answer to both of those questions is likely to be yes,” the cardiologist added.
He noted that the Medtronic ICM, which is one-third the size of a AAA battery, is implanted via a small incision, which is then covered by a adhesive bandage.
“There’s no major surgical technique involved in putting [int ICM] in,” he said.
The REVEAL AF study was sponsored by Medtronic. Dr. Reiffel reported serving as a consultant to the company.
SOURCE: Reiffel JA et al. ACC 2018, Abstract 900-08.
ORLANDO – with other intermittent ambulatory monitoring strategies, in a secondary analysis from the REVEAL AF study.
“If you really want to look for atrial fibrillation because your concern is that the patient has a high-risk profile, and if you saw it you would anticoagulate it and maybe prophylactically use rate control, nothing beats the implanted monitor,” James A. Reiffel, MD, said at the annual meeting of the American College of Cardiology.
As previously reported (JAMA Cardiol. 2017 Oct 1;2[10]:1120-7), the primary outcome – an AF episode lasting for at least 6 minutes – occurred during the first 18 months of the study in 29% of participants. By 30 months, it was 40%. At ACC 2018, Dr. Reiffel presented a new analysis looking at how the insertable cardiac monitor (ICM) would have stacked up against other device-based strategies aimed at detecting silent AF, including a 30-day implantable memory loop, daily transtelephonic ECG monitoring, and one-time or periodic 24- or 48-hour Holter monitoring.
To accomplish this, he and his coinvestigators conducted modeling studies harnessing the REVEAL AF continuous monitoring data. They looked at how many of the real-world patients found to have AF in the study would have been identified had they instead undergone a one-time recording period lasting 1, 2, 7, 14, or 30 days beginning at the time they would have received their ICM. They also looked at the yield of repeated monitoring strategies, including monthly or quarterly 24- or 48-hour Holter monitoring sessions. They repeated the various simulated monitoring strategies 10,000 times each in order to beef up the sample size and stability of the results.
It was no contest, according to Dr. Reiffel, professor of clinical medicine at Columbia University in New York.
That’s because the median time to AF detection in REVEAL AF was 123 days. Thus, any monitoring strategy of 30 days duration or less was doomed to be of comparatively low yield. Indeed, the 12-month AF incidence rate as detected by ICM in REVEAL AF was 27.1%, compared with 1.1%-13.5% for the various modeled monitoring strategies.
Among patients who met the primary endpoint in REVEAL AF, 10.2% had one or more AF episodes lasting 24 hours or more. So a significant proportion of the asymptomatic episodes of AF were not brief.
The take-home lesson of this analysis is straightforward, he said. “While the incidence of screen-detected atrial fibrillation is dependent upon the population screened, it is also strongly dependent upon the duration and intensity of monitoring.”
Session cochair Jeanne E. Poole, MD, observed that while the new REVEAL AF analysis is informative, it leaves unanswered the big questions regarding the clinical importance of these silent episodes of subclinical device-detected AF. That is, are these episodes associated with significantly increased stroke risk, and if so are they just another nonmodifiable risk marker, or are they a risk factor that can be dampened via oral anticoagulation, like symptomatic AF? said Dr. Poole, professor of medicine and director of the clinical cardiac electrophysiology program at the University of Washington, Seattle.
“My own belief is that they are both a risk marker and a risk factor that contributes to stroke,” Dr. Reiffel replied.
He noted that there are two major ongoing clinical trials evaluating the impact of oral anticoagulation in patients with ICM-detected AF. The 3,400-patient German multicenter Non–vitamin K Antagonist Oral Anticoagulants in Patients With Atrial High Rate Episodes (NOAH–AFNET 6 ) trial is testing whether oral anticoagulation with edoxaban (Savaysa) is superior to aspirin or no antithrombotic therapy for prevention of stroke or cardiovascular death. And the 4,000-patient Apixaban for the Reduction of Thrombo-Embolism in Patients With Device-Detected Sub-Clinical Atrial Fibrillation (ARTESIA) trial is randomizing patients to apixaban (Eliquis) or aspirin.
“We’ll know within the next 3-4 years whether patients with high-risk profiles for atrial fibrillation but no clinically manifest atrial fibrillation should in fact be detected and should in fact be anticoagulated if atrial fibrillation is detected. Putting on my ‘Carnac The Magnificent’ hat [made famous by Johnny Carson on the ‘Tonight Show’], I predict the answer to both of those questions is likely to be yes,” the cardiologist added.
He noted that the Medtronic ICM, which is one-third the size of a AAA battery, is implanted via a small incision, which is then covered by a adhesive bandage.
“There’s no major surgical technique involved in putting [int ICM] in,” he said.
The REVEAL AF study was sponsored by Medtronic. Dr. Reiffel reported serving as a consultant to the company.
SOURCE: Reiffel JA et al. ACC 2018, Abstract 900-08.
REPORTING FROM ACC 2018
Key clinical point: Most patients at high risk for previously unidentified atrial fibrillation whose arrhythmia is detected by means of an insertable continuous ECG monitor would go unidentified by any other detection strategy.
Major finding: The median time to insertable cardiac monitor–based detection of a first episode of silent AF of at least 6 minutes length was 123 days.
Study details: This was a multicenter, prospective, single-arm study of 385 patients at high risk for AF who received an insertable cardiac monitor and were followed for 30 months.
Disclosures: The REVEAL AF study was sponsored by Medtronic. The presenter reported serving as a consultant to the company.
Source: Reiffel JA et al. ACC 2018, Abstract 900-08.
Novel targeted cancer drugs cause fewer arrhythmias
ORLANDO – Not all oncology drugs are equal when it comes to their risk of treatment-induced cardiac arrhythmias.
Indeed, compared with anthracycline-based regimens, long the workhorse in treating many forms of cancer, the novel targeted agents – tyrosine kinase inhibitors, immune checkpoint inhibitors, and monoclonal antibodies – were 40% less likely to result in a new arrhythmia diagnosis within 6 months of treatment initiation, in a large, single-center retrospective study reported by Andrew Nickel at the annual meeting of the American College of Cardiology.
Overall, 14% of cancer patients developed a first-ever cardiac arrhythmia within the first 6 months after treatment began. In a Cox multivariate analysis, treatment with a targeted cancer agent was independently associated with a 40% lower risk of arrhythmia, compared with anthracycline-containing therapy. Of note, the incidence of new-onset atrial fibrillation was closely similar in the two groups.
Several patient factors emerged as independent predictors of increased risk of cancer treatment–induced arrhythmia in the multivariate analysis: male sex, with a 1.2-fold increased risk; baseline heart failure, with a 2.2-fold risk; and hypertension, which conferred a 1.6-fold increased risk. These are patient groups in which the novel targeted cancer treatments are a particularly attractive option from the standpoint of mitigating arrhythmia risk, provided their use would be appropriate, he observed.
Mr. Nickel reported having no financial conflicts regarding his study, which was conducted free of commercial support.
SOURCE: Nickel A et al. ACC 18. Abstract 900-06.
ORLANDO – Not all oncology drugs are equal when it comes to their risk of treatment-induced cardiac arrhythmias.
Indeed, compared with anthracycline-based regimens, long the workhorse in treating many forms of cancer, the novel targeted agents – tyrosine kinase inhibitors, immune checkpoint inhibitors, and monoclonal antibodies – were 40% less likely to result in a new arrhythmia diagnosis within 6 months of treatment initiation, in a large, single-center retrospective study reported by Andrew Nickel at the annual meeting of the American College of Cardiology.
Overall, 14% of cancer patients developed a first-ever cardiac arrhythmia within the first 6 months after treatment began. In a Cox multivariate analysis, treatment with a targeted cancer agent was independently associated with a 40% lower risk of arrhythmia, compared with anthracycline-containing therapy. Of note, the incidence of new-onset atrial fibrillation was closely similar in the two groups.
Several patient factors emerged as independent predictors of increased risk of cancer treatment–induced arrhythmia in the multivariate analysis: male sex, with a 1.2-fold increased risk; baseline heart failure, with a 2.2-fold risk; and hypertension, which conferred a 1.6-fold increased risk. These are patient groups in which the novel targeted cancer treatments are a particularly attractive option from the standpoint of mitigating arrhythmia risk, provided their use would be appropriate, he observed.
Mr. Nickel reported having no financial conflicts regarding his study, which was conducted free of commercial support.
SOURCE: Nickel A et al. ACC 18. Abstract 900-06.
ORLANDO – Not all oncology drugs are equal when it comes to their risk of treatment-induced cardiac arrhythmias.
Indeed, compared with anthracycline-based regimens, long the workhorse in treating many forms of cancer, the novel targeted agents – tyrosine kinase inhibitors, immune checkpoint inhibitors, and monoclonal antibodies – were 40% less likely to result in a new arrhythmia diagnosis within 6 months of treatment initiation, in a large, single-center retrospective study reported by Andrew Nickel at the annual meeting of the American College of Cardiology.
Overall, 14% of cancer patients developed a first-ever cardiac arrhythmia within the first 6 months after treatment began. In a Cox multivariate analysis, treatment with a targeted cancer agent was independently associated with a 40% lower risk of arrhythmia, compared with anthracycline-containing therapy. Of note, the incidence of new-onset atrial fibrillation was closely similar in the two groups.
Several patient factors emerged as independent predictors of increased risk of cancer treatment–induced arrhythmia in the multivariate analysis: male sex, with a 1.2-fold increased risk; baseline heart failure, with a 2.2-fold risk; and hypertension, which conferred a 1.6-fold increased risk. These are patient groups in which the novel targeted cancer treatments are a particularly attractive option from the standpoint of mitigating arrhythmia risk, provided their use would be appropriate, he observed.
Mr. Nickel reported having no financial conflicts regarding his study, which was conducted free of commercial support.
SOURCE: Nickel A et al. ACC 18. Abstract 900-06.
REPORTING FROM ACC 2018
Key clinical point: The novel targeted cancer therapies cause markedly fewer cardiac arrhythmias.
Major finding: Cancer patients treated with a tyrosine kinase inhibitor, immune checkpoint inhibitor, or another of the novel targeted therapies were 40% less likely than were those on anthracycline-based therapy to develop a treatment-induced cardiac arrhythmia up to 6 months after treatment initiation.
Study details: This was a retrospective single-center study including more than 5,000 cancer patients.
Disclosures: The presenter reported having no financial conflicts regarding his study, which was conducted free of commercial support.
Source: Nickel A et al. ACC 18, Abstract #900-06.
Cost-effectiveness battle: FFR vs. iFR in DEFINE-FLAIR trial
ORLANDO – The use of an instantaneous wave-free ratio (iFR)–guided strategy to identify physiologically significant coronary stenoses that warrant revascularization proved substantially more cost effective than did a fractional flow reserve (FFR)–based strategy in a prespecified secondary analysis of the randomized DEFINE-FLAIR trial, Manesh R. Patel, MD, reported at the annual meeting of the American College of Cardiology.
The difference in total health care costs over the course of a year of follow-up was $896 per patient in favor of the instantaneous wave-free ratio (iFR) approach, said Dr. Patel, a professor of medicine, the chief of the division of cardiology, and the chief of the division of clinical pharmacology at Duke University in Durham, N.C.
DEFINE-FLAIR was a multicenter study in which 2,492 patients with coronary artery disease were randomized to undergo either iFR- or FFR-guided coronary revascularization. It had previously been established that decision making regarding coronary revascularization or deferral that was guided by FFR leads to better patient outcomes than decision making guided by angiography alone.
DEFINE-FLAIR showed that iFR provides clinical benefits similar to those of FFR. The 1-year primary endpoint, a composite of all-cause mortality, nonfatal MI, or unplanned revascularization, occurred in 6.8% of the iFR group and 7.0% of the FFR group, while the revascularization rate was significantly lower in the iFR group, by a margin of 47.5% to 53.4% (N Engl J Med. 2017 May 11;376(19):1824-34).
Dr. Patel presented a formal study of total health care costs and quality of life in the two study arms through 1 year of follow-up. The cost of coronary physiologic assessment by iFR was lower because, unlike FFR, iFR doesn’t use adenosine for vasodilation. Plus, median procedural time was 4.5 minutes shorter in the iFR group, resulting in lower costs for staff time. After investigators added up the costs of balloons, stents, laboratory testing, and a year’s worth of primary care visits, specialty consults, and unplanned revascularization procedures, the total cost per patient was $7,442.23 in 2017 U.S. dollars in the iFR group and $8,243.39 in the FFR group.
Session cochair Christopher Granger, MD, was favorably impressed.
“With equal clinical outcomes, the iFR – in not using adenosine and by identifying fewer patients needing referral for coronary artery bypass surgery or percutaneous coronary intervention – had a better cost effectiveness by about $900. That’s pretty good,” commented Dr. Granger, a professor of medicine at Duke University.
“At the moment, there is a longer track record for FFR data than iFR data for outcomes, but this is a fairly strong finding in a large population in a well-conducted study, and it shows very positive favorable economic results,” the cardiologist added. “There is no doubt that this [iFR] does have streamlined work flow, lower cost, and the same outcomes. So I think this is actually quite a positive effect.”
Dr. Patel, in acknowledging that there is a spirited ongoing debate among some interventional cardiologists as to which coronary physiology assessment tool should be used, declared, “We should stop arguing about which one to use and just use more of it, first and foremost.”
“I couldn’t agree more,” Dr. Granger said. “Coronary physiology for best decision making, whichever index you decide to choose, will lead to better outcomes and lower cost.”
Dr. Patel estimated that, worldwide, coronary physiology assessment is used in cardiac catheterization laboratories in fewer than 20% of patients. Achieving a substantial increase in that number is a matter of physician education perhaps coupled with payer requirements that interventional cardiologists must demonstrate evidence of ischemia before performing percutaneous coronary intervention on a given coronary lesion. Also, the American College of Cardiology/American Heart Association guidelines, which at present give a Class IIa recommendation for the use of FFR in patients with an intermediate stenosis, probably need to be revisited in light of DEFINE-FLAIR.
“One might argue that the recommendation could be a little stronger. And we have other proven technologies now besides FFR,” he observed.
Dr. Patel reported receiving research grants from Philips Volcano, sponsor of the DEFINE-FLAIR trial, as well as from AstraZeneca, Bayer, Janssen, ProCyrion, and the National Heart, Lung, and Blood Institute. He serves as a consultant to AstraZeneca, Bayer, Janssen, and Medscape.
SOURCE: Patel MR et al. ACC 18, Abstract 402-09.
ORLANDO – The use of an instantaneous wave-free ratio (iFR)–guided strategy to identify physiologically significant coronary stenoses that warrant revascularization proved substantially more cost effective than did a fractional flow reserve (FFR)–based strategy in a prespecified secondary analysis of the randomized DEFINE-FLAIR trial, Manesh R. Patel, MD, reported at the annual meeting of the American College of Cardiology.
The difference in total health care costs over the course of a year of follow-up was $896 per patient in favor of the instantaneous wave-free ratio (iFR) approach, said Dr. Patel, a professor of medicine, the chief of the division of cardiology, and the chief of the division of clinical pharmacology at Duke University in Durham, N.C.
DEFINE-FLAIR was a multicenter study in which 2,492 patients with coronary artery disease were randomized to undergo either iFR- or FFR-guided coronary revascularization. It had previously been established that decision making regarding coronary revascularization or deferral that was guided by FFR leads to better patient outcomes than decision making guided by angiography alone.
DEFINE-FLAIR showed that iFR provides clinical benefits similar to those of FFR. The 1-year primary endpoint, a composite of all-cause mortality, nonfatal MI, or unplanned revascularization, occurred in 6.8% of the iFR group and 7.0% of the FFR group, while the revascularization rate was significantly lower in the iFR group, by a margin of 47.5% to 53.4% (N Engl J Med. 2017 May 11;376(19):1824-34).
Dr. Patel presented a formal study of total health care costs and quality of life in the two study arms through 1 year of follow-up. The cost of coronary physiologic assessment by iFR was lower because, unlike FFR, iFR doesn’t use adenosine for vasodilation. Plus, median procedural time was 4.5 minutes shorter in the iFR group, resulting in lower costs for staff time. After investigators added up the costs of balloons, stents, laboratory testing, and a year’s worth of primary care visits, specialty consults, and unplanned revascularization procedures, the total cost per patient was $7,442.23 in 2017 U.S. dollars in the iFR group and $8,243.39 in the FFR group.
Session cochair Christopher Granger, MD, was favorably impressed.
“With equal clinical outcomes, the iFR – in not using adenosine and by identifying fewer patients needing referral for coronary artery bypass surgery or percutaneous coronary intervention – had a better cost effectiveness by about $900. That’s pretty good,” commented Dr. Granger, a professor of medicine at Duke University.
“At the moment, there is a longer track record for FFR data than iFR data for outcomes, but this is a fairly strong finding in a large population in a well-conducted study, and it shows very positive favorable economic results,” the cardiologist added. “There is no doubt that this [iFR] does have streamlined work flow, lower cost, and the same outcomes. So I think this is actually quite a positive effect.”
Dr. Patel, in acknowledging that there is a spirited ongoing debate among some interventional cardiologists as to which coronary physiology assessment tool should be used, declared, “We should stop arguing about which one to use and just use more of it, first and foremost.”
“I couldn’t agree more,” Dr. Granger said. “Coronary physiology for best decision making, whichever index you decide to choose, will lead to better outcomes and lower cost.”
Dr. Patel estimated that, worldwide, coronary physiology assessment is used in cardiac catheterization laboratories in fewer than 20% of patients. Achieving a substantial increase in that number is a matter of physician education perhaps coupled with payer requirements that interventional cardiologists must demonstrate evidence of ischemia before performing percutaneous coronary intervention on a given coronary lesion. Also, the American College of Cardiology/American Heart Association guidelines, which at present give a Class IIa recommendation for the use of FFR in patients with an intermediate stenosis, probably need to be revisited in light of DEFINE-FLAIR.
“One might argue that the recommendation could be a little stronger. And we have other proven technologies now besides FFR,” he observed.
Dr. Patel reported receiving research grants from Philips Volcano, sponsor of the DEFINE-FLAIR trial, as well as from AstraZeneca, Bayer, Janssen, ProCyrion, and the National Heart, Lung, and Blood Institute. He serves as a consultant to AstraZeneca, Bayer, Janssen, and Medscape.
SOURCE: Patel MR et al. ACC 18, Abstract 402-09.
ORLANDO – The use of an instantaneous wave-free ratio (iFR)–guided strategy to identify physiologically significant coronary stenoses that warrant revascularization proved substantially more cost effective than did a fractional flow reserve (FFR)–based strategy in a prespecified secondary analysis of the randomized DEFINE-FLAIR trial, Manesh R. Patel, MD, reported at the annual meeting of the American College of Cardiology.
The difference in total health care costs over the course of a year of follow-up was $896 per patient in favor of the instantaneous wave-free ratio (iFR) approach, said Dr. Patel, a professor of medicine, the chief of the division of cardiology, and the chief of the division of clinical pharmacology at Duke University in Durham, N.C.
DEFINE-FLAIR was a multicenter study in which 2,492 patients with coronary artery disease were randomized to undergo either iFR- or FFR-guided coronary revascularization. It had previously been established that decision making regarding coronary revascularization or deferral that was guided by FFR leads to better patient outcomes than decision making guided by angiography alone.
DEFINE-FLAIR showed that iFR provides clinical benefits similar to those of FFR. The 1-year primary endpoint, a composite of all-cause mortality, nonfatal MI, or unplanned revascularization, occurred in 6.8% of the iFR group and 7.0% of the FFR group, while the revascularization rate was significantly lower in the iFR group, by a margin of 47.5% to 53.4% (N Engl J Med. 2017 May 11;376(19):1824-34).
Dr. Patel presented a formal study of total health care costs and quality of life in the two study arms through 1 year of follow-up. The cost of coronary physiologic assessment by iFR was lower because, unlike FFR, iFR doesn’t use adenosine for vasodilation. Plus, median procedural time was 4.5 minutes shorter in the iFR group, resulting in lower costs for staff time. After investigators added up the costs of balloons, stents, laboratory testing, and a year’s worth of primary care visits, specialty consults, and unplanned revascularization procedures, the total cost per patient was $7,442.23 in 2017 U.S. dollars in the iFR group and $8,243.39 in the FFR group.
Session cochair Christopher Granger, MD, was favorably impressed.
“With equal clinical outcomes, the iFR – in not using adenosine and by identifying fewer patients needing referral for coronary artery bypass surgery or percutaneous coronary intervention – had a better cost effectiveness by about $900. That’s pretty good,” commented Dr. Granger, a professor of medicine at Duke University.
“At the moment, there is a longer track record for FFR data than iFR data for outcomes, but this is a fairly strong finding in a large population in a well-conducted study, and it shows very positive favorable economic results,” the cardiologist added. “There is no doubt that this [iFR] does have streamlined work flow, lower cost, and the same outcomes. So I think this is actually quite a positive effect.”
Dr. Patel, in acknowledging that there is a spirited ongoing debate among some interventional cardiologists as to which coronary physiology assessment tool should be used, declared, “We should stop arguing about which one to use and just use more of it, first and foremost.”
“I couldn’t agree more,” Dr. Granger said. “Coronary physiology for best decision making, whichever index you decide to choose, will lead to better outcomes and lower cost.”
Dr. Patel estimated that, worldwide, coronary physiology assessment is used in cardiac catheterization laboratories in fewer than 20% of patients. Achieving a substantial increase in that number is a matter of physician education perhaps coupled with payer requirements that interventional cardiologists must demonstrate evidence of ischemia before performing percutaneous coronary intervention on a given coronary lesion. Also, the American College of Cardiology/American Heart Association guidelines, which at present give a Class IIa recommendation for the use of FFR in patients with an intermediate stenosis, probably need to be revisited in light of DEFINE-FLAIR.
“One might argue that the recommendation could be a little stronger. And we have other proven technologies now besides FFR,” he observed.
Dr. Patel reported receiving research grants from Philips Volcano, sponsor of the DEFINE-FLAIR trial, as well as from AstraZeneca, Bayer, Janssen, ProCyrion, and the National Heart, Lung, and Blood Institute. He serves as a consultant to AstraZeneca, Bayer, Janssen, and Medscape.
SOURCE: Patel MR et al. ACC 18, Abstract 402-09.
REPORTING FROM ACC 2018
Key clinical point:
Major finding: A coronary revascularization strategy guided by physiologic information provided by instantaneous wave-free ratio resulted in $896 less in health care costs per patient over 1 year of follow-up than a fractional flow reserve–guided strategy had.
Study details: This was a prespecified analysis of all health care costs during 1 year of follow-up in the 2,492-patient randomized DEFINE-FLAIR study.
Disclosures: The study presenter reported receiving a research grant from Philips Volcano, sponsor of the DEFINE-FLAIR trial.
Source: Patel MR et al. ACC 18, Abstract 402-09.
Nebivolol looks like best beta-blocker for hypertension
ORLANDO – The use of nebivolol as part of a multidrug regimen to treat hypertension was associated with a significantly lower cardiovascular event risk than was combination antihypertensive therapy featuring either metoprolol or atenolol in a large observational study, Brent M. Egan, MD, reported at the annual meeting of the American College of Cardiology.
The primary outcome was hospitalization for acute MI, stroke, heart failure, or angina during a mean 600 days of follow-up. In a Cox proportional hazards regression analysis, the risk of the composite outcome was 1.33-fold greater with atenolol and 1.91-fold greater with metoprolol than in the group on nebivolol for their hypertension.
The risk of hospitalization for MI was 1.47-fold greater in the atenolol group and 2.19-fold greater with metoprolol than in patients on nebivolol. Hospitalization for angina was 2.18 times more likely in the atenolol group and 3.39 times more likely in the metoprolol group than in patients on nebivolol. However, there was no between-group difference between the three beta-blockers in terms of stroke or heart failure rates, according to Dr. Egan of the University of South Carolina, Greenville.
He explained that the impetus for this study was that, even though beta-blockers are universally recognized as a cornerstone of secondary cardiovascular prevention, there are much fewer outcome data to support their use in primary prevention. Since nebivolol is a vasodilatory beta-blocker and atenolol and metoprolol are not, Dr. Egan and his coinvestigators hypothesized that this distinction could result in differences in cardiovascular event rates.
One audience member commented, “this study gives a nice hypothesis-generating rationale for doing a large randomized outcomes trial.” Dr. Egan concurred.
His study was supported by Allergan. He reported receiving research grants from Boehringer Ingelheim and serving as a consultant to Medtronic.
SOURCE: Egan BM et al. ACC 18, Abstract 1324M-11.
ORLANDO – The use of nebivolol as part of a multidrug regimen to treat hypertension was associated with a significantly lower cardiovascular event risk than was combination antihypertensive therapy featuring either metoprolol or atenolol in a large observational study, Brent M. Egan, MD, reported at the annual meeting of the American College of Cardiology.
The primary outcome was hospitalization for acute MI, stroke, heart failure, or angina during a mean 600 days of follow-up. In a Cox proportional hazards regression analysis, the risk of the composite outcome was 1.33-fold greater with atenolol and 1.91-fold greater with metoprolol than in the group on nebivolol for their hypertension.
The risk of hospitalization for MI was 1.47-fold greater in the atenolol group and 2.19-fold greater with metoprolol than in patients on nebivolol. Hospitalization for angina was 2.18 times more likely in the atenolol group and 3.39 times more likely in the metoprolol group than in patients on nebivolol. However, there was no between-group difference between the three beta-blockers in terms of stroke or heart failure rates, according to Dr. Egan of the University of South Carolina, Greenville.
He explained that the impetus for this study was that, even though beta-blockers are universally recognized as a cornerstone of secondary cardiovascular prevention, there are much fewer outcome data to support their use in primary prevention. Since nebivolol is a vasodilatory beta-blocker and atenolol and metoprolol are not, Dr. Egan and his coinvestigators hypothesized that this distinction could result in differences in cardiovascular event rates.
One audience member commented, “this study gives a nice hypothesis-generating rationale for doing a large randomized outcomes trial.” Dr. Egan concurred.
His study was supported by Allergan. He reported receiving research grants from Boehringer Ingelheim and serving as a consultant to Medtronic.
SOURCE: Egan BM et al. ACC 18, Abstract 1324M-11.
ORLANDO – The use of nebivolol as part of a multidrug regimen to treat hypertension was associated with a significantly lower cardiovascular event risk than was combination antihypertensive therapy featuring either metoprolol or atenolol in a large observational study, Brent M. Egan, MD, reported at the annual meeting of the American College of Cardiology.
The primary outcome was hospitalization for acute MI, stroke, heart failure, or angina during a mean 600 days of follow-up. In a Cox proportional hazards regression analysis, the risk of the composite outcome was 1.33-fold greater with atenolol and 1.91-fold greater with metoprolol than in the group on nebivolol for their hypertension.
The risk of hospitalization for MI was 1.47-fold greater in the atenolol group and 2.19-fold greater with metoprolol than in patients on nebivolol. Hospitalization for angina was 2.18 times more likely in the atenolol group and 3.39 times more likely in the metoprolol group than in patients on nebivolol. However, there was no between-group difference between the three beta-blockers in terms of stroke or heart failure rates, according to Dr. Egan of the University of South Carolina, Greenville.
He explained that the impetus for this study was that, even though beta-blockers are universally recognized as a cornerstone of secondary cardiovascular prevention, there are much fewer outcome data to support their use in primary prevention. Since nebivolol is a vasodilatory beta-blocker and atenolol and metoprolol are not, Dr. Egan and his coinvestigators hypothesized that this distinction could result in differences in cardiovascular event rates.
One audience member commented, “this study gives a nice hypothesis-generating rationale for doing a large randomized outcomes trial.” Dr. Egan concurred.
His study was supported by Allergan. He reported receiving research grants from Boehringer Ingelheim and serving as a consultant to Medtronic.
SOURCE: Egan BM et al. ACC 18, Abstract 1324M-11.
REPORTING FROM ACC 2018
Key clinical point:
Major finding: The risk of hospitalization for MI was 1.47-fold greater in patients on atenolol and 2.19-fold greater with metoprolol than in patients on nebivolol as part of a multidrug regimen to treat hypertension.
Study details: This retrospective observational study included three closely propensity score–matched groups, each 16,787 patients in size, on either nebivolol, metoprolol, or atenolol as part of a multidrug antihypertensive regimen.
Disclosures: The study was supported by Allergan. The presenter reported receiving research grants from Boehringer Ingelheim and serving as a consultant to Medtronic.
Source: Egan BM. ACC 2018, Abstract 1324M-11.
MI before age 50? Think familial hypercholesterolemia, substance abuse
ORLANDO – Patients with an MI before age 50 commonly have familial hypercholesterolemia or a substance abuse issue, according to presentations at the annual meeting of the American College of Cardiology.
Not only is the prevalence of familial hypercholesterolemia (FH) increased in patients with an MI at a young age, but 1 year post MI, their LDL remains unacceptably high at 100 mg/dL or more in a high percentage of cases. For that matter, the same is true in patients with an MI before age 50 who don’t have FH, reported Ron Blankstein, MD, director of cardiac computed tomography at Brigham and Women’s Hospital and a cardiologist at Harvard Medical School, Boston.
FH patients after early MI
Dr. Blankstein presented a retrospective study of 1,996 adults with a first confirmed type 1 MI before at 50 who presented at Brigham and Women’s Hospital or Massachusetts General Hospital, of whom 9% met Dutch Lipid Clinic Network criteria for probable or definite FH.
Among patients with an MI before age 50 and a family history of premature CAD, the prevalence of FH was enriched, at 22%. Among those with an LDL of 160 mg/dL or more, the prevalence of FH rose further, to 36%. And by combining all three criteria – MI before age 50, a positive family history of early CAD, and an LDL of at least 160 mg/dL – the prevalence of FH shot up to 64%, Dr. Blankstein said.
Only 89% of patients with an MI prior to turning 50 years old were discharged on a statin. “That’s lower than I would have expected,” he said.
One year post MI, LDL levels had dropped by a mean of 79 mg/dL in the FH group and 39 mg/dL in the non-FH patients. This translated into a 45% reduction in the FH patients, a significantly greater decrease than the 34% drop in the non-FH group. Nonetheless, 43% of FH patients had an LDL of 100 mg/dL or greater at 1 year, as did 26% without FH. These are patients who are particularly likely to benefit from more aggressive lipid-lowering after an acute coronary syndrome. Given that almost 90% of patients with FH remain undiagnosed, assessment for the genetic disorder in young patients with MI is an important means of case finding, the cardiologist observed.
Session cochair Carl E. Orringer, MD, director of preventive cardiovascular medicine at the University of Miami, said he and his colleagues have just initiated a program at that medical center whereby patients with an LDL of 190 mg/dL or more are identified through their electronic medical records and referred to a lipid clinic or cardiovascular prevention program.
“I think this is certainly something to think about for other programs because you want to make sure that if you have lipid intervention services, they actually take care of patients who are at the highest risk,” he said.
Substance abuse plays role
Elsewhere at ACC 2018, Ersilia M. Defilippis, MD, reported on an expanded population of 2,097 patients with a first type 1 MI prior to age 50 at the same two hospitals. Their electronic medical records revealed that 6.0% of them used marijuana and 4.7% used cocaine. During a median 11.2 years of follow-up, the group that used cocaine or marijuana had a 2.2-fold increased risk of cardiovascular death and a 2.0-fold increase in all-cause mortality, compared with nonusers, in an analysis adjusted for baseline differences.
Among these differences, 46% of drug users and 61% of nonusers were hyperlipidemic, 70% of users and 49% of nonusers were smokers, 8% of users and 4% of nonusers presented in cardiac arrest, and the median normalized troponin level was 61 interquartile range (IQR) in users versus 39 IQR in nonusers.
“Given these findings, young patients with MI should be screened for substance abuse and counseled about behavioral change to prevent future adverse events,” concluded Dr. Defilippis of Brigham and Women’s Hospital and Harvard University. She and Dr. Blankstein were coinvestigators in this study. She reported having no financial conflicts of interest. Dr. Blankstein reported receiving research grants from Amgen, Astellas, and Sanofi, and serves as a consultant to Amgen.
Source: Blankstein R. Abstracts 1180M-03 and 1262-436/436.
ORLANDO – Patients with an MI before age 50 commonly have familial hypercholesterolemia or a substance abuse issue, according to presentations at the annual meeting of the American College of Cardiology.
Not only is the prevalence of familial hypercholesterolemia (FH) increased in patients with an MI at a young age, but 1 year post MI, their LDL remains unacceptably high at 100 mg/dL or more in a high percentage of cases. For that matter, the same is true in patients with an MI before age 50 who don’t have FH, reported Ron Blankstein, MD, director of cardiac computed tomography at Brigham and Women’s Hospital and a cardiologist at Harvard Medical School, Boston.
FH patients after early MI
Dr. Blankstein presented a retrospective study of 1,996 adults with a first confirmed type 1 MI before at 50 who presented at Brigham and Women’s Hospital or Massachusetts General Hospital, of whom 9% met Dutch Lipid Clinic Network criteria for probable or definite FH.
Among patients with an MI before age 50 and a family history of premature CAD, the prevalence of FH was enriched, at 22%. Among those with an LDL of 160 mg/dL or more, the prevalence of FH rose further, to 36%. And by combining all three criteria – MI before age 50, a positive family history of early CAD, and an LDL of at least 160 mg/dL – the prevalence of FH shot up to 64%, Dr. Blankstein said.
Only 89% of patients with an MI prior to turning 50 years old were discharged on a statin. “That’s lower than I would have expected,” he said.
One year post MI, LDL levels had dropped by a mean of 79 mg/dL in the FH group and 39 mg/dL in the non-FH patients. This translated into a 45% reduction in the FH patients, a significantly greater decrease than the 34% drop in the non-FH group. Nonetheless, 43% of FH patients had an LDL of 100 mg/dL or greater at 1 year, as did 26% without FH. These are patients who are particularly likely to benefit from more aggressive lipid-lowering after an acute coronary syndrome. Given that almost 90% of patients with FH remain undiagnosed, assessment for the genetic disorder in young patients with MI is an important means of case finding, the cardiologist observed.
Session cochair Carl E. Orringer, MD, director of preventive cardiovascular medicine at the University of Miami, said he and his colleagues have just initiated a program at that medical center whereby patients with an LDL of 190 mg/dL or more are identified through their electronic medical records and referred to a lipid clinic or cardiovascular prevention program.
“I think this is certainly something to think about for other programs because you want to make sure that if you have lipid intervention services, they actually take care of patients who are at the highest risk,” he said.
Substance abuse plays role
Elsewhere at ACC 2018, Ersilia M. Defilippis, MD, reported on an expanded population of 2,097 patients with a first type 1 MI prior to age 50 at the same two hospitals. Their electronic medical records revealed that 6.0% of them used marijuana and 4.7% used cocaine. During a median 11.2 years of follow-up, the group that used cocaine or marijuana had a 2.2-fold increased risk of cardiovascular death and a 2.0-fold increase in all-cause mortality, compared with nonusers, in an analysis adjusted for baseline differences.
Among these differences, 46% of drug users and 61% of nonusers were hyperlipidemic, 70% of users and 49% of nonusers were smokers, 8% of users and 4% of nonusers presented in cardiac arrest, and the median normalized troponin level was 61 interquartile range (IQR) in users versus 39 IQR in nonusers.
“Given these findings, young patients with MI should be screened for substance abuse and counseled about behavioral change to prevent future adverse events,” concluded Dr. Defilippis of Brigham and Women’s Hospital and Harvard University. She and Dr. Blankstein were coinvestigators in this study. She reported having no financial conflicts of interest. Dr. Blankstein reported receiving research grants from Amgen, Astellas, and Sanofi, and serves as a consultant to Amgen.
Source: Blankstein R. Abstracts 1180M-03 and 1262-436/436.
ORLANDO – Patients with an MI before age 50 commonly have familial hypercholesterolemia or a substance abuse issue, according to presentations at the annual meeting of the American College of Cardiology.
Not only is the prevalence of familial hypercholesterolemia (FH) increased in patients with an MI at a young age, but 1 year post MI, their LDL remains unacceptably high at 100 mg/dL or more in a high percentage of cases. For that matter, the same is true in patients with an MI before age 50 who don’t have FH, reported Ron Blankstein, MD, director of cardiac computed tomography at Brigham and Women’s Hospital and a cardiologist at Harvard Medical School, Boston.
FH patients after early MI
Dr. Blankstein presented a retrospective study of 1,996 adults with a first confirmed type 1 MI before at 50 who presented at Brigham and Women’s Hospital or Massachusetts General Hospital, of whom 9% met Dutch Lipid Clinic Network criteria for probable or definite FH.
Among patients with an MI before age 50 and a family history of premature CAD, the prevalence of FH was enriched, at 22%. Among those with an LDL of 160 mg/dL or more, the prevalence of FH rose further, to 36%. And by combining all three criteria – MI before age 50, a positive family history of early CAD, and an LDL of at least 160 mg/dL – the prevalence of FH shot up to 64%, Dr. Blankstein said.
Only 89% of patients with an MI prior to turning 50 years old were discharged on a statin. “That’s lower than I would have expected,” he said.
One year post MI, LDL levels had dropped by a mean of 79 mg/dL in the FH group and 39 mg/dL in the non-FH patients. This translated into a 45% reduction in the FH patients, a significantly greater decrease than the 34% drop in the non-FH group. Nonetheless, 43% of FH patients had an LDL of 100 mg/dL or greater at 1 year, as did 26% without FH. These are patients who are particularly likely to benefit from more aggressive lipid-lowering after an acute coronary syndrome. Given that almost 90% of patients with FH remain undiagnosed, assessment for the genetic disorder in young patients with MI is an important means of case finding, the cardiologist observed.
Session cochair Carl E. Orringer, MD, director of preventive cardiovascular medicine at the University of Miami, said he and his colleagues have just initiated a program at that medical center whereby patients with an LDL of 190 mg/dL or more are identified through their electronic medical records and referred to a lipid clinic or cardiovascular prevention program.
“I think this is certainly something to think about for other programs because you want to make sure that if you have lipid intervention services, they actually take care of patients who are at the highest risk,” he said.
Substance abuse plays role
Elsewhere at ACC 2018, Ersilia M. Defilippis, MD, reported on an expanded population of 2,097 patients with a first type 1 MI prior to age 50 at the same two hospitals. Their electronic medical records revealed that 6.0% of them used marijuana and 4.7% used cocaine. During a median 11.2 years of follow-up, the group that used cocaine or marijuana had a 2.2-fold increased risk of cardiovascular death and a 2.0-fold increase in all-cause mortality, compared with nonusers, in an analysis adjusted for baseline differences.
Among these differences, 46% of drug users and 61% of nonusers were hyperlipidemic, 70% of users and 49% of nonusers were smokers, 8% of users and 4% of nonusers presented in cardiac arrest, and the median normalized troponin level was 61 interquartile range (IQR) in users versus 39 IQR in nonusers.
“Given these findings, young patients with MI should be screened for substance abuse and counseled about behavioral change to prevent future adverse events,” concluded Dr. Defilippis of Brigham and Women’s Hospital and Harvard University. She and Dr. Blankstein were coinvestigators in this study. She reported having no financial conflicts of interest. Dr. Blankstein reported receiving research grants from Amgen, Astellas, and Sanofi, and serves as a consultant to Amgen.
Source: Blankstein R. Abstracts 1180M-03 and 1262-436/436.
REPORTING FROM ACC 18
Key clinical point: Familial hypercholesterolemia is common in young adults with MI.
Major finding: Among patients with MI before age 50, a family history of premature CAD, and an LDL of 160 mg/dL or more, the prevalence of familial hypercholesterolemia was 64%.
Study details: This retrospective study involved 1,996 adults diagnosed with a type 1 MI before age 50.
Disclosures: The study presenter reported receiving research grants from Amgen, Astellas, and Sanofi and serving as a consultant to Amgen.
Source: Blankstein R. Abstracts 1180M-03 and 1262-436/436.