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Aims: The mechanisms responsible for the increased risk of heart failure (HF) post–myocardial infarction (MI) may differ between patients with versus without diabetes. We hypothesized that after high-risk MI, patients with diabetes would demonstrate patterns of remodeling that are suggestive of reduced ventricular compliance and that are associated with an increased risk of death or HF. Methods and Results: We performed quantitative echocardiographic analysis in 153 patients with diabetes and 451 patients without diabetes enrolled in the VALIANT Echo study. Diabetes was associated with a higher risk of death or HF in age-adjusted models (hazard ratio 1.44, 95% CI 1.04-2.00, P = .028). Diabetic patients were similar to nondiabetic patients with respect to left ventricular (LV) volume and ejection fraction but had higher LV mass index (104.1 ± 27.5 vs 97.1 ± 28.6 g/m2, P = .009), relative wall thickness (0.41 ± 0.08 vs 0.38 ± 0.07, P < .0001), and left atrial volume index (LAVi) (26.2 ± 8.1 vs 24.0 ± 8.2 mL/m2, P = .008)—all parameters that were significantly related to the risk of death or HF hospitalization. Changes in LV volume and ejection fraction from baseline to 20 months were not different, although diabetic patients demonstrated greater increase in LAVi (4.4 ± 7.7 vs 2.2 ± 6.7 mL/m2, P = .01). Conclusions: After high-risk MI, diabetic patients were at higher risk of death or HF and demonstrated greater baseline LV mass index, relative wall thickness, and LAVi as well as greater left atrial enlargement at 20-month follow-up. These findings suggest greater baseline concentric remodeling and long-term elevation in LV diastolic pressure post-MI among diabetic patients, which may partially mediate this risk. [ABSTRACT FROM AUTHOR]

Background: Systematic reporting of estimated glomerular filtration rate (eGFR) using the Modification of Diet in Renal Disease (MDRD) Study equation is recommended for detection of chronic kidney disease and prediction of cardiovascular (CV) risk. The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation is a newly developed and validated formula for eGFR that is more accurate at normal or near-normal eGFR. We aimed to assess the incremental prognostic accuracy of eGFRCKD-EPI versus eGFRMDRD in subjects at increased risk for CV disease. Methods: We performed a post hoc analysis of the VALIANT trial that enrolled 14,527 patients with acute myocardial infarction with signs and symptoms of heart failure and/or left ventricular systolic dysfunction. The eGFRMDRD and eGFRCKD-EPI were computed using age, gender, race, and baseline creatinine level. Patients were categorized according to their eGFR using each equation. To assess the incremental prognostic value of eGFRCKD-EPI, the net reclassification improvement was calculated for the composite end point of CV death, recurrent myocardial infarction, heart failure, or stroke. Results: Twenty-four percent of the subjects were reclassified into a different eGFR category using eGFRCKD-EPI. The composite end point occurred in 33% of the subjects in this cohort. Based on eGFRCKD-EPI, subjects reclassified into a higher eGFR experienced fewer events than those reclassified into a lower eGFR (21% vs 43%). In unadjusted analyses, the composite end point risk in subjects with eGFR between 75 and 90 mL/min per 1.73 m2 was comparable with the referent group (eGFR between 90 and 105) using eGFRMDRD (hazard ratio 1.1, 95% CI 0.9-1.2) but was significantly higher using eGFRCKD-EPI (hazard ratio 1.2, 95% CI 1.1-1.4). The net reclassification improvement for eGFRCKD-EPI over eGFRMDRD was 8.7%. Conclusion: The CKD-EPI equation provides more accurate risk stratification than the MDRD Study equation in patients at high risk for CV disease, including identification of increased risk at mildly decreased eGFR. [Copyright &y& Elsevier]

Background: Echocardiographic measurements of left ventricular (LV) function, predominantly LV ejection fraction (LVEF), have been used to define risk in patients after myocardial infarction. However, the extent to which measures of LV structure and function provide incremental prognostic value over clinical variables in survivors of high-risk myocardial infarction has not been well defined. Methods: Predictors of death and development of heart failure were assessed in 603 patients from the Valsartan in Acute Myocardial Infarction (VALIANT) echocardiographic substudy. We used multivariable proportional hazards models to assess the individual predictive value of echocardiographic measures including left ventricular mass index, LVEF, LV volumes, left atrial volume index, right ventricular fractional area change, mitral regurgitation, and deceleration time. We adjusted for the 11 clinical variables found previously to be most associated with all-cause mortality in this cohort. Receiver operating characteristic curves obtained via binary response regression were used to assess the incremental predictive value of echocardiographic measures in predicting outcomes of death and hospital stay for heart failure. Results: Each echocardiographic measure was independently associated with outcome of death or development of heart failure (all P < .002). Left ventricular ejection fraction alone added minimal prognostic value to the clinical assessment, yet adding additional echocardiographic assessments to a multivariable model improved in predicting 17-month survival free of heart failure significantly, increasing the c-statistic from 0.74 to 0.84 (P < .001). Conclusion: Echocardiographic measures of cardiac structure and function beyond LVEF provide important prognostic information beyond the clinical assessment. [Copyright &y& Elsevier]

Background: Advanced age is a well-established prognostic risk factor after acute myocardial infarction (AMI), yet approximately 10% of MIs occur in patients <45 years. We examined characteristics, cardiovascular outcomes, and the influence of risk factors on outcomes in young survivors of AMI. Methods: Fourteen thousand seven hundred three patients enrolled in the VALsartan In Acute myocardial iNfarcTion (VALIANT) trial were divided into 3 age groups: 18 to <45 (n = 803), 45 to <65 (n = 6185), ≥65 years (n = 7715). Multivariate Cox regression was used to compare cardiovascular event rates and assess the impact of risk factors on outcomes. Results: The youngest patients had less diabetes, hypertension, and history of MI and were more likely to be male (18 to <45 years, 88%; ≥65 years, 59.1%), nonwhite (18 to <45 years, 9.6%; ≥65 years, 5%), current smokers (18 to <45 years, 73.7%; ≥65 years, 15.9%), obese (18 to <45 years, 37.9%; ≥65 years, 25.1%), and dyslipidemic at randomization (18 to <45 years, 43.1%; ≥65 years, 32.7%). Adjusted relative risks of smoking (18 to <45 years, hazard ratio [HR] 1.6 [95% confidence interval {CI} 1.1-2.5]; ≥45 years, HR 0.9 [95% CI 0.9-1.1]; P =.014) and hypertension (18 to <45 years, HR 1.8 [95% CI 1.3-2.6]; ≥45 years, HR 1.2 [95% CI 1.1-1.3]; P = .044) were higher in the young, with significant interactions observed between age and these risk factors. Conclusions: After AMI, risk factors and outcomes of the young differ substantively from their older counterparts. The influence of hypertension and smoking is more profound in the young, underscoring the need for aggressive risk factor modification post-AMI. [Copyright &y& Elsevier]

Background: Left ventricular (LV) and right ventricular (RV) function are known predictors of morbidity and mortality after an acute myocardial infarction (MI). However, the prognostic use of a late evaluation of cardiac function after an MI remains unclear. Methods: We analyzed echocardiograms obtained 1 year after MI in patients with LV dysfunction at baseline (ejection fraction [EF] < or = 40%) from 291 patients enrolled in the SAVE echocardiographic substudy who did not develop heart failure (HF) or a recurrent MI during this first year. Left ventricular EF and RV fractional area change were assessed. Results: After a median follow-up of 22 months after the 1-year echocardiogram, a low LVEF (< 30%) at 1 year was associated with an increased risk of death and/or HF (hazards ratio [HR] 2.7, 95% CI 1.3-5.3). Presence of RV dysfunction was also associated with an increased risk of death (HR 8.9, 95% CI 3.5-22.1), development of HF (HR 7.1, 95% CI 3.4-15.0), and the composite end point of death or HF (HR 7.6, 95% CI 4.1-14.2). In multivariate analyses, both low LVEF and RV dysfunction remained independently predictive of the composite end point of death or HF. Patients with biventricular dysfunction were at the greatest risk of death and/or HF (HR 19.4, 95% CI 8.2-46.0) in follow-up. Conclusions: In a stable population of survivors of MI, impaired LV and RV function at 1 year after MI are independently and additively predictive of increased risk of HF or death. [ABSTRACT FROM AUTHOR]

Background: Angiotensin-converting enzyme (ACE) inhibition attenuates ventricular remodeling and improves ventricular function in heart failure patients. Vasopeptidase inhibition has shown similar effects in experimental models. Objectives: The OVERTURE echocardiographic study was designed to test the hypothesis that the vasopeptidase inhibitor omapatrilat would attenuate ventricular remodeling and improve ventricular function to a greater extent than an ACE inhibitor. Methods: Three hundred twenty-one patients with heart failure (New York Heart Association class ≥2) were included in the OVERTURE echocardiographic substudy and were randomized to receive enalapril (10 mg twice a day) or omapatrilat (40 mg every day). Echocardiograms were performed at baseline and at 1 year (n = 214). Left ventricular size was estimated by summation of ventricular areas in apical and short-axis views and by calculation of ventricular volumes. Ejection fraction was calculated from ventricular volumes. Results: Combined diastolic and systolic areas and volumes decreased significantly (mean diastolic area change −8.36 cm2, 95% CI −9.4 to −7.3 cm2; mean systolic change −8.4 cm2, 95% CI −9.5 to −7.3 cm2), and ejection fractions increased significantly (3.6%, 95% CI 2.6% to 4.6%) in both treatment groups from baseline to 1 year. There were no differences in the magnitude of improvement in ventricular size or function based on treatment assignment. Patients who died or were hospitalized for heart failure subsequent to the final assessment demonstrated the least degree of reverse remodeling. Conclusion: Ventricular size and function improved similarly after 1 year with ACE or vasopeptidase inhibition in patients with heart failure. Reverse remodeling was associated with improved outcome. [Copyright &y& Elsevier]