Background: Myocardial injury after noncardiac surgery (MINS) was defined as prognostically relevant myocardial injury due to ischemia that occurs during or within 30 days after noncardiac surgery. The study’s four objectives were to determine the diagnostic criteria, characteristics, predictors, and 30-day outcomes of MINS. Methods: In this international, prospective cohort study of 15,065 patients aged 45 yr or older who underwent in-patient noncardiac surgery, troponin T was measured during the first 3 postoperative days. Patients with a troponin T level of 0.04 ng/ml or greater (elevated “abnormal” laboratory threshold) were assessed for ischemic features (i.e., ischemic symptoms and electrocardiography findings). Patients adjudicated as having a nonischemic troponin elevation (e.g., sepsis) were excluded. To establish diagnostic criteria for MINS, the authors used Cox regression analyses in which the dependent variable was 30-day mortality (260 deaths) and independent variables included preoperative variables, perioperative complications, and potential MINS diagnostic criteria. Results: An elevated troponin after noncardiac surgery, irrespective of the presence of an ischemic feature, independently predicted 30-day mortality. Therefore, the authors’ diagnostic criterion for MINS was a peak troponin T level of 0.03 ng/ml or greater judged due to myocardial ischemia. MINS was an independent predictor of 30-day mortality (adjusted hazard ratio, 3.87; 95% CI, 2.96–5.08) and had the highest population-attributable risk (34.0%, 95% CI, 26.6–41.5) of the perioperative complications. Twelve hundred patients (8.0%) suffered MINS, and 58.2% of these patients would not have fulfilled the universal definition of myocardial infarction. Only 15.8% of patients with MINS experienced an ischemic symptom. Conclusion: Among adults undergoing noncardiac surgery, MINS is common and associated with substantial mortality.

Although supervised exercise programs reduce mortality in survivors of myocardial infarction, the effects of other types of cardiac secondary prevention programs are unknown. To determine the effectiveness of secondary cardiac prevention programs with and without exercise components. The authors searched MEDLINE (1966–2004), the Cochrane Central Register of Controlled Trials, EMBASE, CINAHL, SIGLE, and the Cochrane Effective Practice and Organization of Care Study Registry. They also contacted primary study authors and hand-searched bibliographies provided by the Centers for Medicare & Medicaid Services. Randomized clinical trials. Two reviewers chose studies and extracted data independently; random-effects summary risk ratios were calculated. The authors identified 63 randomized trials (21 295 patients with coronary disease). The summary risk ratio was 0.85 (95% CI, 0.77 to 0.94) for all-cause mortality, but this result differed over time with a risk ratio of 0.97 (CI, 0.82 to 1.14) at 12 months and 0.53 (CI, 0.35 to 0.81) at 24 months. The summary risk ratio was 0.83 (CI, 0.74 to 0.94) for recurrent myocardial infarction over a median follow-up of 12 months. Effects were similar for programs that included risk factor education or counseling with a structured exercise component (risk ratio, 0.88 [CI, 0.74 to 1.04] for mortality and 0.62 [CI, 0.44 to 0.87] for myocardial infarction), for programs that included risk factor education or counseling without an exercise component (risk ratio, 0.87 [CI, 0.76 to 0.99] for mortality and 0.86 [CI, 0.72 to 1.03] for myocardial infarction), and for programs that were solely exercise-based (risk ratio, 0.72 [CI, 0.54 to 0.95] for mortality and 0.76 [CI, 0.57 to 1.01] for myocardial infarction). Most of these programs improved quality of life or functional status, but effect sizes were small. Although these programs may reduce total health care costs, published data on the costs of the programs are inadequate to conclusively comment on their cost-effectiveness. A wide variety of secondary prevention programs improve health outcomes in patients with coronary disease.

Background— The prevalence, prognostic import, and impact of renal insufficiency on the benefits of ACE inhibitors and β-blockers in community-dwelling patients with heart failure are uncertain. Methods and Results— We analyzed data from a prospective cohort of 754 patients with heart failure who had ejection fraction, serum creatinine, and weight measured at baseline. Median age was 69 years, and 43% had an ejection fraction ≥35%. By the Cockcroft-Gault equation, 118 patients (16%) had creatinine clearances ≤30 mL/min and 301 (40%) had creatinine clearances between 30 and 59 mL/min. During follow-up (median 926 days), 385 patients (37%) died. Even after adjustment for all other prognostic factors, survival was significantly associated with renal function ( P =0.002) in patients with either systolic or diastolic dysfunction; patients exhibited a 1% increase in mortality for each 1-mL/min decrease in creatinine clearance. The associations with 1-year mortality reductions were similar for ACE inhibitors (OR 0.46 [95% CI 0.26 to 0.82] versus OR 0.28 [95% CI 0.11 to 0.70]) and β-blockers (OR 0.40 [95% CI 0.23 to 0.70] versus OR 0.41 [95% CI 0.19 to 0.85]) in patients with creatinine clearances <60 mL/min versus ≥60 mL/min, although these drugs were used less frequently in patients with renal insufficiency. Conclusions— Renal insufficiency is more prevalent in patients with heart failure than previously reported and is an independent prognostic factor in diastolic and systolic dysfunction. ACE inhibitors and β-blockers were associated with similar reductions in mortality in patients with and without renal insufficiency.

Heart failure is the fastest growing cardiovascular diagnosis in the United States, with a community prevalence of 2.5% in adults, and the direct and indirect costs of heart failure exceed $33 billion per year.¹ Quiz Ref ID Despite many advances in diagnosis and pharmacotherapy for heart failure during the past 2 decades, morbidity and mortality remain high and quality of life is poor for many patients. Thus, there is increasing enthusiasm for the therapeutic potential of atrial-synchronized biventricular pacemakers (cardiac resynchronization therapy [CRT]) in patients with heart failure and left ventricular (LV) systolic dysfunction. CRT is designed to eliminate the delay in activation of the LV free wall found in many patients with LV systolic dysfunction and thereby improves mechanical synchrony, which in turn increases LV filling time, reduces mitral regurgitation, and reduces septal dyskinesis.

Guidelines recommend that patients with heart failure receive beta-blockers in doses used in the trials that have proven their efficacy. Although the adverse effects of beta-blockade are dose-related, it is unclear whether the benefits are. To determine whether the survival benefits of beta-blockade in heart failure are associated with the magnitude of heart rate reduction or the beta-blocker dose. MEDLINE, EMBASE, CINAHL, SIGLE, Web of Science, and the Cochrane Central Register of Controlled Trials, supplemented by hand-searches of bibliographies. Randomized, placebo-controlled heart failure trials that reported all-cause mortality. Two reviewers independently extracted data on study characteristics, beta-blocker dosing and heart rate reduction, and death. The mean left ventricular ejection fraction in the 23 beta-blocker trials ranged from 0.17 to 0.36, and more than 95% of the 19 209 patients had systolic dysfunction. The overall risk ratio for death was 0.76 (95% CI, 0.68 to 0.84); however, heterogeneity testing revealed moderate heterogeneity among trials (I (2) = 30%), which was associated with the magnitude of heart rate reduction achieved within each trial (P for meta-regression = 0.006). For every heart rate reduction of 5 beats/min with beta-blocker treatment, a commensurate 18% reduction (CI, 6% to 29%) in the risk for death occurred. No significant relationship between all-cause mortality and beta-blocker dosing was observed (risk ratio for death, 0.74 [CI, 0.64 to 0.86]) in high-dose beta-blocker trials vs. 0.78 [CI, 0.63 to 0.96] in low-dose beta-blocker trials; P for meta-regression = 0.69). The analysis is based on aggregate data and resting heart rates. Few patients in these trials had bradycardia or diastolic dysfunction at baseline. The magnitude of heart rate reduction is statistically significantly associated with the survival benefit of beta-blockers in heart failure, whereas the dose of beta-blocker is not.