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In a randomized trial involving patients with a low LVEF and viable myocardium who received optimal medical therapy, PCI did not lead to a lower incidence of death or hospitalization for heart failure.

It is known that the angiotensin-converting–enzyme inhibitor captopril is beneficial in patients with myocardial infarction complicated by left ventricular dysfunction or heart failure. This study compared captopril with valsartan, an angiotensin-receptor blocker, and the combination of the two drugs in such patients. Mortality was the same in the three groups, but there were more side effects with the combination therapy. In patients with heart failure, valsartan is an alternative. Multiple randomized, placebo-controlled trials involving a total of more than 100,000 patients have demonstrated that angiotensin-converting–enzyme (ACE) inhibitors reduce the risk of death as well as the risk of major nonfatal cardiovascular events after myocardial infarction. 1 – 8 The greatest relative and absolute benefits have been obtained with long-term ACE-inhibitor therapy in high-risk patients — specifically, in those with left ventricular dysfunction, signs or symptoms of heart failure, or both. 9 , 10 Angiotensin-receptor blockers offer an alternative approach to the inhibition of the renin–angiotensin system. 11 The identification of a functioning chymase in humans that is capable of generating angiotensin II independently of . . .

Angiotensin II type 1 receptor blockers have favourable effects on haemodynamic measurements, neurohumoral activity, and left-ventricular remodelling when added to angiotensin-converting-enzyme (ACE) inhibitors in patients with chronic heart failure (CHF). We aimed to find out whether these drugs improve clinical outcome. Between March, 1999, and November, 1999, we enrolled 2548 patients with New York Heart Association functional class II–IV CHF and left-ventricular ejection fraction 40% or lower, and who were being treated with ACE inhibitors. We randomly assigned patients candesartan (n=1276, target dose 32 mg once daily) or placebo (n=1272). At baseline, 55% of patients were also treated with β blockers and 17% with spironolactone. The primary outcome of the study was the composite of cardiovascular death or hospital admission for CHF. Analysis was done by intention to treat. The median follow-up was 41 months. 483 (38%) patients in the candesartan group and 538 (42%) in the placebo group experienced the primary outcome (unadjusted hazard ratio 0·85 [95% CI 0·75–0·96], p=0·011; covariate adjusted p=0·010). Candesartan reduced each of the components of the primary outcome significantly, as well as the total number of hospital admissions for CHF. The benefits of candesartan were similar in all predefined subgroups, including patients receiving baseline β blocker treatment. The addition of candesartan to ACE inhibitor and other treatment leads to a further clinically important reduction in relevant cardiovascular events in patients with CHF and reduced left-ventricular ejection fraction. Published online Sept 1, 2003 http://image.thelancet.com/extras/03art7417web.pdf

We investigated the clinical profiles associated with serum uric acid (sUA) levels in a large cohort of patients hospitalized for worsening chronic heart failure with ejection fraction (EF) ≤40%, with specific focus on gender, race, and renal function based interactions. In 3,955 of 4,133 patients (96%) with baseline sUA data, clinical characteristics and outcomes were compared across sUA quartiles. The primary end points were all-cause mortality and a composite of cardiovascular mortality or heart failure hospitalization. Interaction analyses were performed for gender, race, and baseline renal function. Median follow-up was 9.9 months. Mean sUA was 9.1 ± 2.8 mg/dl and was higher in men than in women (9.3 ± 2.7 vs 8.7 ± 3.0 mg/dl, p <0.001) and in blacks than in whites (10.0 ± 2.7 vs 9.0 ± 2.8 mg/dl, p <0.001). Higher sUA was associated with lower systolic blood pressure and EF, higher natriuretic peptides, and more impaired renal function. After accounting for 24 baseline covariates, in patients with enrollment estimated glomerular filtration rate ≥30 ml/min/1.73 m2, sUA was strongly associated with increased all-cause mortality (hazard ratio 1.44, 95% confidence interval 1.22 to 1.69, p <0.001) and the composite end point (hazard ratio 1.44, 95% confidence interval 1.26 to 1.64, p <0.001). However, in patients with estimated glomerular filtration rate <30 ml/min/1.73 m2, sUA was not related with either end point (both p >0.4). Adjusted interaction analyses for gender, race, and admission allopurinol use were not significant. In conclusion, sUA is commonly elevated in patients hospitalized for worsening chronic heart failure and reduced EF, especially in men and blacks. The prognostic use of sUA differs by baseline renal function, suggesting different biologic and pathophysiologic significance of sUA among those with and without significant renal dysfunction. •Mean serum uric acid (sUA) during hospitalization for heart failure is high (∼9 mg/dl).•sUA is associated with lower ejection fraction, higher B-type natriuretic peptide, and impaired renal function.•sUA is independently predictive of postdischarge outcomes in estimated glomerular filtration rate ≥30 ml/min/1.73 m2.

The prognosis associated with prolonged intraventricular conduction on electrocardiogram (ECG) remains uncertain. We aimed to compare clinical outcomes of narrow versus prolonged intraventricular conduction on ECG stratified by QRS morphology and cardiovascular disease (CVD) status. A post-hoc analysis was performed of the randomized-control PRECISION trial. Patients with centrally adjudicated, nonpaced baseline ECGs were included. QRS duration was classified narrow (≤100 ms) versus prolonged (>100 ms) with additional categorization into left (LBBB) or right (RBBB) bundle branch block or nonspecific intraventricular conduction delay (IVCD). IVCD was subclassified if left ventricular conduction delay (LVCD) was present (L-IVCD) or absent (O-IVCD). The primary outcome was adjudicated all-cause and cardiovascular (CV) mortality. Of 24,081 patients randomized, 22,067 (92%) were included with follow-up 34 ± 13 months. Study patients were 63 ± 9 years, 64% female, 75% Caucasian, 23% with established CVD. The prevalence of QRS prolongation was 5.6% (1,240): 760 right bundle branch block (3.4%), 313 LBBB (1.4%), and 161 IVCD (0.7%), 95 subclassified L-IVCD (0.4%). After adjustment, LBBB and L-IVCD were similarly associated with increased all-cause (LBBB: 2.3 [1.4 to 3.8], p = 0.001; L-IVCD: 4.0 [2.1 to 7.9], p <0.001) and CV (LBBB: 3.6 [2.0 to 6.5], p <0.001; L-IVCD 3.6 [1.3 to 9.7], p = 0.001) mortality. The presence of LVCD (LBBB or L-IVCD) was associated with all-cause (2.8 [1.8 to 4.2], p <0.001) and CV (3.6 [2.2 to 6.1], p <0.001) mortality exceeding the observed risks of coronary artery disease, left ventricular hypertrophy, or diabetes. The LVCD hazard persisted across QRS durations (100 to 120 vs >120 ms) and CVD status. In conclusion, LVCD, whether LBBB or L-IVCD, was strongly associated with increased mortality in patients with and at-risk for CVD.

Patients who have had a myocardial infarction resulting in a reduced left ventricular ejection fraction are at risk for ventricular arrhythmias and sudden death. In this large trial, patients were randomly assigned to receive an implantable defibrillator or conventional therapy. During the follow-up period, which lasted up to four years, the mortality rate was lower in the defibrillator group than in the conventional-therapy group (14.2 percent vs. 19.8 percent). Patients with a reduced left ventricular ejection fraction received either an implantable defibrillator or conventional therapy. The mortality rate was lower in the defibrillator group. Patients with myocardial infarction and reduced left ventricular function are at risk for congestive heart failure and arrhythmia-related sudden death. In 1996, the implantation of a defibrillator was reported to improve survival in patients with coronary heart disease, reduced ventricular function, unsustained ventricular tachycardia, and inducible ventricular tachycardia, 1 and this finding was confirmed in 1999. 2 In both studies, patients underwent invasive electrophysiological testing to determine their risk of arrhythmia. The prognostic value of electrophysiological testing for the identification of patients with coronary heart disease who are at risk for ventricular arrhythmias is uncertain. 3 We reasoned that in patients with a . . .

Background The left ventricular performance index (LVGFI) as a comprehensive marker of cardiac performance integrates LV structure with global function within one index. In a prospective cohort study of healthy individuals the LVGFI demonstrated a superior prognostic value as compared to LV ejection fraction (LVEF). In patients after ST-segment elevation myocardial infarction (STEMI), however, the role of the LVGFI is unknown. Aim of this study was to investigate the relationship between the LVGFI and infarct characteristics as well as prognosis in a large multicenter STEMI population. Methods In total 795 STEMI patients reperfused by primary angioplasty (<12 h after symptom onset) underwent cardiovascular magnetic resonance (CMR) at 8 centers. CMR was completed within one week after infarction using a standardized protocol including LV dimensions, mass and function for calculation of the LVGFI. The primary clinical endpoint of the study was the occurrence of major adverse cardiac events (MACE). Results The median LVGFI was 31.2 % (interquartile range 25.7 to 36.6). Patients with LVGFI < median had significantly larger infarcts, less myocardial salvage, a larger extent of microvascular obstruction, higher incidence of intramyocardial hemorrhage and more pronounced LV dysfunction ( p  < 0.001 for all). MACE and mortality rates were significantly higher in the LVGFI < median group ( p  < 0.001 and p  = 0.003, respectively). The LVGFI had an incremental prognostic value in addition to LVEF for prediction of all-cause mortality. Conclusions The LVGFI strongly correlates with markers of severe myocardial and microvascular damage in patients with STEMI, offering prognostic information beyond traditional cardiac risk factors including the LVEF. Trials registration ClinicalTrials.gov: NCT00712101

Background Ischemic cardiomyopathy and severe left ventricular dysfunction are well established to represent the main determinants of poor survival and premature death compared with preserved ventricular function. However, the role of myocardial revascularization as a therapeutic alternative is not known to improve the long-term prognosis in this group of patients. This study will investigate whether myocardial revascularization contributes to a better prognosis for patients compared with those treated with drugs alone and followed over the long term. Methods The study will include 600 patients with coronary artery disease associated with ischemic cardiomyopathy. The surgical or drug therapy option will be randomized, and the events considered for analysis will be all-cause mortality, nonfatal infarction, unstable angina requiring additional revascularization, and stroke. The events will be analyzed according to the intent-to-treat principle. Patients with multivessel coronary disease and left ventricular ejection fraction measurements of less than 35% will be included. In addition, myocardial ischemia will be documented by myocardial scintigraphy. Markers of myocardial necrosis will be checked at admission and after the procedure. Discussion The role of myocardial revascularization (CABG) in the treatment of patients with coronary artery disease and heart failure is not clearly established. The surgical option of revascularizing the myocardium is a procedure designed to reduce the load of myocardial hibernation in patients with heart failure caused by coronary artery disease. On the other hand, the assessment of myocardial viability is frequently used to identify patients with left ventricular ischemic dysfunction in which CABG may add survival benefit. However, the effectiveness of this option is uncertain. The great difficulty in establishing the efficacy of surgical intervention is based on the understanding of viability without ischemia. Thus, this study will include only patients with viable and truly ischemic myocardium to correct this anomaly. Trial registration Evaluation of a randomized comparison between patients with coronary artery disease associated with ischemic cardiomyopathy submitted to medical or surgical treatment: MASS-VI (HF), ISRCTN77449548 , Oct 10th, 2019 (retrospectively registered).

In the studies of left ventricular dysfunction (SOLVD), enalapril reduced mortality in patients with symptomatic but not asymptomatic left ventricular systolic dysfunction during the trial. We did a 12-year follow-up of SOLVD to establish if the mortality reduction with enalapril among patients with heart failure was sustained, and whether a subsequent reduction in mortality would emerge among those with asymptomatic ventricular dysfunction. Of the 6797 patients previously enrolled in the SOLVD prevention and treatment trials, we ascertained the subsequent vital status of 5165 individuals who were alive when the trials had been completed. Follow-up was done through direct contacts in Belgium and linkages with national death registries and federal beneficiary or historic tax summary files in the USA and Canada. Follow-up was 99·8% (6784/6797) complete. In the prevention trial, 50·9% (1074/2111) of the enalapril group had died compared with 56·4% (1195/2117) of the placebo group (generalised Wilcoxon p=0·001). In the treatment trial, 79·8% (1025/1285) of the enalapril group had died compared with 80·8% (1038/1284) of the placebo group (generalised Wilcoxon p=0·01). The reductions in cardiac deaths were significant and similar in both trials. When data for the prevention and treatment trials were combined, the hazard ratio for death was 0·90 for the enalapril group compared with the placebo group (95% CI 0·84–0·95, generalised Wilcoxon p=0·0003). Enalapril extended median survival by 9·4 months in the combined trials (95% CI 2·8–16·5, p=0·004). Treatment with enalapril for 3–4 years led to a sustained improvement in survival beyond the original trial period in patients with left ventricular systolic dysfunction, with an important increase in life expectancy.

Mechanical left ventricular dyssynchrony (MLVD) might contribute in the therapeutic decision-making in patients with heart failure (HF) prior to cardiac resynchronization therapy (CRT). Our aim was to assess MLVD in patients with HF prior to implantable cardioverter-defibrillator (ICD) compared to patients with CRT-D. In a prospective study, patients with LVEF ≤ 35% who were scheduled for ICD or CRT-D, underwent gated SPECT myocardial perfusion imaging with technetium 99m sestamibi within 3 months prior procedure. MLVD was measured by phase analysis. The study cohort consisted of 143 patients, 71 with ICD and 72 with CRT-D. Age 68.3 ± 11 and LVEF 24 ± 6%. Phase standard deviation (SD) was 62.5 ± 18 and 59.7 ± 20 (P = NS), respectively. During follow-up of 23.7 ± 12.1 months, there were 10 vs 14 cardiac death in ICD and CRT-D, respectively (P = NS), hospitalization for HF, in 34 vs 53 (P < .001). In multivariate analysis, Phase SD was the independent predictor for cardiac death [HR 2.66 (95% CI 1.046-6.768), P = .04]. Kaplan-Meier curves of phase SD of 60° significantly identified ICD patients with and without cardiac deaths and hospitalization for HF exacerbation. MLVD by phase SD can identify patients with cardiac events and predict cardiac death in patients treated with ICD.