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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.

Cardiosphere-derived cells (CDCs) reduce scarring after myocardial infarction, increase viable myocardium, and boost cardiac function in preclinical models. We aimed to assess safety of such an approach in patients with left ventricular dysfunction after myocardial infarction. In the prospective, randomised CArdiosphere-Derived aUtologous stem CElls to reverse ventricUlar dySfunction (CADUCEUS) trial, we enrolled patients 2–4 weeks after myocardial infarction (with left ventricular ejection fraction of 25–45%) at two medical centres in the USA. An independent data coordinating centre randomly allocated patients in a 2:1 ratio to receive CDCs or standard care. For patients assigned to receive CDCs, autologous cells grown from endomyocardial biopsy specimens were infused into the infarct-related artery 1·5–3 months after myocardial infarction. The primary endpoint was proportion of patients at 6 months who died due to ventricular tachycardia, ventricular fibrillation, or sudden unexpected death, or had myocardial infarction after cell infusion, new cardiac tumour formation on MRI, or a major adverse cardiac event (MACE; composite of death and hospital admission for heart failure or non-fatal recurrent myocardial infarction). We also assessed preliminary efficacy endpoints on MRI by 6 months. Data analysers were masked to group assignment. This study is registered with ClinicalTrials.gov, NCT00893360. Between May 5, 2009, and Dec 16, 2010, we randomly allocated 31 eligible participants of whom 25 were included in a per-protocol analysis (17 to CDC group and eight to standard of care). Mean baseline left ventricular ejection fraction (LVEF) was 39% (SD 12) and scar occupied 24% (10) of left ventricular mass. Biopsy samples yielded prescribed cell doses within 36 days (SD 6). No complications were reported within 24 h of CDC infusion. By 6 months, no patients had died, developed cardiac tumours, or MACE in either group. Four patients (24%) in the CDC group had serious adverse events compared with one control (13%; p=1·00). Compared with controls at 6 months, MRI analysis of patients treated with CDCs showed reductions in scar mass (p=0·001), increases in viable heart mass (p=0·01) and regional contractility (p=0·02), and regional systolic wall thickening (p=0·015). However, changes in end-diastolic volume, end-systolic volume, and LVEF did not differ between groups by 6 months. We show intracoronary infusion of autologous CDCs after myocardial infarction is safe, warranting the expansion of such therapy to phase 2 study. The unprecedented increases we noted in viable myocardium, which are consistent with therapeutic regeneration, merit further assessment of clinical outcomes. US National Heart, Lung and Blood Institute and Cedars-Sinai Board of Governors Heart Stem Cell Center.

In this randomized, placebo-controlled trial, investigators evaluated the effects of the sodium–glucose cotransporter 2 inhibitor dapagliflozin in patients with heart failure and a reduced ejection fraction with or without type 2 diabetes. The risk of worsening heart failure or cardiovascular death was lower among those who received dapagliflozin, regardless of the presence or absence of diabetes.

In this comparative-effectiveness trial, biventricular pacing prevented the reduction in left ventricular ejection fraction that is seen with right ventricular pacing. The deleterious effect of nonphysiologic right ventricular apical pacing on left ventricular systolic function has been recognized since the 1920s. 1 In the Dual Chamber and VVI Implantable Defibrillator (DAVID) trial, the unexpected increased rates of death and hospital admission for heart failure among patients who were randomly assigned to the dual-chamber, rate-adaptive (DDDR) mode were purportedly due to the adverse effect of right ventricular apical pacing on left ventricular structural remodeling. 2 Results of subsequent trials have supported the notion that right ventricular apical pacing might lead to adverse clinical outcomes in patients with standard pacing indications. 3 – 7 Nevertheless, right ventricular . . .

This review focuses on the available data regarding the utility of advanced left ventricular (LV) imaging in aortic stenosis (AS) and its potential impact for optimising the timing of aortic valve replacement. Ejection fraction is currently the only LV parameter recommended to guide intervention in AS. The cut-off value of 50%, recommended for decision-making in asymptomatic patients with AS, is currently under debate. Several imaging parameters have emerged as predictors of disease progression and clinical outcomes in this setting. Global longitudinal LV strain by speckle tracking echocardiography is useful for risk stratification of asymptomatic patients with severe AS and preserved LV ejection fraction. Its prognostic value was demonstrated in these patients, but further work is required to define the best thresholds to aid the decision-making process. The assessment of myocardial fibrosis is the most studied application of cardiac magnetic resonance in AS. The detection of replacement fibrosis by late gadolinium enhancement offers incremental prognostic information in these patients. Clinical implementation of this technique to optimise the timing of aortic valve intervention in asymptomatic patients is currently tested in a randomised trial. The use of T1 mapping techniques can provide an assessment of interstitial myocardial fibrosis and represents an expanding field of interest. However, convincing data in patients with AS is still lacking. All these imaging parameters have substantial potential to influence the management decision in patients with AS in the future, but data from randomised clinical trials are awaited to define their utility in daily practice.

In this trial, patients with mild-to-moderate heart failure were randomly assigned to receive an implantable cardioverter–defibrillator (ICD) alone or an ICD plus cardiac-resynchronization therapy. Patients in the latter group had lower rates of death and hospitalization for heart failure. The use of implantable cardioverter–defibrillators (ICDs) improves survival among patients who have New York Heart Association (NYHA) class II or III heart failure with left ventricular systolic dysfunction despite optimal medical therapy. 1 Cardiac-resynchronization therapy (CRT) improves symptoms of heart failure, quality of life, exercise capacity, 2 – 6 and left ventricular function 7 when used in patients with NYHA functional class III or ambulatory class IV heart failure with a wide QRS complex. CRT has also been shown to reduce mortality among patients not receiving an ICD. 8 However, studies have not shown a survival benefit of CRT in patients with NYHA class II . . .

Patients with CAD and LV dysfunction were assigned to either medical therapy alone or medical therapy plus CABG. At 5 years, there was no significant difference between the two study groups in the rate of death from any cause. It is estimated that 5.8 million patients in the United States 1 and 15 million in Europe 2 have heart failure. Coronary artery disease is the most common substrate for heart failure in industrialized nations. 3 However, the role of coronary-artery bypass grafting (CABG) in the treatment of patients with coronary artery disease and heart failure has not been clearly established. In three landmark clinical trials in the 1970s, a total of 2234 patients with chronic stable angina were randomly assigned to undergo CABG or receive medical therapy alone. 4 – 6 The findings from these trials led to recommendations supporting the use of CABG . . .

Current guidelines on the use of β-blockers in post–acute myocardial infarction (MI) patients without reduced left ventricular ejection fraction (LVEF) are based on studies before the implementation of modern reperfusion and secondary prevention therapies. It remains unknown whether β-blockers will reduce mortality and recurrent MI in contemporary revascularized post-MI patients without reduced LVEF. BETAMI is a prospective, randomized, open, blinded end point multicenter study in 10,000 MI patients designed to test the superiority of oral β-blocker therapy compared to no β-blocker therapy. Patients with LVEF ≥40% following treatment with percutaneous coronary intervention or thrombolysis and/or no clinical signs of heart failure are eligible to participate. The primary end point is a composite of all-cause mortality or recurrent MI obtained from national registries over a mean follow-up period of 3 years. Safety end points include rates of nonfatal MI, all-cause mortality, ventricular arrhythmias, and hospitalizations for heart failure obtained from hospital medical records 30 days after randomization, and from national registries after 6 and 18 months. Key secondary end points include recurrent MI, heart failure, cardiovascular and all-cause mortality, and clinical outcomes linked to β-blocker therapy including drug adherence, adverse effects, cardiovascular risk factors, psychosocial factors, and health economy. Statistical analyses will be conducted according to the intention-to-treat principle. A prespecified per-protocol analysis (patients truly on β-blockers or not) will also be conducted. The results from the BETAMI trial may have the potential of changing current clinical practice for treatment with β-blockers following MI in patients without reduced LVEF. EudraCT number 2018-000590-75.

Background Liraglutide is an antidiabetic agent with cardioprotective effect. The purpose of this study is to test efficacy of liraglutide to improve diabetic cardiomyopathy in patients with diabetes mellitus type 2 (DM2) without cardiovascular disease. Methods Patients with DM2 were randomly assigned to receive liraglutide 1.8 mg/day or placebo in this double-blind trial of 26 weeks. Primary outcome measures were LV diastolic function (early (E) and late (A) transmitral peak flow rate, E/A ratio, early deceleration peak (Edec), early peak mitral annular septal tissue velocity (Ea) and estimated LV filling pressure (E/Ea), and systolic function (stroke volume, ejection fraction, cardiac output, cardiac index and peak ejection rate) assessed with CMR. Intention-to-treat analysis of between-group differences was performed using ANCOVA. Mean estimated treatment differences (95% confidence intervals) are reported. Results 23 patients were randomized to liraglutide and 26 to placebo. As compared with placebo, liraglutide significantly reduced E (− 56 mL/s (− 91 to − 21)), E/A ratio (− 0.17 (− 0.27 to − 0.06)), Edec (− 0.9 mL/s 2  * 10 −3 (− 1.3 to − 0.2)) and E/Ea (− 1.8 (− 3.0 to − 0.6)), without affecting A (3 mL/s (− 35 to 41)) and Ea (0.4 cm/s (− 0.9 to 1.4)). Liraglutide reduced stroke volume (− 9 mL (− 16 to − 2)) and ejection fraction (− 3% (− 6 to − 0.1)), but did not change cardiac output (− 0.4 L/min (− 0.9 to 0.2)), cardiac index (− 0.1 L/min/m 2 (− 0.4 to 0.1)) and peak ejection rate (− 46 mL/s (− 95 to 3)). Conclusions Liraglutide reduced early LV diastolic filling and LV filling pressure, thereby unloading the left ventricle. LV systolic function reduced and remained within normal range. Future studies are needed to investigate if liraglutide-induced left ventricular unloading slows progression of diabetic cardiomyopathy into symptomatic stages. Trial registration ClinicalTrials.gov: NCT01761318.

Cardiac resynchronization improves left ventricular function and functional status in patients who have left ventricular systolic dysfunction and interventricular dyssynchrony due to a conduction delay. In a randomized trial comparing medical therapy alone with medical therapy plus cardiac resynchronization, combined therapy was associated with a significant reduction in the risk of death from any cause. In a randomized trial comparing medical therapy alone with medical therapy plus cardiac resynchronization, combined therapy was associated with a significant reduction in the risk of death from any cause. Despite improvements in pharmacologic treatment, many patients with heart failure have severe and persistent symptoms, and their prognosis remains poor. 1 , 2 Such patients commonly have regions of delayed myocardial activation and contraction, leading to cardiac dyssynchrony. In a series of trials lasting up to six months, cardiac resynchronization decreased symptoms and improved exercise capacity, the quality of life, and ventricular function. 3 – 7 The Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) trial showed that cardiac-resynchronization therapy alone or combined with an implantable defibrillator reduced the composite end point of death from any cause or hospitalization during a . . .