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Cardiac allograft vasculopathy is characterized by increased coronary intimal thickness and is a leading cause of death in heart transplant (HTx) recipients despite the routine use of statins. The experience with inhibitors of proprotein convertase subtilisin-kexin type 9 in HTx recipients is limited. Our hypothesis was that lowering cholesterol with the proprotein convertase subtilisin–kexin type 9inhibitor evolocumab would reduce coronary intimal thickness in these patients without compromising safety.

The randomized controlled High‐Intensity Interval Training in De Novo Heart Transplant Recipients in Scandinavia (HITTS) study compared 9 months of high‐intensity interval training (HIT) with moderate intensity continuous training in de novo heart transplant recipients. In our 3‐year follow‐up study, we aimed to determine whether the effect of early initiation of HIT on peak oxygen consumption (VO2peak) persisted for 2 years postintervention. The study's primary end point was the change in VO2peak(mL/kg/min). The secondary end points were muscle strength, body composition, heart rate response, health‐related quality of life, daily physical activity, biomarkers, and heart function. Of 78 patients who completed the 1‐year HITTS trial, 65 entered our study and 62 completed the study tests. VO2peakincreased from baseline to 1 year and leveled off thereafter. During the intervention period, the increase in VO2peakwas larger in the HIT arm; however, 2 years later, there was no significant between‐group difference in VO2peak. However, the mean change in the anaerobic threshold and extensor muscle endurance remained significantly higher in the HIT group. Early initiation of HIT after heart transplantation appears to have some sustainable long‐term effects. Clinical trial registration number: NCT01796379. High‐ compared to moderate‐intensity interval training for 1 year after heart transplantation results in comparable peak oxygen consumption but improved anaerobic threshold and muscle endurance 2 years later.

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AbstractPurpose:Diagnostic and prognostic evaluation remains challenging in arrhythmogenic right ventricular cardiomyopathy (ARVC). We measured plasma concentration of soluble ST2 (sST2) and assessed its association with right ventricular (RV) function and ventricular arrhythmias in patients with ARVC.Methods:We included patients with ARVC and genotype positive relatives. Soluble ST2 was determined by ELISA. We assessed myocardial function by echocardiography including strain by speckle tracking technique.Results:We included 44 subjects (age 41 ± 15 years, 21 (48%) female). Soluble ST2 was associated with RV global strain (r = 0.44; p = 0.008), as well as with left ventricular (LV) function. Plasma levels of sST2 were higher in patients with ventricular arrhythmias than in patients without ventricular arrhythmias (35 ± 13 ng/mL vs. 26 ± 7 ng/mL, p = 0.009). The association between sST2 and ventricular arrhythmias remained significant even after adjusting for RV function (Wald = 5.2; p = 0.02).Conclusions:Soluble ST2 is associated with RV and LV function in patients with ARVC. Soluble ST2 may aid in the determination of disease severity in ARVC.

This study sought to evaluate whether a panel of biomarkers improved prognostication in patients with heart failure (HF) and reduced ejection fraction of ischemic origin using a systematized approach according to suggested requirements for validation of new biomarkers.

ObjectiveInterleukin-6 (IL-6) is a driver of inflammation and associated endothelial cell activation in acute coronary syndromes. We evaluated the effect of the IL-6 receptor antagonist tocilizumab on coronary microvascular function and endothelial dysfunction measured by coronary flow reserve (CFR) and markers of endothelial cell activation in patients with non-ST-elevation myocardial infarction (NSTEMI).MethodsThis substudy was part of a two-centre, double-blind, randomised, placebo-controlled trial evaluating the effect of a single dose of tocilizumab in NSTEMI. Markers of endothelial cell activation (vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule-1 and von Willebrand factor) were assessed in 117 patients. In 42 of these patients, 20 assigned to placebo and 22 to tocilizumab, we measured CFR. Blood samples were obtained at seven consecutive time points between day 1 and 3. CFR was measured by transthoracic echocardiography during hospitalisation and after 6 months.ResultsTocilizumab did not affect CFR during hospitalisation (tocilizumab: 3.4±0.8 vs placebo: 3.3±1.2, p=0.80). CFR improved significantly in both groups at 6 months. Patients in the tocilizumab group had significantly higher area under the curve for VCAM-1 (median 622 vs 609 ng/mL/hour, tocilizumab and placebo respectively, p=0.003). There were inverse correlations between VCAM-1 and CFR in the placebo (hospitalisation: r=−0.74, p<0.01, 6 months: r=−0.59, p<0.01), but not in the tocilizumab group (hospitalisation: r=0.20, p=0.37, 6 months r=−0.28, p=0.20).ConclusionsTocilizumab did not affect CFR during hospitalisation or after 6 months. Tocilizumab increased VCAM-1 levels during hospitalisation, but this was not associated with reduced CFR in these patients.

Cardiotoxicity from anthracyclines or cardiac radiation therapy is detrimental to left ventricular (LV) function. However, the long-term effects on right ventricular (RV) performance are largely unknown. The aim of this study was to investigate the long-term impact of cardiotoxic treatment on RV function among adult cancer survivors.

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The role of speckle-tracking echocardiography in the assessment of chronic aortic regurgitation (AR) is not established. Load dependency may encumber the interpretation of strain measurements in the chronically overloaded left ventricle. The aim of this study was to investigate the mechanisms of left ventricular (LV) contraction patterns in asymptomatic patients with moderate to severe AR and preserved ejection fractions.