In patients with heart failure and reduced LVEF, chronic ACE inhibition with enalapril prevents progressive LV dilatation and systolic dysfunction (increased ESV). These effects probably result from a combination of altered remodeling and sustained reduction in preload and afterload.

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Chronic ACE inhibitor treatment slows or reverses LV dilatation in patients with asymptomatic LV systolic dysfunction. Compared with symptomatic patients, asymptomatic patients manifest a slower rate of spontaneous LV dilatation and less reduction in LV volumes by enalapril.

Spironolactone administration in patients with CHF has opposite effects on circulating levels of natriuretic peptides (which decrease) and aldosterone and AII (which increase). The reduction in natriuretic peptides might be related to changes in left ventricular diastolic filling pressure and/or compliance, whereas the increase in AII and aldosterone probably reflects activated feedback mechanisms. Further studies are needed to link these changes to the beneficial effects on survival and to determine whether the addition of an AII antagonist could be useful in this setting.

Without revascularization, presence of dysfunctional viable myocardium by DE-CMR is an independent predictor of mortality in patients with ischemic LV dysfunction. This observation may be useful for pre-operative selection of patients for revascularization.

Aims Myostatin (Mstn), a member of the transforming growth factors (TGF)‐β family that regulate skeletal muscle growth, has been identified as a regulator of cardiomyocyte growth. The aim of our study was to measure Mstn plasma concentrations in patients with congestive heart failure (CHF) and to evaluate their relationship with other neurohormones released in CHF. Methods and results concentrations of Mstn were measured using a competitive immunoassay, in 76 CHF patients who were receiving optimal treatment and 60 healthy controls. Circulating levels of other neurohormones N‐terminal pro‐atrial natriuretic peptide (NT‐proANP), B‐type natriuretic peptide (BNP), N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP), and Big ET‐1 were also measured. Plasma Mstn was higher in CHF patients than in controls (63.0 vs. 43.0 ng/mL; P < 0.001). In CHF, Mstn levels correlated positively with NT‐proANP (r = 0.25; P = 0.03), BNP (r = 0.33; P < 0.01), NT‐proBNP (r = 0.32; P < 0.01), and Big ET‐1 (r = 0.26; P = 0.02). No significant correlations were observed with age and creatinine. Conclusion Our results demonstrate that plasma concentrations of Mstn are significantly increased in CHF patients and that Mstn correlates with biomarkers related to HF severity. Our study confirms the activation of Mstn in patients with heart failure.

BackgroundApolipoprotein B100 (apoB) is a superior indicator of CV risk than total or LDL-C. Non-HDL-C represents a simple surrogate for apoB in hypertriglyceridemic and/or T2DM patients. ApoB and non-HDL-C show high correlation, although the degree of mutual concordance remains debated in CV risk evaluation.ObjectivesWe used the Discriminant Ratio (DR) methodology to compare the performance of non-HDL-C with that of apoB to rank diabetic patients according to dyslipidemia and to establish the underlying relationship between these variables taking measurement noise and intra-/intersubject variation into account, and to derive an unbiased equivalence equation.MethodsFasting total C, HDL-C, apoB and triglycerides were measured in 45 diabetic patients. The DR of the underlying between-subject standard deviation (SD) to the within-subject SD was calculated from duplicates. Correlation coefficients between pairs were adjusted to include an estimate of the underlying correlation.ResultsMean values [day 1 (1SD)] were 143 (36) mg/dl (non-HDL-C) and 98 (24) mg/dl (apoB). The DR's of both parameters were similar (1.76 and 1.83) (p = 0.83). Pearson's product-moment correlation coefficient between tests was very high (0.94), reaching unity (1.00) after attenuation adjustment. The unbiased equation of equivalence relating apoB to non-HDL-C had a slope of 0.65 and an intercept of 6.3 mg/dl.ConclusionsThe discrimination power of non-HDL-C is similar to that of apoB to rank diabetic patients according to atherogenic cholesterol and lipoprotein burden. Since true correlation between variables reached unity, non-HDL-C may provide not only a metabolic surrogate but also a candidate biometrical equivalent to apoB, as non-HDL-C calculation is readily available.

Cardiovascular outcomes of adult patients with nonischemic DCM do not appear to be influenced by the degree of trabeculation. This argues against a noncompaction phenotype designating a more severe form of DCM.