Left ventricular hypertrophy (LVH) is growth in left ventricular mass caused by increased cardiomyocyte size. LVH can be a physiological adaptation to strenuous physical exercise, as in athletes, or it can be a pathological condition, which is either genetic or secondary to LV overload. Physiological LVH is usually benign and regresses upon reduction/cessation of physical activity. Pathological LVH is a compensatory phenomenon, which eventually may become maladaptive and evolve towards progressive LV dysfunction and heart failure (HF). Both interstitial and replacement fibrosis play a major role in the progressive decompensation of the hypertrophied LV. Coronary microvascular dysfunction (CMD) and myocardial ischemia, which have been demonstrated in most forms of pathological LVH, have an important pathogenetic role in the formation of replacement fibrosis and both contribute to the evolution towards LV dysfunction and HF. Noninvasive imaging allows detection of myocardial fibrosis and CMD, thus providing unique information for the stratification of patients with LVH. (Circ J 2016; 80: 555-564).

Aging is associated with an increasing burden of morbidity, especially for cardiovascular diseases (CVDs). General cardiovascular risk factors, ischemic heart diseases, heart failure, arrhythmias, and cardiomyopathies present a significant prevalence in older people, and are characterized by peculiar clinical manifestations that have distinct features compared with the same conditions in a younger population. Remarkably, the aging heart phenotype in both healthy individuals and patients with CVD reflects modifications at the cellular level. An improvement in the knowledge of the physiological and pathological molecular mechanisms underlying cardiac aging could improve clinical management of older patients and offer new therapeutic targets.

Background and Aims: The prediction of the first major arrhythmic event (MAE) is still an unmet need in the recently defined scenario of non-dilated left ventricular cardiomyopathy (NDLVC). Methods: A cohort of 337 patients with NDLVC and no history of MAE was retrospectively identified at two large centres. Patient-tailored diagnostic workup included cardiac magnetic resonance (CMR), endomyocardial biopsy, and genetic testing. The primary endpoint was the occurrence of the first MAE, including sustained ventricular tachycardia (VT), ventricular fibrillation, or appropriate implantable cardioverter-defibrillator therapy, by 60-month follow-up. A pool of 216 NDLVC patients from 11 European centres served as a validation cohort. Results: In the study cohort (mean age 37 ± 15 years, 62% male), the mean left ventricular ejection fraction (LVEF) was 52 ± 8%, and 79% of patients had late gadolinium enhancement (LGE) at baseline CMR. By 60-month follow-up, 51 patients (15%) experienced a MAE. The primary endpoint was predicted by male sex [hazard ratio (HR) 2.4, 95% confidence interval (CI) 1.3–4.4, P = .007], baseline non-sustained VT (HR 3.1, 95% CI 1.7–5.6, P < .001), LVEF < 45% (HR 5.5, 95% CI 2.7–11.0, P < .001), septal (HR 2.0, 95% CI 1.0–4.0, P = .046) and ring-like pattern of LGE (HR 1.3, 95% CI .6–2.6, P = .54), pathogenic/likely pathogenic variants in guideline-defined high-risk genes (HR 4.6, 95% CI 2.3–9.1, P < .001), and biopsy/CMR-proven myocardial inflammation (HR 15.7, 95% CI 6.1–40.3, P < .001). The results were confirmed in the validation cohort (Uno’s C-index 0.81, 95% CI .75–.88). A novel risk score was subsequently derived. Conclusions: In NDLVC, male sex, non-sustained VT, LVEF < 45%, septal and ring-like LGE, high-risk genotypes, and myocardial inflammation predicted the first episode of MAE by 60 months.

Over recent years, preclinical and clinical evidence has implicated myocardial inflammation (M-Infl) in the pathophysiology and phenotypes of traditionally genetic cardiomyopathies. M-Infl resembling myocarditis on imaging and histology occurs frequently as a clinical manifestation of classically genetic cardiac diseases, including dilated and arrhythmogenic cardiomyopathy. The emerging role of M-Infl in disease pathophysiology is leading to the identification of druggable targets for molecular treatment of the inflammatory process and a new paradigm in the field of cardiomyopathies. Cardiomyopathies constitute a leading cause of heart failure and arrhythmic sudden death in the young population. The aim of this review is to present, from bedside to bench, the current state of the art about the genetic basis of M-Infl in nonischemic cardiomyopathies of the dilated and arrhythmogenic spectrum in order to prompt future research towards the identification of novel mechanisms and treatment targets, with the ultimate goal of lowering disease morbidity and mortality.

Detrended Fluctuation Analysis (DFA) is a popular method for assessing the fractal characteristics of biosignals, recently adapted for evaluating the heart‐rate multifractal and/or multiscale characteristics. However, the existing methods do not consider the beat‐by‐beat sampling of heart rate and have relatively low scale resolutions and were not applied to cardiovascular signals other than heart rate. Therefore, aim of this work is to present a DFA‐based method for joint multifractal/multiscale analysis designed to address the above critical points and to provide the first description of the multifractal/multiscale structure of interbeat intervals (IBI), systolic blood pressure (SBP), and diastolic blood pressure (DBP) in male and female volunteers separately. The method optimizes data splitting in blocks to reduce the DFA estimation variance and to evaluate scale coefficients with Taylor’s expansion formulas and maps the scales from beat domains to temporal domains. Applied to cardiovascular signals recorded in 42 female and 42 male volunteers, it showed that scale coefficients and degree of multifractality depend on the temporal scale, with marked differences between IBI, SBP, and DBP and with significant sex differences. Results may be interpreted considering the distinct physiological mechanisms regulating heart‐rate and blood‐pressure dynamics and the different autonomic profile of males and females.