Imaging techniques for the assessment of adverse cardiac remodeling in metabolic syndrome.

Metabolic syndrome (MetS) includes different metabolic conditions (i.e. abdominal obesity, impaired glucose tolerance, hypertriglyceridemia, decreased HDL cholesterol, and/or hypertension) that concour in the development of cardiovascular disease and diabetes. MetS individuals often show adverse cardiac remodeling and myocardial dysfunction even in the absence of overt coronary artery disease or valvular affliction. Diastolic impairment and hypertrophy are hallmarks of MetS-related cardiac remodeling and represent the leading cause of heart failure with preserved ejection fraction (HFpEF). Altered cardiomyocyte function, increased neurohormonal tone, interstitial fibrosis, coronary microvascular dysfunction, and a myriad of metabolic abnormalities have all been implicated in the development and progression of adverse cardiac remodeling related to MetS. However, despite the enormous amount of literature produced on this argument, HF remains a leading cause of morbidity and mortality in such population. The early detection of initial adverse cardiac remodeling would enable the optimal implementation of effective therapies aiming at preventing the progression of the disease to the symptomatic phase. Beyond conventional imaging techniques, such as echocardiography, cardiac tomography, and magnetic resonance, novel post-processing tools and techniques provide information on the biological processes that underlie metabolic heart disease. In this review, we summarize the pathophysiology of MetS-related cardiac remodeling and illustrate the relevance of state-of-the-art multimodality cardiac imaging to identify and quantify the degree of myocardial involvement, prognosticate long-term clinical outcome, and potentially guide therapeutic strategies.

Right ventricle dysfunction assessment for transcatheter tricuspid valve repair: A matter of debate.

Newer approaches in transcatheter tricuspid valve replacement (TTVR) have recently showed optimistic data of efficacy and safety in patients at high risk for surgery. However, the absence of residual regurgitation (and subsequently higher likelihood for developing afterload mismatch) with TTVR compared with transcatheter tricuspid valve intervention may become a critical concern if RV dysfunction is misdiagnosed. Indeed, such sudden increase in afterload on the right ventricle (RV) may not be tolerable, resulting in higher risk of acute right heart failure in the early postoperative period. In this context, strain imaging may find a further application to provide a more comprehensive stratification of the severity of RV dysfunction and thus help to better define the eligibility criteria and timing for TTVR. Meanwhile, it is of paramount importance to underline the contribution given by the Trivalve study on the understanding of the role of RV function in TTVI, that so far was largely undefined, being evaluated only in small noncontrolled cohorts.