August 2021 at a glance: focus on cardiomyopathies, medical treatment and devices

Cardiomyopathies are an important and heterogeneous cause of heart failure (HF).1, 2 In a retrospective study, 52% of patients with dystrophin gene (DMD) mutation and without severe skeletal myopathy presented dilated cardiomyopathy at first evaluation, or developed it during a median follow-up of 8 years. Major adverse cardiac events, including end-stage HF and sudden cardiac death (SCD), occurred in 22% of patients with dilated cardiomyopathy. Left ventricular dimensions and function were associated with poor outcomes.3 Cardiac amyloidosis is another important cause of HF.1, 4 Left atrial (LA) structure and function were evaluated in 1225 African-Americans in sinus rhythm genotyped for the transthyretin (TTR) valine-to-isoleucine substitution (V122I). V122I TTR variant carriers had greater LA enlargement and worse LA contractile longitudinal strain, compared to non-carriers. After adjusting for possible confounders, the risk of LA abnormalities was twofold higher in V122I TTR carriers.5 Sudden cardiac death is a feared complication in patients with cardiovascular (CV) disease.6, 7 Independent predictors of SCD were investigated in 8399 patients with HF and reduced ejection fraction (HFrEF) enrolled in PARADIGM-HF. Beyond single time-point measures, dynamic changes in clinical and laboratory variables were important determinants of SCD risk. The subgroups with the highest risk were characterized by either baseline N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels <3516 pg/mL, increasing levels of total bilirubin and worsening New York Heart Association functional class during follow-up or by baseline NT-proBNP levels ≥3516 pg/mL, no implantable cardioverter-defibrillator and low total cholesterol.8 The efficacy of sodium-glucose co-transporter 2 (SGLT2) inhibitors has been widely established in patients with HFrEF.9-12 It remains uncertain whether even patients with HF and preserved ejection fraction (HFpEF) may have potential benefits. Anker et al.13 described the pathophysiological mechanisms underneath HFpEF, the pharmacodynamic profile of SGLT2 inhibitors, and the potential benefits of SGLT2 inhibitors in HFpEF based on early clinical data. A novel position paper from the European Society of Cardiology, focusing on cardiac, renal and metabolic effects of this class of agents, is published in this issue.14 Baseline characteristics of patients enrolled in the VICTORIA (VerICiguaT Global Study in Subjects With Heart Failure With Reduced Ejection Fraction) trial were previously published.15 Ponikowski et al.16 evaluated the relationship between atrial fibrillation (AF), outcome and treatment effect in this population. History of AF was associated with increased risk of CV death. Beneficial effects of vericiguat were independent of AF status at baseline. New-onset AF after randomization was not influenced by the treatment with vericiguat and was associated with increased rates of HF hospitalization and CV death. Kidney function is another major determinant of outcome in HF.17, 18 Another study showed that there was no significant difference in renal function trajectories between vericiguat- and placebo-treated patients, during 48 weeks of treatment. Vericiguat had beneficial effects, irrespective of renal function at baseline and incident worsening renal function.19 Valvular heart disease (VHD) is a major determinant of outcome in patients with HF.20-24 Medical treatment may have a meaningful impact on VHD and this has been thoroughly reviewed by Gill et al.25 Elderly age is considered one of the main factors contributing to suboptimal treatment in HFrEF patients.26 However, undertreatment may occur also at younger ages. Butler et al.27 evaluated treatment patterns and clinical outcomes during 1-year periods before and after a worsening HF event, in 4460 commercially insured patients, aged <65 years. Interestingly, the use of HF medications increased before and decreased after the worsening HF event. HF-related and all-cause hospitalizations and outpatient visits reached the highest rate in the 0–3 months after the worsening HF event. The best candidates for percutaneous edge-to-edge mitral valve repair by MitraClip still need to be better defined.28-30 Data from the Italian Society of Interventional Cardiology (GIse) registry Of Transcatheter treatment of mitral valve regurgitaTiOn (GIOTTO) registry are presented in this issue. Among 1659 patients undergoing MitraClip, 59.4% had functional mitral regurgitation (MR) and 40.6% degenerative MR. Procedural success was similar between the two aetiologies, but functional MR was associated with worse mid-term outcome compared with degenerative aetiology. Residual MR 1+ after MitraClip was associated with reduced risk of 1-year mortality, compared with residual MR 2+ and 3/4+, especially in patients with functional MR.31 In a retrospective analysis of MitraClip performed in Germany from 2011 to 2017, an increase in annual numbers of procedures was observed over time. In-hospital mortality did not differ according to centre procedural volume, although patients treated in high-volume centres had a higher risk profile.32 A relatively wide proportion of patients with advanced HF may benefit from left ventricular assist device (LVAD) implantation, namely the HeartMate 3 (HM3), a fully magnetically levitated centrifugal-flow pump.33, 34 Patients receiving HM3 in the single-arm prospective continuous access protocol (CAP) phase, following the MOMENTUM 3 enrolment, had similar survival and primary outcome than those implanted in the pivotal cohort. On the other hand, accumulating post-pivotal trial experience showed a lower burden of complications and hospitalizations in CAP patients.35 In a retrospective study including 254 LVAD patients, bloodstream infection prior to implantation was an independent predictor of 1-year post-procedural mortality and infections. Other possible risk factors were other infections (non-bloodstream), INTERMACS profile ≤2, higher serum creatinine, lower serum albumin, nasal Staphylococcus aureus colonization and specific gut microbial composition.36