Revista española de cardiología (English ed.)最新文献

Introduction and objectives: Left ventricular reverse remodeling (LVRR) is a key therapeutic goal in dilated cardiomyopathy (DCM). However, its genetic predictors and prognostic impact remain uncertain.

Methods: We analyzed genotyped DCM patients with serial echocardiograms from the Spanish DCM study. The main objective was to assess the influence of genotype on LVRR, defined by improvement in ejection fraction within 12± 6 months. Secondary endpoints included major adverse cardiovascular events, end-stage heart failure (HF), and malignant ventricular arrhythmias.

Results: A total of 711 patients were included (67% male, mean age 50.8 years, baseline ejection fraction 31%, 44% genotype positive). LVRR occurred in 39% of genotype-positive vs 47% of genotype-negative patients (P=.036). Independent predictors of LVRR were TTN variants, lower baseline ejection fraction, and HF admission at diagnosis. In contrast, desmosomal, nuclear envelope and motor sarcomeric gene variants were associated with a lower likelihood of LVRR. During a median follow-up of 4.5 years, 26% of patients with initial LVRR showed subsequent deterioration, which was more frequent among genotype-positive individuals (32% vs 22%, P=.054). Compared with patients with sustained LVRR, those with deterioration had worse outcomes, including higher rates of major cardiovascular events (25% vs 7%), end-stage HF (18% vs 1%), and ventricular arrhythmia (12% vs 4%) (all P <.05).

Conclusions: Genotype is a major determinant of both initial and long-term LVRR. Loss of ejection fraction improvement is common and strongly associated with adverse outcomes.

Introduction and objectives: Among cancer survivors, mitral regurgitation (MR) may reflect therapy-related cardiotoxicity or incidental coexistence given the high prevalence of both conditions. We evaluated the efficacy and safety of mitral transcatheter edge-to-edge repair (M-TEER) in this setting.

Methods: We conducted a retrospective, multicenter observational study using the Spanish M-TEER registry. Patients with and without prior cancer diagnosis were matched 1:1 using propensity score matching. The primary endpoint was a composite of all-cause mortality or unplanned heart failure hospitalization at mid-term follow-up. Secondary endpoints were residual MR grade and New York Heart Association functional class at 1 year.

Results: Of 1237 patients (73 ± 11 years, 34% female), 164 (13.3%) had a prior cancer diagnosis. Propensity score matching yielded 163 pairs. The most common malignancies were breast (20.9%), leukemia/lymphoma (19.6%), prostate (12.9%), and colorectal (12.3%). The median [interquartile range] time from cancer diagnosis to M-TEER was 7 [3-17] years. MR was attributable to cardiotoxicity in 38.7%. MR type was associated with cancer location, anthracycline exposure, and left-sided chest radiotherapy (P < .001). After a median follow-up of 24 [11-43] months, the primary endpoint occurred in 80 (49.1%) cancer survivors and 69 (42.3%) controls (HR, 1.23; 95%CI, 0.89-1.70; P = .202). At 1-year, residual MR grade and New York Heart Association class were similar between groups. Among cancer survivors, independent predictors of worse outcomes included hematologic malignancy, mediastinal radiotherapy, diabetes mellitus, anemia, and EuroSCORE II.

Conclusions: A prior cancer diagnosis did not impact mid-term mortality, heart failure hospitalizations, or 1-year functional and echocardiographic outcomes after M-TEER.