RESUMO
Background: The use of beta-blockers in hypertrophic obstructive cardiomyopathy (HOCM) patients after alcohol septal ablation (ASA) lacks data support. We aimed to evaluate the effect of metoprolol on exercise capacity, hemodynamic and laboratory parameters, and quality of life in HOCM patients after ASA. Methods: This was a prospective randomized single-center open-label crossover trial in 21 HOCM patients after ASA. Patients received metoprolol and no beta-blocker for two periods of three months. The endpoints were: peak oxygen uptake (pVO2), maximal left ventricular outflow tract (LVOT) pressure gradient at peak exercise, a ratio of mitral peak velocity of the early filling (E) to early diastolic mitral annular velocity (e') (E/e') at rest, Kansas City Cardiomyopathy Questionnaire (KCCQ) overall summary score, and N-terminal prohormone of brain natriuretic peptide (NT-proBNP) plasmatic concentration. Results: No significant association was found between the treatment and any of the endpoints in the assessed patients: 1) pVO2 (19.5 ± 5.3 ml/kg/min vs. 19.4 ± 4.1 ml/kg/min, p = 0.90), 2) exercise-induced pressure gradient in LVOT 32 ± 37 mmHg vs. 32 ± 30 mmHg, p = 0.84, 3) E/e' ratio at rest (11 ± 4 vs. 10 ± 4, p = 0.23), 4) KCCQ overall summary score (78 ± 11 vs. 77 te ± 15, p = 0.56), 5) NT-proBNP (215 pg/ml [121-333] vs. 153 pg/ml [102-228], p = 0.19). Conclusions: In HOCM patients after successful ASA, metoprolol treatment did not improve exercise capacity, hemodynamic and laboratory parameters, or quality of life.
RESUMO
BACKGROUND: The genetic background of patients with hypertrophic cardiomyopathy (HCM) treated with alcohol septal ablation (ASA) and its relationship to the outcomes are not known. We aimed to investigate whether the outcome of genotype positive (G+) patients differs from genotype negative (G-) patients treated with ASA. METHODS: We included 129 HCM patients (mean age 54±13 years) treated with ASA in a tertiary cardiovascular center and performed next generation sequencing (NGS) based genomic testing. All patients were followed-up three months after the procedure and yearly thereafter. RESULTS: A total of 30 (23%) HCM patients were G+ patients. At the 3-months follow-up, both groups of patients had similar left ventricular outflow tract PG (16.9±15.7 mmHg in G+ vs. 16.3±18.8 mmHg in G-, P=0.73) and symptoms (follow-up NYHA class 1.40±0.62 vs. 1.37±0.53, P=0.99, follow-up CCS class 0.23±0.52 vs. 0.36±0.65, P=0.36). The independent predictors of all-cause mortality were baseline interventricular septum (IVS) thickness (HR 1.12, 95% CI: 1.00-1.26, P=0.049) and age at the time of ASA (HR 1.11, 95% CI: 1.06-1.17, P<0.01). The adjusted all-cause mortality rate did not differ significantly between G+ and G- patients (P=0.52). The adjusted combined mortality event rate did not differ between both groups (P=0.78). CONCLUSIONS: Despite more severe phenotype in G+ HCM patients, ASA is an equally effective treatment for LVOTO in G+ patients as it is for treating LVOTO in G- patients. The long-term outcome after ASA is similar in G+ and G- patients.
