Dilatatív cardiomyopathia talaján kialakult, súlyosan csökkent balkamra- (BK-) funkcióval (EF: 30%) járó szívelégtelenség miatt kardiáliskontraktilitás-modulátor (CCM) pacemakert implantáltunk egy 65 éves férfinak, keskeny QRS-komplex és optimális gyógyszeres kezelés ellenére perzisztáló NYHA III panaszok mellett. Betegünk esetében a szívkontraktilitás-moduláció reverz remodellinget eredményezett, amit a BK-funkció növekedése (EF: 46%), a BK végszisztolés térfogatának (ESV) >15%-os csökkenése, valamint a funkcionális kapacitás javulása (NYHA I) reprezentált. CCMpacemaker beültetése szóba jöhet optimális gyógyszeres terápia mellett 25-45% közötti EF-jú, NYHA II-III funkcionális stádiumú, iszkémiás, vagy noniszkémiás etiológiájú szívelégtelen betegek számára, ahol a CRT kritériumai nem teljesülnek, vagy CRT nonrespondernek bizonyultak.

Conduction system pacing (CSP) is increasingly accepted as an alternative to biventricular pacing in heart failure (HF) patients with left bundle branch block (LBBB) and non-LBBB. However, its efficiency in right bundle branch block (RBBB) is ill-defined. Herein, we report on the clinical outcomes of CSP in HFrEF patients with wide QRS complex and RBBB morphology. His-bundle (HBP) or LBB-area pacing (LBBAP) was attempted as a primary strategy in patients with RBBB, QRS duration ≥130 ms and left ventricular ejection fraction (LV EF) <35% and NYHA class II to IV HF despite optimized medical treatment for at least 6 months. Data on functional status, NT-pro-BNP levels and echocardiographic parameters were collected during follow-up and expressed as mean ± SEM, Statistical significance was calculated with Student’s paired t-test and chi square distribution. CSP was performed in 12 RBBB-HF patients (age 64.3±2.9 years) with mean QRS duration of 150±4 msec and baseline LV EF of 25.4±2.3%. The aetiology of HF was ischaemic (6 patients) and non-ischaemic cardiomyopathy (6 patients). During the procedure, HBP was achieved in 7 and LBBAP in 5 patients, resulting in a significant reduction in the QRS-duration (115±2.6 msec, P130msec and RBBB morphology.

Uremic cardiomyopathy, characterized by diastolic dysfunction, left ventricular hypertrophy (LVH), and fibrosis, is a common cardiovascular complication of chronic kidney disease (CKD). Men are at a higher risk for cardiovascular and renal diseases, compared to age-matched, pre-menopausal women. We aimed to investigate the influence of sex on the severity of uremic cardiomyopathy through the characterization of functional and molecular indices of myocardial remodeling in a rat model. CKD was induced by a 5/6 nephrectomy in 9-week-old male and female Wistar rats. Serum and urine tests, transthoracic echocardiography, left ventricular (LV) histology, and quantitative reverse transcription polymerase chain reaction (RT-qPCR) were performed at week 8 or 9. Moreover, LV alterations were also tested in permeabilized cardiomyocytes (CMs) by force measurements and Western immunoblotting. CKD resulted in the development of a more severe uremic cardiomyopathy in male rats—including LVH, LV diastolic dysfunction, and fibrosis—than in female rats, where only LVH was observed. A uremic cardiomyopathy was also associated with a decrease in maximal Ca²⁺-activated force (F_max) in CMs of male rats. Additionally, increases in CM Ca²⁺-independent passive stiffness (F_passive) and decreases in cardiac myosin-binding protein C (cMyBP-C) phosphorylation levels were significantly larger in male than female rats. In conclusion, a uremic cardiomyopathy involved cardiac remodeling in both sexes. Nevertheless, male rats exhibited more pronounced signs of macroscopic and microscopic alterations than their female counterparts, illustrating a sex-dependent component of uremic cardiomyopathy.