BACKGROUND:In hypoplastic left heart syndrome with aortic atresia, the non-functional left ventricle may influence right ventricular performance. We evaluated serial changes in tricuspid and mitral valve diameters after the Norwood procedure and their relationship to right ventricular function. METHODS:Of 150 patients who underwent the Norwood procedure (2001-2020), 47 died before total cavopulmonary connection. Of the 103 survivors, 76 with sufficient serial echocardiographic data were analysed (1,399 examinations). Tricuspid and mitral valve diameters were measured, and right ventricular function was assessed. Right ventricular dysfunction was defined as any degree of impairment. Mixed-effects models were used to account for repeated measures. RESULTS:Median follow-up was 4.6 years (IQR 2.4-11.8). Right ventricular dysfunction was observed in 15.9% of examinations. Patients with right ventricular dysfunction had significantly larger tricuspid valve diameters than those with normal function (24.3 mm vs 23.4 mm, p = 0.006), whereas mitral valve diameters showed no significant difference (7.6 mm vs 7.1 mm, p = 0.120). The mitral/tricuspid ratio was similar between groups (0.320 versus 0.324, p = 0.340). Mixed-effects modelling showed that the tricuspid valve diameter remained 0.618 mm larger in the dysfunction group after adjusting for growth over time (p = 0.029). Tricuspid valve diameter differences emerged at the bidirectional cavopulmonary shunt stage and accelerated through Fontan completion (p < 0.001). CONCLUSIONS:In hypoplastic left heart syndrome with aortic atresia, right ventricular dysfunction is associated with progressive tricuspid valve enlargement but not with changes in the mitral/tricuspid ratio. While the stable ratio suggests proportional annular growth, a comprehensive volumetric assessment is needed to clarify ventricular-ventricular interactions.
BACKGROUND:The best management of coronary artery disease in patients with severe aortic stenosis undergoing transcatheter aortic valve implantation (TAVI) is debated. We investigated the clinical impact of the residual extent of myocardium at risk in patients undergoing TAVI. METHODS:Patients enrolled in the REVASC-TAVI (Management of Myocardial Revascularization in Patients Undergoing TAVI With Coronary Artery Disease) international multicenter registry were stratified according to the myocardium jeopardized by coronary artery disease using the British Cardiovascular Intervention Society Jeopardy Score (BCIS-JS) after a planned coronary revascularization. A planned revascularization included percutaneous coronary interventions performed before TAVI, during TAVI, or within 1 month after TAVI. The study population was divided according to the residual BCIS-JS (rBCIS-JS): patients with extensive residual myocardial at risk (rBCIS-JS >4 group) and patients without extensive residual myocardial at risk (rBCIS-JS ≤4 group). The primary study end point was the composite of all-cause death, nonfatal myocardial infarction, nonfatal stroke, and rehospitalization for heart failure at 2 years. RESULTS:Among the 2407 patients enrolled, 294 pairs of patients were selected by propensity matching and compared. At 2-year follow-up, the incidence of the primary end point was higher in patients with rBCIS-JS >4 compared with patients with rBCIS-JS ≤4 (37.5% versus 23.0%, P=0.004). A significantly lower rate of myocardial infarction was reported in patients with BCIS-JS ≤4 (8.2% versus 2.6%, P=0.011). At multivariate analysis, rBCIS-JS >4 (hazard ratio, 1.43 [95% CI, 1.11-1.84]; P=0.005) independently predicted 2-year major adverse cardiac and cerebrovascular events. CONCLUSIONS:In patients with concomitant coronary artery disease and severe aortic stenosis, the residual myocardial risk significantly affects TAVI outcomes. In particular, a rBCIS-JS >4 is associated with higher rates of major adverse cardiac and cerebrovascular events at 2 years.
Patients on direct-acting oral anticoagulants (DOACs) are at high risk of perioperative bleeding complications. Intraoperative hemoadsorption is a novel strategy to reduce perioperative bleeding in patients on DOACs undergoing non-deferable cardiac surgery. The international STAR-registry reports real-world clinical outcomes associated with this application. The hemoadsorption device was incorporated into the cardiopulmonary bypass (CPB) circuit and active for the duration of the pump run. Patients on DOACs undergoing CABG and/or single valve surgery before completing the recommended washout were included. Outcome measurements included bleeding events according to standardized definitions and 24-hour chest-tube-drainage (CTD). A total of 62 patients were included from 7 institutions in Austria, Germany, Sweden, and the UK (mean age 69.9 ± 7.5years, 71
AIMS:Age-associated clonal haematopoiesis of indeterminate potential (CHIP) has been linked to increased incidence and worse prognosis of chronic heart failure (CHF). CHIP arises from somatic mutations in haematopoietic stem and progenitor cells. Mosaic loss of Y chromosome (LOY), the most common somatic mutation in male blood cells, increases with age, drives clonal expansion of myeloid cells, and has been experimentally associated with cardiac fibrosis and heart failure in mice. However, its prognostic value and interplay with CHIP in CHF patients remain unclear. METHODS AND RESULTS:We analysed 781 male CHF patients across the full spectrum of left ventricular ejection fraction to assess the prevalence and prognostic relevance of LOY and the two most common CHIP-driver mutations, DNMT3A and TET2. Both LOY and CHIP mutations increased with age and co-occurred in 27.1% of men >70 years. LOY independently predicted all-cause mortality in patients with heart failure with reduced ejection fraction (HFrEF). The co-occurrence of LOY and DNMT3A/TET2 mutations further increased mortality among CHIP carriers. This detrimental prognostic effect of LOY was confirmed in a validation cohort of HFrEF patients. Single-cell RNA sequencing of peripheral blood mononuclear cells from HFrEF patients with ischaemic heart failure revealed elevated pro-fibrotic signalling in LOY monocytes, characterized by increased inflammatory and remodelling markers (S100A8, TLR2, CLEC4D) and decreased expression of transforming growth factor-β inhibitors (SMAD7, TGIF2). In patients with both LOY and DNMT3A mutations, monocytes showed enhanced pro-inflammatory gene expression, including alarmins (S100A8, HMGB2) and interferon-related genes (IFNGR1, TRIM56, CD84). CONCLUSIONS:Somatic mutations in blood cells-particularly LOY-are associated with increased mortality in male CHF patients, with LOY emerging as an independent prognostic marker.
