Transthyretin amyloid cardiomyopathy in patients with unexplained increased left ventricular wall thickness.

Amyloid cardiomyopathy (CA) was previously considered a rare disease; however, rapid advancements in imaging modalities have led to an increased frequency of its diagnosis. The aim of this prospective study was to assess the prevalence and clinical phenotype of transthyretin amyloidosis (ATTR) cardiomyopathy in patients exhibiting unexplained increased left ventricular (LV) wall thickness. From 2020 to 2022, we enrolled 100 consecutive adults with unexplained increased LV wall thickness in the study. The analysis included clinical data, electrocardiography, transthoracic echocardiography, single-photon emission computed tomography/computed tomography with 3,3-disphono-1,2-propanodicarboxylic acid, genetic testing. Overall, 18% of patients were diagnosed with CA, comprising 5% with light-chain amyloidosis, and 12% with ATTR. To evaluate associations with the ATTR diagnosis, a LOGIT model and multivariate analysis were applied. Notably, age, polyneuropathy, gastropathy, carpal tunnel syndrome, lumbar spine stenosis, low voltage, ventricular arrhythmia, LV mass, LV ejection fraction, global longitudinal strain (GLS), E/A, E/E', right ventricle (RV) thickness, right atrium area, RV VTI, TAPSE, apical sparing, ground glass appearance of myocardium, thickening of interatrial septum, thickening of valves, and the "5-5-5" sign were found to be significantly associated with ATTR (p < 0.05). The best predictive model for ATTR diagnoses exhibited an area under the curve of 0.99, including LV mass, GLS and RV thickness. This study, conducted at a cardiology referral center, revealed that a very considerable proportion of patients with unexplained increased LV wall thickness may suffer from underlying CA. Moreover, the presence of ATTR should be considered in patients with increased LV mass accompanied by reduced GLS and RV thickening.

Elevated carbonylated proteins are associated with major cardiovascular events in patients with chronic coronary syndrome: A cohort study.

BACKGROUND: Protein carbonylation is reported in atherosclerosis, but its predictive value is unknown. AIMS: We evaluated plasma carbonylated protein (PC) levels in association with clinical outcomes in coronary artery disease (CAD) in long-term follow-up. METHODS: In patients with advanced stable CAD, we assessed plasma PC content along with fibrin clot properties, i.e., permeability (Ks) and clot lysis time, and its determinants: plasminogen activator inhibitor-1 (PAI-1) and thrombin-activatable fibrinolysis inhibitor. We recorded a composite of myocardial infarction, ischemic stroke, systemic embolism, and cardiovascular death during a follow-up of 8.3 (1.8) years. RESULTS: The analysis involved 178 patients aged 64.0 (57.0-70.0) years. The baseline PC content was 2.9 (2.2-3.7) nmol/mg protein and was elevated above the reference value obtained for a control group (2.03 nmol/mg protein) in 82.6% of patients. In linear regression models, high PC adjusted for age was associated with lower Ks, longer clot lysis time, and elevated PAI-1 and thrombin-activatable fibrinolysis inhibitor. Baseline PC was 48% higher in patients with the composite endpoint (n = 67, 37.6%) compared with others (P <0.001). Patients with PC in the highest quartile (3.7-5.1 nmol/mg protein) were more likely to develop the composite endpoint compared to the lowest quartile (hazard ratio [HR] 4.9; 95% confidence interval, 2.1-11.3; P <0.001). CONCLUSIONS: This is the first study showing that in CAD the extent of protein carbonylation, in part via its antifibrinolytic effects, predisposes to cardiovascular events in long-term follow-up, highlighting the role of persistent oxidative protein modifications in atherosclerotic vascular disease.

Balloon aortic valvuloplasty for severe aortic stenosis may reduce mitral regurgitation in mid-term follow-up.

Introduction: Mitral regurgitation (MR) is a frequent complication in patients with severe aortic stenosis (AS). Material and methods: Echocardiographic assessment of MR was performed at baseline, at 30 days and at 6 months after balloon aortic valvuloplasty (BAV). Results: Data of 271 patients were included in our final analysis, of which 21.2% (n = 85) had at least moderate MR at baseline (in 19 (22.3%) subjects MR was diagnosed as primary). Both groups showed similar severity of AS, but patients in the MR group had a greater left ventricle (LV) size (p = 0.003 for LVESD, p = 0002 for LVEDD) and slightly lower LV ejection fraction (p = 0.04). Mitral regurgitation parameters significantly improved both at 30 days and 6 months after BAV in the MR group (MR jet area: 7.2 (4.5-9.9) vs. 3.6 (2.3-7.2) cm2, and 7.2 (4.5-9.9) vs. 3.2 (2.1-6.7) cm2; %MR/left atrial area 34.5 (23.4-42.7) vs. 17.5 (9.3-29.5) and 34.5 (23.4-42.7) vs. 14.5 (8.3-24.5), p < 0.001 for all). In multivariate logistic regression analysis, the change at 30 days, from baseline, in the LVESD (OR = 1.87; 95% CI: 1.23-2.87; p < 0.001) and LVEF (OR = 0.95; 95% CI: 0.87-1.01; p < 0.001); MR jet area (OR = 2.2, 95% CI: 1.5-4.6; p < 0.001) and the presence of primary MR (OR = 3.2, 95% CI: 1.04-5.98; p < 0.001) were retained as independent predictors of significant persisting MR at 6 months. Conclusions: Balloon aortic valvuloplasty may reduce MR in mid-term follow-up. Predictors of persistent MR at 6 months after BAV included an increase of LVESD and MR jet area and decrease of LVEF at 30 days.