Pislaru, Sorin V.

Abstract Aims Prevalent right ventricular (RV) dysfunction (RVD) is associated with increased mortality in patients with heart failure with preserved ejection fraction (HFpEF), but no study has characterized long-term changes in RV structure and function within the same patient. Methods and results Patients with unequivocal HFpEF defined by either invasive haemodynamics or hospitalization for pulmonary oedema (n = 271) underwent serial echocardiographic evaluations >6 months apart. Clinical, structural, functional, and haemodynamic characteristics were examined. Over a median of 4.0 years (interquartile range 2.1–6.1), there was a 10% decline in RV fractional area change and 21% increase in RV diastolic area (both P < 0.0001). These changes greatly exceeded corresponding changes in the left ventricle. The prevalence of tricuspid regurgitation increased by 45%. Of 238 patients with normal RV function at Exam 1, 55 (23%) developed RVD during follow-up. Development of RVD was associated with both prevalent and incident atrial fibrillation (AF), higher body weight, coronary disease, higher pulmonary artery and left ventricular filling pressures, and RV dilation. Patients with HFpEF developing incident RVD had nearly two-fold increased risk of death (adjusted hazard ratio 1.89, 95% confidence interval 1.01–3.44; P = 0.04). Conclusion While previous attention has centred on the left ventricle in HFpEF, these data show that right ventricular structure and function deteriorate to greater extent over time when compared with changes in the left ventricle. Further study is required to evaluate whether interventions targeting modifiable risk factors identified for incident RVD, including abnormal haemodynamics, AF, coronary disease, and obesity, can prevent RVD and thus improve outcomes.

Grading severity of AS in AF is complicated by varying stroke volumes associated with fluctuating maximum velocities and pressure gradients across the aortic valve. Current guidelines recommend averaging five continuous‐wave peak velocity and mean gradient (MG) Doppler signals across the aortic valve when estimating severity of AS in AF. However, it is unknown when grading severity of AS how the average of multiple Doppler signals vs the highest Doppler signal in AF compares to the Doppler signals when the patient is in normal sinus rhythm. We present a series of patients with AS who had two echocardiograms performed within 2‐4 months of each other, one when in normal sinus rhythm and one when in AF, and compare the aortic valve hemodynamics associated with the two rhythms.

Background Mitral regurgitation is a heterogeneous disease. Determining which patients derive optimal outcomes from transcatheter edge‐to‐edge mitral valve repair (TMVR) remains challenging. We sought to determine whether baseline mitral valve anatomic characteristics are predictive of left atrial pressure (LAP) changes during TMVR with MitraClip. Methods and Results Consecutive patients with severe mitral regurgitation undergoing TMVR (n=112) underwent continuous intraprocedural LAP monitoring and retrospective echocardiographic analysis for specific mitral anatomic characteristics. Procedural success (optimal LAP reduction) was defined as ≥40% reduction in left atrial V‐wave pressure compared with baseline. Echocardiographic predictors of optimal LAP reduction and increased postprocedure mean diastolic gradient were evaluated. Mean age was 79±14 years, and 36 patients (32%) were women. Primary, mixed, and secondary mitral regurgitation were present in 78 patients (70%), 22 patients (20%), and 12 patients (10%), respectively. Baseline mean LAP and V‐wave were 22±6 and 38±13 mm Hg; after TMVR, these decreased to 19±5 and 27±10 mm Hg, respectively ( P <0.0001 for both). Independent predictors of optimal LAP reduction were the presence of a flail scallop, mitral regurgitation localized to a single scallop, and high‐quality 3‐dimensional echocardiographic imaging. Independent predictors of elevated postprocedure mean diastolic gradient were elevated preprocedure mean diastolic gradient, mitral annular calcification, and implantation of multiple clips. Conclusions Mitral valve pathoanatomic features, including a flail leaflet and single jet, are predictive of optimal LAP reduction with TMVR. High‐quality 3‐dimensional imaging may help select patients with the highest likelihood of optimal hemodynamic results with TMVR. These data expand current knowledge about patient selection for TMVR and deserve further study in larger cohorts.

AbstractIntroductionTricuspid valve regurgitation (TR) is a frequent finding in patients with pulmonary arterial hypertension (PAH). However, its prognostic significance and relation to PAH, while suspected, are poorly understood. We assessed 727 consecutive patients with newly diagnosed PAH who underwent transthoracic echocardiographic evaluation of tricuspid valve function.ObjectivesThe study objective was to determine the association of TR presence and severity with patient characteristics, pulmonary artery hemodynamics and outcome.MethodsConsecutive patients with newly diagnosed PAH (N = 727 with group 1 pulmonary hypertension) underwent transthoracic echocardiographic evaluation of tricuspid valve function at diagnosis. The primary study end point was all‐cause mortality or lung transplantation.ResultsIn this population, 702 patients (96.5%) had TR; in 165 patients (23%), TR was severe. Compared with those with no or mild TR by echocardiography criteria, patients with severe TR had shorter mean (SD) 6‐minute walk distances (285 [125] m vs 360 [121] m; P = .02) and higher levels of B‐type natriuretic peptide (695 [672] pg/dL vs 328 [300] pg/dL; P < .05). Severe TR was associated with greater right atrial dilatation (91% vs 47%; P = .004) and right ventricular (RV) dilatation (92% vs 51%; P = .008), greater right atrial pressure (mean [SD] 15 [7] mm Hg vs 10 [6] mm Hg; P < .001) and lower cardiac index (mean [SD], 2.2 [0.7] L/min/m2 vs 2.8 [0.9] L/min/m2; P < .001). Severe TR was strongly predictive of greater 5‐year mortality risk after adjustment for age, sex, functional class, 6‐minute walk distance, diffusing capacity, RV size and pulmonary vascular resistance index (adjusted hazard ratio, 1.83; 95% CI, 1.38‐2.41; P < .001).ConclusionsSevere TR was a significant predictor of long‐term mortality rate in PAH, and TR severity correlated with PAH severity.

AbstractObjectivesTo investigate the feasibility, procedural success, and outcomes of paravalvular leak (PVL) closure in patients with prior transcatheter aortic valve replacement (TAVR).BackgroundPVL after TAVR is associated with adverse patient outcomes and increased mortality. Percutaneous PVL closure has emerged as a therapeutic strategy for addressing this issue, but data for transcatheter PVL repair after TAVR remains limited.MethodsThis is a single center retrospective review of PVL closure after TAVR. Patients with balloon‐expandable or self‐expanding prostheses were included. Baseline patient demographics, procedural characteristics, complications, and clinical outcomes were reviewed.ResultsA total of 18 patients with clinically significant PVL after TAVR referred for PVL closure were identified during the study period. Procedural success resulting in successful transcatheter occluder plug delivery was 78% (14 cases). Balloon postdilatation (2/4) and valve‐in‐valve (2/4) were used effectively in the remaining patients after an unsuccessful PVL closure attempt. PVL grading by echocardiography decreased from moderate or severe to < moderate in 13 patients (72%). Adverse events including cardiac tamponade and acute kidney injury occurred in 1 case each. One‐month all‐cause mortality was 11%.ConclusionIn selected patients, percutaneous PVL repair following TAVR is feasible and effective for both balloon‐expandable and self‐expanding prostheses. Most patients undergoing PVL closure after TAVR require a single occluder plug placement for reduction in PVL to mild or less.

Background: Heart failure (HF) with preserved ejection fraction (HFpEF) is a heterogeneous syndrome. Phenotyping patients into pathophysiologically homogeneous groups may enable better targeting of treatment. Obesity is common in HFpEF and has many cardiovascular effects, suggesting that it may be a viable candidate for phenotyping. We compared cardiovascular structure, function, and reserve capacity in subjects with obese HFpEF, those with nonobese HFpEF, and control subjects. Methods: Subjects with obese HFpEF (body mass index ≥35 kg/m 2 ; n=99), nonobese HFpEF (body mass index <30 kg/m 2 ; n=96), and nonobese control subjects free of HF (n=71) underwent detailed clinical assessment, echocardiography, and invasive hemodynamic exercise testing. Results: Compared with both subjects with nonobese HFpEF and control subjects, subjects with obese HFpEF displayed increased plasma volume (3907 mL [3563–4333 mL] versus 2772 mL [2555–3133 mL], and 2680 mL [2380–3006 mL]; P <0.0001), more concentric left ventricular remodeling, greater right ventricular dilatation (base, 34±7 versus 31±6 and 30±6 mm, P =0.0005; length, 66±7 versus 61±7 and 61±7 mm, P <0.0001), more right ventricular dysfunction, increased epicardial fat thickness (10±2 versus 7±2 and 6±2 mm; P <0.0001), and greater total epicardial heart volume (945 mL [831–1105 mL] versus 797 mL [643–979 mL] and 632 mL [517–768 mL]; P <0.0001), despite lower N-terminal pro-B-type natriuretic peptide levels. Pulmonary capillary wedge pressure was correlated with body mass and plasma volume in obese HFpEF ( r =0.22 and 0.27, both P <0.05) but not in nonobese HFpEF ( P ≥0.3). The increase in heart volumes in obese HFpEF was associated with greater pericardial restraint and heightened ventricular interdependence, reflected by increased ratio of right- to left-sided heart filling pressures (0.64±0.17 versus 0.56±0.19 and 0.53±0.20; P =0.0004), higher pulmonary venous pressure relative to left ventricular transmural pressure, and greater left ventricular eccentricity index (1.10±0.19 versus 0.99±0.06 and 0.97±0.12; P <0.0001). Interdependence was enhanced as pulmonary artery pressure load increased ( P for interaction <0.05). Compared with those with nonobese HFpEF and control subjects, obese patients with HFpEF displayed worse exercise capacity (peak oxygen consumption, 7.7±2.3 versus 10.0±3.4 and12.9±4.0 mL/min·kg; P <0.0001), higher biventricular filling pressures with exercise, and depressed pulmonary artery vasodilator reserve. Conclusions: Obesity-related HFpEF is a genuine form of cardiac failure and a clinically relevant phenotype that may require specific treatments.