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Paravalvular prosthetic regurgitation is common, affecting 5-10% of surgical prostheses and 40-70% of transcatheter valves. While many patients may suffer no significant morbidity, paravalvular prosthetic regurgitation can lead to heart failure and haemolytic anaemia, and, in some studies, has been associated with impaired survival. Over the past several years, percutaneous repair of paravalvular prosthetic regurgitation has been demonstrated to be a highly efficacious therapy. When performed in experienced centres, procedural success with percutaneous repair occurs in 90% of patients. Due to the complex nature of the techniques, there is a significant learning curve with a high potential for prolonged procedures (∼2.5 h) and complications (∼5%), although death is rare (∼0.5%). Percutaneous repair of paravalvular prosthetic regurgitation requires a close collaboration between imaging specialists, surgeons and the interventional operators. Importantly, successful percutaneous repair obviates the need for open surgical correction, which can be high risk or prohibitive due to the need for reoperation in the setting of comorbidities. Herein, we discuss appropriate patient selection, the catheter-based techniques and outcomes of percutaneous repair for symptomatic paravalvular prosthetic regurgitation.

Low-gradient (LG) severe aortic stenosis (AS) and preserved EF with reduced stroke volume are associated with an adverse prognosis, but the relationship of stroke volume index (SVI) with mortality among a range of values is unknown. We investigated the prognostic impact of SVI in this population.We examined 405 consecutive patients with preserved EF (≥50%) and severe AS (valve area1.0 cm(2)) with LG (40 mm Hg) using echocardiography. Patients were stratified into quartiles based on SVI distribution (group 1:38 mL/m(2) (n=90), group 2: 38-43 mL/m(2) (n=105), group 3: 43-48 mL/m(2) (n=104) and group 4:48 mL/m(2) (n=106)).Groups 1 and 2 had poorer survival with medical management compared with 3 and 4 (3-year estimate 46% and 67% vs. 78% and 73%, respectively, p=0.002) although aortic valve replacement referral rate was similar (53%-62%, p=0.57). An inverse relationship was observed between SVI and mortality (HR 1.28 (1.11 to 1.46) per every 5 mL/m(2) decrease in SVI). After multivariable analysis, SVI was the strongest predictor of mortality (HR 0.92 (0.89 to 0.95), p0.0001). Using different SVI cutpoints, SVI35 was associated with highest mortality (HR 2.36 (1.49 to 3.73), p0.001), followed by SVI38 (HR 2.09 (1.39 to 3.16), p0.001) and by SVI43 (HR 2.05 (1.38 to 3.05), p0.001). Survival with SVI ≥43 was similar to age and sex-matched controls (3-year estimate 84%, p=0.24); survival for SVI43 was significantly worse (3-year estimate 63%, p0.001).Lower SVI is incrementally associated with mortality in LG severe AS with preserved EF. These findings have implications for classification of AS severity, identification of high-risk groups and subsequent management.

Background: Severe tricuspid regurgitation, constrictive pericarditis and restrictive cardiomyopathy can all present with signs and symptoms of right heart failure and similar haemodynamic findings of elevation and equalisation of diastolic pressures at catheterisation. Although catheterisation findings of enhancement of ventricular interaction are a reliable parameter to distinguish constrictive pericarditis from restrictive cardiomyopathy, this also may be present in severe tricuspid regurgitation. Objective: To identify unique haemodynamic parameters that differentiate severe tricuspid regurgitation from constrictive pericarditis. Methods: Haemodynamic findings from simultaneous right and left heart catheterisation of 14 patients (age 59 years; men 71%) with documented severe tricuspid regurgitation (group I) were compared with those of 14 patients with surgically proven constrictive pericarditis (group II). Results: Findings of elevated right atrial pressure, early rapid ventricular filling and expiratory equalisation of ventricular diastolic pressures were similar in both groups. Ventricular interdependence, assessed by interaction of left ventricular (LV) and right ventricular (RV) systolic pressures, was also present in both groups. Relative changes in LV and RV diastolic pressures during respiration reliably distinguished group I from group II. During inspiration, the difference between the LV and RV diastolic pressures widened in group I but narrowed in group II. The height and slope of the early rapid filling wave in RV pressure trace was accentuated during inspiration in group I but did not change in group II. Conclusions: The haemodynamic findings at cardiac catheterisation in patients with severe, symptomatic tricuspid regurgitation are similar to those of constrictive pericarditis. Careful analysis of the relationship of the LV and RV diastolic pressures during respiration can help differentiate the two entities.

To examine whether percutaneous alcohol septal ablation affects coronary flow reserve (CFR) in patients with hypertrophic cardiomyopathy (HCM).CFR was measured immediately before and after septal ablation in patients with symptomatic obstructive HCM. CFR was also obtained in normal subjects (NL) for comparison.Patients with HCM (n = 11), compared with NL (n = 22), had a lower mean (SD) baseline CFR (1.96 (0.5) vs 3.0 (0.7), p0.001), a lower coronary resistance (1.04 (0.45) vs 3.0 (2.6), p = 0.002), a higher coronary diastolic/systolic velocity ratio (DSVR; 5.1 (3.0) vs 1.8 (0.5), p = 0.04) and a lower hyperaemic coronary flow per left ventricular (LV) mass (0.73 (0.4) vs 1.1 (0.6) ml/min/g, p = 0.007). Septal ablation in the HCM group (n = 7) reduced the outflow tract gradient but not the left atrial or LV diastolic pressures. Ablation resulted in immediate normalisation of CFR (to 3.1 (1), p = 0.01) and DSVR (to 1.9 (0.8), p = 0.09) and an increase in coronary resistance (to 1.91 (0.6), p = 0.02). This was probably related to an improvement in the systolic coronary flow.This study demonstrates that successful septal ablation in patients with symptomatic HCM results in immediate improvement in CFR, which is reduced in HCM partly because of the increased systolic contraction load.