Vascular complications with a plug-based vascular closure device after transcatheter aortic valve replacement: Predictors and bail-outs

Background: The MANTA vascular closure device (VCD) is dedicated to large bore access closure and associated with favorable results in selected study populations. Anatomical predictors for access site complications are lacking. Aim: To evaluate MANTA in a real-world population and identify predictors for vascular complications. Methods: All patients undergoing transfemoral transcatheter aortic valve replacement (TAVR) between January 2016 and May 2020 with MANTA closure were included. Baseline characteristics were collected, pre-procedural computed tomography and post-deployment femoral angiograms were analyzed for anatomical differences. The primary endpoint was a composite of access site related major and minor vascular complications at 30 days follow-up according to the VARC-2 definitions. Secondary endpoints included bleeding, time to hemostasis, procedural length and incomplete arteriotomy closure or arterial occlusion by angiography. A Cox proportional hazards model was used to compare all-cause mortality for patients with and without an access site complication. Results: The 512 patients underwent TAVR with MANTA access closure. Median age was 80 (IQR 75–85), 53% was male, median BMI was 26.4 kg/m2 (IQR 23.4–29.7). Access site related major- or minor vascular complication occurred in 20 (4%) and 23 (4%) of patients respectively. Median time to hemostasis was 42 s (IQR 28–98). Post deployment angiogram showed an occlusion in 24 patients (5%), incomplete closure in 60 patients (12%) or both in three patients (1%). Of these 87 patients, 36 (41%) had a vascular complication. Femoral artery diameter (OR 0.70 [0.53–0.93]), low- (OR 3.47 [1.21–10.00]) and high (OR 2.43 [1.16–5.10]) arteriotomies were independent predictors for vascular complications. Conclusion: In this contemporary TAVR population, access-site related complications occurred in 8% of patients and were mainly due to percutaneous closure device failure. Small artery diameter and off-target punctures were independent predictors

Sildenafil treatment in established right ventricular dysfunction improves diastolic function and attenuates interstitial fibrosis independent from afterload

Right ventricular (RV) function is an important determinant of prognosis in congenital heart diseases, pulmonary hypertension, and heart failure. Preventive sildenafil treatment has been shown to enhance systolic RV function and improve exercise capacity in a model of fixed RV pressure load. However, it is unknown whether sildenafil has beneficial effects when treatment is started in established RV dysfunction, which is clinically more relevant. Our aim was to assess the effects of sildenafil treatment on RV function and fibrosis in a model of established RV dysfunction due to fixed afterload. Rats were subjected to pulmonary artery banding (PAB), which induced RV dysfunction after 4 wk, characterized by reduced exercise capacity, decreased tricuspid annular plane systolic excursion, and RV dilatation. From week 4 onward, 50% of rats were treated with sildenafil (100 mg.kg(-1).day(-1), n = 9; PAB-SIL group) or vehicle (n = 9; PAB-VEH group). At 8 wk, exercise capacity was assessed using cage wheels, and RV function was assessed using invasive RV pressure-volume measurements under anesthesia. Sildenafil treatment, compared with vehicle, improved RV ejection fraction (44 +/- 2% vs. 34 +/- 2%, P <0.05, PAB-SIL vs. PAB-VEH groups), reduced RV end-diastolic pressure (2.3 +/- 0.5 vs. 5.1 +/- 0.9 mmHg, P <0.05), and RV dilatation (end-systolic volume: 468 +/- 45 vs. 643 +/- 71 mu l, P = 0.05). Sildenafil treatment also attenuated RV fibrosis (30 +/- 6 vs. 17 +/- 3%, P <0.05) but did not affect end-systolic elastance, exercise capacity, or PKG or PKA activity. In conclusion, sildenafil improves RV diastolic function and attenuates interstitial fibrosis in rats with established RV dysfunction, independent from afterload. These results indicate that sildenafil treatment has therapeutic potential for established RV dysfunction

Clinical symptoms of right ventricular failure in experimental chronic pressure load are associated with progressive diastolic dysfunction

Background: Right ventricular failure (RVF) due to pressure load is a major cause of death in congenital heart diseases and pulmonary hypertension. The mechanisms of RVF are unknown. We used an experimental approach based upon clinical signs of RVF to delineate functional and biological processes associated with RVF. Methods and results: Wistar rats were subjected to a pulmonary artery banding (PAB n = 12) or sham surgery (CON, n = 7). After 52 5 days, 5/12 PAB rats developed clinical symptoms of RVF (inactivity, ruffled fur, dyspnea, ascites) necessitating termination (PAR + CF). We compared these to PAR rats with RVF without clinical symptoms (PAB). PAB resulted in reduced cardiac output, RV stroke volume, TAPSE, and increased end diastolic pressure (all p <0.05 vs. CON) in all rats, but PAB + CF rats were significantly more affected than PAR, despite similar pressure load (p = ns). Pressure-volume analysis showed enhanced contractility (end systolic elastance) in PAB and PAR + CF, but diastolic function (end diastolic elastance, end diastolic pressure) deteriorated especially in PAB + CF. In PAB + CF capillary density was lower than in PAR. Gene-array analysis revealed down-regulation of both fatty acid oxidation and carbohydrate metabolism in PAB + CF. Conclusion: Chronic PAR led to different degrees of RVF, with half of the rats developing severe clinical symptoms of RVF, associated with progressive deterioration of diastolic function, hypoxia-prone myocardium, increased response to oxidative stress and suppressed myocardial metabolism. This model represents clinical RVF and allows for unraveling of mechanisms involved in the progression from RV adaptation to RV failure and the effect of intervention on these mechanisms. (C) 2014 Elsevier Ltd. All rights reserved