Background: Prosthesis-patient mismatch (PPM) following transcatheter aortic valve replacement (TAVR) is common, but the incidence, predictors and outcome of PPM are still controversial. Methods: A total of 18 articles incorporating 72,016 patients were identified form PubMed and Embase online database. Results: The pooled incidences of overall, and severe PPM following TAVR were 32.0% and 10.0% separately. Comparing to surgical aortic valve replacement (SAVR), TAVR had lower incidence of overall (OR, 0.31, 95% CI, 0.20–0.50) and severe PPM (OR, 0.38, 95% CI, 0.28–0.52). PPM was associated with a larger body surface area (BSA), larger body mass index (BMI) and previous myocardial infarction in comparison with those patients without PPM. Although PPM was not rare after TAVR, no significant differences were observed both in short- and mid-term all-cause mortality (30 day: OR: 1.51, 95% CI, 0.79–2.87, 1 year: OR: 1.02, 95% CI, 0.96–1.08, and 2 years: OR: 0.99, 95% CI, 0.79–1.24) between patients with PPM and those without PPM. Conclusions: Despite the fact that the incidence of PPM was lower than that of SAVR, PPM was not seen to have an impact on short- and mid-term survival.

Pulmonary hypertension (PH) is one of the most devastating cardiovascular diseases worldwide and it draws much attention from numerous scientists. As an indispensable part of pulmonary artery, smooth muscle cells are worthy of being carefully investigated. To elucidate the pathogenesis of PH, several theories focusing on pulmonary artery smooth muscle cells (PASMC), such as hyperproliferation, resistance to apoptosis, and cancer theory, have been proposed and widely studied. Here, we tried to summarize the studies, concentrating on the role of PASMC in the development of PH, feasible molecular basis to intervene, and potential treatment to PH.

Background: Gut Microbiome can produce numerous metabolites which may be absorbed into the circulation and play a critical role in the development of diseases. Our study wants to find out the roles of faecal microbiota and its metabolite in the development of pulmonary hypertension.Methods: SD rats were expose to either normoxia (Control, n=8) or chronic hypoxia (10% O2) (n=16).Rats in chronic hypoxia were randomly received sodium butyrate (500 mg/kg) (n=8) or volumematched saline (n=8) once a day. Rats in normoxia condition also received volume-matched saline once a day. RVSP and lung vascular features were assessed after 3 week's treatment. Rats' fecal samples were collected and analyzed by GCMS and 6S/18S Amplicon Sequencing. Activation of HIF-1α, HMGB2, TLR4, TNF-α, HDAC5 and PCNA was assessed using Western blot analysis. The effect of sodium butyrate on proliferation of pulmonary artery smooth muscle cell, induced by PDGF or hypoxia (1% O2), was evaluated by CCK-8, EDU assay and wound healing assay. Results: Hypoxia significantly increased RVSP and induced a significant decrease in butyrateproducing bacteria, but a slight decrease of SCFAs without statistic difference. Administration of sodium butyrate remarkably attenuated the RVSP and improved lung vascular features. Decreased expression of HDAC5, PCNA, HIF-1α, HMGB2, TLR4, TNF-α and inhibited proliferation of PASMC were found in rats or cells with sodium butyrate. Conclusions: Decreased butyrate-producing bacteria may contribute to the development of PH, and sodium butyrate supplement can effectively attenuate hypoxia-induced PH in rats probably by inhibiting the proliferation and migration of PASMC. EDU: 5-Ethynyl-2 ' -deoxyuridine SCFAs: Short chain fatty acids MCT: Monocrotaline NS: Normal saline SB: Sodium Butyrate Declarations Ethics approval and consent to participateThe rats experiment protocol was approved by the Animal Research Committee

Background: Gut Microbiome can produce numerous metabolites which may be absorbed into the circulation and play a critical role in the development of diseases. Our study wants to find out the roles of faecal microbiota and its metabolite in the development of pulmonary hypertension. Methods: SD rats were expose to either normoxia (Control, n=8) or chronic hypoxia (10% O 2 ) (n=16). Rats in chronic hypoxia were randomly received sodium butyrate (500 mg/kg) (n=8) or volume-matched saline (n=8) once a day. Rats in normoxia condition also received volume-matched saline once a day. RVSP and lung vascular features were assessed after 3 week’s treatment. Rats’ fecal samples were collected and analyzed by GCMS and 6S/18S Amplicon Sequencing. Activation of HIF-1α, HMGB2, TLR4, TNF-α, HDAC5 and PCNA was assessed using Western blot analysis. The effect of sodium butyrate on proliferation of pulmonary artery smooth muscle cell, induced by PDGF or hypoxia (1% O 2 ), was evaluated by CCK-8, EDU assay and wound healing assay. Results: Hypoxia significantly increased RVSP and induced a significant decrease in butyrate-producing bacteria, but a slight decrease of SCFAs without statistic difference. Administration of sodium butyrate remarkably attenuated the RVSP and improved lung vascular features. Decreased expression of HDAC5, PCNA, HIF-1α, HMGB2, TLR4, TNF-α and inhibited proliferation of PASMC were found in rats or cells with sodium butyrate. Conclusions: Decreased butyrate-producing bacteria may contribute to the development of PH, and sodium butyrate supplement can effectively attenuate hypoxia-induced PH in rats probably by inhibiting the proliferation and migration of PASMC.