Prognostic Implication of Pulmonary Arterial Pressure in Surgical Repair of Predominantly Congenital Mitral Valve Regurgitation-Based Intracardiac Abnormalities.

INTRODUCTION: Knowledge is limited regarding the significance of pulmonary arterial pressure (PAP) in predominantly congenital mitral valve regurgitation (MR)-based intracardiac abnormalities. METHODS: From a prospective cohort, we included 200 patients with congenital MR regardless of other associated intracardiac abnormalities (mean age 60.4 months, 67% female, systolic PAP (sPAP) 54.2 mm Hg) surgically repaired in 2012-2019 and followed up to 2020 (median 30.0 months). Significant pulmonary hypertension (PH) was defined as sPAP >50 mm Hg at rest or mean PAP >25 mm Hg on right heart catheterization. By perioperative sPAP changes, patients were stratified as group I (pre-normotension to post-normotension), group II (pre-hypertension to post-normotension), or group III (pre-hypertension to post-hypertension). Primary outcomes were the recurrence of MR (defined as the regurgitation grade of moderate or greater) and the progression of MR (defined as any increase in the magnitude of regurgitation grade after surgery). Cox proportional hazard and Kaplan-Meier curve were performed. RESULTS: There was no association between preoperative PH and the recurrent MR (adjusted hazard ratios [aHR]: 1.146 [95% CI: 0.453-2.899]) and progressive MR (aHR: 1.753 [95% CI: 0.807-3.804]), respectively. There were no significant differences among group I, group II, and group III in the recurrent MR but in the progressive MR. A dose dependency was identified for preoperative sPAP with recurrent MR (aHR: 1.050 [95% CI: 1.029-1.071]) and progressive MR risks (aHR: 1.037 [95% CI: 1.019-1.055]), respectively. CONCLUSIONS: Preoperative higher sPAP is associated with worse outcomes, warranting heightened attention to the identification of perioperative sPAP.

Activation of the CaR-CSE/H2S pathway confers cardioprotection against ischemia-reperfusion injury.

Ischemia-reperfusion (I/R) injury is a multifactorial process triggered when an organ is subjected to transiently reduced blood supply. The result is a cascade of pathological complications and organ damage due to the production of reactive oxygen species following reperfusion. The present study aims to evaluate the role of activated calcium-sensing receptor (CaR)-cystathionine γ-lyase (CSE)/hydrogen sulfide (H2S) pathway in I/R injury. Firstly, an I/R rat model with CSE knockout was constructed. Transthoracic echocardiography, TTC and HE staining were performed to determine the cardiac function of rats following I/R Injury, followed by TUNEL staining observation on apoptosis. Besides, with the attempt to better elucidate how CaR-CSE/H2S affects I/R, in-vitro culture of human coronary artery endothelial cells (HCAECs) was conducted with gadolinium chloride (GdCl3, a CaR agonist), H2O2, siRNA against CSE (siCSE), or W7 (a CaM inhibitor). The interaction between CSE and CaM was subsequently detected. Plasma oxidative stress indexes, H2S and CSE, and apoptosis-related proteins were all analyzed following cell apoptosis. We found that H2S elevation led to the improvement whereas CSE knockdown decreased cardiac function in rats with I/R injury. Moreover, oxidative stress injury in I/R rats with CSE knockout was aggravated, while the increased expression of H2S and CSE in the aortic tissues resulted in alleviated the oxidative stress injury. Moreover, increased H2S and CSE levels were found to inhibit cell apoptotic ability in the aortic tissues after I/R injury, thus attenuating oxidative stress injury, accompanied by inhibited expression of apoptosis-related proteins. In HCAECs following oxidative stress treatment, siCSE and CaM inhibitor were observed to reverse the protection of CaR agonist. Coimmunoprecipitation assay revealed the interaction between CSE and CaM. Taken together, all above-mentioned data provides evidence that activation of the CaR-CSE/H2S pathway may confer a potent protective effect in cardiac I/R injury.

The role of microRNA-1 targeting of MAPK3 in myocardial ischemia-reperfusion injury in rats undergoing sevoflurane preconditioning via the PI3K/Akt pathway.

Recent studies have uncovered the vital roles played by microRNAs in regulating cardiac injury. Among them, the cardiac enriched microRNA-1 (miR-1) has been extensively studied and proven to be detrimental to cardiac myocytes. Hence, the current study aimed to explore whether miR-1 affects myocardial ischemia-reperfusion injury (MIRI) in rats undergoing sevoflurane preconditioning and the underlying mechanism. After successful model establishment, rats with MIRI were transfected with mimics or inhibitors of miR-1, or siRNA against MAPK3, and then were injected with sevoflurane. A luciferase reporter gene assay was conducted to evaluate the targeting relationship between miR-1 and MAPK3. Reverse transcription quantitative polymerase chain reaction and Western blot analysis were employed to evaluate the expressions of miR-1, MAPK3, phosphatidylinositol 3-kinase (PI3K), and Akt. Additionally, the concentration of lactate dehydrogenase (LDH) was determined. Cell apoptosis and viability were assessed using TUNEL and cell counting kit-8 assays, and the ischemic area at risk and infarct size were detected using Evans blue and triphenyltetrazolium chloride staining. MAPK3 was found to be the target gene of miR-1. miR-1 expressed at a high level whereas MAPK3 expressed at a low level in MIRI rats. Overexpressing miR-1 or silencing MAPK3 blocked the PI3K/Akt pathway to increase cell apoptosis, ischemic area at risk, and infarct area but decreased cell viability and increased LDH concentration. In contrast, miR-1 downregulation abrogated the effects induced by miR-1 mimics or siRNA against MAPK3. These findings indicate that inhibition of miR-1 promotes MAPK3 to protect against MIRI in rats undergoing sevoflurane preconditioning through activation of the PI3K/Akt pathway.

Can Renal Resistive Index Predict Acute Kidney Injury After Acute Type A Aortic Dissection Repair?

BACKGROUND: This study sought to determine whether assessment of the renal resistive index (RRI) can predict the short-term reversibility of acute kidney injury (AKI) after repair of acute type A aortic dissection (TAAD). METHODS: This prospective study included 62 patients undergoing repair of acute TAAD. Doppler-based RRIs were obtained preoperatively, immediately after the surgical procedure, and 6, 24, and 48 hours postoperatively. The occurrence of AKI was evaluated daily according to Acute Kidney Injury Network criteria. Persistent AKI was defined as AKI lasting longer than 3 days. The association between the maximum RRI level at different time points and persistent AKI was analyzed by the receiver-operating characteristic curve. RESULTS: Of the 62 patients, 22 (35.5%) had no AKI, 21 (33.9%) had transient AKI, and 19 (30.6%) had persistent AKI. The maximum RRI was 0.67 ± 0.03 (0.62 to 0.71), 0.71 ± 0.05 (0.59 to 0.79), and 0.78 ± 0.05 (0.70 to 0.92) in the no AKI, transient AKI, and persistent AKI groups, respectively. The maximum level of RRI was significantly correlated with that of SCr during the first 48 hours postoperatively (rho = 0.606; p < 0.001). RRI could predict persistent AKI with an area under the receiver-operating characteristic curve of 0.918 (95% confidence interval, 0.850 to 0.986; p < 0.001). A postoperative RRI of 0.725 or higher was a marker for early detection of persistent AKI with high sensitivity and specificity (94.7% and 72.1%, respectively). CONCLUSIONS: An elevated maximum RRI may be a predictor of persistent AKI after repair of acute TAAD. This is helpful for management decision making and improving the prognosis of patients with AKI.

[Palliative percutaneous transluminal renal angioplasty and stenting in elderly patients for serious coronary heart disease with renal arterial stenosis].

OBJECTIVE: To investigate the feasibility of palliative percutaneous transluminal renal angioplasty (PTRA) and stenting in patients with serious coronary heart disease and renal arterial stenosis. METHODS: Thirty-four (23 male and 11 female) patients with a mean age of 61.0+/-11.8 years (ranging from 55 to 78 years) with serious coronary heart disease and renal arterial stenosis, who were unwilling or not suitable to undergo percutaneous coronary intervention and coronary artery bypass grafting, were enrolled in this study. All the cases underwent PTRA and were followed up for 17-53 months (average 35.0+/-9.3 months). The patients' renal and cardiac functions and left ventricular ejection fraction (LVEF) were measured in transthoracic echocardiography with the score of SF-36 Health Survey recorded. RESULTS: During the follow-up, the weekly incidence of angina pectoris reduced from 14.0+/-3.9 to 6.5+/-3.3 (P<0.01) and LVEF increased from (40.2+/-10.4)% to (45.3+/-7.8)% (P<0.05). The SF-36 scores were significantly improved from 56.5+/-8.0 to 80.1+/-16.8 (P<0.01), with also significant improvement in the subscales of health and daily activity, self-feeling, and general health. CONCLUSION: Palliative PTRA and stenting is feasible and necessary in elderly patients with serious coronary heart disease and renal arterial stenosis when percutaneous coronary intervention or coronary artery bypass graft therapy is not possible.