2023年 · 第03卷第01期

Objective: Data comparing the outcomes of MiStent (Micell Technologies, Durham, North Carolina, USA) microcrystalline biodegradable polymer (BP) drug-eluting stent (DES) and those of another post-marketing BP-DES, TIVOLI (EssenTech, Beijing, China) are rare. This study sought to compare the angiographic efficacy and clinical outcomes of the microcrystalline BP sirolimus-eluting stent (SES) system MiStent and those of TIVOLI BP-SES. Methods: The DESSOLVE-C trial was a prospective, single-blinded, multicenter, randomized trial (NCT02448524), which randomly assigned patients with de novo coronary lesions to receive MiStent or TIVOLI BP-SES by a 1:1 ratio. The primary endpoint was a non-inferiority comparison of in-stent late lumen loss (LLL) by quantitative coronary angiography at 9 months. The secondary endpoint was device-related clinical cardiovascular composite events (target lesion failure (TLF), composite of cardiac death, target vessel myocardial infarction (MI), and clinically driven target lesion revascularization) and 1-year outcomes. Results: A total of 428 patients (216 patients in the MiStent group and 212 patients in the TIVOLI group) were enrolled and included in an intention-to-treat analysis. MiStent was not only non-inferior but superior to TIVOLI for in-stent LLL at 9 months ((0.23 ± 0.37) mm vs. (0.34 ± 0.48) mm, P for non-inferiority <0.001, P for superiority = 0.02). Although without significant difference, the rate of TLF in MiStent was quantitatively lower than that in TIVOLI (3.70% vs. 6.60%; P = 0.17). Conclusion: Compared with TIVOLI BP-SES, the MiStent system was superior in in-stent LLL at 9 months and had a comparable clinical benefit at 1 year in de novo coronary lesions.

Objective: While evidence-based clinical guidelines recommend chordal-sparing mitral valve replacement, rather than mitral valve repair, in patients with severe ischemic mitral regurgitation (IMR) undergoing coronary artery bypass grafting, there are no similar recommendations for patients undergoing left ventricular reconstruction (LVR). This study aimed to compare the clinical outcomes of mitral valve repair and replacement in patients undergoing LVR complicated by more than moderate IMR. Methods: In this single-center cohort study, a total of 74 consecutive patients who underwent LVR and mitral valve surgery (repair group: 59; replacement group: 15), during the period from March 2000 to March 2021 at Fuwai Hospital (Beijing, China) were retrospectively enrolled. Survival rates were calculated with the Kaplan-Meier method and compared using the log-rank test. Univariate Cox analysis was performed to evaluate possible confounders, followed by adjustment in multivariate analysis. The primary outcome was survival free of major adverse cardiovascular and cerebrovascular events (MACCE). Results: Median follow-up time was 59.4 months. Compared with mitral valve replacement, mitral valve repair was associated with increased risk of perioperative use of ventricular assist device (22.0% vs. 0, P = 0.045). There was no difference in overall survival (hazard ratio (HR), 1.10; 95% confidence interval (CI), 0.31-3.93; Plogrank = 0.888) and MACCE-free survival (HR, 1.54; 95% CI, 0.65-3.65; Plogrank = 0.319), even after multivariate Cox regression (HR, 1.35; 95% CI, 0.37-4.88; PCox = 0.646; and HR, 1.41; 95% CI, 0.57-3.44; PCox = 0.455, respectively). Furthermore, while no differences were observed in ejection fraction and left ventricular end-diastolic diameter on follow-up echocardiography, mitral valve repair was associated with an increased risk of recurrent mitral regurgitation (P = 0.041). Conclusions: In patients undergoing LVR complicated by more than moderate IMR, both concomitant mitral valve repair and replacement can be successfully achieved with comparable overall and MACCE-free survival outcomes; however, mitral valve replacement may be superior to mitral valve repair for persistent correction of mitral dysfunction.

Objective: Dopamine, via its receptors, plays a vital role in the maintenance of blood pressure by modulating renal sodium transport. However, the role of the D4 dopamine receptor (D4 receptor) in renal proximal tubules (PRTs) is still unclear. This study aimed to verify the hypothesis that activation of D4 receptor directly inhibits the activity of the Na+-K+-ATPase (NKA) in RPT cells. Methods: NKA activity, nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) levels were measured in RPT cells treated with the D4 receptor agonist PD168077 and/or the D4 receptor antagonist L745870, the NO synthase inhibitor NG-nitro-L-arginine-methyl ester (L-NAME) or the soluble guanylyl cyclase inhibitor 1H-[1,2,4] oxadiazolo-[4,3-a] quinoxalin-1-one (ODQ). Total D4 receptor expression and its expression in the plasma membrane were investigated by immunoblotting in RPT cells from Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs). Results: Activation of D4 receptors with PD168077, inhibited NKA activity in RPT cells from WKY rats in a concentration- and time-dependent manner. The inhibitory effect of PD168077 on NKA activity was prevented by the addition of the D4 receptor antagonist L745870, which by itself had no effect. The NO synthase inhibitor L-NAME and the soluble guanylyl cyclase inhibitor ODQ, which by themselves had no effect on NKA activity, eliminated the inhibitory effect of PD168077 on NKA activity. Activation of D4 receptors also increased NO levels in the culture medium and cGMP levels in RPT cells. However, the inhibitory effect of D4 receptors on NKA activity was absent in RPT cells from SHRs, which could be related to decreased plasma membrane expression of D4 receptors in SHR RPT cells. Conclusions: Activation of D4 receptors directly inhibits NKA activity via the NO/cGMP signaling pathway in RPT cells from WKY rats but not SHRs. Aberrant regulation of NKA activity in RPT cells may be involved in the pathogenesis of hypertension.

Objective: Many studies have shown that blood glucose fluctuations (GFs) are more harmful to patients with diabetes mellitus (DM) than sustained hyperglycemia. However, the effect of GF on electrocardiogram (ECG) parameters and vulnerability to ventricular tachycardia/fibrillation (VT/VF) remains poorly characterized. This study aimed to assess the effect of GF on ECG parameters and induction of VT/VF in streptozotocin (STZ)-induced diabetic Sprague-Dawley rats. Methods: Male Sprague-Dawley rats were injected with STZ and randomly divided into 3 treatment groups: controlled STZ-induced diabetic rats (C-STZ) (n = 10); uncontrolled STZ-induced diabetic rats (U-STZ) (n = 10); and STZ-induced diabetic rats with glucose fluctuations (GF-STZ) (n = 10). After 12 weeks, baseline ECG recordings were taken and a VT/VF test was performed with the administration of caffeine and dobutamine. Hematoxylin & eosin and masson staining were used to evaluate pathological cardiac changes after intervention. Results: No significant difference in heart rate, RR interval, P wave (duration and height), PR segment, PR interval, QRS wave duration, and T wave height was observed among the 3 groups (P > 0.05). Compared with the C-STZ group, the U-STZ and GF-STZ groups both had a longer T wave duration ((62.41 ± 2.38) ms vs. (78.37 ± 4.64) ms and (96.06 ± 4.60) ms, P < 0.05), QT interval ((83.66 ± 2.31) ms vs. (101.75 ± 4.56) ms and (119.14 ± 4.88) ms, P < 0.05), and QTc interval ((77.45 ± 1.36) ms vs. (91.36 ± 3.49) ms and (104.55 ± 3.01) ms, P < 0.05), all of which were longest in the GF-STZ group (P < 0.05). Additionally, the GF-STZ group had the highest VT/VF occurrence and duration and the highest arrhythmia score. Conclusion: This study revealed GF can significantly prolong the QT interval, QTc interval, and T wave duration, as well as increase vulnerability to VT/VF in rats, which may be an important electrophysiological mechanism of GF-related ventricular arrhythmia.

Objective: The aim of this study was to investigate the efficacy and safety of tolvaptan, as well as the impact of its treatment dose and duration in heart failure patients with congestive signs. Methods: The PubMed, Embase, Cochrane Library, and ClinicalTrials.gov databases were searched to collect data from all randomized controlled trials (RCT) examining the efficacy and safety of tolvaptan in heart failure patients with congestive signs compared with placebo or blank control until March 4, 2021. Urine volume, change in body weight, improvement in dyspnea, and reduction of edema were evaluated as efficacy indicators. All-cause mortality, worsening heart failure, and adverse events were considered safety indicators. The quality of eligible publications was assessed using the Cochrane risk of bias for RCTs. Results: Ten RCTs with 5,980 patients were included in this analysis. Compared with control, tolvaptan significantly reduced weight in the short term (day 1, 7 RCTs, weighted mean difference (WMD): -1.09, 95% confidence interval (CI): -1.27 to -0.91; day 2, 2 RCTs, WMD: -1.67, 95% CI: -3.00 to -0.33; day 7, 4 RCTs, WMD: -0.95, 95% CI: -1.25 to -0.66), increased urine volume (WMD: 1,825.72, 95% CI: 1,438.38-2,213.07), and relieved dyspnea (risk ratio (RR): 1.12, 95% CI: 1.05-1.19) without increasing the mortality rate (RR: 0.96, 95% CI: 0.87-1.06). Furthermore, the weight loss and increase in urine volume were not dose-dependent effects, and prolonged medication did not lead to sustained weight loss. In addition, there seemed to be more adverse events (RR: 1.17, 95% CI: 1.03-1.32) after treatment with tolvaptan. Further analysis revealed that patients treated with tolvaptan were more likely to report thirst (RR: 6.09, 95% CI: 3.37-11.00) and dry mouth (RR: 6.36, 95% CI: 4.09-9.90), as well as develop hypernatremia (RR: 12.76, 95% CI: 3.52-46.32). Conclusions: The meta-analysis shows that tolvaptan can improve congestion with no increase in mortality rate, but should be used to guard against adverse events. Deserve to be mentioned, the number of RCTs included was limited, suggesting that the observed results should be interpreted with caution. Additional robust clinical studies are warranted to validate the present findings.

Cardiovascular disease (CVD) is the leading cause of mortality worldwide. Multiple factors are involved in CVD, and emerging data indicate that lipoprotein(a) (Lp(a)) may be associated with atherosclerotic cardiovascular disease (ASCVD) independent of other traditional risk factors. Lp(a) has been identified as a novel therapeutic target. Previous studies on the influence of Lp(a) in CVD have mainly used in western populations. In this review, the association of plasma Lp(a) concentration with ASCVD was summarized, with regards to epidemiological, population-based observational, and pathological studies in Chinese populations. Lp(a) mutations and copy number variations in Chinese populations are also explored. Finally, the impact of plasma Lp(a) levels on patients with type 2 diabetes mellitus, cancer, and familial hypercholesterolemia are discussed.

High altitude brings a great physiological change in human beings, both during short-term exposure and in lifelong residents, especially in the cardiovascular system. Hypoxia notably induces pulmonary vasoconstriction, thus resulting in a moderate increase in pulmonary arterial pressure. Acclimatized inhabitants exhibit lower pulmonary pressure and better exercise capacity than lowlanders during short-term high-altitude exposure. Rapid ascent to high altitude without adequate acclimatization can cause high-altitude pulmonary edema in susceptible individuals, with a rapid increase in pulmonary pressure. Cardiac output increases initially following acute high-altitude exposure and returns to normal as at sea level after a few days of acclimatization. Ventricular volumes at high altitude change consistently with decreases in plasma volume. Left ventricular systolic function is enhanced after acute high-altitude exposure and during chronic acclimatization. However, there are controversies on whether right ventricular systolic function is preserved or decreases after high-altitude exposure, probably due to variable hypoxic pulmonary vasoconstriction. High altitude induces altered ventricular diastolic patterns. Recently, a new perspective has emerged, whereby ventricular intrinsic relaxation is not impaired, as assessed by untwisting through speckle-tracking imaging. Persistent hypoxic pulmonary hypertension probably induced right ventricular dilation and hypertrophy, and even right heart failure, described as high-altitude heart diseases. Descent to lower altitude should be the best treatment for them, and potential pharmacological agents majorly focus on the inhabitation of pulmonary vasoconstriction, such as phosphodiesterase-5 inhibitors and endothelin receptor antagonists. Evidence on the risks of high-altitude exposure for patients with previous cardiovascular diseases is limited, and thus they should be prudent when ascending to high altitude. Further randomized large-scale studies are needed to explore cardiac performance at high altitudes and provide more evidence for the prevention and clinical management of medical complications at high altitude.

A 43-year-old male was admitted to General Hospital of Northern Theater Command with exacerbation of chest pain for 10 d. Computed tomographic angiography (CTA) showed an irregular aortic arch aneurysm involving the left subclavian artery (LSA), with penetrating aortic ulcer and intramural hematoma. A modified fenestrated thoracic endovascular aortic repair (TEVAR) technique was performed successfully. Follow-up CTA showed that stent grafts were well-apposed, without endoleaks, migration, or branch artery occlusion, and the hematoma was almost completely absorbed. In this case, precise fenestrations were created by measurements based on three-dimensional CT reconstruction and angiography. Furthermore, the physician chose an LSA approach to catch the guide wire and deployed branched stent grafts, considering the oblique direction of this branch and the small size of the fenestration. This case shows that pre-fenestrated and inner bare stent enhancing TEVAR is a safe and feasible technique for repair of complicated aortic arch aneurysm.