Effect of different doses of atorvastatin on collateral formation in coronary artery disease patients with coronary atherosclerosis.

OBJECTIVE: The study aimed to explore the effect of different doses of atorvastatin on collateral formation in coronary artery disease (CAD) patients with coronary atherosclerosis. METHODS: The study included 218 CAD patients who received treatment between January 2017 and January 2020 at our hospital. They were assigned to the high-dose group (40 mg atorvastatin) and the low-dose group (20 mg atorvastatin) using the random table method with 109 patients per group. The blood lipid levels, TNF-α, hs-CRP, NO, and coronary atherosclerosis collateral formation before and after treatment in the two groups were compared, and favorable factors of good coronary artery collateral circulation were analyzed by multivariate logistic regression analysis. RESULTS: LDL-C, TG, and TC levels decreased, whereas HDL-C levels increased in the two groups after treatment. The high-dose group had lower LDL-C, TG, and TC levels but higher HDL-C levels than the low-dose group, and the difference was statistically significant ( P < 0.05). TNF-α and hs-CRP levels decreased while NO levels increased in both groups after treatment. The high-dose group had lower TNF-α and hs-CRP levels but higher NO levels than the low-dose group, and the difference was statistically significant ( P < 0.05). CONCLUSION: High-dose atorvastatin could blood lipid levels of modulate CAD patients and promote coronary atherosclerosis collateral formation. In addition, hypertension, LDL-C, HDL-C, TNF-α, hs-CRP, and NO were independent determinants of good coronary artery collateral circulation.

Effects of Combined Lipid-Lowering Therapy on Low-Density Lipoprotein Cholesterol Variability and Cardiovascular Adverse Events in Patients with Acute Coronary Syndrome.

INTRODUCTION: To investigate the effect of combined lipid-lowering therapy on low-density lipoprotein cholesterol (LDL-C) variability and cardiovascular adverse events in patients with acute coronary syndrome (ACS). METHODS: A total of 200 patients with acute coronary syndrome, admitted to the first Hospital of Hebei Medical University from January 2018 to June 2019, were randomly divided into the observation group (100 cases were treated with combined lipid-lowering drugs, including 10 mg/day atorvastatin and 10 mg/day ezetimibe) and the control group (100 cases were given an intensive statin regimen, including 40 mg/day atorvastatin). The levels of blood lipids, creatine kinase (CK), alanine transaminase (ALT), matrix metalloproteinase-9 (MMP-9) and high-sensitivity C-reactive protein (hsCRP) were observed and compared between the two groups. Focus was laid on the concentration of the above-mentioned parameters and follow-up results including the drug safety and incidence of cardiovascular adverse events. RESULTS: Before treatment, there was no significant difference in total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), CK, ALT, MMP-9, hsCRP and LDL-C between the two groups (P > 0.05). After 6 months, 12 months and 24 months of treatment, TC, HDL-C, CK, ALT, MMP-9, hsCRP and LDL-C were improved in both groups, and TC, HDL-C, CK, ALT, MMP-9, hsCRP and LDL-C in the observation group elicited greater results than those in the control group with significant difference (P < 0.05). In the course of treatment, the drug safety of the two groups was compared (P > 0.05), and the incidence of cardiovascular adverse events in the observation group was significantly lower than that in the control group (6.59% vs. 11.96%) (P < 0.05). CONCLUSION: Combination therapy with atorvastatin and ezetimibe potentially provides remarkable effects in terms of treating acute coronary syndrome, controlling the variation of LDL-C, alleviating the inflammatory state and reducing the incidence of cardiovascular adverse events with a safe profile. Combined lipid-lowering drugs are considered valid and alternative approaches for wide clinical practice.

Transcatheter closure through single venous approach for young children with patent ductus arteriosus: A retrospective study of 686 cases.

The objective is to explore the feasibility and safety of transcatheter closure of patent ductus arteriosus (PDA) through single venous approach in Chinese young children.A total of 1088 patients aged between 9 months old to 3 years old who underwent transcatheter closure of PDA from May 2004 to May 2015 were retrospectively reviewed. All the procedures were under ultrasound monitoring. The shape and size of PDA as well as immediate therapeutic results were recorded by angiography and ultrasonography. The size of occluder was individually selected according to the smallest diameter of the PDAs. Echocardiography was respectively performed 3 days, 1month, 6 months, and 12 months after the procedure to evaluate the outcomes.Among the total 1088 children, transcatheter closure of PDA was accomplished through single venous approach that was performed in 686 cases. The average weight and age of the children were 10.9 ±â€Š3.6 kg (5.0-14.3 kg) and 1.8 ±â€Š1.6 years (9 months-3 years), respectively. The fluoroscopic time was about 5.1 to 11.6 minutes. Successful device placement with the initially selected occluder was achieved in 662 cases. In other 14 cases, the procedure was eventually completed after being replaced with a larger occluder; while in the other 10 cases, smaller occluders were applied to replace the initial ones. Technically, all the procedures were successfully performed. All the patients were followed up for 15.6 ±â€Š8.2 years. No serious complications and death were observed during the follow-up.Transcatheter closure of PDA with occluder by single venous approach is an effective and reliable method in vast majority of young children.

Chronic intermittent hypobaric hypoxia attenuates monocrotaline-induced pulmonary arterial hypertension via modulating inflammation and suppressing NF-κB/p38 pathway.

OBJECTIVES: Inflammation is involved in various forms of pulmonary arterial hypertension (PAH). Although the pathophysiology of PAH remains uncertain, NF-κB and p38 mitogen-activated protein kinase (p38 MAPK) has been reported to be associated with many inflammatory mediators of PAH. This study aimed to evaluate the effect of chronic intermittent hypobaric hypoxia (CIHH) on pulmonary inflammation and remodeling in monocrotaline (MCT) induced PAH in rats. MATERIALS AND METHODS: An in vivo model of PAH induced by MCT was employed. Statistical analyses were done using one-way analysis of variance (ANOVA) or Fisher's LSD test for multiple comparisons. RESULTS: Four weeks of CIHH exposure following MCT injection resulted in significant reduction of mean pulmonary artery pressure (mPAP) level and improvement of right ventricular hypertrophy (RVH). Morphometric analyses showed decreased wall thickness of pulmonary arterioles in MCT+CIHH treated rats. These findings are consistent with the decrease in Ki-67 immunostaining. Following CIHH treatments, apoptotic analysis showed a consistent decrease in T lymphocytes together with lower levels of CD4+ T cell subset as measured in spleen and blood samples. Furthermore, CIHH treatment resulted in markedly reduced expression of TNF-α and IL-6 via the inhibition of NF-κB and p38 MAPK activity in rat lungs. CONCLUSION: Altogether, these results provide new evidence relating to the mode of action of CIHH in the prevention of PAH induced by MCT.

Uncovering the rare variants of DLC1 isoform 1 and their functional effects in a Chinese sporadic congenital heart disease cohort.

Congenital heart disease (CHD) is the most common birth defect affecting the structure and function of fetal hearts. Despite decades of extensive studies, the genetic mechanism of sporadic CHD remains obscure. Deleted in liver cancer 1 (DLC1) gene, encoding a GTPase-activating protein, is highly expressed in heart and essential for heart development according to the knowledge of Dlc1-deficient mice. To determine whether DLC1 is a susceptibility gene for sporadic CHD, we sequenced the coding region of DLC1 isoform 1 in 151 sporadic CHD patients and identified 13 non-synonymous rare variants (including 6 private variants) in the case cohort. Importantly, these rare variants (8/13) were enriched in the N-terminal region of the DLC1 isoform 1 protein. Seven of eight amino acids at the N-terminal variant positions were conserved among the primates. Among the 9 rare variants that were predicted as "damaging", five were located at the N-terminal region. Ensuing in vitro functional assays showed that three private variants (Met360Lys, Glu418Lys and Asp554Val) impaired the ability of DLC1 to inhibit cell migration or altered the subcellular location of the protein compared to wild-type DLC1 isoform 1. These data suggest that DLC1 might act as a CHD-associated gene in addition to its role as a tumor suppressor in cancer.

A Large Institutional Study on Outcomes and Complications after Transcatheter Closure of a Perimembranous-Type Ventricular Septal Defect in 890 Cases.

PURPOSE: To investigate the incidence, cause, and prevention of complications associated with interventional therapy for perimembranous ventricular septal defects (pmVSDs). METHODS: A retrospective analysis was performed on 890 patients with pmVSDs after interventional therapy. The complications were then analyzed by electrocardiography and echocardiography during or after interventional therapy. During the follow-up period of 12-52 (mean of 26.9 ± 21.6) months, the technical success rate was 97.9% (871/890). RESULTS: The incidence of serious complication was 1.12% (10/890), including five cases of third-degree atrioventricular block, two of severe tricuspid valve regurgitation, one of cerebral infarction in the basal ganglia area, and two of femoral artery thrombosis. No death was reported during patient follow-up. CONCLUSIONS: Transcatheter closure of pmVSDs in selected patients was found to be effective and safe. KEY WORDS: Complication; Interventional therapy; Ventricular septal defect.