Case report: pulmonary artery perforation during transseptal puncture for left atrial appendage closure requires emergency cardiac operation.

Patients with atrial fibrillation who take a high bleeding risk and are not candidates for oral anticoagulation therapy are increasingly being referred for left atrial appendage closure (LAAC) as an alternative method of stroke prevention. However, certain manipulations performed during the LAAC procedure, such as transseptal puncture (TSP), may potentially result in vessel injury and lead to cardiac tamponade or even fatality. Clinical significance and management strategies associated with these complications remain controversial. A 74-year-old female patient with atrial fibrillation was referred for left atrial appendage occlusion. During the puncture of the atrial septum, the catheter sheath inadvertently exited through the roof of the right atrium and continued to advance, resulting in pulmonary artery perforation. The patient underwent immediate pericardiocentesis and drainage, followed by surgical exploration for suturing the tear in the pulmonary artery and ligation of the left atrial appendage. This represents the first reported case of a pulmonary artery perforation occurring during a transseptal puncture procedure for left atrial appendage closure. The case exemplifies the feasibility of emergency cardiac surgery as a therapeutic intervention.

Effect of evolocumab on the progression of intraplaque neovascularization of the carotid based on contrast-enhanced ultrasonography (EPIC study): A prospective single-arm, open-label study.

Background and Purpose: The aim of this study was to explore the effect of half a year of evolocumab plus moderate-intensity statin treatment on carotid intraplaque neovascularization (IPN) and blood lipid levels. Methods: A total of 31 patients with 33 carotid plaques who received evolocumab plus statin treatment were included. Blood lipid levels, B-mode ultrasound and contrast-enhanced ultrasonography (CEUS) at baseline and after half a year of evolocumab plus statin therapy were collected. The area under the curve (AUC) reflected the total amount of acoustic developer entering the plaque or lumen within the 180 s measurement period. The enhanced intensity reflected the peak blood flow intensity during the monitoring period, and the contrast agent area reflected the area of vessels in the plaques. Results: Except for high-density lipoprotein cholesterol (HDL-c), all other lipid indices decreased. Compared with baseline, low-density lipoprotein cholesterol (LDL-c) decreased by approximately 57% (p < 0.001); total cholesterol (TC) decreased by approximately 34% (p < 0.001); small dense low-density lipoprotein (sd-LDL) decreased by approximately 52% (p < 0.001); and HDL-c increased by approximately 20% (p < 0.001). B-mode ultrasonography showed that the length and thickness of the plaque and the hypoechoic area ratio were reduced (p < 0.05). The plaque area, calcified area ratio, and lumen cross-sectional area changed little (p > 0.05). CEUS revealed that the area under the curve of plaque/lumen [AUC (P/L)] decreased from 0.27 ± 0.13 to 0.19 ± 0.11 (p < 0.001). The enhanced intensity ratio of plaque/lumen [intensity ratio (P/L)] decreased from 0.37 ± 0.16 to 0.31 ± 0.14 (p = 0.009). The contrast agent area in plaque/area of plaque decreased from 19.20 ± 13.23 to 12.66 ± 9.59 (p = 0.003). The neovascularization score decreased from 2.64 ± 0.54 to 2.06 ± 0.86 (p < 0.001). Subgroup analysis based on statin duration (<6 months and ≥6 months) showed that there was no significant difference in the AUC (P/L) or intensity ratio (P/L) at baseline or after half a year of evolocumab treatment. Conclusion: This study found that evolocumab combined with moderate-intensity statins significantly improved the blood lipid profile and reduced carotid IPN. Clinical Trial Registration: https://www.clinicaltrials.gov; identifier: NCT04423406.

Case report: Treatment of a patient with STEMI and cardiogenic shock caused by RCA originating from LAD.

The right coronary artery (RCA) originating from the left anterior descending artery (LAD) is a very rare variation of coronary artery anomaly. This kind of anomaly is usually considered to be clinically benign. Here, we present an acute myocardial infarction patient with a single coronary artery (SCA), in whom the LAD and RCA are both occlusive at the same time. He suffered from ventricular fibrillation, cardiogenic shock, and severe bradyarrhythmias many times. Fortunately, this patient survived from death through our effective medical procedures.

Physiological cyclic stretch up-regulates angiotensin-converting enzyme 2 expression to reduce proliferation and migration of vascular smooth muscle cells.

Angiotensin-converting enzyme 2 (ACE2) is considered as an endogenous negative regulator of renin-angiotensin system (RAS), exerting multiple cardiovascular protective roles. Whether mechanical stretch modulates ACE2 expression remains unknown. The present study aimed at investigating whether ACE2 is involved in physiological stretch (10% elongation, 1 Hz) mediated cellular functions and the underlying mechanism. Cultured human aortic smooth muscle cells (HASMCs) were exposed to 10% stretch for indicated time, and real-time PCR and Western blot analysis showed 10% stretch increased ACE2 expression and activity significantly compared with static conditions and increased Ang-(1-7) level, but decreased Ang II level; Brdu incorporation assay and Scratch test showed that ACE2 was involved in the inhibition of HASMCs proliferation and migration by 10% stretch; the Dual-Luciferase Reporter Assay demonstrated that 10% increased ACE2 promoter activity, but had no effect on ACE2 mRNA stability; kinase inhibition study and Electrophoretic mobility shift assay (EMSA) showed that JNK1/2 and PKCßII pathway, as well as their downstream transcription factors, AP-1 and NF-κB, were involved in 10% stretch induced ACE2 expression. In conclusion, our study indicates ACE2 is a mechanosensitive gene, and may represent a potential therapeutic target for mechanical forces related vascular diseases.

Upregulation of miR-142-5p in atherosclerotic plaques and regulation of oxidized low-density lipoprotein-induced apoptosis in macrophages.

MicroRNA (miR)­142­5p is a member of the miR­142 family, which have been shown to be associated with tumors, stem cells and disorders of the immune system. However, the role of miR­142­5p in atherosclerosis has yet to be investigated. In the present study, an atherosclerotic apolipoprotein E­deficient (apoE­/­) mouse model was constructed and fed a high­fat diet. The expression levels of miR­142­5p in the murine atherosclerotic plaques were detected by gene microarray analysis. In addition, an in vitro assay was used to determine the expression levels of miR­142­5p in human endothelial cells, smooth muscle cells and macrophages, which were treated with oxidized low­density lipoprotein (ox­LDL). Furthermore, a miR­142­5p inhibitor and mimic was transfected into cultured human macrophages, in order to observe the effects on transforming growth factor­ß2 (TGF­ß2) expression. The effects of co­transfection of the miR­142­5p inhibitor or mimic with TGF­ß2, in human macrophages, on the rate of apoptosis was analyzed. The expression levels of miR­142­5p were 6.84­fold higher in mice with stable atherosclerotic plaques, and 2.69­fold higher in mice with vulnerable atherosclerotic plaques, as compared with the controls. Furthermore, the expression levels of miR­142­5p were upregulated in the cultured human macrophages. The percentage of apoptotic cells was lowest in the macrophages transfected with both TGF­ß2 and miR­142­5p inhibitors and treated with ox­LDL. The expression levels of miR­142­5p were upregulated in the atherosclerotic plaques of the apoE­/­ mice. The findings of the present study have shown that the upregulation of miR­142­5p expression may regulate apoptosis in human macrophages by targeting TGF­ß2. This effect may have an important role in the progression of atherosclerosis.