Cardiology Research and Practice

Secreted frizzled related protein 4 (SFRP4), a member of the SFRPs family, contributes to a significant function in metabolic and cardiovascular diseases. However, there is not enough evidence to prove the antiatherosclerosis effect of SFRP4 in ApoE knock-out (KO) mice. ApoE KO mice were fed a western diet and injected adenovirus (Ad)-SFRP4 through the tail vein for 12 weeks. Contrasted with the control cohort, the area of atherosclerotic plaque in ApoE KO mice overexpressing SFRP4 was reduced significantly. Plasma high-density lipoprotein cholesterol was elevated in the Ad-SFRP4 group. RNA sequence analysis indicated that there were 96 differentially expressed genes enriched in 10 signaling pathways in the mRNA profile of aortic atherosclerosis lesions. The analysis data also revealed the expression of a number of genes linked to metabolism, organism system, and human disease. In summary, our data demonstrates that SFRP4 could play an important role in improving atherosclerotic plaque formation in the aorta.

Background. Percutaneous coronary intervention using a drug-eluting stent (DES) is a common therapeutic option for acute coronary syndrome (ACS). However, stent-associated complications, such as bleeding associated with dual antiplatelet therapy, in-stent restenosis, stent thrombosis, and neoatherosclerosis, remain. Drug-coated balloons (DCBs) are expected to reduce stent-associated complications. This study aimed to assess the efficacy of DCB therapy and compare it with that of DES therapy in patients with ACS. Materials and Methods. In this single-center, retrospective, observational study, we examined all patients with ACS treated with DCB or DES between July 2014 and November 2020. Patients with left main trunk lesions were excluded. The primary outcome was a composite of major adverse cardiovascular events (MACE: cardiac death, myocardial infarction, and target lesion revascularization) at one year. Results. Three hundred and seventy-two patients were treated with DES, and 83 patients were treated with DCB. MACE occurred in 10 (12.0%) patients in the DCB group and in 50 (13.4%) patients in the DES group (). Conclusions. DCB is a valuable and effective therapy for patients with ACS. Moreover, DCB may become an alternative therapy for DES in patients with ACS.

Background. Chronic Chagas heart disease (CCHD) and systemic arterial hypertension (SAH) frequently coexists in areas where Chagas disease is endemic. The effects of the association of both conditions (CCHD-SAH) on the extracellular matrix (ECM) remodeling are unknown. Matrix metalloproteinases (MMP) 2 and 9 are involved in ECM remodeling. The aim of this study was to evaluate MMP 2 and MMP9 in CCHD-SAH patients and to correlate their levels with those of the profibrogenic cytokine TGF-beta. Methods. We included 19 patients with CCHD-SAH, 14 patients with CCHD alone, and 19 controls matched by sex and age. MMP-2 and MMP-9 plasma levels were studied by gel zymography and showed as optical densities (OD). TGF-beta plasma levels were measured by double-ligand ELISA and expressed as pg/mL. Results. Median (5^th, 95^th) MMP-2 plasma levels were 1224.7 OD (1160, 1433.5) in patients with CCHD alone, 1424.1 OD (1267.5, 1561) in patients with CCHD-SAH, and 940 OD (898.1, 1000.8) in controls (). MMP-9 plasma levels were 1870 OD (1740, 1904.1) in patients with CCHD alone, 1754.6 OD (1650, 2049) in those with CCHD-SAH and 89.7 OD (80, 96) in controls (). MMP-9 plasma levels were higher than those of MMP 2 in patients with CCHD-SAH (). No correlation was found between TGF-beta plasma levels with MMP-2 serum levels (r = 0.12; ), but a moderate negative correlation (r = −0.46; ) was observed between TGF-beta and MMP-9 plasma levels. Conclusions. MMP-2 and especially MMP-9 may play a role in the ECM remodeling process in patients with CCHD-SAH. TGF-Beta may counteract the MMP effect on the ECM remodeling process in patients with CCHD-SAH.

Background. Endothelial cell senescence is one of the key mechanistic factors in the pathogenesis of atherosclerosis. In terms of molecules, the phosphatidylinositol 3-kinase/protein kinase B/endothelial nitric oxide synthase (PI3K/Akt/eNOS) signaling plays an important role in the prevention and control of endothelial cell senescence, while hydrogen sulfide (H2S) improves the induced precocious senescence of endothelial cells through the PI3K/Akt/eNOS pathway. Comparatively, replicative senescence in endothelial cells is more in line with the actual physiological changes of human aging. This study aims to investigate the mechanism by which H2S improves endothelial cell replicative senescence and the involvement of the PI3K/Akt/eNOS pathway. Methods. we established a model of replicative senescence in human umbilical vein endothelial cells (HUVECs) and explored the effect of 200 μmol/L sodium hydrosulfide (NaHS; a donor of H2S) on senescence, which was determined by cell morphology, the expression level of plasminogen activator inhibitor 1 (PAI-1), and the positive rate of senescence-associated β-galactosidase (SA-β-Gal) staining. Cell viability was detected by MTT assay to evaluate the effect of NaHS and the PI3K inhibitor, LY294002. Meanwhile, the protein expression of PI3K, Akt, p-Akt, and eNOS in endothelial cells of each group was detected by Western blot. Results. the replicative senescence model was established in HUVECs at the passage of 16 cumulative cell population doubling values (CPDL). Treatment with NaHS not only significantly reduced the expression of PAI-1 and the positive rate of SA-β-Gal in HUVEC’s replicative senescence model but also notably increased the expression of PI3K, p-Akt, p-eNOS, and the content of nitric oxide(NO). However, the effects of NaHS on the expression of the pathway and the content of NO in HUVECs were abolished when LY294002 specifically inhibited PI3K. Conclusion. NaHS improves the replicative senescence of HUVECs with the contribution of the PI3K/Akt/eNOS pathway.

Background. The optimal exercise prescription for coronary artery disease (CAD) remains under debate. The aim of our meta-analysis is to investigate the efficacy of high-intensity interval training (HIIT) versus moderate-intensity continuous training (MICT) of coronary artery disease patients. Methods. Electronic databases were searched from their inception date until October 23, 2021, and the articles include randomized controlled trials. The mean differences and 95% confidence intervals were calculated, and heterogeneity was assessed using the I² test. Results. The study standards were met by seventeen studies. The pooled studies included 902 patients. HIIT resulted in improvement in peak oxygen uptake (1.50 ml/kg/min, 95% confidence interval: 0.48 to 2.53, n = 853 patients, and low quality evidence) compared with MICT. There was no discernible difference between the individuals in the HIIT group and the MICT group in terms of systolic/diastolic blood pressure or peak/resting heart rate. Conclusion. This systematic review and meta-analysis reported the superiority of HIIT versus MICT in enhancing peak oxygen uptake in CAD patients.

Background. Acute kidney injury (AKI) is a common complication of percutaneous coronary intervention (PCI) that has been associated with high morbidity and mortality in patients with STEMI. Acute tubular damage may be reflected by serum creatinine (Scr) values that do not meet the criteria for AKI. Methods. This analysis included 19,424 patients from the Improving Care for Cardiovascular Disease in China, Acute Coronary Syndrome Project (n = 5,221 (36.8%), patients with a small increase in Scr within 48 h of hospitalization; n = 14,203 patients with no increase in Scr). The primary outcome was the incidence of major adverse cardiovascular events (MACE). Secondary outcomes included the incidence of massive hemorrhage, in-hospital death, atrial fibrillation, heart failure, cardiogenic shock, cardiac arrest, and stroke. Logistic regression analysis was used to evaluate associations between a small increase in Scr within 48 h of hospitalization (>0.1 to <0.3 mg/dl) and MACE or massive hemorrhage during hospitalization. Results. Patients with a small increase in Scr within 48 h of hospitalization were significantly more likely to experience MACE (11.2% vs. 9.1%; ) or massive hemorrhage (3.2% vs. 2.2%; ) compared to patients with no increase in Scr, but there was no significant difference in in-hospital mortality (0.8% vs. 0.9%; ). Logistic regression analysis showed that a small increase in Scr within 48 h of hospital admission was a risk factor for MACE (OR, 1.168; 95% CI, 1.044–1.306; ) or massive hemorrhage (OR, 1.413; 95% CI, 1.164–1.715; ). Other risk factors included age ˃65 years, history of heart failure, use of glycoprotein IIb/IIIa inhibitors, aspirin or ACEI/ARB, LVEF <40%, Killip class III-IV, and increased SBP and heart rate. Conclusion. A small increase in Scr during hospitalization in patients with STEMI undergoing primary PCI that does not meet the criteria for AKI is a risk factor for in-hospital adverse outcomes. This effect is maintained in patients with normal Scr at hospitalization. Trial Registration. Clinical trial registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT02306616.