The impact of MicroRNA-155 on the effect of cryoablation in paroxysmal atrial fibrillation.

Elevated plasma MicroRNA-155 (miR-155) levels are strongly associated with cardiac fibrosis and chronic inflammation processes. However, the relationship between miR-155 and paroxysmal atrial fibrillation (PAF) recurrence following cryoablation remains poorly explored. We aimed to evaluate whether elevated miR-155 is related to long-term AF recurrence following cryoablation. Preoperative miR-155 levels were determined in PAF patients undergoing initial cryoablation. Multivariate-adjusted Cox models were constructed to determine the relationship between miR-155 levels and PAF recurrence. Multivariate logistic regression analyses were performed to determine predictors of PAF recurrence.  Of the 66 enrolled patients, 13 patients (19.7%) had recurrence at the 12-month following-up. These patients had significantly higher baseline miR-155 levels than those without PAF recurrence ((AAA ± BBB) vs. (AAA ± BBB), P < 0.05). The study results showed that miR-155 expression levels were significantly higher in the experimental group than in the control group. Additionally, logistic regression analysis revealed that miR-155 expression was positively correlated with PAF recurrence after cryoablation. Elevated preoperative miR-155 levels are related to a higher risk of AF recurrence and can independently predict AF recurrence following cryoablation.

Regulator of G-protein signaling 5 protects cardiomyocytes against apoptosis during in vitro cardiac ischemia-reperfusion in mice by inhibiting both JNK1/2 and P38 signaling pathways.

Ischemic heart disease is one of the most common diseases in modern society. Ischemic myocardium can be salvaged by vascular recanalization therapy, but its benefit is attenuated by injury that can occur during reperfusion. And apoptotic cell death plays an important part in myocardial ischemia-reperfusion (IR) injury. Regulator of G-protein signaling 5 (RGS5), highly expressed in different cell types of the human adult heart, is a guanosine triphosphatase-activating protein to inhibit many signaling pathways such as c-Jun NH2-terminal kinase 1/2 (JNK1/2) and p38 which promote cardiac IR-induced apoptosis. However the role of RGS5 in cardiac IR-induced apoptosis remains unclear. An in vitro IR model was applied to the isolated hearts of wild type mice (WT), RGS5-transgenic mice (TG), and RGS5-knockout mice (KO). Our results revealed that compared with either WT or KO mice, TG mice showed inhibition of cardiomyocyte apoptosis as indicated by a greater increase of B cell lymphoma/lewkmia-2 (Bcl-2), and an obvious reduction in the positive expression of the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), Bcl-2 Associated X protein (Bax), and active caspase-3. Moreover, the inhibition of both JNK1/2 and p38 signaling markedly reversed IR-induced cardiomyocyte apoptosis in RGS5-KO mice. These studies show that RGS5 protects cardiomyocytes against apoptosis during IR through inhibiting both JNK1/2 and p38 signaling pathways.

Association Between Dietary Inflammatory Index and Heart Failure: Results From NHANES (1999-2018).

Objective: To explore the relationship between dietary inflammatory index (DII) and heart failure (HF) in participants with cardiovascular and cerebrovascular diseases. Methods: NHANES (1998-2018) data were collected and used to assess the association of HF with DII. Twenty-four-hour dietary consumptions were used to calculate the scores of DII. Demographic characteristics and physical and laboratory examinations were collected for the comparison between HF and non-HF groups. Logistic regression analysis and random forest analysis were performed to calculate the odds rate and determine the potential beneficial dietary components in HF. Results: A total of 19,067 cardiac-cerebral vascular disease participants were categorized as HF (n = 1,382; 7.25%) and non-HF (n = 17,685; 92.75%) groups. Heart failure participants had higher levels of DII score compared with those in the non-HF group (0.239 ± 1.702 vs. -0.145 ± 1.704, p < 0.001). Compared with individuals with T1 (DII: -3.884 to -0.570) of DII, those in T3 (DII: 1.019 to 4.598) had a higher level of total cholesterol (4.49 ± 1.16 vs. 4.75 ± 1.28 mmol/L, p < 0.01), globulin (29.92 ± 5.37 vs. 31.29 ± 5.84 g/L, p < 0.001), and pulse rate (69.90 ± 12.22 vs. 72.22 ± 12.77, p < 0.001) and lower levels of albumin (40.76 ± 3.52 vs. 39.86 ± 3.83 g/L, p < 0.001), hemoglobin (13.76 ± 1.65 vs. 13.46 ± 1.77 g/dl, p < 0.05), and hematocrit (40.83 ± 4.69 vs. 40.17 ± 5.01%, p < 0.05). The odds rates of HF for DII from the logistic regression were 1.140, 1.158, and 1.110 in models 1, 2, and 3, respectively. In addition, from the results of random forest analysis, dietary magnesium, fiber, and beta carotene may be essential in HF. Conclusion: Dietary inflammatory index was positively associated with HF in US adults, and dietary intervention might be a promising method in the therapy of HF.

The relationship of MicroRNA-21 and plaque stability in acute coronary syndrome.

Acute coronary syndrome (ACS) leads to clinical symptoms such as chest pain, dyspnea, and arrhythmia. The occurrence of ACS is mainly related to the vulnerable plaques in the coronary arteries. MicroRNA-21 (miR-21) is widely expressed in cardiovascular disease and considered as a marker of myocardial infarction, but its role in vulnerable atherosclerotic plaque of ACS is poorly studied. The cases of ACS and control group were selected in 2 years. Our results revealed that miR-21 was highly positively correlated with the maximum lipid core area, the number of diseased vessels, the number of macrophages, the number of vulnerable plaques, and negatively correlated with the thickness of fiber caps. In the high expression group, the number of coronary artery lesions, the number of vulnerable plaques, the core area of lipid pools and the number of macrophages were significantly higher than those in the low expression group and the middle expression group. But the high expression group of the thickness of the fiber cap was significantly lower than that of the low expression group and the medium expression group. These studies show that miR-21 is an important factor leading to vulnerable plaque instability in ACS, and it can be a predictor of acute adverse events in coronary heart disease.

MiR-155 Knockout in Fibroblasts Improves Cardiac Remodeling by Targeting Tumor Protein p53-Inducible Nuclear Protein 1.

Cardiac remodeling caused by acute myocardial infarction (AMI) represents a major challenge for heart failure research. MiR-155 has been identified as a key mediator of cardiac inflammation and hypertrophy. In this study, we investigate the role of miR-155 in cardiac remodeling induced by AMI. We demonstrate that miR-155 expressed in cardiac fibroblasts is a potent contributor to cardiac remodeling. We reveal that in vivo, miR-155 knockout improves left ventricular function, reduces infarct size, and attenuates collagen deposition, whereas overexpression of miR-155 produces the opposite effects. MiR-155 knockout also inhibits cardiac fibroblast proliferation and differentiation into myofibroblasts. In addition, downregulation of tumor protein p53-inducible nuclear protein 1 (TP53INP1) by small interfering RNA reverses the effects of miR-155 knockout on cardiac fibroblasts. Our data reveal that knockout of miR-155 in cardiac fibroblasts improves cardiac remodeling by targeting TP53INP1, which may be a novel treatment strategy for cardiac remodeling.

Comparison of efficacy of different treatments for pulmonary embolism.

An optimal therapy for pulmonary embolism (PE) was explored by comparing three different methods in order to alleviate the sufferings of PE patients and reduce the mortality. Eighty patients with PE diagnosed by computed tomography angiography (CTA) were treated with thrombolysis, anticoagulation only, or surgery/intervention. The clinical efficacy of different treatments were compared and analyzed. Twenty-four out of the 26 patients (92%) in anticoagulation only group showed improvement in CTA and clinical presentations, which was significantly higher than that in the thrombolysis group (87%, n=39, P<0.05). However, there was no significant difference in the rate of mortality between thrombolysis group and anticoagulation only group. In the surgery/interventional group (n=15), the success rate was 47%, and the mortality rate was 14%. Both of them were significantly different from those in thrombolysis and anticoagulation only groups (both P<0.05). Log-rank analysis of the data of 5-year follow-up revealed that the survival time in surgery/intervention group was significantly shorter than in the other two groups (P<0.05). It was suggested that it is of importance to choose the appropriate therapeutic regimen for PE patients. Mortality may be reduced and prognosis may be improved with anticoagulation only and thrombolysis therapy.