Objective:Dysfunction of cardiac autonomic nerve system is considered as one of risk factors for coronary atherosclerotic heart disease. Heart rate variability (HRV) has been used to study the correlation between damage of coronary artery and dysfunction of autonomic nervous system. We hypothesize the correlation between damage of coronary artery and dysfunction of autonomic nervous system by HRV among subjects with stable angina.Methods:A 236 subjects who diagnosed as stable angina pectoris by elective coronary angiography, were divided into two groups by Gensini score system (GS):GS≤32 (GS1) and GS2>32 (GS2). Subgroups were divided based on location of stenosis lesions and the number of coronary artery disease. 86 subjects suspicious with stable angina pectoris with normal coronary angiography were selected as the control group. All subjects were received 24-hour ambulatory electrocardiogram and the result of time-domain HRV was analyzed (SDNN, SDANN, SDNNind, RMSSD, PNN50).Results:Compared with control group, SDNN, SDNNind and RMSSD lower in GS1, and SDNN, SDANN, SDNNind, RMSSD, PNN50 lower in GS2; ccompared with GS1, SDNN was lower in GS2. Compared with control group, SDNN in one-vessel, SDNN, SDANN in two-vessel diseased and in three-vessel diseased were lower, and compared with two-vessel diseased, SDNN, SDANN lower in three-vessel diseased. Compared with right-coronary artery diseased, SDNN and SDANN in left-coronary artery diseased group were lower, while compared with lesions in left circumflex, SDNN in lesions in left anterior descending artery lower.Conclusion:HRV may be play a crucial role in estimating the correlation between damage of coronary artery and dysfunction of autonomic nerve system.

The outcome of patients with acute type B aortic dissection (BAAD) is largely dictated by whether or not the case is “complicated.” The purpose of this study was to investigate the risk factors leading to in-hospital death among patients with BAAD and then to develop a predictive model to estimate individual risk of in-hospital death. A total of 188 patients with BAAD were enrolled. Risk factors for in-hospital death were investigated with univariate and multivariable logistic regression analysis. Significant risk factors were used to develop a predictive model. The in-hospital mortality rate was 9% (17 of 188 patients). Univariate analysis revealed 7 risk factors to be statistically significant predictors of in-hospital death ( P < .1). In multivariable analysis, the following variables at admission were independently associated with increased in-hospital mortality: hypotension (odds ratio [OR], 4.85; 95% confidence interval [CI], 1.12–18.90; P = .04), ischemic complications (OR, 8.24; 95% CI, 1.25–33.85; P < .001), renal dysfunction (OR, 12.32; 95% CI, 10.63–76.66; P < .001), and neutrophil percentage ≥80% (OR, 5.76; 95% CI, 2.58–12.56; P = .03). Based on these multivariable results, a reliable and simple prediction model was developed, a total score of 4 offered the best point value. Independent risk factors associated with in-hospital death can be predicted in BAAD patients. The prediction model could be used to identify the prognosis for BAAD patients and assist physicians in their choice of management.

Hyperactivity of the sympathetic nervous system is a major driver of cardiac remodeling, exerting its effects through both α-, and β-adrenoceptors (α-, β-ARs). As the relative contribution of subtype α1-AR to cardiac stress responses remains poorly investigated, we subjected mice to either subcutaneous perfusion with the β-AR agonist isoprenaline (ISO, 30 mg/kg × day) or to a combination of ISO and the stable α1-AR agonist phenylephrine (ISO/PE, 30 mg/kg × day each). Telemetry analysis revealed similar hemodynamic responses under both ISO and ISO/PE treatment i.e., permanently increased heart rates and only transient decreases in mean blood pressure during the first 24 h. Echocardiography and single cell analysis after 1 week of exposure showed that ISO/PE-, but not ISO-treated animals established α1-AR-mediated inotropic responsiveness to acute adrenergic stimulation. Morphologically, additional PE perfusion limited concentric cardiomyocyte growth and enhanced cardiac collagen deposition during 7 days of treatment. Time-course analysis demonstrated a diverging development in transcriptional patterns at day 4 of treatment i.e., increased expression of selected marker genes Xirp2, Nppa, Tgfb1, Col1a1, Postn under chronic ISO/PE treatment which was either less pronounced or absent in the ISO group. Transcriptome analyses at day 4 via RNA sequencing demonstrated that additional PE treatment caused a marked upregulation of genes allocated to extracellular matrix and fiber organization along with a more pronounced downregulation of genes involved in metabolic processes, muscle adaptation and cardiac electrophysiology. Consistently, transcriptome changes under ISO/PE challenge more effectively recapitulated early transcriptional alterations in pressure overload-induced experimental heart failure and in human hypertrophic cardiomyopathy.