Objective A novel index based on fi-equency-domain analysis of heart rate variability （HRV） was tested on patients with reduced left ventricular systolic function. This index, namely VHFI, was defined as the very hi...Objective A novel index based on fi-equency-domain analysis of heart rate variability （HRV） was tested on patients with reduced left ventricular systolic function. This index, namely VHFI, was defined as the very high frequency （VHF） component of the power spectrum normalized to represent its relative value in proportion to the total power minus the very low frequency component. Methods Patients （n = 130） were divided into a study group, consisting 66 patients with decreased left ventricular systolic function, and a control group, consisting 64 patients with normal heart structure and function and without severe coronary artery stenosis （〈 50%）. Results VHFI in the study group was significantly higher than that in the control group （19.17 ± 13.35 vs 11.37 ± 10.77, P 〈 0.001）. Cardiac events occurred in 18 patients during follow-up （33.34 i 3.26 months）. Defining the positive test as VHFI =15 and negative test as VHFI 〈15, achieved a sensitivity of 57.58% and a specificity of78.13% for predicting decreased left ventricular systolic function, and achieved a sensitivity of 66.67% and a specificity of 64.29% for predicting cardiac events. Univariate Cox regression analysis showed that positive VHFI test was an independent variable in predictive cardiac events. Conclusions The results suggest that VHFI is a useful tool for quick evaluation of left ventricular systolic function and prediction of prognosis展开更多
Subjective: To observe the effect of electroacupuncture (EA) of acupoints of the Heart Meridian and Lung Meridian on ischemic cardiac systolic ability for analyzing the relative specific relationship between the Heart...Subjective: To observe the effect of electroacupuncture (EA) of acupoints of the Heart Meridian and Lung Meridian on ischemic cardiac systolic ability for analyzing the relative specific relationship between the Heart Meridian and the heart. Methods: Acute myocardial ischemia (AMI) was produced by intravenous infusion of pituitrin (40 u + 5% glucose injection 500 ml, 60 drips/min) in the rabbit. Left intraventricular pressure (LVP), maximal rising velocity of LVP (dp/dt max), isovolumetric pressure (IP) and end-diastolic pressure (EDP) of the left cardiac ventricle were used as the indexes. Three points of Heart Meridian [HM, from 'Shenmen' (HT 7) to 'Lingdao' (HT 4)] and the three points of Lung Meridian [LM, from 'Taiyuan' (LU 9) to 'Lieque' (LU 7)] were punctured with filiform needles and stimulated with hand-manipulation and electrically with ZY2-1 EA Therapeutic Apparatus. 30 rabbits anesthetized with urethane (1 g/kg) were randomly and evenly divided into control group, HM group and LM group. Result-s: The effects of EA of HM points were evidently superior to those of EA of LM points in promoting the recovery of both AMI-induced decrease of LVP and dp/dtmax, and AMI-induced increase of IP and EDP. Conclusion: Acupoints of Heart Meridian has a relatively specific connection with the heart in comparison with those of Lung Meridian; and the Heart Meridian is a functional whole.展开更多
To test the hypothesis that transient nonischemic stimulation of hypertrophy would render the heart resistant to subsequent ischemic stress,short-term transverse aortic constriction(TAC)was performed in mice and then ...To test the hypothesis that transient nonischemic stimulation of hypertrophy would render the heart resistant to subsequent ischemic stress,short-term transverse aortic constriction(TAC)was performed in mice and then withdrawn for several days by aortic debanding,followed by subsequent myocardial exposure to ischemia/reperfusion(I/R).Following I/R injury,the myocardial infarct size and apoptosis were markedly reduced,and contractile function was significantly improved in the TAC preconditioning group compared with the control group.Mechanistically,hypertrophic preconditioning remarkably alleviated I/R-induced oxidative stress,as evidenced by the increased reduced nicotinamide adenine dinucleotide phosphate(NADPH)/nicotinamide adenine dinucleotide phosphate(NADP)ratio,increase in the reduced glutathione(GSH)/oxidized glutathione(GSSH)ratio,and reduced mitochondrial reactive oxygen species(ROS)production.Moreover,TAC preconditioning inhibited caspase-3 activation and mitigated the mitochondrial impairment by deacetylating isocitrate dehydrogenase 2(IDH2)via a sirtuin 3(SIRT3)-dependent mechanism.In addition,the expression of a genetic deacetylation mimetic IDH2 mutant(IDH2 K413R)in cardiomyocytes,which increased IDH2 enzymatic activity and decreased mitochondrial ROS production,and ameliorated I/R injury,whereas the expression of a genetic acetylation mimetic(IDH2 K413Q)in cardiomyocytes abolished these protective effects of hypertrophic preconditioning.Furthermore,both the activity and expression of the SIRT3 protein were markedly increased in preconditioned mice exposed to I/R.Treatment with an adenovirus encoding SIRT3 partially emulated the actions of hypertrophic preconditioning,whereas genetic ablation of SIRT3 in mice blocked the cardioprotective effects of hypertrophic preconditioning.The present study identifies hypertrophic preconditioning as a novel endogenous self-defensive and cardioprotective strategy for cardiac I/R injury that induces IDH2 deacetylation through a SIRT3-dependent mechanism.A therapeutic strategy targeting IDH2 may be a promising treatment for cardiac ischemic injury.展开更多
文摘Objective A novel index based on fi-equency-domain analysis of heart rate variability （HRV） was tested on patients with reduced left ventricular systolic function. This index, namely VHFI, was defined as the very high frequency （VHF） component of the power spectrum normalized to represent its relative value in proportion to the total power minus the very low frequency component. Methods Patients （n = 130） were divided into a study group, consisting 66 patients with decreased left ventricular systolic function, and a control group, consisting 64 patients with normal heart structure and function and without severe coronary artery stenosis （〈 50%）. Results VHFI in the study group was significantly higher than that in the control group （19.17 ± 13.35 vs 11.37 ± 10.77, P 〈 0.001）. Cardiac events occurred in 18 patients during follow-up （33.34 i 3.26 months）. Defining the positive test as VHFI =15 and negative test as VHFI 〈15, achieved a sensitivity of 57.58% and a specificity of78.13% for predicting decreased left ventricular systolic function, and achieved a sensitivity of 66.67% and a specificity of 64.29% for predicting cardiac events. Univariate Cox regression analysis showed that positive VHFI test was an independent variable in predictive cardiac events. Conclusions The results suggest that VHFI is a useful tool for quick evaluation of left ventricular systolic function and prediction of prognosis
基金grants of State Scientific-technological Scale Project
文摘Subjective: To observe the effect of electroacupuncture (EA) of acupoints of the Heart Meridian and Lung Meridian on ischemic cardiac systolic ability for analyzing the relative specific relationship between the Heart Meridian and the heart. Methods: Acute myocardial ischemia (AMI) was produced by intravenous infusion of pituitrin (40 u + 5% glucose injection 500 ml, 60 drips/min) in the rabbit. Left intraventricular pressure (LVP), maximal rising velocity of LVP (dp/dt max), isovolumetric pressure (IP) and end-diastolic pressure (EDP) of the left cardiac ventricle were used as the indexes. Three points of Heart Meridian [HM, from 'Shenmen' (HT 7) to 'Lingdao' (HT 4)] and the three points of Lung Meridian [LM, from 'Taiyuan' (LU 9) to 'Lieque' (LU 7)] were punctured with filiform needles and stimulated with hand-manipulation and electrically with ZY2-1 EA Therapeutic Apparatus. 30 rabbits anesthetized with urethane (1 g/kg) were randomly and evenly divided into control group, HM group and LM group. Result-s: The effects of EA of HM points were evidently superior to those of EA of LM points in promoting the recovery of both AMI-induced decrease of LVP and dp/dtmax, and AMI-induced increase of IP and EDP. Conclusion: Acupoints of Heart Meridian has a relatively specific connection with the heart in comparison with those of Lung Meridian; and the Heart Meridian is a functional whole.
基金supported by the National Natural Science Foundation of China(81870290,81521001,81800235,and 81800238)。
文摘To test the hypothesis that transient nonischemic stimulation of hypertrophy would render the heart resistant to subsequent ischemic stress,short-term transverse aortic constriction(TAC)was performed in mice and then withdrawn for several days by aortic debanding,followed by subsequent myocardial exposure to ischemia/reperfusion(I/R).Following I/R injury,the myocardial infarct size and apoptosis were markedly reduced,and contractile function was significantly improved in the TAC preconditioning group compared with the control group.Mechanistically,hypertrophic preconditioning remarkably alleviated I/R-induced oxidative stress,as evidenced by the increased reduced nicotinamide adenine dinucleotide phosphate(NADPH)/nicotinamide adenine dinucleotide phosphate(NADP)ratio,increase in the reduced glutathione(GSH)/oxidized glutathione(GSSH)ratio,and reduced mitochondrial reactive oxygen species(ROS)production.Moreover,TAC preconditioning inhibited caspase-3 activation and mitigated the mitochondrial impairment by deacetylating isocitrate dehydrogenase 2(IDH2)via a sirtuin 3(SIRT3)-dependent mechanism.In addition,the expression of a genetic deacetylation mimetic IDH2 mutant(IDH2 K413R)in cardiomyocytes,which increased IDH2 enzymatic activity and decreased mitochondrial ROS production,and ameliorated I/R injury,whereas the expression of a genetic acetylation mimetic(IDH2 K413Q)in cardiomyocytes abolished these protective effects of hypertrophic preconditioning.Furthermore,both the activity and expression of the SIRT3 protein were markedly increased in preconditioned mice exposed to I/R.Treatment with an adenovirus encoding SIRT3 partially emulated the actions of hypertrophic preconditioning,whereas genetic ablation of SIRT3 in mice blocked the cardioprotective effects of hypertrophic preconditioning.The present study identifies hypertrophic preconditioning as a novel endogenous self-defensive and cardioprotective strategy for cardiac I/R injury that induces IDH2 deacetylation through a SIRT3-dependent mechanism.A therapeutic strategy targeting IDH2 may be a promising treatment for cardiac ischemic injury.
