ABSTRACT
Objectives: To explore the impact of coronary atherosclerosis on diastolic function in patients with coronary heart disease. Methods: Present study included 600 patients with suspected coronary heart disease (CHD) admitted to our hospital between September 2014 to August 2017, coronary arteriography(CAG)was performed in all patients. Patients were divided into control group (n=150, CAG negative patients) , atherosclerosis group (n=150 ), and coronary heart disease group (n=300). Echocardiography, CAG, left ventriculography were measured in all patients, left ventricular diastolic function, coronary volume and pressure were compared among groups. Results: Left ventricular end-diastolic volume(LVEDV), left atrial volume index(LAVI) and left ventricular diastolic time constant (T) were significantly higher, while the ratio of early-to-late diastolic velocity (E/A) , the maximal rise velocity of left ventricular pressure (+dp/dtmax) , the maximum decrease velocity of left ventricular pressure (-dp/dtmax), the first third diastolic filling fraction (1/3 FF)and the last third of the diastolic filling fraction (p1/3 FF) were significantly reduced in the coronary atherosclerosis group and the coronary heart disease group as compared to control group (all P<0.05); left ventricular ejection fraction (LVEF) in CHD group was lower than that in control group (P<0.05); incidence of E/A<1.2 was significantly different among the 3 groups (P<0.01). Multivariate logistic regression analysis indicated that Gensini score was an independent risk factor for diastolic dysfunction(OR=1.93, 95%CI:1.31~2.68, P=0.01). The coronary artery end-diastolic volume (CEDV) , the coronary artery end-systolic volume ( CESV) , the maximum decrease velocity of coronary artery pressure (C-dp/dtmax), the maximum rise velocity of coronary artery pressure (C+dp/dtmax) were significantly decreased in the coronary sclerosis group (P<0.05) ; CEDV, CESV, C-dp/dtmax, C+dp/dtmaxwere significantly decreased in the coronary heart disease group (P<0.01) as compared with the control group. Compared with the coronary atherosclerosis group, the CEDV, CESV, C-dp/dtmax, C+dp/dtmaxwere significantly decreased in CHD group (P<0.05). CESV, C-dp/dtmax, C+dp/dtmax in the coronary sclerosis group were significantly decreased (P<0.05), CEDV, CESV, C-dp/dtmax, C+dp/dtmaxin the coronary heart disease group were significantly decreased (P<0.01).Compared with the coronary atherosclerosis group, the CEDV, CESV, C-dp/dtmax, C+dp/dtmaxwere significantly decreased in CHD group (P<0.05). Spearman correlation analysis showed that Gensini score was negatively correlated with C-dp /dtmax(r=-0.43, P<0.01). Conclusions:Diastolic dysfunction is a sensitive index of myocardial ischemia in patients with coronary heart disease. In patients with coronary atherosclerosis, cardiac diastolic dysfunction could be shown in the absence of cardiac systolic dysfunction. The severity of coronary atherosclerosis is positively related to coronary diastolic dysfunction, which may lead to decrease of coronary vascular compliance, thus induce cardiac diastolic dysfunction.
ABSTRACT
OBJECTIVE@#To investigate the protective effect of glucagon-like peptid-1 (GLP-1) against cardiac microvascular endothelial cell (CMECs) injured by high glucose.@*METHODS@#CMECs were isolated and cultured. Superoxide assay kit and dihydroethidine (DHE) staining were used to assess oxidative stress. TUNEL staining and caspase 3 expression were used to assess the apoptosis of CMECs. H89 was used to inhibit cAMP/PKA pathway; fasudil was used to inhibit Rho/ROCK pathway. The protein expressions of Rho, ROCK were examined by Western blot analysis.@*RESULTS@#High glucose increased the production of ROS, the activity of NADPH, the apoptosis rate and the expression level of Rho/ROCK in CMECs, while GLP-1 decreased high glucose-induced ROS production, the NADPH activity and the apoptosis rate and the expression level of Rho/ROCK in CMECs, the difference were statistically significant (P<0.05).@*CONCLUSIONS@#GLP-1 could protect the cardiac microvessels against oxidative stress and apoptosis. The protective effects of GLP-1 are dependent on downstream inhibition of Rho through a cAMP/PKA-dependent manner, resulting in a subsequent decrease in the expression of NADPH oxidase.
ABSTRACT
Objective: To investigate the protective effect of glucagon-like peptid-1 (GLP-1) against cardiac microvascular endothelial cell (CMECs) injured by high glucose. Methods: CMECs were isolated and cultured. Superoxide assay kit and dihydroethidine (DHE) staining were used to assess oxidative stress. TUNEL staining and caspase 3 expression were used to assess the apoptosis of CMECs. H89 was used to inhibit cAMP/PKA pathway; fasudil was used to inhibit Rho/ROCK pathway. The protein expressions of Rho, ROCK were examined by Western blot analysis. Results: High glucose increased the production of ROS, the activity of NADPH, the apoptosis rate and the expression level of Rho/ROCK in CMECs, while GLP-1 decreased high glucose-induced ROS production, the NADPH activity and the apoptosis rate and the expression level of Rho/ROCK in CMECs, the difference were statistically significant (. P<0.05). Conclusions: GLP-1 could protect the cardiac microvessels against oxidative stress and apoptosis. The protective effects of GLP-1 are dependent on downstream inhibition of Rho through a cAMP/PKA-dependent manner, resulting in a subsequent decrease in the expression of NADPH oxidase.