Objectives To evaluate the association of coronary artery endothelial function and plasma levels of low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) in patients with Type 2 ...Objectives To evaluate the association of coronary artery endothelial function and plasma levels of low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) in patients with Type 2 Diabetes Mellitus (DM). Methods We investigated 90 participants from our institution between October 2007 to March 2010: non-DM(n = 60) and DM(n = 30). As an indicator of coronary endothelial dysfunction, we used non-invasive Doppler echocardiography to quantify coronary flow velocity reserve (CFVR) in the distal part of the left descending artery after rest and after intravenous adenosine administration. Results Plasma level of LDL-C was significantly higher in patients with DM than in non-DM (3.21 ±0.64 vs. 2.86 ±0.72 mmo/L, P < 0.05), but HDL-C level did not differ between the groups (1.01 ±0.17 vs. 1.05 ±0.19 mmo/L). Furthermore, the CFVR value was lower inDMpatients than non-diabetics (2.45 ±0.62 vs. 2.98 ±0.68, P < 0.001). Plasma levels of LDL-C were negatively correlated with CFVR in all subjects (r = ��0.35, P < 0.001; 95% confidence interval (CI): ��0.52 –��0.15) and in the non-DM(r = ��0.29, P < 0.05; 95% CI: ��0.51–��0.05), with an even stronger negative correlation in the DM group (r = ��0.42, P < 0.05; 95%CI: ��0.68 –��0.06). Age (β= ��0.019, s = 0.007, sβ= ��0.435, 95% CI: ��0.033 –��0.005, P = 0.008), LDL-C (β= ��0.217, s = 0.105, sβ= ��0.282, 95% CI: ��0.428 –��0.005, P = 0.045) remained independently correlated with CFVR in the DM group. However, we found no correlation between HDL-C level and CFVR in any group. Conclusions Diabetes may contribute to coronary artery disease (CAD) by inducing dysfunction of the coronary artery endothelium. Increased LDL-C level may adversely impair coronary endothelial function in DM. HDL-C may lose its endothelial-protective effects, in part as a result of pathological conditions, especially under abnormal glucose metabolism.展开更多
Background： Pressure overload-induced myocardial hypertrophy is a key step leading to heart failure. Previous cellular and animal studies demonstrated that deteriorated excitation-contraction coupling occurs as early...Background： Pressure overload-induced myocardial hypertrophy is a key step leading to heart failure. Previous cellular and animal studies demonstrated that deteriorated excitation-contraction coupling occurs as early as the compensated stage of hypertrophy before the global decrease in left ventricular ejection fraction （LVEF）. This study was to evaluate the cardiac electromechanical coupling time in evaluating cardiac systolic function in the early stage of heart failure. Methods： Twenty-six patients with Stage B heart failure （SBHF） and 31 healthy controls （CONs） were enrolled in this study. M-mode echocardiography was performed to measure LVEF. Tissue Doppler imaging （TDI） combined with electrocardiography （ECG） was used to measure cardiac electromechanical coupling time. Results： There was no significant difference in LVEF between SBHF patients and CONs （64.23 ± 8.91% vs. 64.52 ± 5.90%; P= 0.886）. However, all four electromechanical coupling time courses （Qsb： onset of Q wave on ECG to beginning of S wave on TDI, Qst： onset of Q wave on ECG to top of S wave on TDI, Rsb： top of R wave on ECG to beginning orS wave on TDI, and Rst： top of R wave on ECG to top orS wave on TDI） of SBHF patients were significantly longer than those of CONs （Qsb： 119.19 ± 35.68 ms vs. 80.30 ± 14.81 ms, P 〈 0.001 ; Qst： 165.42 ± 60.93 ms vs. 129.04 ± 16.97 ms, P = 0.006; Rsb： 82.43 ± 33.66 ms vs. 48.30 ± 15.18 ms, P 〈 0.001; and Rst： 122.37 ± 36.66 ins vs. 93.25 ± 16.72 ms, P = 0.001 ）, and the Qsb, Rsb, and Rst time showed a significantly higher sensitivity than LVEF （Rst： P =0.032; Rsb： P = 0.003; and Qsb： P = 0.004）. Conclusions： The cardiac electromechanical coupling time is more sensitive than LVEF in evaluating cardiac systolic function.展开更多
基金Acknowledgements This work was supported by the National Natural Sciences Foundation of China （81400177, CHEN SM） and Beijing Natural Science Foundation （7154249, CHEN SM）. The authors have no financial disclosures.
文摘Objectives To evaluate the association of coronary artery endothelial function and plasma levels of low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) in patients with Type 2 Diabetes Mellitus (DM). Methods We investigated 90 participants from our institution between October 2007 to March 2010: non-DM(n = 60) and DM(n = 30). As an indicator of coronary endothelial dysfunction, we used non-invasive Doppler echocardiography to quantify coronary flow velocity reserve (CFVR) in the distal part of the left descending artery after rest and after intravenous adenosine administration. Results Plasma level of LDL-C was significantly higher in patients with DM than in non-DM (3.21 ±0.64 vs. 2.86 ±0.72 mmo/L, P < 0.05), but HDL-C level did not differ between the groups (1.01 ±0.17 vs. 1.05 ±0.19 mmo/L). Furthermore, the CFVR value was lower inDMpatients than non-diabetics (2.45 ±0.62 vs. 2.98 ±0.68, P < 0.001). Plasma levels of LDL-C were negatively correlated with CFVR in all subjects (r = ��0.35, P < 0.001; 95% confidence interval (CI): ��0.52 –��0.15) and in the non-DM(r = ��0.29, P < 0.05; 95% CI: ��0.51–��0.05), with an even stronger negative correlation in the DM group (r = ��0.42, P < 0.05; 95%CI: ��0.68 –��0.06). Age (β= ��0.019, s = 0.007, sβ= ��0.435, 95% CI: ��0.033 –��0.005, P = 0.008), LDL-C (β= ��0.217, s = 0.105, sβ= ��0.282, 95% CI: ��0.428 –��0.005, P = 0.045) remained independently correlated with CFVR in the DM group. However, we found no correlation between HDL-C level and CFVR in any group. Conclusions Diabetes may contribute to coronary artery disease (CAD) by inducing dysfunction of the coronary artery endothelium. Increased LDL-C level may adversely impair coronary endothelial function in DM. HDL-C may lose its endothelial-protective effects, in part as a result of pathological conditions, especially under abnormal glucose metabolism.
基金This study was supported by grants from the National Natural Science Foundation of China （no. 91339105 and no. 81625001） and the Beijing Municipal Science and Technology Commission （no. Z 141100000214006）.
文摘Background： Pressure overload-induced myocardial hypertrophy is a key step leading to heart failure. Previous cellular and animal studies demonstrated that deteriorated excitation-contraction coupling occurs as early as the compensated stage of hypertrophy before the global decrease in left ventricular ejection fraction （LVEF）. This study was to evaluate the cardiac electromechanical coupling time in evaluating cardiac systolic function in the early stage of heart failure. Methods： Twenty-six patients with Stage B heart failure （SBHF） and 31 healthy controls （CONs） were enrolled in this study. M-mode echocardiography was performed to measure LVEF. Tissue Doppler imaging （TDI） combined with electrocardiography （ECG） was used to measure cardiac electromechanical coupling time. Results： There was no significant difference in LVEF between SBHF patients and CONs （64.23 ± 8.91% vs. 64.52 ± 5.90%; P= 0.886）. However, all four electromechanical coupling time courses （Qsb： onset of Q wave on ECG to beginning of S wave on TDI, Qst： onset of Q wave on ECG to top of S wave on TDI, Rsb： top of R wave on ECG to beginning orS wave on TDI, and Rst： top of R wave on ECG to top orS wave on TDI） of SBHF patients were significantly longer than those of CONs （Qsb： 119.19 ± 35.68 ms vs. 80.30 ± 14.81 ms, P 〈 0.001 ; Qst： 165.42 ± 60.93 ms vs. 129.04 ± 16.97 ms, P = 0.006; Rsb： 82.43 ± 33.66 ms vs. 48.30 ± 15.18 ms, P 〈 0.001; and Rst： 122.37 ± 36.66 ins vs. 93.25 ± 16.72 ms, P = 0.001 ）, and the Qsb, Rsb, and Rst time showed a significantly higher sensitivity than LVEF （Rst： P =0.032; Rsb： P = 0.003; and Qsb： P = 0.004）. Conclusions： The cardiac electromechanical coupling time is more sensitive than LVEF in evaluating cardiac systolic function.
