摘要
Background Coronary endothelial shear stress （ESS） triggered the development of atherosclerosis. However, the effect of calcium channel antagonist on the distribution of ESS remained unclear. Methods Twenty consecutive patients with acute coronary syndrome （ACS） 48 hours after maximal medication with single left anterior descending artery stenosis 〈50% were studied. Nicardipine was intravenously injected at 1 μg/kg after a bolus of 10 mg in order to achieve mean blood pressure （MBP） reduced by 10% or more, or the heart rate increased by 10-15 beats/min. Hemodynamic variables and angiogram at baseline and during injection of nicardipine were recorded, respectively. Coronary artery 3-D reconstruction was used for the analysis of ESS. Results Distal reference-vessel-diameter and minimal lumen diameter decreased significantly from （2.42±0.41） mm and （1.47±0.49） mm at baseline to （2.22±0.35） mm and （1.35±0.49） mm at maximal drug-dosage （P=0.018 and 0.020, respectively）. Nicardipine did not change blood velocity. Lowest mean shear stress at segments 2-mm distal to plaque increased significantly from （0.034±0.519） Pa at baseline to （0.603±0.728） Pa （P=0.013） at peak effect of drug. Conclusions Nicardipine was associated with the constriction of diseased vessel segment that adapted to the reduction of blood pressure, without dynamic change of blood velocity at each stage of whole cardiac cycle. Increased ESS value at segments distal to plaque reflected the cardioprotection by nicardipine （ChiCTR-TRC-10000964）.
Background Coronary endothelial shear stress （ESS） triggered the development of atherosclerosis. However, the effect of calcium channel antagonist on the distribution of ESS remained unclear. Methods Twenty consecutive patients with acute coronary syndrome （ACS） 48 hours after maximal medication with single left anterior descending artery stenosis 〈50% were studied. Nicardipine was intravenously injected at 1 μg/kg after a bolus of 10 mg in order to achieve mean blood pressure （MBP） reduced by 10% or more, or the heart rate increased by 10-15 beats/min. Hemodynamic variables and angiogram at baseline and during injection of nicardipine were recorded, respectively. Coronary artery 3-D reconstruction was used for the analysis of ESS. Results Distal reference-vessel-diameter and minimal lumen diameter decreased significantly from （2.42±0.41） mm and （1.47±0.49） mm at baseline to （2.22±0.35） mm and （1.35±0.49） mm at maximal drug-dosage （P=0.018 and 0.020, respectively）. Nicardipine did not change blood velocity. Lowest mean shear stress at segments 2-mm distal to plaque increased significantly from （0.034±0.519） Pa at baseline to （0.603±0.728） Pa （P=0.013） at peak effect of drug. Conclusions Nicardipine was associated with the constriction of diseased vessel segment that adapted to the reduction of blood pressure, without dynamic change of blood velocity at each stage of whole cardiac cycle. Increased ESS value at segments distal to plaque reflected the cardioprotection by nicardipine （ChiCTR-TRC-10000964）.
