Klein R M, Schwartzkopff B, Strauer B E
Department of Medicine, Division of Cardiology, Heinrich Heine University of Düsseldorf, Germany.
Am Heart J. 1998 Sep;136(3):389-97. doi: 10.1016/s0002-8703(98)70211-x.
Recent reports indicate that myocarditis can be associated with acute myocardial ischemia and even myocardial infarction in patients with normal arteriograms. We therefore tested the hypothesis that patients with biopsy-proven myocarditis have endothelial dysfunction despite angiographically smooth epicardial coronary arteries.
Graded concentrations of the endothelium-dependent vasodilator acetylcholine (10(-6) to 10(-4) mol/L) and for comparison, the non-endothelium-dependent vasodilator nitroglycerin (0.3 mg intracoronary), were infused into the left coronary arteries of 18 patients (mean age 47+/-9 years, 8 women and 10 men) with biopsy-proven myocarditis but without angiographically demonstrable coronary artery disease. Vascular responses were analyzed by quantitative coronary angiography. Three patients had an intact vasodilator response to acetylcholine concentrations of up to 10(-4) mol/L in all segments of the left coronary artery, with a mean dilatation of +9.9%+/-2%. In contrast, paradoxical constriction by acetylcholine occurred in 9 patients, who showed a mean change in coronary artery diameter of - 11%+/-3%. Six patients had no significant change in any segments in response to acetylcholine (-2.5%+/-4%). There was a significant inverse correlation between the number of T-lymphocytes in the myocardium and the response of the epicardial coronary arteries to acetylcholine (Pearson correlation coefficient -0.49, P=.03).
It can be assumed that the process of myocarditis is associated with impairment of endothelium-dependent vasodilation in response to acetylcholine in most patients. Vasoconstriction in the presence of acetylcholine in myocarditis is likely to reflect an abnormality of endothelial function. Endothelial dysfunction of coronary arteries may explain the occurrence of myocardial ischemia in patients with myocarditis.
近期报告表明,在动脉造影正常的患者中,心肌炎可能与急性心肌缺血甚至心肌梗死相关。因此,我们检验了这样一个假设:尽管心外膜冠状动脉造影显示正常,但经活检证实为心肌炎的患者存在内皮功能障碍。
将内皮依赖性血管扩张剂乙酰胆碱(浓度从10⁻⁶至10⁻⁴mol/L)以及作为对照的非内皮依赖性血管扩张剂硝酸甘油(冠状动脉内注入0.3mg),分别注入18例经活检证实为心肌炎但冠状动脉造影未显示有冠状动脉疾病的患者(平均年龄47±9岁,8名女性和10名男性)的左冠状动脉。通过定量冠状动脉造影分析血管反应。3例患者对左冠状动脉各节段中浓度高达10⁻⁴mol/L的乙酰胆碱有完整的血管扩张反应,平均扩张幅度为+9.9%±2%。相比之下,9例患者出现乙酰胆碱引起的矛盾性收缩,冠状动脉直径平均变化为-11%±3%。6例患者对乙酰胆碱的反应在任何节段均无显著变化(-2.5%±4%)。心肌中T淋巴细胞数量与心外膜冠状动脉对乙酰胆碱的反应之间存在显著负相关(Pearson相关系数-0.49,P = 0.03)。
可以假定,在大多数患者中,心肌炎的过程与对乙酰胆碱的内皮依赖性血管舒张功能受损有关。心肌炎患者在乙酰胆碱存在时出现的血管收缩可能反映了内皮功能异常。冠状动脉内皮功能障碍可能解释了心肌炎患者心肌缺血的发生。