Krüger Dietmar, Al Mokhtari Nour Eddine, Wieckhorst Arne, Rausche Tim, Simon-Herrmann Gunhild, Simon Rüdiger
Department of Cardiology, University Hospital Kiel, Germany.
Coron Artery Dis. 2008 Jun;19(4):249-55. doi: 10.1097/MCA.0b013e3283030b4b.
Aim of our study was to evaluate the coronary flow patterns and therapeutic effects of nitroglycerin (NTG) in patients with isolated large coronary artery aneurysms (CA). CA are defined as nonobstructive lesions of the epicardial coronary arteries with a luminal dilation >or=two-fold of the normal diameters. The pathophysiology of a potential coronary insufficiency in this entity is still unknown.
A coronary sinus study with incremental atrial pacing before and after the administration of 0.2 mg NTG was performed in 19 patients with bilateral large fusiform nonstenotic CA to evaluate an exercise-induced myocardial ischemia. The average peak velocity in the aneurysmatic segment of the proximal left anterior descending artery was simultaneously measured by a 14/1000 inch Doppler flow wire. The coronary flow volumes and vascular resistances were calculated.
Evidence of exercise-induced myocardial ischemia was found in all patients presenting with a frank cardiac lactate production (10.2+/-3.3%) which was significantly aggravated by NTG (26.0+/-7.5%, P<0.003). 0.2 mg NTG provoked a long-lasting and significant decrease in coronary flow volume (from 140.2+/-34.2 to 91.2+/-21.8 ml/min, P<0.002), a marked increase in coronary vascular resistance (from 0.62 to 0.92 mmHG x ml/min(-1), P<0.002) and an inadequate increase in coronary flow volume under cardiac pacing.
CA were identified as an entity of nonobstructive ischemic coronary artery disease with an exercise-induced myocardial ischemia and impaired flow volume. NTG exerted an adverse vasoactive effect in CA.
我们研究的目的是评估孤立性大冠状动脉瘤(CA)患者的冠状动脉血流模式以及硝酸甘油(NTG)的治疗效果。CA被定义为心外膜冠状动脉的非阻塞性病变,管腔直径扩张至正常直径的两倍或以上。该实体中潜在冠状动脉供血不足的病理生理学仍不清楚。
对19例双侧大梭形非狭窄性CA患者进行冠状动脉窦研究,在给予0.2mg NTG前后进行递增性心房起搏,以评估运动诱发的心肌缺血。同时用14/1000英寸多普勒血流导线测量左前降支近端动脉瘤段的平均峰值速度。计算冠状动脉血流量和血管阻力。
所有出现明显心脏乳酸生成(10.2±3.3%)的患者均有运动诱发心肌缺血的证据,NTG使其显著加重(26.0±7.5%,P<0.003)。0.2mg NTG引起冠状动脉血流量持续显著下降(从140.2±34.2降至91.2±21.8ml/min, P<0.002),冠状动脉血管阻力显著增加(从0.62增至0.92mmHg×ml/min(-1),P<0.002),且在心脏起搏时冠状动脉血流量增加不足。
CA被确定为一种非阻塞性缺血性冠状动脉疾病实体,伴有运动诱发的心肌缺血和血流量受损。NTG在CA中发挥了不良血管活性作用。