Pupita G, Maseri A, Kaski J C, Galassi A R, Gavrielides S, Davies G, Crea F
Cardiovascular Unit, Royal Postgraduate Medical School, Hammersmith Hospital, London, United Kingdom.
N Engl J Med. 1990 Aug 23;323(8):514-20. doi: 10.1056/NEJM199008233230804.
In patients with stable coronary artery disease, the ischemic threshold for the production of effort-related angina is often quite variable. Although this feature is commonly attributed to changes in the caliber of coronary arteries at the site of stenosis, it could also be caused by the constriction of distal vessels, collateral vessels, or both.
In order to test this hypothesis, we studied 11 patients with stable angina, total occlusion of a single coronary artery that was supplied by collateral vessels, normal ventricular function, no evidence of coronary-artery spasm, and no other coronary stenoses. These conditions precluded the modulation of coronary flow by vasomotion at the site of the coronary stenosis.
The ischemic threshold--assessed by multiplying the heart rate by the systolic blood pressure at a 1-mm depression of the ST segment during exercise testing--increased by 19 percent after the administration of nitroglycerin (P less than 0.05) and decreased by 18 percent after the administration of ergonovine (P less than 0.01). Ambulatory electrocardiographic monitoring of the patients when not receiving treatment detected 73 ischemic episodes that, in keeping with the history, showed variations of 25 to 52 beats per minute in the heart rate at a 1-mm depression of the ST segment; 12 episodes of sinus tachycardia exceeded the lowest ischemic heart rate by a mean (+/- SD) of 22 +/- 13 beats per minute without ST-segment depression. Furthermore, 21 ischemic episodes occurred at a heart rate more than 25 beats per minute below that at a 1-mm depression of the ST segment during exercise testing. Delayed and reduced filling of collateral and collateralized vessels associated with depression of the ST segment similar to that observed during ambulatory monitoring was detected on angiographic evaluation after the intracoronary administration of ergonovine in three patients.
We propose that the constriction of distal coronary arteries, collateral vessels, or both may cause myocardial ischemia in patients with chronic stable angina.
在稳定型冠状动脉疾病患者中，与运动相关的心绞痛产生的缺血阈值通常变化很大。虽然这一特征通常归因于狭窄部位冠状动脉管径的改变，但也可能是由远端血管、侧支血管或两者的收缩引起的。
为了验证这一假设，我们研究了11例稳定型心绞痛患者，这些患者单支冠状动脉完全闭塞且有侧支血管供血，心室功能正常，无冠状动脉痉挛证据，也无其他冠状动脉狭窄。这些情况排除了冠状动脉狭窄部位血管运动对冠状动脉血流的调节作用。
通过运动试验中ST段压低1 mm时的心率乘以收缩压来评估缺血阈值，在给予硝酸甘油后缺血阈值升高了19%（P<0.05），给予麦角新碱后降低了18%（P<0.01）。在未接受治疗时对患者进行动态心电图监测发现73次缺血发作，与病史一致，ST段压低1 mm时心率每分钟变化25至52次；12次窦性心动过速发作时，平均（±标准差）心率超过最低缺血心率22±13次/分钟，且无ST段压低。此外，21次缺血发作时的心率比运动试验中ST段压低1 mm时的心率低25次/分钟以上。在3例患者冠状动脉内注射麦角新碱后进行血管造影评估，发现侧支血管和侧支供血血管的充盈延迟和减少，伴有类似于动态监测中观察到的ST段压低。
我们提出，远端冠状动脉、侧支血管或两者的收缩可能导致慢性稳定型心绞痛患者发生心肌缺血。
