Vejar M, Hackett D, Brunelli C, Spallarossa P, Ianetti M, Galassi A R, Lipkin D, Caponnetto S, Patrono C, Maseri A
Cardiovascular Research Unit Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.
Circulation. 1990 Jan;81(1 Suppl):I4-11; discussion I22-3.
Episodic platelet activation has been shown to occur in unstable angina, and aspirin should have an important therapeutic role in the management of these patients. The response to aspirin alone or to aspirin in combination with vasodilators such as heparin and beta-blockers has been assessed in 41 patients with unstable angina. Therapy was added sequentially in the event of recurrence of transient myocardial ischemia. Patients were randomly assigned to two groups. Group 1 (21 patients) received an intravenous infusion of isosorbide dinitrate and oral diltiazem, and group 2 (20 patients) received intravenous aspirin (60 mg the first day and 20 mg on successive days). This dose of aspirin reduced serum thromboxane B2 from 160 +/- 88 ng/ml (mean +/- SD) to undetectable values (less than 6 ng/ml, p less than 0.01). If episodes of ischemic ST segment shift continued, the therapy of group 1 was added to that of group 2 or vice versa; if further ST segment changes were documented, intravenous heparin and oral beta-blockers were added; if episodes of myocardial ischemia persisted, urgent coronary arteriography and myocardial revascularization were performed. Nine patients in group 1 and six in group 2 (p = 0.8) had no further episodes of myocardial ischemia on their initial therapy; 12 additional patients had no further episodes when taking combined therapy of aspirin and vasodilators. Thus, the administration of aspirin alone was not superior to coronary dilators; 30% of all patients continued to have episodes of myocardial ischemia or had a myocardial infarction develop when heparin and beta-blockers were added. Myocardial infarction occurred in one patient on vasodilator therapy alone, in two on combined therapy, and in two on full therapy. These results suggest that in some patients, the stimulus to coronary thrombosis and vasoconstriction occasionally becomes so strong that it cannot be inhibited by certain antagonist drugs. The unstable tendency to continuation of ischemia or evolution to myocardial infarction is not related to the severity of the persisting stenosis. Those patients not promptly responding to combined therapy immediately from admission should have early coronary angiography and aggressive treatment.
已证实在不稳定型心绞痛中会出现间歇性血小板激活，阿司匹林在这些患者的治疗中应具有重要的治疗作用。对41例不稳定型心绞痛患者评估了单独使用阿司匹林或阿司匹林与血管扩张剂（如肝素和β受体阻滞剂）联合使用的效果。如果短暂性心肌缺血复发，则依次添加治疗方法。患者被随机分为两组。第1组（21例患者）接受静脉输注硝酸异山梨酯和口服地尔硫䓬，第2组（20例患者）接受静脉注射阿司匹林（第1天60mg，随后每天20mg）。该剂量的阿司匹林可使血清血栓素B2从160±88ng/ml（平均值±标准差）降至无法检测的值（小于6ng/ml，p<0.01）。如果缺血性ST段移位发作持续存在，则将第1组的治疗方法添加到第2组，反之亦然；如果记录到进一步的ST段变化，则添加静脉注射肝素和口服β受体阻滞剂；如果心肌缺血发作持续存在，则进行紧急冠状动脉造影和心肌血运重建。第1组9例患者和第2组6例患者（p = 0.8）在初始治疗时没有进一步的心肌缺血发作；另外12例患者在接受阿司匹林和血管扩张剂联合治疗时没有进一步发作。因此，单独使用阿司匹林并不优于冠状动脉扩张剂；当添加肝素和β受体阻滞剂时，所有患者中有30%继续出现心肌缺血发作或发生心肌梗死。仅接受血管扩张剂治疗的1例患者发生心肌梗死，联合治疗的2例患者发生心肌梗死，接受全面治疗的2例患者发生心肌梗死。这些结果表明，在某些患者中，冠状动脉血栓形成和血管收缩的刺激偶尔会变得非常强烈，以至于某些拮抗药物无法抑制。缺血持续或演变为心肌梗死的不稳定倾向与持续狭窄的严重程度无关。那些从入院起就未对联合治疗迅速做出反应的患者应尽早进行冠状动脉造影并积极治疗。
