Marzilli M
Cardio Thoracic Department, University of Pisa, Italy.
Rev Port Cardiol. 2000 Nov;19 Suppl 5:V25-30.
Patients with Angina Pectoris benefit from therapy with nitrates, beta-blockers, and calcium channel antagonists. All these drugs, through different action mechanisms, tend to reduce cardiac work and restore the balance between myocardial metabolic demand and blood supply. Failure of this conventional haemodynamic treatment in controlling symptoms and preventing ischemia is however frequent, and many such patients are then referred for myocardial revascularization. This scenario has been innovated by Trimetazidine, an anti-ischemic agent that exerts its beneficial effects by increasing cell tolerance to ischemia and improving functional recovery at the time of reperfusion. Compared with classic "hemodynamic" agents, Trimetazidine demonstrated similar efficacy in reducing frequency and severity of ischemic attacks and in increasing exercise tolerance, with a lower incidence of side effects. The adjunct of Trimetazidine to propranolol was found superior to nitrates in reducing ischemic episodes. In angina patients not controlled by CA-antagonists, Trimetazidine lowered the frequency of ischemic attacks and prolonged the time to ischemia during exercise. More recently, Trimetazidine has been shown to improve left ventricular dysfunction in patients with congestive heart failure, and in ischemic patients undergoing PTCA. In chronic coronary artery disease, Trimetazidine improved regional dysfunction at rest and during dobutamine stress echocardiography. Given the metabolic mechanism of action of Trimetazidine, focused on improving energy metabolism and restoring membrane homeostasis, it is expected to especially benefit patients in whom metabolic alteration contribute to the pathogenesis of ischemia, namely diabetic patients. Preliminary data from a multicenter study do support this hypothesis. In conclusion, available data indicate that the cardioprotective effect of Trimetazidine results in improvement of symptoms and preservation of left ventricular function in patients with acute and chronic ischemic syndromes.
心绞痛患者可从硝酸盐、β受体阻滞剂和钙通道拮抗剂治疗中获益。所有这些药物通过不同的作用机制，倾向于减少心脏做功，恢复心肌代谢需求与血液供应之间的平衡。然而，这种传统的血液动力学治疗在控制症状和预防缺血方面常常失败，许多此类患者随后会被转诊进行心肌血运重建。曲美他嗪革新了这种情况，它是一种抗缺血药物，通过增加细胞对缺血的耐受性和改善再灌注时的功能恢复发挥有益作用。与经典的“血液动力学”药物相比，曲美他嗪在减少缺血发作的频率和严重程度以及提高运动耐量方面显示出相似的疗效，且副作用发生率较低。发现曲美他嗪与普萘洛尔联用在减少缺血发作方面优于硝酸盐。在未被钙拮抗剂控制的心绞痛患者中，曲美他嗪降低了缺血发作的频率，并延长了运动时出现缺血的时间。最近，已证明曲美他嗪可改善充血性心力衰竭患者以及接受经皮冠状动脉腔内血管成形术（PTCA）的缺血患者的左心室功能障碍。在慢性冠状动脉疾病中，曲美他嗪改善了静息时以及多巴酚丁胺负荷超声心动图检查期间的局部功能障碍。鉴于曲美他嗪的代谢作用机制专注于改善能量代谢和恢复膜稳态，预计它对代谢改变促成缺血发病机制的患者（即糖尿病患者）尤其有益。一项多中心研究的初步数据确实支持这一假设。总之，现有数据表明曲美他嗪的心脏保护作用可改善急性和慢性缺血综合征患者的症状并保留左心室功能。
