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A pathophysiological compass to personalize antianginal drug treatment
Nature Reviews Cardiology ( IF 41.7 ) Pub Date : 2021-07-07 , DOI: 10.1038/s41569-021-00573-w
Edoardo Bertero 1 , Gerd Heusch 2 , Thomas Münzel 3, 4 , Christoph Maack 1, 5
Affiliation  

Myocardial ischaemia results from coronary macrovascular or microvascular dysfunction compromising the supply of oxygen and nutrients to the myocardium. The underlying pathophysiological processes are manifold and encompass atherosclerosis of epicardial coronary arteries, vasospasm of large or small vessels and microvascular dysfunction — the clinical relevance of which is increasingly being appreciated. Myocardial ischaemia can have a broad spectrum of clinical manifestations, together denoted as chronic coronary syndromes. The most common antianginal medications relieve symptoms by eliciting coronary vasodilatation and modulating the determinants of myocardial oxygen consumption, that is, heart rate, myocardial wall stress and ventricular contractility. In addition, cardiac substrate metabolism can be altered to alleviate ischaemia by modulating the efficiency of myocardial oxygen use. Although a universal agreement exists on the prognostic importance of lifestyle interventions and event prevention with aspirin and statin therapy, the optimal antianginal treatment for patients with chronic coronary syndromes is less well defined. The 2019 guidelines of the ESC recommend a personalized approach, in which antianginal medications are tailored towards an individual patient’s comorbidities and haemodynamic profile. Although no antianginal medication improves survival, their efficacy for reducing symptoms profoundly depends on the underlying mechanism of the angina. In this Review, we provide clinicians with a rationale for when to use which compound or combination of drugs on the basis of the pathophysiology of the angina and the mode of action of antianginal medications.



中文翻译:

个性化抗心绞痛药物治疗的病理生理学指南针

心肌缺血是由于冠状动脉大血管或微血管功能障碍损害心肌的氧和营养供应而引起的。潜在的病理生理过程是多方面的,包括心外膜冠状动脉的动脉粥样硬化、大小血管的血管痉挛和微血管功能障碍——其临床相关性越来越受到重视。心肌缺血可具有广泛的临床表现,统称为慢性冠状动脉综合征。最常见的抗心绞痛药物通过引起冠状血管舒张和调节心肌耗氧量的决定因素(即心率、心肌壁应力和心室收缩力)来缓解症状。此外,可以通过调节心肌氧利用效率来改变心脏底物代谢以减轻缺血。尽管阿司匹林和他汀类药物治疗生活方式干预和事件预防的预后重要性存在普遍共识,但慢性冠状动脉综合征患者的最佳抗心绞痛治疗尚不明确。ESC 2019 年指南推荐了一种个性化方法,其中抗心绞痛药物是根据个体患者的合并症和血流动力学特征量身定制的。尽管没有抗心绞痛药物可以提高生存率,但其减轻症状的功效在很大程度上取决于心绞痛的潜在机制。在这篇综述中,我们根据心绞痛的病理生理学和抗心绞痛药物的作用方式,为临床医生提供何时使用哪种化合物或药物组合的基本原理。

更新日期:2021-07-08
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