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Reappraisal of Ischemic Heart Disease: Fundamental Role of Coronary Microvascular Dysfunction in the Pathogenesis of Angina Pectoris

机译:缺血性心脏病重新评估:冠状动脉微血管功能障碍在心绞痛发病机制中的基本作用

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In recent years, it has become apparent that coronary microvascular dysfunction plays a pivotal pathogenic role in angina pectoris. Functional and structural mechanisms can affect the physiological function of the coronary microvasculature and lead to myocardial ischemia in people without coronary atheromatous disease and also in individuals with obstructive coronary artery disease. Abnormal dilatory responses of the coronary microvessels, coronary microvascular spasm, and extravascular compressive forces have been identified as pathogenic mechanisms in both chronic and acute forms of ischemic heart disease. The condition characterized by anginal symptoms and evidence of myocardial ischemia triggered by coronary microvascular dysfunction, in the absence of obstructive coronary disease, is known as microvascular angina. The concept of microvascular angina, however, may extend further to include patients with obstructive coronary artery disease and individuals with angina after coronary revascularization or heart transplantation because coronary microvascular dysfunction contributes to myocardial ischemia in many such patients. Patients with microvascular angina constitute a sizeable proportion of all cases of stable angina undergoing diagnostic coronary angiography and of those with persisting angina after successful coronary revascularization. Coronary microvascular dysfunction is also often responsible for angina in individuals with cardiomyopathy and heart valve disease as well as acute coronary syndrome cases such as Takotsubo syndrome and myocardial infarction with no obstructive coronary artery disease. Patients with stable microvascular angina present typically with effort or rest chest pain and a reduced coronary flow reserve or microvascular spasm. This condition, which affects women and men, can markedly impair quality of life and prognosis and represents a substantial cost burden to healthcare systems and individuals alike. In recent years, progress in the diagnosis of myocardial ischemia and the use of tests to investigate functional and structural causes for a reduced coronary flow reserve and microvascular spasm have allowed the identification of an increased number of cases of microvascular angina in everyday clinical practice. Although some of the available anti-anginal drugs may be helpful, treatment of coronary microvascular dysfunction remains a major challenge. The present article discusses the fundamental role that coronary microvascular dysfunction plays in the pathogenesis of ischemic heart disease, the clinical characteristics of patients presenting with microvascular angina, and possible diagnostic and therapeutic strategies.
机译:近年来,显而易见的是,冠状动脉微血管功能障碍在心绞痛中发挥枢轴病原作用。功能性和结构机制可以影响冠状动脉微血管生理的生理功能,导致没有冠状动脉疾病的人的心肌缺血,并且在具有阻塞性冠状动脉疾病的个体中。冠状动脉微血管,冠状动脉微血管痉挛和血管外压缩力的异常膨胀反应已被鉴定为缺血性心脏病的慢性和急性形式的致病机制。在没有阻塞性冠状病的情况下,冠状动脉微血管功能障碍引发的角度症状和心肌缺血的证据表征的病症被称为微血管心绞痛。然而,微血管心绞痛的概念可能进一步扩展,包括冠状动脉血运重建或心脏移植后患有阻塞性冠状动脉疾病和患有心绞痛的个体的患者,因为冠状动脉微血管功能障碍有助于许多此类患者的心肌缺血。微血管心绞痛患者构成了所有稳定心绞痛诊断冠状动脉造影和冠状动脉血运重建后持久性心绞痛的患者的大量比例。冠状动脉微血管功能障碍通常也负责心肌病和心脏瓣膜病的个体心绞痛以及急性冠状动脉综合征病例,如TAGOSUBO综合征和心肌梗死,没有阻塞性冠状动脉疾病。患有稳定的微血管心绞痛的患者通常具有努力或静止胸部疼痛和降低的冠状动脉流量储备或微血管痉挛。这种影响妇女和男性的条件,可以显着损害生活质量和预后,并代表了医疗保健系统和个人的大量成本负担。近年来,在心肌缺血的诊断和使用试验中探讨了冠状动脉流量储备和微血管痉挛的使用和结构原因的进展使鉴定日常临床实践中的微血管心绞痛患者数量增加。虽然一些可用的抗角虫药物可能有用,但冠状动脉微血管功能障碍的治疗仍然是一个重大挑战。本文讨论了冠状动脉血管功能障碍在缺血性心脏病发病机制中发挥的基本作用,患有微血管心绞痛的患者的临床特征,以及可能的诊断和治疗策略。

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