The BHF Centre of Excellence and the NIHR Biomedical Research Centre at the School of Cardiovascular Medicine and Sciences, King's College London, London, UK.
Curr Opin Cardiol. 2020 Nov;35(6):720-725. doi: 10.1097/HCO.0000000000000788.
Nearly one-third of patients presenting with angina have unobstructed epicardial coronary arteries and evidence of coronary microvascular disease. Up until recently, the pathophysiology of coronary microvascular disease has been poorly understood, resulting in limited effective therapeutic options in these patients. As a result, patients with coronary microvascular disease continue to suffer from a poor quality of life and adverse cardiovascular outcomes.
Recent mechanistic studies have improved our understanding of the pathophysiology underlying coronary microvascular dysfunction; these studies have implicated the nitric oxide and endothelin pathways as the main drivers. The aim of this article is to review our current understanding of the pathophysiology of ischaemia in patients with coronary microvascular disease.
Patients with angina who have coronary microvascular disease, but no obstructive coronary artery disease, are unable to augment their coronary blood flow in response to physiological stress, thereby predisposing them to myocardial ischaemia as a result of supply:demand mismatch in the myocardium. In addition to abnormalities of vascular resistance, perturbations in cardiac-coronary coupling also contribute to ischaemia in these patients. Although impaired flow reserve is the diagnostic hallmark, mechanistic studies have demonstrated that the underlying pathophysiology is heterogeneous. At present, two main endotypes have been identified, which can be readily differentiated on the basis of minimal microvascular resistance. A better understanding of the pathophysiology and mechanisms driving ischaemia in coronary microvascular dysfunction may stimulate the development of individualised therapies that may lead to an improvement in patients' quality of life and prognosis.
约三分之一的心绞痛患者存在无阻塞性的冠状动脉心外膜和冠状动脉微血管疾病的证据。直到最近，冠状动脉微血管疾病的病理生理学仍未被充分理解，导致这些患者的有效治疗选择有限。因此，患有冠状动脉微血管疾病的患者仍然生活质量较差，心血管不良结局风险较高。
最近的机制研究提高了我们对冠状动脉微血管功能障碍基础病理生理学的理解；这些研究表明，一氧化氮和内皮素途径是主要的驱动因素。本文的目的是回顾我们目前对冠状动脉微血管疾病患者缺血病理生理学的理解。
有冠状动脉微血管疾病但无阻塞性冠状动脉疾病的心绞痛患者无法在生理应激时增加冠状动脉血流，从而导致心肌缺血，因为心肌中的供需不匹配。除了血管阻力异常外，心脏-冠状动脉偶联的改变也会导致这些患者发生缺血。尽管血流储备受损是诊断的标志，但机制研究表明，潜在的病理生理学是异质的。目前，已经确定了两种主要的内型，根据最小的微血管阻力可以很容易地进行区分。对冠状动脉微血管功能障碍导致缺血的病理生理学和机制的更好理解，可能会刺激个体化治疗的发展，从而提高患者的生活质量和预后。
