Purpose of review
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.