Coronary microvasculature in the infarct-related territory

The coronary microvasculature in the infarct-related territory refers to the network of pre-arterioles, arterioles, and capillaries within the myocardial region affected by an acute myocardial infarction (AMI) [1]. Despite successful restoration of flow in the epicardial "culprit" artery, this microvascular bed often remains poorly perfused due to microvascular obstruction (MVO) or the "no-reflow" phenomenon [2]. The pathophysiology of this dysfunction includes distal embolization of atherothrombotic debris, endothelial injury, and extrinsic compression by myocardial edema [3]. As a therapeutic target, the microvasculature is addressed using intracoronary vasodilators to reduce resistance and improve myocardial salvage [1,4]. Improving microvascular perfusion is a critical clinical goal, as MVO is a strong independent predictor of adverse left ventricular remodeling and increased mortality [2]. Pharmacological agents such as adenosine and sodium nitroprusside are commonly employed to induce microvascular vasodilation and mitigate the effects of ischemia-reperfusion injury [1,5]. The integrity of this microvascular territory is often assessed using invasive measures like the Index of Microcirculatory Resistance (IMR) or non-invasive imaging like Cardiac Magnetic Resonance (CMR) [2]. References: [1] Heusch G. (2019) Circ Res. [2] Niccoli G, et al. (2016) JACC. [3] Kloner RA. (2011) JACC. [4] Crea F, Camici PG. (2014) NEJM. [5] StatPearls, Adenosine.

Other names

Microvascular obstructionMVONo-reflow phenomenonCoronary microcirculationInfarct-related microvasculature

Pharmacological agents target the microvasculature to induce vasodilation, reduce microvascular resistance, and prevent platelet-mediated obstruction, thereby restoring myocardial tissue perfusion [1,4].