Pathophysiology and diagnosis of coronary microvascular dysfunction in ST-elevation myocardial infarction

Abstract

Early mechanical reperfusion of the epicardial coronary artery by primary percutaneous coronary intervention (PCI) is the guideline-recommended treatment for ST-elevation myocardial infarction (STEMI). Successful restoration of epicardial coronary blood flow can be achieved in over 95% of PCI procedures. However, despite angiographically complete epicardial coronary artery patency, in about half of the patients perfusion to the distal coronary microvasculature is not fully restored, which is associated with increased morbidity and mortality. The exact pathophysiological mechanism of post-ischaemic coronary microvascular dysfunction (CMD) is still debated. Therefore, the current review discusses invasive and non-invasive techniques for the diagnosis and quantification of CMD in STEMI in the clinical setting as well as results from experimental in vitro and in vivo models focusing on ischaemic-, reperfusion-, and inflammatory damage to the coronary microvascular endothelial cells. Finally, we discuss future opportunities to prevent or treat CMD in STEMI patients.

Balloon Deflation Strategy during Primary Percutaneous Coronary Intervention in Acute ST-Segment Elevation Myocardial Infarction: A Randomized Controlled Clinical Trial and Numerical Simulation-Based Analysis

“…When no-reflow occurs during primary PCI, it significantly attenuates the beneficial impact of reperfusion therapy, resulting in poor clinical and functional outcomes. Previous studies indicate that no-reflow is a multifactorial phenomenon, and its mechanisms include pre-existing microvascular dysfunction, distal micro-thrombo-embolization, ischemic injury, reperfusion injury, and individual susceptibility [ 3 – 6 ].…”

“…Although timely and successful reperfusion with primary percutaneous coronary intervention (PCI) is the most effective method for reducing infarct size and improving the outcome in patients with acute ST-segment elevation myocardial infarction (STEMI) [ 1 , 2 ], PCI is also associated with a serious problem known as no-reflow phenomenon, which significantly attenuates the beneficial effects of reperfusion therapy, resulting in poor clinical and functional outcomes. This phenomenon may develop in 5–50% of STEMI patients during primary PCI [ 3 – 6 ]. No-reflow is thought to be caused by a variety of pathophysiological factors, such as distal embolization, ischemia-reperfusion injury, and the susceptibility of coronary microcirculation to injury [ 3 – 6 ].…”

“…This phenomenon may develop in 5–50% of STEMI patients during primary PCI [ 3 – 6 ]. No-reflow is thought to be caused by a variety of pathophysiological factors, such as distal embolization, ischemia-reperfusion injury, and the susceptibility of coronary microcirculation to injury [ 3 – 6 ].…”

Ischaemic cardiomyopathy. Pathophysiological insights, diagnostic management and the roles of revascularisation and device treatment. Gaps and dilemmas in the era of advanced technology

“…9 At the ultrastructural level, prolonged period of ischaemia followed by reperfusion is associated with severe endothelial dysfunction with reduced secretion of intrinsic vasodilators such nitric oxide and increased secretion of potent vasoconstrictors such as endothelin, endothelial swelling, loss of pinocytotic vesicles within the endothelium, visible breaks of the endothelial lining with aggregation of platelets, fibrin tactoids and neutrophils in the same region and extra-cellular erythrocytes with rouleaux formation and luminal obstruction. 10 In addition, destabilisation of the cellular junctions is associated with increased permeability and interstitial oedema, which can further enhance microvascular bed compression and increase infarct size. [11][12][13][14] Finally, intramyocardial haemorrhage represents the most severe and irreversible form of coronary microvascular injury with destruction of coronary capillaries, extravasation of erythrocytes, necrosis, cellular debris within the infarct core.…”

ST-segment elevation myocardial infarction: Historical perspective and new horizons

“…However, poor myocardial reperfusion as documented by an absent or poor myocardial blush on angiography and sustained ST elevation is a clear sign of extensive irreversible damage. Although the clinical correlates are well described, the fundamental pathophysiology is poorly understood [23,41,42]. Distal embolisation no-reflow, reperfusion injury and probably several other as yet undefined mechanisms form the next barrier to further improve outcomes of primary PCI, in particular in patients with cardiogenic shock, and to prevent late progression to heart failure.…”