Coronary Microcirculation: The Next Frontier in the Management of STEMI

Abstract

Although the widespread adoption of timely invasive reperfusion strategies over the last two decades has significantly improved the prognosis of patients with ST-segment elevation myocardial infarction (STEMI), up to half of patients after angiographically successful primary percutaneous coronary intervention (PCI) still have signs of inadequate reperfusion at the level of coronary microcirculation. This phenomenon, termed coronary microvascular dysfunction (CMD), has been associated with impaired prognosis. The aim of the present review is to describe the collected evidence on the occurrence of CMD following primary PCI, means of assessment and its association with the infarct size and clinical outcomes. Therefore, the practical role of invasive assessment of CMD in the catheterization laboratory, at the end of primary PCI, is emphasized, with an overview of available technologies including thermodilution- and Doppler-based methods, as well as recently developing functional coronary angiography. In this regard, we review the conceptual background and the prognostic value of coronary flow reserve (CFR), index of microcirculatory resistance (IMR), hyperemic microvascular resistance (HMR), pressure at zero flow (PzF) and angiography-derived IMR. Finally, the so-far investigated therapeutic strategies targeting coronary microcirculation after STEMI are revisited.

Microvascular dysfunction following deferred stenting strategy in ST-segment elevation myocardial infarction: a case report

“…Should significant recovery be evidenced by the 5th day, this might reinforce the utilization of these coronary physiology tools, particularly when contemplating deferred stenting strategies. 17 Given the current uncertainty surrounding this recovery kinetics, we introduce a speculative algorithm with the intent of sparking discussion on how understanding microcirculatory function might potentially influence clinical decision-making ( Figure 5 ).…”

The follow-up of myocardial injury and left ventricular function after spontaneous coronary artery dissection

“…Although larger studies are needed to confirm this, the emergence and withdrawal mechanisms of MVO and IMH in SCAD-related myocardial infarction with ST-elevation (STEMI) may differ in comparison to type 1 STEMI patients. The exact pathophysiological mechanism of post-ischemic CMD is still being debated ( 17 , 18 ), along with future opportunities for preventing or treating CMD in STEMI patients. Pathophysiological mechanisms of CMD in AMI are divided into intraluminal obstruction (such as thromboembolism, plugging, and vasospasm) and extravascular expression (such as IMH, interstitial and cellular edema, and increased end-diastole pressure of the left ventricle) ( 18 ).…”

“…The exact pathophysiological mechanism of post-ischemic CMD is still being debated ( 17 , 18 ), along with future opportunities for preventing or treating CMD in STEMI patients. Pathophysiological mechanisms of CMD in AMI are divided into intraluminal obstruction (such as thromboembolism, plugging, and vasospasm) and extravascular expression (such as IMH, interstitial and cellular edema, and increased end-diastole pressure of the left ventricle) ( 18 ). Future research may focus on identifying the predominant pathophysiological mechanisms that contribute to CMD in SCAD.…”