Etiology and Clinical Implications of Microvascular Dysfunction in Patients With Acute Myocardial Infarction

Abstract

SummaryIn patients with acute myocardial infarction (MI), coronary microvasculatures are often damaged irreversibly due to myocardial ischemia and reperfusion, and fl ow to the previously ischemic myocardium is markedly reduced, a phenomenon known as the "no-refl ow phenomenon". Percutaneous coronary intervention (PCI) may accelerate embolization of plaque gruels and microthrombi to the microvessels, which further reduces tissue perfusion. The extent of the no-refl ow zone correlates with infarct size, and it has additional prognostic information. Recent advances in imaging modalities have enabled us to diagnose the no-refl ow phenomenon and to assess the mechanisms of the no-refl ow phenomenon. Pharmacological interventions and catheter-based devices to retrieve embolic materials have been proposed, and some of them are associated with improvement in clinical outcomes. Thus, we should keep in mind that only the achievement of complete microvascular perfusion is associated with better functional and clinical outcomes in patients with acute MI. (Int Heart J 2014; 55: 185-189) Key words: Echocardiography, Myocardial perfusion, Reperfusion, Myocardial ischemia, Microcirculation, Myocardial viability, Prognosis, Ventricular function A cute myocardial infarction (MI) is caused by obstruction of a coronary artery by a thrombus on a ruptured plaque. Salvaging threatened myocardium after acute coronary occlusion has been a key therapeutic objective. Percutaneous coronary intervention (PCI) with coronary stenting is widely performed for this purpose. PCI, however, does not necessarily guarantee the recovery of blood fl ow at the microvascular level, because myocardial ischemia often injures the coronary microvasculature structurally.1-3) This is called the noreflow phenomenon.4) If this phenomenon occurs, it significantly attenuates the benefi cial impacts of reperfusion therapy, resulting in poor clinical and functional outcomes. [1][2][3]5) The PCI procedure itself may worsen the microvascular function. Balloon inflation and stenting may introduce embolization of plaque and thrombus debris, resulting in obstruction in distal coronary small arteries and arterioles. Atheroembolism and/or thromboembolism could limit the effi cacy of PCI. 6)Attention is currently shifting from "no-fl ow" to "no-refl ow". We should ascertain the patency to determine the status of the coronary microvasculature in each patient with acute MI in order perform risk stratifi cation. With the advancement of imaging modalities, which include myocardial contrast echocardiography, Doppler guidewire, and cardiac magnetic resonance imaging, the number of patients with the no-refl ow phenomenon has increased compared to the rates that we deemed. Our ultimate therapeutic goal is to achieve successful microvascular reperfusion. In this review, I attempt to provide an in-depth understanding of the no-refl ow phenomenon from the bench to the bedside.

Sonoreperfusion Therapy Kinetics in Whole Blood Using Ultrasound, Microbubbles and Tissue Plasminogen Activator

“…This occurs in up to 55% of patients following PCI and portends poor clinical outcome (Kloner et al 1974; van Kranenburg et al 2014; Wu et al 1998). MVO, largely caused by obstruction of the microcirculation with atherothrombotic debris, results in local inflammation, platelet aggregation, myocardial edema due to dysfunctional endothelium, and formation of in situ microvascular thrombi (Ito 2014; Robbers et al 2013). While many preventative and curative strategies have been employed (Bernink et al 2014; Fröhlich et al 2013; Galasso et al 2014), there has been no consistently efficacious therapeutic approach.…”

Impact of Doctor Car with Mobile Cloud ECG in Reducing Door-to- Balloon Time of Japanese ST-Elevation Myocardial Infarction Patients

“…17) Recently, it has been reported that reducing the door-toballoon time is not sufficient for in-hospital mortality. 26,27) We may pay more attention to pre-hospital activity such as first medical contact (FMC) to balloon time. There were 55 cases of suspected AMI for which our Doctor Car was required.…”

Nicorandil Attenuates Ischemia-Reperfusion Injury Via Inhibition of Norepinephrine Release From Cardiac Sympathetic Nerve Terminals

“…33) NICO has both ATP-sensitive KATP channel opener and nitrate properties, and it has a protective effect on myocardial I/R injury in animal models 10,11) and humans. [34][35][36] Ishii, et al 37) reported in a randomized study that the addition of intravenous NICO to percutaneous coronary intervention prevented cardiovascular events in patients with acute myocardial infarction, although NICO did not limit infact size in a multicenter study that was performed using a lower dose of NICO compared to a previous study.…”