Microvasculature in Acute Myocardial Ischemia: Part II

Abstract

I n the setting of suspected acute myocardial infarction (AMI), a cardiologist needs to know three things: (1) whether there is actually an ongoing infarction, (2) whether reperfusion therapy has succeeded, and (3) how much myocardium was salvaged by reperfusion. Myocardial contrast echocardiography (MCE) can answer the first question by demonstrating the presence of a perfusion defect resulting from reduced microvascular flow because of the presence of a thrombus in an epicardial coronary artery. In a recent multicenter study of 203 patients without ST-segment elevation who presented to the emergency department with chest pain, 21 had AMI, and MCE only missed 1 such patient (sensitivity of 95%). 1 Panel A in Figure 1 demonstrates a MCE perfusion defect in a patient presenting to the emergency department with chest pain who was subsequently ruled in for an AMI. The success of reperfusion and degree of myocardial salvage are equally important to know in patients even with ST-elevation AMI. Coronary angiography is not reliable in this regard. 2 The success of attempted reperfusion can also be accurately assessed with MCE. Most currently used clinical and electrocardiographic parameters are accurate in Ϸ75% of the cases, whereas MCE has an almost 100% accuracy. Panel B in Figure 1 depicts MCE images that were obtained immediately after thrombolysis and showed that most of the myocardium was reperfused. A small region in the apex showed no reflow and failed to exhibit improvement in function weeks later, whereas the reperfused myocardium showed complete recovery in function. In several cases of STelevation AMI, perfusion is normal at the time of cardiac catheterization despite a wall motion abnormality, and when angiography is performed, the infarct-related artery is found to be open, either spontaneously or from treatment with aspirin and heparin. No-Reflow PhenomenonAlthough MCE immediately after reperfusion can provide an accurate assessment of the success of reperfusion, it might underestimate the degree of no reflow because of reactive hyperemia. 3,4 The degree of reactive hyperemia is influenced by the amount of capillary damage and the degree of residual stenosis in the infarct-related artery. The no-reflow zone also changes dynamically in the first several hours after reperfusion because of vasospasm, myocardial edema, etc. Therefore, the ideal time to measure no reflow to determine the extent of myocardial necrosis is after 48 hours following reperfusion. 5,6 At that time, dynamic changes in resting tissue perfusion have subsided, and the extent of no reflow correlates well with infarct size and denotes a region of irreversible tissue damage.The "no-reflow" phenomenon in the heart was originally described in a canine model of coronary artery ligation followed by reperfusion. 7 Despite an open infarct-related artery, regions within the myocardium showed low flow, which were located exclusively within irreversibly injured myocardium. Consequently, the size of the no-reflow zone approximated infarct size. Elec...

New Modality for Evaluating Plaque Characteristics of the Culprit Lesion in a Patient With Acute Coronary Syndrome and No Reflow Phenomenon

“…Clinical factors associated with this phenomenon include age, male sex, hyperglycemia, increased white blood cell count, and absence of preinfarction angina. [11][12][13] The most consistent risk factors for this phenomenon, determined by gray-scale IVUS, are the presence of an attenuated plaque, large plaque burden, lipid pool-like imaging, and positive vessel remodeling. 3,4) However, there are still some limitations such as instrument settings and expertise of the interpreter.…”

Renin-Angiotensin System Inhibitors Can Prevent Intravenous Lipid Infusion-Induced Myocardial Microvascular Dysfunction and Leukocyte Activation

“…15 We postulated that the FFA-induced reduction in myocardial microvascular velocity is due to increased resistance in capillaries, because these vessels are responsible for 75% of the total microvascular resistance in maximally dilated coronary vasculature. 27, 28 In fact, the amount of time required for whole blood to pass through a microchannel array of capillaries with the same inner lumen diameter (7×4.5 μm), which reflects capillary resistance, was significantly prolonged after the lipid/heparin infusion. The numbers of adherent or clumped leukocytes in the ex vivo capillary model were also significantly increased after lipid/ heparin infusion.…”

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

“…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][2][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.…”

“…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.…”

“…Myocardial contrast echocardiography: Until now, myocardial contrast echocardiography (MCE) has been the gold standard examination for diagnosing the no-refl ow phenomenon. [1][2][3]5,11,12) MCE uses intravascular contrast agents that contain microbubbles as blood tracers, and it enables us the assessment of microvascular integrity and blood flow dynamics in myocardial capillaries. The no-refl ow zone is documented as the region of contrast perfusion defect (Figure 2).…”