Prati et al. report an important study in this issue,showing that platetet GP IIb/IIIa inhibition limits microcirculatory impairment in the setting of angioplasty for acute coronary syndromes. Prior studies suggest that abciximab use in unstable angina and myocardial infarction may limit cardiac enzyme surge and improve clinical outcomes. Improved outcomes are hypothesized to result from improved microcirculatory function, presumably by limiting or preventing platelet thrombi from causing microvascular obstruction. Prati et al. hypothesize that if platelet thrombus and plugging are correct, then abciximab could be a useful option to limit microvascular obstruction. The study inferred microvascular thrombus using myocardial blush from left ventricular video densitometry, a twodimensional projection image with substantial limitations. Nevertheless, the study showed abciximab provided a protective effect, with improved blush scores. This is important from the standpoint that microvascular flow is inferred but not directly measured, and a therapeutic attempt proved at least partially successful. The importance of microvessels and their obstruction is only recently coming into focus.
MICROVASCULAR OBSTRUCTIONMicrovascular obstructive has been hypothesized for many years [1][2][3]. Acutely obstructing the cardiac microvessels causes myocyte necrosis and endothelial cell sloughing within the intramyocardial capillaries. Leukocytes (most polys) appear, and the capillary lumina have RBC plugging. There myocyte swelling, and occlusive microthrombi consistent with plateletfibrin clot. This microanatomic picture occurs with acute myocardial injury due to vascular occlusion, embolization, and subsequent reperfusion injury. Microvascular obstruction is emerging as a key component to long-term cardiac complications following myocardial infarction [4]. It is typically observed in the catheterization laboratory as low flow or the noreflow phenomenon, promotes left ventricular enlargement (adverse remodeling) and heart failure, and has key prognostic implications [5,6]. One study used MRI to diagnose microvascular obstruction (MVO) and followed patients for 16 months after an acute infarction [4]. The study endpoints were death, nonfatal MI, heart failure, and transient ischemic attack. All patients had coronary angiograms. Interestingly, 17% of patients with angiographic TIMI III flow had MVO, while 60% with TIMI 0, I, or II had no MVO. In patients with MVO, long-term end-diastolic volumes rose by 89% vs. 10% in those without MVO. End-systolic volumes in patients with MVO rose 166% compared to 3% in those without MVO. More importantly, 46% of MVO patients had events compared with 9% in those without it. Multiple regression analysis found MVO to be an important prognostic marker when controlling for infarct size.The emerging data thus imply three intriguing and important conclusions about MVO: first, it is a common complication of acute coronary syndromes; second, it is often unrecognized; third, it is responsible for serious long...