Characterization of spatial patterns of flow within the reperfused myocardium by myocardial contrast echocardiography. Implications in determining extent of myocardial salvage.

Villanueva, Flordeliza S.; Glasheen, William P.; Sklenar, Jiri; Kaul, Sanjiv

doi:10.1161/01.cir.88.6.2596

Cited by 155 publications

(80 citation statements)

References 44 publications

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“…9 MCE has been clinically shown to be superior for the detection of acute coronary syndromes in the emergency department compared with routine evaluation. 10 A day or two after reperfusion (when hyperemia has abated), it can define the region with no-reflow, which approximates infarct size.…”

Section: Acute Myocardial Infarctionmentioning

confidence: 99%

Myocardial Contrast Echocardiography

et al. 2004

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Section: Acute Myocardial Infarctionmentioning

confidence: 99%

Myocardial Contrast Echocardiography

et al. 2004

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“…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.…”

Section: No-reflow Phenomenonmentioning

confidence: 99%

“…25 Capillary obstruction often progresses for several minutes to hours after coronary recanalization, possibly as a result of reperfusion injury, and thus, the size and clinical presentation of the no-reflow phenomenon vary greatly with time. 3,4 Continuous monitoring of CBF velocity with Doppler flow wire shows that the systolic flow reversal is seen in only half the patients with no reflow immediately after reperfusion 26 ; the other half develop this abnormality later. Great cardiac vein flow often decreases gradually until the day after reperfusion, and functional recovery in those with this finding is worse than in those without it.…”

Section: No-reflow Phenomenonmentioning

confidence: 99%

Microvasculature in Acute Myocardial Ischemia: Part II

2004

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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...

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“…These results support the speculations by previous investigators that damage or interruption to the coronary microvascular network (ie, damaged intramyocardial capacitance vessels) exists in clinical or experimental cases of 'no-reflow'. [14][15][16][17][18] …”

Section: Capillary Morphological Abnormalities and Capillary Volume Fmentioning

confidence: 99%