Automated quantification of the spatial extent of perfusion defects and viability on myocardial contrast echocardiography.

The spatial extent of hypoperfusion or viability is important in the treatment of patients with coronary artery disease. We hypothesized that computerized pixel intensity threshold analysis (PITA) could be used for the automated analysis of perfusion defect size during myocardial contrast echocardiography (MCE). For calibration studies, MCE was performed in 6 dogs undergoing ischemia and reperfusion. Infarct size was determined by PITA, which automatically calculates the percentage of pixels within the myocardium that fail to exceed a predetermined threshold of maximum contrast enhancement. A threshold of 10% of maximum yielded infarct sizes that most closely correlated with those determined by histologic staining. For clinical validation, MCE was performed in 30 patients with acute myocardial infarction before primary percutaneous coronary intervention (PCI) for measurement of risk area; and within 5 days and at 4 weeks after PCI to determine infarct size. The defect size by PITA with a 10% threshold value closely correlated with those measured by expert reader planimetry on background-subtracted color-coded image sets (r = 0.95, P < .001). We conclude that automated analysis of perfusion defect size on MCE is possible by PITA. This technique may be useful for rapid and objective analysis of the extent of ischemia and viability, and for clinical experimentation where accurate and sequential analysis of perfusion defect size is imperative.

Improvement in microvascular reflow and reduction of infarct size with adenosine in patients undergoing primary coronary stenting.

The aim of this study was to use myocardial contrast echocardiography to evaluate the effect of intravenous adenosine on microvascular reflow in patients with acute myocardial infarction who underwent primary coronary stenting (PCS). Thirty patients who underwent primary PCS for acute myocardial infarction were randomized to intravenous adenosine (50 to 70 mug/kg/min) or vehicle for 3 hours. Myocardial contrast echocardiography was performed before and sequentially after PCS to determine the risk area during coronary occlusion and infarct size. The risk area was similar in the adenosine- and placebo-treated patients. The infarct size as a ratio to the risk area was smaller in patients treated with adenosine when measured at 3 to 5 days (0.37 +/- 0.29 vs 0.68 +/- 0.25, p <0.01) and at 4 weeks (0.34 +/- 0.26 vs 0.60 +/- 0.21, p <0.01) after PCS. This effect was greatest when patency was achieved <4 hours after symptom onset (0.18 +/- 0.18 vs 0.74 +/- 0.31, p <0.05), with little effect after 4 hours. The relative microvascular blood volume in the risk area at 4 weeks was higher in patients receiving adenosine than in those receiving placebo (0.73 +/- 0.22 vs 0.57 +/- 0.20, p <0.01), and was highest when patency was achieved in <4 hours. In conclusion, the adjunctive use of intravenous adenosine after PCS reduces the infarct size relative to the risk area. This beneficial effect occurs primarily in those undergoing early intervention.