Effect of clinical variables on the correlation between amount of ST elevation and myocardial scintigraphic perfusion defect during coronary occlusion.

PURPOSE: We investigated if the correlation between the amount of ST elevation (STE) and myocardial ischemia could be altered by variables such as hypertension or body mass index (BMI). METHODS: A 12-lead electrocardiogram and a technetium-99m tetrofosmin injection were performed during balloon coronary occlusion in 34 patients with single-vessel disease. RESULTS: The sum of STE correlated with scintigraphic extent of ischemia (r = 0.441; P = .009), but this correlation improved significantly in men and patients with BMI of 28 kg/m2 or less and was highest in nonhypertensive patients (r = 0.763; P < .001). In contrast, it was poor in women and patients with BMI greater than 28 kg/m2 or arterial hypertension, being lowest in the latter subset (r = 0.110; P = .664). Moreover, 8 (80%) of 10 patients with extensive hypoperfusion but with low SigmaSTE (< or =20 mm) were hypertensive. CONCLUSIONS: If confirmed by larger studies, electrocardiographic underestimation of transmural ischemia during coronary occlusion in patients with hypertension or increased BMI may lead to adjustments in STE criteria for reperfusion therapy.

Relation of myocardial perfusion defects and nonsignificant coronary lesions by angiography with insights from intravascular ultrasound and coronary pressure measurements.

Several studies have demonstrated a correlation between myocardial ischemia and severity of coronary lesions as determined by intravascular ultrasound (IVUS) and fractional flow reserve (FFR) measurements. However, their value for the assessment of mild coronary stenoses that are associated with myocardial perfusion abnormalities has not been well studied. The objective of this study was to prospectively compare the results of myocardial perfusion as determined by exercise/dipyridamole myocardial single-photon emission computed tomography with IVUS and FFR measurements in patients who had angiographically mild coronary stenosis (< 50% diameter stenosis by quantitative coronary angiography). Forty-eight patients who had stable coronary disease (61 +/- 11 years of age; 6 women) were included. All had mild coronary stenosis in the proximal/middle segment of > or = 1 coronary artery and had undergone maximal exercise myocardial technetium-99m tetrofosmin single-photon emission computed tomography within 48 hours before coronary angiography. IVUS measurements included lesion lumen area, external elastic membrane area, lesion plaque burden (calculated as external elastic membrane minus lumen area, divided by external elastic membrane, and multiplied by 100), and lumen area stenosis (calculated as reference lumen area minus lesion lumen area, divided by reference lumen area, multiplied by 100). Fifty-three coronary lesions were studied, with a mean percent diameter stenosis of 34.9 +/- 7.9% on angiography. Myocardial perfusion defects were demonstrated by single-photon emission computed tomography in 11 patients (12 myocardial regions) with no differences in lesion percent diameter stenosis compared with those without perfusion defects. The presence of reversible perfusion defects was associated with a higher lesion plaque burden as evaluated by IVUS (67.4 +/- 8.1% vs 60.2 +/- 9.3%, p = 0.01). FFR values did not differ in the presence or absence of perfusion defects (0.90 +/- 0.06 vs 0.92 +/- 0.07, respectively; p = NS). In conclusion, plaque burden as determined by IVUS may partly explain the presence of myocardial perfusion defects in cases of angiographically nonsignificant coronary lesions. However, the high FFR values associated with these lesions suggest that other mechanisms, such as endothelial/microvascular dysfunction, might also account for perfusion abnormalities in these patients.

[Post-infarction ventricular septal defect treated during the acute phase by transcatheter closure with an Amplatzer septal occluder]. / Comunicación interventricular postinfarto de miocardio tratada en fase aguda mediante cierre percutáneo con el dispositivo Amplatzer.

A 75-year-old man had a large anterior myocardial infarction complicated by a ventricular septal defect, which was treated in the first 48 h by transcatheter closure using the Amplatzer septal occluder. Treatment was successful (with only mild residual post-procedure shunting) and coronary angioplasty with stent implantation at the point of occlusion of the middle left anterior descending artery was performed in a later intervention. However, the patient died 7 days after the procedure as a result of sepsis and ventricular failure.

Comunicación interventricular postinfarto de miocardio tratada en fase aguda mediante cierre percutáneo con el dispositivo Amplatzer / Post-Infarction ventricular septal defect treated during the acute phase by transcatheter closure with an amplatzer septal occluder

Presentamos el caso de un paciente de 75 años afectado de un infarto anterior extenso complicado con una comunicación interventricular muscular apical que se trató mediante la implantación percutánea de una prótesis de tipo Amplatzer dentro de las primeras 48 h de evolución del infarto. Con este tratamiento se consiguió cerrar de forma eficaz el defecto interventricular (ligero shunt residual posprocedimiento), y posteriormente se practicó con éxito una angioplastia con implantación de stent en una oclusión de la descendente anterior media. Sin embargo, el paciente falleció 7 días después del procedimiento por sepsis y fallo ventricular (AU)

Coronary smooth muscle reactivity to muscarinic stimulation after ischemia-reperfusion in porcine myocardial infarction.

This study tested whether ischemia-reperfusion alters coronary smooth muscle reactivity to vasoconstrictor stimuli such as those elicited by an adventitial stimulation with methacholine. In vitro studies were performed to assess the reactivity of endothelium-denuded infarct-related coronary arteries to methacholine (n = 18). In addition, the vasoconstrictor effects of adventitial application of methacholine to left anterior descending (LAD) coronary artery was assessed in vivo in pigs submitted to 2 h of LAD occlusion followed by reperfusion (n = 12), LAD deendothelization (n = 11), or a sham operation (n = 6). Endothelial-dependent vasodilator capacity of infarct-related LAD was assessed by intracoronary injection of bradykinin (n = 13). In vitro, smooth muscle reactivity to methacholine was unaffected by ischemia-reperfusion. In vivo, baseline methacholine administration induced a transient and reversible drop in coronary blood flow (9.6 +/- 4.6 to 1.9 +/- 2.6 ml/min, P < 0.01), accompanied by severe left ventricular dysfunction. After ischemia-reperfusion, methacholine induced a prolonged and severe coronary blood flow drop (9.7 +/- 7.0 to 3.4 +/- 3.9 ml/min), with a significant delay in recovery (P < 0.001). Endothelial denudation mimics in part the effects of methacholine after ischemia-reperfusion, and intracoronary bradykinin confirmed the existence of endothelial dysfunction. Infarct-related epicardial coronary artery shows a delayed recovery after vasoconstrictor stimuli, because of appropriate smooth muscle reactivity and impairment of endothelial-dependent vasodilator capacity.