In this study, 6 patients underwent angiographic assessment prior to and subsequent to acute myocardial infarction. The mean inter-angiographic interval was 36 months and the mean infarct to angiography interval was 8 months. Left ventricular ejection fraction decreased from 0.69 to 0.45 after infarction. The degree of left ventricular dysfunction after infarction did not necessarily relate to the site or type of infarction. All patients had significant progression of their coronary lesions with occlusion of a major coronary vessel in the interval. Coronary artery occlusion with infarction produces a variable degree of damage and subsequent left ventricular dysfunction.
We investigated the feasibility of using intravascular ultrasound imaging to analyze vascular physiology in various arterial beds. Canine superficial femoral, external iliac, and common carotid arteries were harvested and suspended and perfused in a bath of oxygenated, heated, physiologic salt solution. A 6-Fr, 20-MHz ultrasound imaging catheter was inserted into the lumen of the arteries and serial images were acquired after bolus injections of either serotonin or normal saline into the extravascular bathing medium. Serotonin resulted in a significant time- and dose-dependent decrease in cross-sectional area in muscular femoral arteries (P less than .001): -5.2% with 10(-8) M serotonin, -15% with 10(-7) M, and -28% with 10(-6) M. Histologically transitional iliac arteries demonstrated less marked changes, while elastic carotid arteries demonstrated no significant changes. Our results indicate that intravascular ultrasound may be used to quantify and differentiate responses to vasoconstrictive agents in different vascular beds.
Left ventricular thrombus formation is a well-described complication of acute myocardial infarction, and two-dimensional echocardiography is a reliable method for its detection.'.2The echocardiographic detection of biventricular thrombi in this setting, however, has not previously been rep o d .
