EFFECT OF INFARCT SIZE MEASURED FROM ANTIMYOSIN SINGLE-PHOTON EMISSION COMPUTED TOMOGRAPHIC SCANS ON LEFT-VENTRICULAR REMODELING

To evaluate the effect of infarct size on left ventricular volumes and geometric remodeling, 26 patients with a first acute Q wave myocardial infarction (anterior in 14, inferior in 12) had the infarct sized from single-photon emission computed tomographic (SPECT) imaging of indium-111 antimyosin. All patients underwent gated blood pool scintigraphy before hospital discharge for determination of ejection fraction and end-diastolic and end-systolic volume indexes. Infarct size was quantitated from indium-111 antimyosin uptake in coronal slices with use of a threshold technique for edge detection. Nineteen of 26 patients had additional simultaneous acquisitions of indium-111 and thallium-201 uptake and the infarct was expressed as a percent of the total left ventricle. Infarct size was larger (59 +/- 16 vs. 33 +/- 16 g), predischarge ejection fraction lower (35 +/- 5% vs. 60 +/- 9%) and end-systolic volume index higher (57 +/- 13 vs. 36 +/- 10 ml/m2) in the group with anterior infarction. Despite these differences, predischarge end-diastolic volume index was not significantly different between the group with anterior (88 +/- 17 ml/m2) versus inferior (89 +/- 14 ml/m2) infarction. There was a significant inverse correlation between percent infarct size and ejection fraction for patients with dual isotope imaging (r = -0.90) and a significant direct correlation between infarct size and end-systolic volume index (r = 0.79, p < 0.01). Fourteen patients without subsequent myocardial infarction or coronary artery bypass grafting had a repeat gated blood pool study late (26 +/- 15 months) after infarction. Patients with an anterior infarction had a significant increase in end-diastolic volume index (+10 +/- 11 ml/m2), which was also significantly different from the change in end-diastolic volume index in the group with inferior infarction (-5 +/- 5.2 ml/m2). These data suggest that infarct size and location have a profound effect on left ventricular function and chamber size. Anterior infarcts, because they are larger, cause more severe left ventricular dysfunction and higher end-systolic volume early. The consequent increases in end-systolic wall stress may be the driving mechanism for late left ventricular chamber enlargement. This method for measuring infarct size has potential usefulness for selecting patients who will benefit from pharmacologic intervention to prevent late left ventricular dilation.