Diagnosis of right ventricular acute myocardial infarction by dual isotope thallium-201 and indium-111 antimyosin SPECT imaging.

To assess the diagnostic value of indium-111 antimyosin for detecting right ventricular (RV) wall acute infarction, 30 patients with electrocardiographic-documented left ventricular inferior (posterior) wall acute myocardial infarction underwent simultaneous dual isotope indium-111 antimyosin and thallium-201 single-photon emission computed tomography (SPECT) within 2 days of admission. RV necrosis was defined as uptake of indium-111 antimyosin anterior and to the right of septal thallium uptake. Twenty-nine of the 30 patients (97%) had indium-111 antimyosin uptake in the inferior, posterior or lateral walls of the left ventricle and 14 of 30 (47%) had additional RV antimyosin uptake. Three different patterns of RV uptake of indium-111 antimyosin were observed: crescent-shaped, focal and apical. Twenty-seven patients underwent gated blood pool scanning before hospital discharge. Twelve of the 14 patients with RV antimyosin uptake had gated blood pool scintigraphy and 7 of 12 had RV dysfunction; 5 had normal RV function. Except for 1 patient who had questionable RV antimyosin uptake and had RV dysfunction, no patient without RV antimyosin uptake had RV dysfunction. In summary, right and left ventricular necrosis can be detected on tomographic images of indium-111 antimyosin uptake in patients with inferior infarctions when simultaneous uptake of a perfusion tracer, thallium-201, is imaged and used as an aid to reconstruction and anatomic localization.

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 less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)

Dual isotope thallium and indium antimyosin SPECT imaging to identify acute infarct patients at further ischemic risk.

Forty-two patients (28 men and 14 women) with acute myocardial infarction (35 Q, seven non-Q wave) were injected with 2.0 mCi indium 111-labeled antimyosin (AM) monoclonal antibody (111In AM) within 48 hours of the onset of chest pain. Forty-eight hours later (72-96 hours after onset of chest pain), patients were injected with 2.2 mCi thallium 201, and two sets of single-photon emission computed tomography (SPECT) images were obtained simultaneously using dual energy windows set for the 247 keV indium photopeak and the 70 keV thallium peak. Seventeen patients had repeat scans at 4 hours. 111In AM uptake and 201Tl defects were localized to one or more of 24 coronal and sagittal segments. Scans with only 201Tl defects and corresponding 111In AM uptake were classified as matches; scans with unmatched 201Tl defects in addition to matching regions corresponding to electrocardiographic infarct location were classified as mismatches; and scans with 201Tl and 111In AM uptake in the same segments were classified as overlap. Scan patterns were correlated with clinical evidence for residual ischemia occurring within 6 weeks of infarct and including infarct extension, recurrent angina, and positive predischarge low-level or 6-week symptom-limited stress tests and with coronary anatomy. Fourteen patients had only matching patterns (group 1), 23 had mismatches (group 2), and five had 201Tl-111In overlap as the predominant pattern. None of the patients in group 1 had previous myocardial infarction; in each, the matched area corresponded to the Q wave location on electrocardiogram, and none had further in-hospital ischemic events or positive stress tests.(ABSTRACT TRUNCATED AT 250 WORDS)