CLINICAL STUDY
Relation of thallium uptake to morphologic features of chronic ischemic heart disease: evidence for myocardial remodeling in noninfarcted myocardium
Jamshid Shirani, MD, FACCa,
Jaetae Lee, MD ,
Rebecca Quigg, MD, FACC,
Ruth Pick, MD ,
Stephen L. Bacharach, PhD and
Vasken Dilsizian, MD, FACC ||
a Albert Einstein College of Medicine, New York, New York, USA
Kyungpook National University Hospital, Taegu, South Korea
Columbia Michael Reese Hospital and Medical Center, Chicago, Illinois, USA
Department of Nuclear Medicine, National Institutes of Health, Bethesda, Maryland, USA
|| Cardiology Branch, National Heart, Lung and Blood Institute, Bethesda, Maryland, USA
Manuscript received May 19, 2000;
revised manuscript received March 7, 2001,
accepted March 23, 2001.
Address for correspondence: Dr. Vasken Dilsizian, National Institutes of Health, Cardiology Branch, NHLBI, Building 10, Room 7B-15, Bethesda, Maryland 20892-1650 dilsizian{at}nmdhst.cc.nih.gov
OBJECTIVES
The aim of this study was to investigate the disparity between the extent of myocardial injury as assessed by thallium and the severity of left ventricular (LV) dysfunction in chronic ischemic heart disease.
BACKGROUND
Although it is believed that thallium differentiates between viable and nonviable myocardium, in some patients with chronic ischemic heart disease, viable regions by thallium may fail to improve function after revascularization.
METHODS
Thirteen transplant candidates with chronic ischemic heart disease (LV ejection fraction = 14 ± 6% at rest) were studied prospectively with stress-redistribution-reinjection thallium single-photon emission computed tomography. We examined pretransplantation quantitative thallium uptake and post-transplantation extent and the histological distribution of collagen replacement in infarcted and noninfarcted myocardium and in 13 age-matched control hearts.
RESULTS
The volume fraction of collagen varied inversely with wall thickness (r = 0.70, p < 0.001) and was higher in irreversible (30.9 ± 15.8%) compared with reversible (20.2 ± 12.6%, p < 0.001) or normal thallium segments (15.0 ± 8.7%, p < 0.001). The irreversible thallium segments had lower wall thickness and more severe coronary artery narrowing (9.7 ± 2.8 mm and 95 ± 8%) compared with reversible (11.7 ± 2.7 mm and 87 ± 13%, p < 0.001) and normal thallium segments (12.8 ± 2.6 mm and 80 ± 14%, p < 0.001). Mean volume fraction of collagen was significantly lower in noninfarcted than it was in infarcted segments (13 ± 6% vs. 36 ± 13%, p < 0.001) but exceeded that in the control hearts (4 ± 2%, p < 0.001). Noninfarcted segments had predominantly interstitial fibrosis with either microscopic or patchy areas of replacement fibrosis.
CONCLUSIONS
In chronic ischemic heart disease with severe LV dysfunction, patterns of normal, reversible and irreversible thallium uptake correlated with the magnitude of collagen replacement, segmental wall thickness and severity of coronary artery narrowing. The finding of scattered areas of replacement fibrosis in noninfarcted myocardium may explain the observed disparity between LV contractile dysfunction and the extent of myocardial injury assessed by thallium.
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Abbreviations and Acronyms
| | LV | = left ventricle | | LVEF | = left ventricular ejection fraction | | SPECT | = single-photon emission computed tomography |
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