Long-term survival of patients with coronary artery disease and left ventricular dysfunction: Implications for the role of myocardial viability assessment in management decisions,☆☆,,★★,

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Abstract

Objectives: Our purpose was to evaluate the long-term benefit of myocardial viability assessment for stratifying risk and selecting patients with low ejection fraction for coronary artery bypass grafting and to determine the relation between the severity of anginal symptoms, the amount of ischemic myocardium, and clinical outcome. Methods: We studied 93 consecutive patients with severe coronary artery disease and low ejection fraction (median, 25%) who underwent positron emission tomography to delineate the extent of perfusion-metabolism mismatch (reflecting hibernating myocardium) for potential myocardial revascularization. Median follow-up was 4 years (range, 0 to 6.2 years). Results: Fifty patients received medical therapy, and 43 patients underwent bypass grafting. In Cox survival models, heart failure class, prior myocardial infarction, and positron emission tomographic mismatch were the best predictors of survival. Patients with positron emission tomographic mismatch receiving bypass grafting had improved 4-year survival compared with those on medical therapy (75% versus 30%; P = .007) and a significant improvement in angina and heart failure symptoms. In patients without positron emission tomographic mismatch, bypass grafting tended to improve survival and symptoms only in those patients with severe angina (100% versus 60%; P = .085), whereas no survival advantage was apparent in patients with minimal or no anginal symptoms (63% versus 52%; P = .462). Conclusions: Patients with low ejection fraction and evidence of viable myocardium by positron emission tomography have improved survival and symptoms with coronary bypass grafting compared with medical therapy. In patients without evidence of viability, survival and symptom improvement with bypass grafting are apparent only among those patients with severe angina. (J Thorac Cardiovasc Surg 1998; 116:997-1004)

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From the Division of Nuclear Medicine, Department of Medical and Molecular Pharmacology, UCLA School of Medicine, Los Angeles, Califa; and the Departments of Internal Medicine and Radiology, Wayne State University School of Medicine, Detroit, Mich.b

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Dr Di Carli is the recipient of a Scientist Development Grant from the American Heart Association, Dallas, Texas.

Address for reprints: Marcelo F. Di Carli, MD, Division of Cardiology, Harper Hospital, 3990 John R., Detroit, MI 48201.

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*Current address: Department of Nuclear Medicine, Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195.

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