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Detection of viable myocardium in patients with known severe heart disease
Coronary artery disease remains a major health problem in Australia despite the substantial decline in age-adjusted mortality rates over the last 20 years. It is still our leading cause of death, accounting for approximately 30,000 deaths each year.
Coronary artery occlusion can result in injury to the heart muscle (myocardium) because of the deficiency in blood flow. As a consequence, the myocardium in that region of the heart fails to contract normally. It has been shown that the abnormally contracting region contains a mix of non-viable and injured, but potentially viable, myocardium. Restoration of blood flow of this potentially viable myocardium may result in improved contractility. Such an improvement is highly desirable as ventricular function is the major determinant of prognosis in patients with coronary artery disease. Therefore, one of the clinical challenges in diagnosing and treating coronary artery disease is to assess the amount of residual viable tissue present.
In coronary artery disease, PET uses radioisotopes such as N-13 ammonia (13NH3) and 18F-FDG PET to evaluate qualitatively and quantitatively regional coronary blood flow and ongoing active metabolism, hence myocardial viability. Regions with depressed contractile function in which there is reduced coronary flow but still active or increased FDG uptake have been shown to predict reversibility of cardiac dysfunction in 85 per cent of cardiac segments after revascularisation. Conversely, the absence of ongoing metabolism correctly predicted irreversibility of cardiac dysfunction in up to 92 per cent of segments. PET is currently regarded as the gold standard for the detection of myocardial viability.
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Cardiology
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Neurology
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Oncology
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