Detection and characterization of hibernating myocardium.
Since Tennant and Wiggers observed that coronary occlusion caused a reduction in cardiac contractile function, a lot has been written about the concept of hibernating myocardium. Known as the 'smart heart', hibernating myocardium is characterized by a persistent ventricular myocardial dysfunction with preserved viability, which improves with the relief of the ischaemia; this chronic downregulation in contractile function being a protective mechanism to reduce oxygen demand and thus ensure myocyte survival. This improvement usually results in an enrichment in the quality of life as well as enhanced ventricular function. In fact, it has been observed that the cardiac event rate in patients with viable dysfunctional left ventricular segments who are medically treated, is higher than the event rate in patients with comparable viability who are revascularized. Different degrees of histological alteration have been seen in hibernating myocardium, ranging from cellular de-differentiation (fetal phenotype) to cellular degeneration. Cellular de-differentiation has been associated with repetitive stunning. On the other hand, cellular degeneration (with more extensive fibrosis) has been associated with chronic low myocardial blood flow and a longer time to recovery after revascularization. These histological patterns may suggest an evolution from cellular de-differentiation to degeneration, which ends in scar formation if no revascularization is performed. In fact, several studies have described the clinical value of identifying and revascularizing hibernating segments as early as possible, to minimize fibrosis and morbidity from adverse events. Detection of hibernating myocardium still remains an important clinical problem. Imaging modalities to assess myocardial viability must differentiate potentially functional tissue from myocardium with no potential for functional recovery. These techniques fall into three broad categories: ventricular function assessment, myocardial perfusion imaging and myocardial metabolic imaging. PET imaging with fluorine-18 fluorodeoxyglucose (18F-FDG) and 11C-acetate, single photon emission computed tomography (SPECT) with thallium and 99mTc-sestamibi, dobutamine echocardiograpy, magnetic resonance imaging (MRI) and fast computed tomography (CT) have been used for this purpose. PET imaging, in both perfusion and glucose metabolic activity, has become a standard for myocardial viability assessment, however, similar information may be available from carefully performed studies with perfusion tracers alone.
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Radiology Department, Nuclear Medicine Division, Stanford Hospital, Stanford University School of Medicine, 300 Pasteur Drive, Room H0101, Stanford, California 94305-5281, USA. drmari@stanford.edu
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D003324:Coronary Artery Disease / Q000150:complications; D019788:Fluorodeoxyglucose F18; D006321:Heart / Q000000981:diagnostic imaging; D006334:Heart Function Tests; D006801:Humans; D017682:Myocardial Stunning / Q000175:diagnosis / Q000000981:diagnostic imaging* / Q000209:etiology / Q000473:pathology; D009943:Organophosphorus Compounds; D015609:Organotechnetium Compounds; D019275:Radiopharmaceuticals; D017256:Technetium Tc 99m Sestamibi; D013794:Thallium Radioisotopes; D014055:Tomography, Emission-Computed; D015899:Tomography, Emission-Computed, Single-Photon; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000209:etiology
D009943:Organophosphorus Compounds; D015609:Organotechnetium Compounds; D019275:Radiopharmaceuticals; D013794:Thallium Radioisotopes; D019788:Fluorodeoxyglucose F18; C078700:technetium tc-99m tetrofosmin; D017256:Technetium Tc 99m Sestamibi