Quantcast

Myokardialer Vitalitätsnachweis mit der Dobutamin-Echokardiografie: Aktuelle Übersicht

Research paper by Heinz Völler, U. Nixdorff, F. A. Flachskampf

Indexed on: 01 Oct '00Published on: 01 Oct '00Published in: Zeitschrift fur Kardiologie



Abstract

Myocardial stunning (contractile dysfunction in the presence of normalized perfusion) and myocardial hibernation (contractile dysfunction matching reduced perfusion) have represented separate concepts of viable, but dyssynergic myocardium in the past. However, in vivo experimental and clinical work suggests that repetitive ischemia due to coronary artery disease may induce a gradual transition between stunned and hibernating myocardium. Myocardial hibernation itself can result from a spectrum of ischemic conditions ranging from impaired myocardial blood flow reserve to frank hypoperfusion. With increasing severity and duration of ischemia, degeneration of cardiac myocytes, accumulation of glycogen and cell death ensue. Additonally, there is an increase of extracellular matrix protein content leading to reparative fibrosis, which in turn limits functional recovery.    In the light of these structural features, the available methods for detection of viable myocardium, in particular dobutamine echocardiography and nuclear imaging techniques, offer complementary rather than contradictory information. Dobutamine echo has satisfactory sensitivity, excellent specificity, and high diagnostic accuracy for the detection of viable dyssynergic myocardium. While in the past only its predictive accuracy for segmental recovery has been validated, newer data show an improved survival after revascularization if at least four viable dyssynergic left ventricular segments in a 16 segment model can be identified by dobutamine echocardiography. The complete (low and high dose) dobutamine protocol can elicit several types of contractile responses (sustained improvement in contraction or monophasic response, biphasic response, new wall motion abnormality) which should be interpreted in view of other clinical data including a previous infarction. The test protocol can be used safely at the end of the first week after myocardial infarction. If ischemia or viability is documented, revascularization should be performed promptly. A similar strategy should be followed in the setting of chronic coronary heart disease with left ventricular dysfunction. Since the structural changes of hibernating myocardium are progressive, time to revascularization is critical. On the other hand, responsible therapeutic planning requires proof of ischemia or viability before initiating a potentially hazardous revascularization procedure.