Myocardial stunning (contractile dysfunction in the presence of normalized
perfusion) and myocardial hibernation (contractile dysfunction matching red
uced perfusion) have represented separate concepts of viable, but dyssynerg
ic 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. Myocardia
l hibernation itself can result from a spectrum of ischemic conditions rang
ing from impaired myocardial blood flow reserve to frank hypoperfusion. Wit
h increasing severity and duration of ischemia, degeneration of cardiac myo
cytes, 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 detect
ion of viable myocardium, in particular dobutamine echocardiography and nuc
lear imaging techniques, offer complementary rather than contradictory info
rmation. Dobutamine echo has satisfactory sensitivity, excellent specificit
y, and high diagnostic accuracy for the detection of viable dyssynergic myo
cardium. While in the past only its predictive accuracy for segmental recov
ery has been validated, newer data show an improved survival after revascul
arization if at least four viable dyssynergic left ventricular segments in
a 16 segment model can be identified by dobutamine echocardiography. The co
mplete (low and high dose) dobutamine protocol can elicit several types of
contractile responses (sustained improvement in contraction or monophasic r
esponse, biphasic response, new wall motion abnormality) which should be in
terpreted in view of other clinical data including a previous infarction. T
he test protocol can be used safely at the end of the first week after myoc
ardial infarction. If ischemia or viability is documented, revascularizatio
n should be performed promptly. A similar strategy should be followed in th
e setting of chronic coronary heart disease with left ventricular dysfuncti
on. Since the structural changes of hibernating myocardium are progressive,
time to revascularization is critical. On the other hand, responsible ther
apeutic planning requires proof of ischemia or viability before initiating
a potentially hazardous revascularization procedure.