Myocardial hibernation is defined as a state of chronically reduced contractility in response to a reduction in blood supply and the ability to recover function after revascularization. There is controversy about the chronicity of a reduction in myocardial perfusion for induction of the adaptive mechanisms of hibernation. A search was conducted of the clinical literature for evidence showing that myocardial perfusion is chronically reduced in hibernating myocardium. Ninety-three clinical studies in patients with dysfunctional but viable myocardium (hibernating myocardium) and revascularization were reviewed. Contractile function, as assessed by ventriculography, radionuclide ventriculography, or echocardiography, was measured before revascularization in 91 studies (97.8%). Viability was assessed before revascularization using nuclear imaging--particularly 18-fluorodeoxyglucose positron emission tomography (PET) or (201)thallium-201 single-photon emission tomography (SPECT)--or pharmacologic stress echocardiography in 66 studies (71%). Myocardial perfusion measurements using (99m)Tc sestamibi SPECT, (13)N-ammonia, or (15-)O-water in PET, were obtained before revascularization in 68 studies (73.1%). There were no studies that measured myocardial perfusion more than once before revascularization. After revascularization, contractile function was assessed in 85 studies (91.4%), viability in 19 studies (20.4%), and myocardial perfusion in 28 studies (30.1%). Multiple measurements of perfusion, viability, and contractile function were performed after revascularization in two (2.2%), two (2.2 %), and ten (10.8%) studies, respectively. There was a lack of evidence in the clinical literature for chronic reduction in myocardial perfusion in patients with hibernating myocardium, because multiple measurements of perfusion have not been systematically performed at different time points with respect to revascularization.