New Answers, Still More Questions!
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In the early 1980s, Rahimtoola1 reviewed the results of coronary bypass surgery trials and identified patients with coronary artery disease and chronic left ventricular dysfunction that improved upon revascularization. He proposed the concept of hibernating myocardium as “prolonged ischemia… in which myocardial metabolism and ventricular function are reduced to match the reduced blood supply…, a new equilibrium… whereby necrosis is prevented, and the myocardium is capable of returning to normal or near-normal function on restoration of an adequate blood supply.”1 This clinically based concept quickly found its experimental counterpart in a number of studies that characterized acute and subacute ischemia by proportionate reductions in blood supply and contractile function, ie, perfusion-contraction matching.2 Also, the recovery of initially disturbed substrate and energy metabolism during ongoing ischemia supported the notion that downregulation of contractile function permitted the myocardium to recover its metabolism and sustain its viability.3
Emerging Controversies: Reduced Versus Normal Baseline Flow; Short-Term Versus Chronic Hibernation
Vanoverschelde et al4 using PET in patients with collateral-dependent myocardium found a significant 19% reduction in blood flow in dysfunctional versus remote reference regions; because this degree of flow reduction was modest in relation to the severity of dysfunction, they reasoned that this was a situation of cumulative stunning with normal flow rather than hibernation with reduced resting flow. The majority of PET studies in patients with chronic hibernation report reduced resting flow; the amount of blood flow reduction is only modest (20% to 30%) as compared to the severity of dysfunction.5 However, in these PET studies, transmural resolution was lacking and more severe subendocardial ischemia …