Correspondence 1907 Chronic Myocardial Hiberation

Chronic Myocardial Hiberation The study of Vanoverschelde et al' demonstrated significant abnormalities on morphological analysis of myocardial biopsies from patients with chronic myocardial hibernation. These morphological changes are very similar to those described previously2 and do not occur in stunning; thus, the investigators correctly state that their patients with left ventricular dysfunction had chronic myocardial hibernation. The authors proposed that in their patients, myocardial hibernation was the result of, or followed, repeated episodes of myocardial stunning. Their rationale for invoking stunning was based on "no reduction" of resting myocardial blood flow (MBF) to areas of resting left ventricular (LV) wall motion abnormalities. This conclusion was based on the demonstration of similar blood flow measured by positron emission tomography (PET) to collateral-dependent myocardium in a group of 26 patients, 17 of whom had reduced function (group 2) and 9 who had normal function (group 1). Thus, the question that arises is whether MBF in group 2 patients would be expected to be the same as in group 1 patients. MBF is importantly determined by myocardial oxygen demand: The group 2 patients had 5.6% higher rate-pressure product and 21.7% larger LV volume than group 1 patients; thus, MBF in group 2 patients would be expected to be higher than in group 1 patients. Indeed, MBF in normally functioning LV segments in group 2 patients was higher than in group 1 patients (95.5±26.7 versus 82.7±18.0 mL/min per 100 g, P<.05). MBF in the dysfunctional LV segments in group 2 patients was significantly lower than in normally functioning LV segments in the group 2 patients (77.1±24.6 versus 95.5±26.7 mL/min per 100 g, P<.001).' These data demonstrate that MBF to the dysfunctional LV segments was reduced (and not "not reduced," which the authors repeatedly assert). Conversano et al3 also have demonstrated using PET that MBF in hibernating myocardium was lower than in normal subjects (40±5 versus 113±33 mL/min per 100 g). It is possible that MBF to normally functioning LV segments in at least some of their patients, all of whom had coronary artery disease, may have been somewhat reduced, because small reductions of MBF may not necessarily be associated with LV dysfunction.4 The values for MBF in their group 1 patients (82.7±18.0 mL/min per 100 g) are lower than those previously reported in normal subjects using PET (117±33 mL/min per 100 g).3 Thus, MBF to the dysfunctional LV segments in group 2 patients (hibernating myocardial segments) may be reduced to a greater extent when compared with normal subjects than would be apparent by comparing it with group 1 patients or even those in group 2. Data of Conversano et a13 support this hypothesis (vide supra). It also would have been very useful to know whether the patients in groups 1 and 2 had disease of coronary arteries (and the percent stenosis in the diseased arteries) other than the totally occluded