Relation of contractile reserve of hibernating myocardium to myocardial structure in humans.

Myocardium to Myocardial Structure in Humans To the Editor: Nagueh and colleagues1 investigated the relationship between myocardial ultrastructure and the inotropic contractile reserve of the hibernating myocardium. They suggested that the amount of interstitial fibrosis in a dysfunctional myocardial segment is an important determinant of both inotropic contractile reserve during dobutamine stimulation and of the recovery of function after revascularization. The authors showed that myocardium with $30% interstitial fibrosis does not respond to dobutamine and that its function does not improve after revascularization. This is in agreement with earlier reports, which also demonstrated that the presence of this magnitude of interstitial fibrosis is associated with irreversible myocardial dysfunction.2,3 We suggest, therefore, that myocardial segments with these characteristics be removed from the analysis because they represent irreversibly damaged scar tissue rather than hibernating myocardium. Nagueh et al1 conclude that the contractile response to dobutamine inversely correlates with the extent of interstitial fibrosis. However, close analysis of their data does not support this conclusion. Two groups of hibernating segments are reported. Group 3 consisted of segments with near-normal ultrastructure and minimal fibrosis (1%) that exhibited inotropic contractile reserve and recovered function after revascularization; in group 2, despite the modest amount of fibrosis (9%), 50% of the segments that had improved function after revascularization (ie, hibernating) did not exhibit inotropic contractile reserve. No continuous relationship between fibrosis and inotropic contractile reserve can be demonstrated in these segments. Thus, in hibernating myocardium, which is defined by the occurrence of improved systolic function after revascularization, the amount of interstitial fibrosis is low and seems unlikely to impair the response to adrenergic stimulation. A number of studies, including our own, have also reported the lack of inotropic contractile reserve in a substantial number of hibernating myocardial segments,4,5 particularly in those from patients with severe left ventricular dysfunction. Our work indicated that hibernating myocardial segments (defined by contractile improvement after revascularization) without inotropic contractile reserve have an amount of fibrosis ('14%) similar to that in segments that exhibit a response to dobutamine but a greater number of myocytes with marked myofibrillar loss (26% versus 11%).6 This known ultrastructural “adaptation” of hibernating myocardium provides a plausible explanation for the lack of response to adrenergic stimulation. We suggest that the lack of inotropic contractile reserve found in many hibernating myocardial segments, which can be identified as viable by PET scanning and as hibernating by postoperative recovery of function, is due to the abundance of myocytes depleted of contractile units rather than the presence of fibrosis.