Histological alterations in chronically hypoperfused myocardium. Correlation with PET findings.

Abstract

Background In patients with chronic coronary artery disease (CAD)

Medical and Cellular Implications of Stunning, Hibernation, and Preconditioning

“…Human hibernating myocardium has a distinctive histological appearance with myolysis, glycogen accumulation, and increased interstitial fibrosis (Fig 3). 134,[152][153][154] It has been suggested that these histopathological changes may represent a dedifferentiation of the myocytes. 153 When advanced, such changes indicate a poor prognosis for recovery even with adequate revascularization.…”

Structural remodelling of cardiomyocytes in the border zone of infarcted rabbit heart

“…After revascularisation, the hibernating segments often show a delayed recovery of function which can take a few months to more than one year in a fraction of patients with chronic hibernating myocardium [8]. It has been suggested that the structural remodelling found in chronic hibernating myocardium is at least partially responsible for this delayed recovery of function [9][10][11]. In recent studies we have also characterized the dedifferentiation process in an in vitro model by co-culturing adult rabbit CM's with cardiac fibroblasts [12,13].…”

Downregulation of Immunodetectable Connexin43 and Decreased Gap Junction Size in the Pathogenesis of Chronic Hibernation in the Human Left Ventricle

“…Histological and electron microscopic examination of biopsy material obtained from hibernating regions reveal a variable degree of fibrous tissue replacement, with a proportion of the myocytes showing depleted contractile material, numerous and small mitochondria, and irregular nuclear envelopes. 3,4 Although early studies suggested that such altered myocytes characterized the hibernating state 3 and could explain the delay in recovery in contractile function after successful revascularization, 5 more recent reports have described them in equal frequency in both hibernating and nonhibernating ventricular segments. 4,6 Similar cellular features have also been described in ventricular specimens from patients with dilated, nonischemic cardiomyopathy 7 as well as in rat cardiac myocytes after a short period of unloading.…”

“…3,4 Although early studies suggested that such altered myocytes characterized the hibernating state 3 and could explain the delay in recovery in contractile function after successful revascularization, 5 more recent reports have described them in equal frequency in both hibernating and nonhibernating ventricular segments. 4,6 Similar cellular features have also been described in ventricular specimens from patients with dilated, nonischemic cardiomyopathy 7 as well as in rat cardiac myocytes after a short period of unloading. 8 It can therefore be hypothesized that these are secondary features of cells contracting against a low afterload and are not characteristic of hibernation.…”