[Hibernating myocardium. An incomplete adaptation to ischemia]

Area of Science:

• Cardiology
• Cardiovascular Pathology
• Cellular Biology

Background:

• Hibernating myocardium is a state of impaired cardiac function due to reduced oxygen supply.
• The prevailing hypothesis suggested this was an adaptive response to chronic ischemia.

Purpose of the Study:

• To investigate the cellular and molecular basis of hibernating myocardium.
• To determine if hibernating myocardium represents adaptation or degeneration.

Main Methods:

• Utilized angiography, radionuclide ventriculography, thallium scintigraphy, and dobutamine echocardiography to identify hibernating myocardium in 38 patients.
• Performed cardiac biopsies for electron microscopy, immunohistochemistry, and in situ hybridization to analyze myocardial structure and protein expression.
• Assessed apoptosis using terminal deoxynucleotidyl transferase end-labeling and electron microscopy.

Main Results:

• Biopsies revealed structural degeneration with reduced protein/mRNA expression and disorganization of contractile proteins.
• Significant reparative fibrosis was observed due to increased extracellular matrix proteins.
• Apoptosis was detected, indicating programmed cell death.
• Postoperative radionuclide ventriculography showed significant improvement in regional function (23.5% to 48%).
• Echocardiographic wall-motion score improved from 3.4 to 1.8.
• Severity of morphological changes correlated with functional recovery; severe degeneration (stage 3) resulted in only partial recovery.

Conclusions:

• Hibernating myocardium is characterized by cellular degeneration, not adaptation.
• The extent of degeneration progressively diminishes the potential for complete structural and functional recovery.
• Early revascularization is recommended for patients with hibernating myocardium to maximize recovery potential.