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Cardiac hypothermia evaluated by ultrastructural studies in man
The Journal of Thoracic and Cardiovascular Surgery
|April 1, 1978
Summary
Cardiac hypertrophy, not ischemia, caused cellular damage in patients undergoing cardiopulmonary bypass. Deep hypothermia protected mitochondria during surgery, but structural changes persisted.
Area of Science:
- Cardiovascular Surgery
- Cardiac Pathology
- Cellular Biology
Background:
- Cardiopulmonary bypass (CPB) involves cardiac arrest, posing risks to myocardial tissue.
- Deep hypothermia is used to protect the heart during CPB, but its effects on hypertrophic myocardium require further investigation.
Purpose of the Study:
- To investigate the structural changes in hypertrophic myocardium during CPB with deep hypothermia.
- To differentiate between cellular damage caused by intraoperative ischemia and that resulting from cardiac hypertrophy.
Main Methods:
- Transmural left ventricular biopsies were obtained from 13 patients undergoing CPB.
- Biopsies were collected at baseline, after aortic cross-clamping, and after reperfusion.
- Deep hypothermia (15°C) was employed during ischemic arrest.
Main Results:
- Mitochondrial structure remained normal throughout the procedure.
- Cellular alterations, including widened intercalated discs, edema, myelin figures, and myofibrillar lysis, were observed.
- No clear correlation was found between the severity of structural injuries and the duration of aortic cross-clamping.
Conclusions:
- The observed cellular alterations in hypertrophic myocardium are likely a consequence of cardiac hypertrophy itself.
- Deep hypothermia effectively protected mitochondrial integrity during CPB.
- Intraoperative ischemia time did not appear to be the primary driver of observed cellular damage in this cohort.