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Mechanical and electrical properties of cardiomyopathic hearts of Syrian hamsters
J M Capasso1, G Olivetti, P Anversa
1Department of Pathology, New York Medical College, Valhalla 10595.
Insights
Cardiomyopathy in Syrian hamsters impairs heart muscle function and electrical activity. This leads to earlier and more severe arrhythmias when exposed to glycosides, suggesting a link to disease progression.
Area of Science:
- Cardiology
- Physiology
- Pharmacology
Background:
- Cardiomyopathy precedes congestive heart failure in Syrian hamsters.
- Myocardial dysfunction involves mechanical and electrical alterations.
Purpose of the Study:
- To investigate mechanical and electrical changes in cardiomyopathic hamster hearts.
- To assess the arrhythmogenic potential of glycoside exposure in this model.
Main Methods:
- In vitro study of left ventricular posterior papillary muscles.
- In vivo electrocardiographic response to ouabain infusion.
Main Results:
- Decreased myocardial tension, prolonged contraction timing, and increased action potential duration observed.
- Reduced velocity of muscle shortening and relengthening.
- Glycoside infusion induced earlier and more severe arrhythmias (PVCs, VT, VF) in diseased hamsters.
Conclusions:
- Impaired mechanical performance and abnormal electrical activity contribute to disease progression.
- These alterations are linked to lethal arrhythmias in the cardiomyopathic hamster model.
Abstract:
To determine whether the cardiomyopathy that develops in the Syrian hamster before the occurrence of congestive heart failure is associated with mechanical and electrical alterations consistent with myocardial dysfunction, left ventricular posterior papillary muscles of control and cardiomyopathic animals at 120 days of age were studied in vitro. Moreover, the electrocardiographic response to ouabain was investigated in vivo to analyze the arrhythmogenic potential of the cardiomyopathic heart to glycoside exposure. Results showed a decreased tension-generating ability of the myocardium in the diseased animals, which was accompanied by a prolongation of the timing parameters of contraction and an increase in the duration of the repolarization phase of the transmembrane action potential. Furthermore, the velocity of isotonic muscle shortening and relengthening was depressed at all physiological loads. Glycoside infusion elicited premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation in diseased hamsters much earlier in time than in healthy controls. The impairment in mechanical performance in association with the abnormality in membrane electrical activity may be responsible for the progression of the disease process and the occurrence of lethal arrhythmias in this animal model.