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Relation between ventricular and myocyte function with tachycardia-induced cardiomyopathy
F G Spinale1, B M Fulbright, R Mukherjee
1Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston.
Circulation Research
|July 1, 1992
Summary
Chronic supraventricular tachycardia (SVT) leads to heart muscle cell dysfunction and structural changes, causing SVT cardiomyopathy. This study reveals primary defects in myocyte contractile performance and calcium responsiveness in SVT cardiomyopathy.
Area of Science:
- Cardiology
- Cell Biology
- Physiology
Background:
- Chronic supraventricular tachycardia (SVT) is known to cause left ventricular (LV) dilatation and dysfunction.
- Alterations in myocyte function and structure are suspected contributors to SVT-induced cardiomyopathy.
Purpose of the Study:
- To investigate LV function and isolated myocyte structure and function in pigs with pacing-induced SVT cardiomyopathy.
- To determine the cellular mechanisms underlying SVT cardiomyopathy.
Main Methods:
- Pacing-induced SVT cardiomyopathy in pigs (3 weeks at 240 bpm) compared to controls.
- Assessment of LV function via echocardiography and catheterization.
- Evaluation of isolated myocyte function using computer-assisted video microscopy, examining contractile performance in attached and unattached states, and calcium responsiveness.
Main Results:
- LV fractional shortening and peak +dP/dt were significantly reduced in SVT pigs.
- Isolated SVT myocytes exhibited significantly lower shortening extent and velocity in both attached and unattached states compared to controls.
- SVT myocytes showed blunted responsiveness to extracellular calcium and reduced myofibril volume.
Conclusions:
- SVT cardiomyopathy likely results from primary defects in isolated myocyte contractile performance.
- Reduced myocyte contractile function in SVT cardiomyopathy is associated with cytoarchitectural abnormalities and impaired calcium responsiveness.