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Left ventricular dysfunction and dilatation resulting from chronic supraventricular tachycardia
The Journal of Thoracic and Cardiovascular Surgery
|July 1, 1987
Summary
Chronic supraventricular tachycardia significantly impairs ventricular function, causing cardiac enlargement. While ejection fraction recovers, enlarged ventricles persist even after tachycardia elimination, indicating lasting functional changes.
Area of Science:
- Cardiology
- Cardiac Electrophysiology
- Ventricular Function
Background:
- Chronic supraventricular tachycardia (SVT) is suspected to cause impaired ventricular function.
- Resolution of SVT through surgical procedures may restore normal ventricular function.
Purpose of the Study:
- To investigate the functional consequences of prolonged supraventricular tachycardia.
- To assess reversibility of tachycardia-induced cardiac changes.
Main Methods:
- Implanted permanent asynchronous atrial pacemakers in 12 awake dogs to induce chronic tachycardia (190 +/- 5 bpm).
- Utilized serial radionuclide angiograms to monitor ventricular function over 3 months.
- Assessed recovery of ventricular function in 5 dogs over 12 weeks post-tachycardia.
Main Results:
- Prolonged tachycardia significantly reduced ejection fraction (49% to 29%) and increased left ventricular end-diastolic volume (69 to 105 ml).
- Stroke volume and cardiac output remained unchanged during tachycardia.
- Following tachycardia cessation, ejection fraction normalized, but end-diastolic volume remained persistently elevated (67 to 91 ml).
Conclusions:
- Prolonged supraventricular tachycardia induces significant functional cardiac changes, including cardiac enlargement.
- These tachycardia-induced functional changes and cardiac enlargement are not immediately reversible after eliminating the arrhythmia.