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Converting enzyme inhibition normalizes QT interval in spontaneously hypertensive rats
C Baillard1, P Mansier, P V Ennezat
1U127-INSERM, Hôpital Lariboisiere, Paris, France.
Hypertension (Dallas, Tex. : 1979)
|September 16, 2000
Summary
Spontaneously hypertensive rats (SHR) show increased QT interval and left ventricular mass due to heart pressure overload. Converting enzyme inhibition reversed these changes, demonstrating SHR
Area of Science:
- Cardiology
- Physiology
- Pharmacology
Background:
- The QT interval, a measure of cardiac repolarization, is not well-characterized in rats.
- Spontaneously hypertensive rats (SHR) develop pressure-overloaded hearts.
- Assessing QT interval changes in response to cardiac mechanical overload is crucial.
Purpose of the Study:
- To quantify the QT interval in spontaneously hypertensive rats (SHR).
- To investigate the effect of converting enzyme inhibition on QT interval and cardiac remodeling in SHR.
- To establish SHR as a model for studying QT interval adaptations during mechanical overload.
Main Methods:
- Implanted telemetry system for ECG and RR interval recording in freely moving rats.
- Manual QT duration determination using a calibrated gauge.
- Echocardiography for sequential assessment of left ventricular mass.
- Time-frequency domain analysis for heart rate variability evaluation.
Main Results:
- 12-month-old SHR exhibited higher left ventricular mass, QT, and RR intervals compared to Wistar rats.
- Trandolapril treatment (2 months) reduced systolic blood pressure, left ventricular mass, and QT interval in SHR.
- A positive correlation was observed between QT interval and left ventricular mass.
- Heart rate variability remained unchanged throughout the study.
Conclusions:
- The QT interval in SHR reflects phenotypic changes associated with mechanical heart overload.
- SHR are suitable for longitudinal QT interval studies, aiding in vivo determination of cardiac adaptation.
- Converting enzyme inhibition demonstrates a reversible increase in QT interval in pressure-overloaded hearts.