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Potentiation of reperfusion-associated ventricular fibrillation by left ventricular hypertrophy
A L Taylor1, R Winter, F Thandroyen
1Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas.
Insights
Left ventricular hypertrophy significantly increases the risk of reperfusion ventricular fibrillation after ischemia. Lidocaine protects against ischemia but not reperfusion arrhythmias in hypertrophied hearts.
Area of Science:
- Cardiology
- Electrophysiology
- Cardiac Hypertrophy
Background:
- Electrophysiological changes in hypertrophied myocytes can predispose hearts to arrhythmias.
- Hypertrophy combined with ischemia is linked to sudden cardiac death.
- The effect of hypertrophy on reperfusion arrhythmias remains undescribed.
Purpose of the Study:
- To investigate the hypothesis that left ventricular hypertrophy potentiates reperfusion-associated arrhythmias.
- To determine if left ventricular hypertrophy influences the incidence of ventricular fibrillation during reperfusion following coronary artery occlusion.
Main Methods:
- 37 unsedated dogs underwent 15 minutes of coronary artery occlusion and reperfusion.
- 17 dogs had induced left ventricular hypertrophy; 20 served as controls.
- All dogs received lidocaine to assess its protective effects during ischemia and reperfusion.
Main Results:
- Reperfusion ventricular fibrillation occurred in 7/17 dogs with left ventricular hypertrophy vs. 1/18 controls (p <= 0.05).
- Hypertension presence did not significantly affect reflow ventricular arrhythmias.
- Increased heart rate before reperfusion correlated with increased ventricular fibrillation incidence.
Conclusions:
- Left ventricular hypertrophy significantly increases the incidence of reperfusion-induced ventricular fibrillation.
- This effect is independent of hypertension.
- Lidocaine protected against ischemia-induced ventricular fibrillation but not reperfusion-induced ventricular fibrillation in hypertrophied hearts.
Abstract:
Important electrophysiological alterations that may predispose hearts to arrhythmias have been described for hypertrophied myocytes, and hypertrophy coupled with ischemia has been associated with an increased incidence of sudden death; however, an influence of hypertrophy on reperfusion arrhythmias has not been previously described. We hypothesized that reperfusion-associated arrhythmias would be potentiated by left ventricular hypertrophy. After induction of renovascular hypertension, 37 awake, unsedated dogs (17 with left ventricular hypertrophy and 20 without hypertrophy) underwent 15 minutes of coronary artery occlusion and reperfusion. All dogs were pretreated with lidocaine bolus injections and with lidocaine by continuous infusion during coronary occlusion and reperfusion. Reperfusion-associated ventricular fibrillation occurred in seven of 17 dogs with left ventricular hypertrophy versus one of 18 dogs without hypertrophy (p less than or equal to 0.05). The presence of hypertension was not significantly associated with an increased incidence of reflow ventricular arrhythmias. Neither QT interval nor area-at-risk was different between the dogs with and without reperfusion ventricular fibrillation; however, increased heart rate just before reperfusion did correlate with an increased incidence of ventricular fibrillation at reperfusion. Thus, 1) left ventricular hypertrophy was associated with a significantly increased incidence of reperfusion-induced ventricular fibrillation after 15 minutes of ischemia, 2) this increased incidence was independent of the presence of hypertension, and 3) lidocaine protected control and hypertrophied hearts against ventricular fibrillation during ischemia but was ineffective in protecting hypertrophied hearts against reperfusion-induced ventricular fibrillation.