Key result
Complete heart block in rats decreased heart rate by ~50% and increased stroke volume 2.5 times (P < 0.01), leading to cardiomegaly without congestive heart failure.
Why the study?
Does complete heart block alter myocardial function, morphology, and energy metabolism in a rat model?
Does complete heart block alter myocardial function, morphology, and energy metabolism in a rat model?
p-value: p=<0.01
A rat model of complete heart block demonstrates that severe sustained bradycardia induces compensatory stroke volume increases and eccentric hypertrophy without progressing to congestive heart failure over 12 weeks.
Does not support changes in clinical management of heart block; leaves open whether similar adaptations occur in patients.
AIMS: Severe sustained bradycardia may cause acute and possibly chronic congestive heart failure (CHF). The aim of this study was to investigate acute and chronic effects of complete heart block (CHB) on cardiac function, morphology, and creatine (Cr) metabolism. METHODS AND RESULTS: CHB was induced in male Sprague-Dawley rats (approximately 250 g, n = 11) by means of electrocautery applied to the region of AV node and were compared with controls (n = 15). The rats were investigated at 1, 3, and 12 weeks after CHB induction with transthoracic echocardiography. Invasive haemodynamic assessment of left and right ventricular pressures was performed at 12 weeks. After the sacrifice, the hearts were freeze-clamped for analysis of myocardial Cr, and high energy phosphometabolites. The efficacy of operative procedure was 54%. The peri-operative mortality rate was 20%. Heart rate (HR) decreased by approximately 50% (P < 0.01) while stroke volume (SV) increased 2.5 times (P < 0.01) in the CHB rats. Cardiac index remained unchanged. The rats with CHB grew normally and were in no apparent distress. Filling pressures in left and right ventricles were normal. The CHB rats developed marked cardiomegaly with biventricular dilatation and eccentric left ventricular hypertrophy (P < 0.01). There was no change in the myocardial content of Cr and high energy phosphometabolites. CONCLUSION: Rats with CHB are compensating for reduction in HR with increased SV without haemodynamic and biochemical characteristics of CHF. This model may be useful to study the effects of CHB and bradycardia on myocardial structure, function, electrophysiology, and metabolism as well as for studies of cell therapy for reparation of AV conductance.
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Gizurarson et al. (2007) studied Complete heart block (n=26). Complete heart block (CHB) induction via electrocautery vs. Controls was evaluated on Cardiac function, morphology, and creatine metabolism (p=<0.01). Complete heart block in rats decreased heart rate by ~50% and increased stroke volume 2.5 times (P < 0.01), leading to cardiomegaly without congestive heart failure.
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