Premature ventricular complexes
Premature ventricular complexes (PVCs) are an electrocardiographic (ECG) conduction abnormality of the canine heart which results in left systolic dysfunction.
This cardiac disorder is characterized by cardiac impulses initiated within the ventricles instead of the sinus node due to increased automaticity of the ventricle or reentry stimulation/
PVCs are characterized by a premature ventricular contraction without a preceding P wave, with a duration of more than 0.12 seconds (P waves dissociated from the QRS complex). The QRS complex is usually wide and bizarre.
While the presence of PVCs may carry adverse prognosis especially in structural heart disease, PVCs in general are thought to be benign or secondary to the cardiomyopathic process. Studies have demonstrated improvement of left ventricular function after successful PVC suppression strategy.
PVCs are often caused by:
- ventricular concentric hypertrophy or eccentric hypertrophy due to underlying cardiomyopathy
- Anemia, hypomagnesemia
- Cardiac neoplasia - e.g. myxoma, chemodectoma, paraganglioma, rhabdomyosarcoma, right atrial hemangiosarcoma
- Gastric dilation and volvulus
- Congestive heart failure
- Metabolic derangements - acidosis, hypokalemia, hypocalcemia, puerperal hypocalcemia
- Traumatic myocarditis, endocarditis or myocardial ischemia/reperfusion injuries
- Neoplasia, Immune-mediated disease
- Toxicity due to digoxin, barbiturates, antiarrhythmic agents, sparfloxacin, grepafloxacin
- Occult dilated cardiomyopathy in Dobermans
- Juvenile ventricular arrhythmia (PVCs and ventricular tachycardia) in German Shepherds
- Arrythmogenic right ventricular cardiomyopathy in the Boxer - >100 PVCs in a 24 hour period (using a Holter) is generally considered diagnostic
- Doxorubicin-induced myocardial failure
- Brody effect following blood loss
- Atrial or ventricular bigeminy or chronic atrioventricular block, which result in increased action potential duration, early afterdepolarization and torsade de pointes.
Clinically affected dogs usually present with weakness, exercise intolerance, syncope and sudden death, and these symptoms should be differentiated from ventricular tachycardia and ventricular fibrillation.
Treatment for congenital arrhythmias usually requires specific arrhythmia drugs such as mexiletine (8 mg/kg PO q8 h) or sotalol (2.5 mg/kg PO q12 h).
Lignocaine can also be used in emergency situations, given at 2 - 4 mg/kg slow IV, then repeated every 5 - 10 minutes to maximum of 8 mg/kg, followed by 25 - 75 μg/kg/min as constant rate infusion.
Premature ventricular complexes should be avoided as the risk of ventricular fibrillation and death are significant. Prediction of ventricular fibrillation secondary to PVCs is often based on tachycardia, which, if present, is an strong indicator to initiate anti-arrhythmic therapy. However, VPCs in dogs with normal or low heart rates are not considered life threatening.
- Pacchia CF et al (2012) Atrial Bigeminy Results in Decreased Left Ventricular Function: An Insight into the Mechanism of PVC-Induced Cardiomyopathy. Pacing Clin Electrophysiol 35(10):1232-1235
- Huizar JF et al (2011) Left ventricular systolic dysfunction induced by ventricular ectopy: a novel model for premature ventricular contraction-induced cardiomyopathy. Circ Arrhythm Electrophysiol 4(4):543-549
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- Watanabe I et al (2011) Effect of the ATP-sensitive K⁺ channel opener nicorandil in a canine model of proarrhythmia. Int Heart J 52(5):318-322