Premature ventricular complexes

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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.

In dogs, PVCs commonly coexist with and are a reversible cause of cardiomyopathy[1], and is observed commonly in large-breed dogs, especially the Boxer and Doberman.

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[2]. Studies have demonstrated improvement of left ventricular function after successful PVC suppression strategy[3].

PVCs are often caused by:

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.

References

  1. 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
  2. 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
  3. ogun F et al (2007) Radiofrequency ablation of frequent, idiopathic premature ventricular complexes: Comparison with a control group without intervention. Heart Rhythm 4:863–867
  4. Hennan JK et al (2009) GAP-134 ([2S,4R]-1-[2-aminoacetyl]4-benzamidopyrrolidine-2-carboxylic acid) prevents spontaneous ventricular arrhythmias and reduces infarct size during myocardial ischemia/reperfusion injury in open-chest dogs. J Cardiovasc Pharmacol Ther 14(3):207-214
  5. Wess G et al (2010) Ability of a 5-minute electrocardiography (ECG) for predicting arrhythmias in Doberman Pinschers with cardiomyopathy in comparison with a 24-hour ambulatory ECG. J Vet Intern Med 24(2):367-371
  6. Cruickshank J et al (2009) Genetic analysis of ventricular arrhythmia in young German Shepherd Dogs. J Vet Intern Med 23(2):264-270
  7. Gelzer AR et al (2010) Combination therapy with mexiletine and sotalol suppresses inherited ventricular arrhythmias in German shepherd dogs better than mexiletine or sotalol monotherapy: a randomized cross-over study. J Vet Cardiol 12(2):93-106
  8. Meurs KM et al (2010) Genome-wide association identifies a deletion in the 3' untranslated region of striatin in a canine model of arrhythmogenic right ventricular cardiomyopathy. Hum Genet 128(3):315-324
  9. Ker J et al (2009) The Brody effect induced by premature ventricular complexes in the ovine heart. Onderstepoort J Vet Res 76(4):443-448
  10. 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