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Ventricular Ectopy in the normal heart ... When should we worry? 06 July 2010 BCS Editorial Ventricular ectopy in the setting of a structurally normal heart has historically been thought of as a benign phenomenon [1, 2] and, whilst many patients are symptomatic, it was thought that the presence of ectopy per se conferred no long term risk. There have, however, been several studies over the past few years investigating the association between frequent ventricular ectopy and the development of impaired left ventricular function.
In the most recent paper by Baman et al[3], the aim was to investigate how many is too many in respect of PVC count. The authors used a selected cohort of 174 patients who had all been referred for ablation of frequent PVCs. 90 % were symptomatic of the ectopy. The patients had failed to respond to initial therapies (usually beta-blockers or calcium antagonists) and coronary disease had been ruled out. All patients underwent echocardiography and holter monitoring at baseline and 3 months and 6 months after ablation to determine EF and ectopy burden.
The authors determined that LV dysfunction was significantly associated with a higher PVC burden, and went onto report that using a cut-off value of 24% results in a sensitivity and specificity of approximately 80%, whilst cautioning that a PVC burden of under 24% may still cause or aggravate existing cardiomyopathy and therapy targeting PVC burden of >10% in these cases may be appropriate.
Whilst the study clearly identifies a link between cardiomyopathy and frequent PVCs, it also highlights the importance of reversibility after ablation, which is clearly important. It is also important to note that this study identifies patients who had already been referred for therapy targeting their ectopy and as such this is likely to introduce a degree of bias and, perhaps, over estimate the prevalence of LV dysfunction in this group of patients.
In a previous study by Niwano and colleagues [4] the focus was directed to those patients with frequent ventricular ectopy and preserved LV function at baseline, demonstrating a significant decrease in LV function in approximately 20% of those cases.
These studies suggests that we should give thought to left ventricular function in patients with frequent PVCs and consider ablation therapy not only as a therapeutic measure, but perhaps as a preventative one.
REFERENCES
1. Conti, C.R., Ventricular arrhythmias: a general cardiologist's assessment of therapies in 2005. Clin Cardiol, 2005. 28(7): p. 314-6.
2. Gaita, F., et al., Long-term follow-up of right ventricular monomorphic extrasystoles. J Am Coll Cardiol, 2001. 38(2): p. 364-70.
3. Baman, T.S., et al., Relationship between burden of premature ventricular complexes and left ventricular function. Heart Rhythm.
4. Niwano, S., et al., Prognostic significance of frequent premature ventricular contractions originating from the ventricular outflow tract in patients with normal left ventricular function. Heart, 2009. 95(15): p. 1230-7.
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