By Joshua D. Moss, MD
Associate Professor of Clinical Medicine, Cardiac Electrophysiology, Division of Cardiology, University of California, San Francisco
Dr. Moss reports no financial relationships relevant to this field of study.
SYNOPSIS: Several echocardiographic and electrocardiographic features were identified that can help predict if a cardiomyopathy is caused purely by frequent premature ventricular complexes and whether left ventricular function will normalize with ablative therapy.
SOURCE: Penela D, Fernández-Armenta J, Aguinaga L, et al. Clinical recognition of pure premature ventricular complex-induced cardiomyopathy at presentation. Heart Rhythm 2017; Jul 27. pii: S1547-5271(17)30893-7. doi: 10.1016/j.hrthm.2017.07.025. [Epub ahead of print].
Frequent premature ventricular complexes (PVCs) can both independently cause a cardiomyopathy and worsen an existing cardiomyopathy. In patients with normal left ventricular (LV) function and frequent PVCs, several factors have been identified as possible predictors of future cardiomyopathy, including higher PVC burden, longer PVC-QRS duration, non-sustained ventricular tachycardia (VT), and presence of multiple PVC morphologies. In patients with cardiomyopathy caused “purely” by frequent PVCs, LV function often recovers completely after successful suppression of the PVCs with catheter ablation. In contrast, LV function may improve only partially or minimally if the PVCs are merely worsening a nonischemic cardiomyopathy with another principal etiology.
In this prospective study at five centers, Penela et al sought to determine what characteristics could predict which patients would gain complete recovery of LV function with successful PVC ablation. Over a 5.5-year period, 105 patients with a PVC burden > 4% on 24-hour Holter monitoring, LV ejection fraction < 50% that was not known to pre-date the diagnosis of PVCs, and no evidence of ischemic heart disease underwent catheter ablation after at least three months of guideline-directed medical therapy. Acute success was achieved in 93 (89%), with sustained success through 12 months of follow-up in 74 (71%). All patients with sustained successful reduction in PVC burden by at least 80%, as well as those with partial suppression but complete recovery of LV function, were included in the analysis.
There were two independent predictors of any significant echocardiographic response to PVC ablation: shorter sinus rhythm QRS duration and larger baseline PVC burden (with a pre-ablation burden > 12% conferring 98% sensitivity and 90% specificity for response). About half the patients demonstrated complete normalization of LV function with sustained or partial suppression of PVCs and were deemed to have a “pure” PVC-induced cardiomyopathy. Findings independently associated with such a cardiomyopathy included shorter sinus rhythm QRS duration and PVC-QRS duration, higher PVC burden (with a pre-ablation burden > 17% conferring 97% sensitivity and 78% specificity for the diagnosis), and smaller LV end-diastolic and end-systolic diameters. An algorithm was derived to distinguish patients prior to therapy: The presence of an intrinsic QRS > 130 msec, baseline PVC burden < 17%, or LV end-diastolic dimension > 63 mmHg was predictive of PVC-worsened cardiomyopathy, while the absence of all three suggested a pure PVC-induced cardiomyopathy with 85% sensitivity and 98% specificity.
COMMENTARY
This study provides more information for cardiologists to use in identifying cardiomyopathy patients who could benefit most from additional ambulatory ECG monitoring and referral for ablative therapy. By evaluating a relatively simple set of parameters that typically are collected during routine evaluation of cardiomyopathy, clinicians can give a better explanation of the potential effect of PVC ablation (particularly when the PVCs themselves are not very symptomatic). More meaningful long-term prognoses can be discussed, and primary prevention ICD implantation may be delayed successfully or deferred completely.
One could argue that incomplete recovery of LV systolic function after successful PVC ablation does not rule out the possibility that some irreversible structural disease has developed purely because of long-standing PVCs. In fact, one patient of 13 who exhibited complete normalization in ejection fraction and followed longer than 12 months eventually developed worsening LV function again. However, the definition of a “pure” PVC-induced cardiomyopathy is largely semantic. What the authors effectively have described is a means of predicting complete recovery, with the best prognosis conferred by narrow sinus QRS, PVC burden > 17%, and non-dilated LV.
Equally interesting are those factors that were not predictive. Older age did not confer a lower likelihood of pure PVC-induced cardiomyopathy and probability of complete recovery with ablation; neither did lower LV ejection fraction. Whereas older patients with severely decreased LV systolic function instinctively might seem to carry a poorer prognosis, their chance for recovery with PVC ablation may be as good as everyone else’s. The absence of pathological late gadolinium enhancement on cardiac MRI also may help predict recovery, although this study likely was underpowered when it comes to answering that question.
One management option not addressed is antiarrhythmic drug therapy, and whether PVC suppression with medications could confer the same benefits as successful catheter ablation. Many cardiologists and patients may be more comfortable with non-invasive therapies without associated procedural risks. Nevertheless, PVC ablation has been shown in multiple studies to be both safe and effective, and antiarrhythmic drugs (particularly amiodarone) are by no means risk-free. Notably, in the present study, procedure-related complications were infrequent, including one femoral pseudoaneurysm and two pericardial effusions (none required surgical intervention). Patients undergoing evaluation and treatment for cardiomyopathy should be considered for ambulatory ECG monitoring to assess PVC burden, particularly if they exhibit any ectopy on a routine 12-lead ECG or suggestive symptoms. Referral to an electrophysiologist for discussion of the relative risks and benefits of antiarrhythmic drug therapy vs. catheter ablation is appropriate for any cardiomyopathy patient with > 5-10% PVC burden, and especially if a pure PVC-induced cardiomyopathy is identified using the criteria above.
Several echocardiographic and electrocardiographic features were identified that can help predict if a cardiomyopathy is caused purely by frequent premature ventricular complexes and whether left ventricular function will normalize with ablative therapy.
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