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Class IC antiarrhythmic drugs for suspected premature ventricular contraction-induced cardiomyopathy
Matthew C Hyman1, Danielle Mustin1, Gregory Supple1
1Section of Cardiac Electrophysiology, Division of Cardiovascular Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania.
Insights
Class IC antiarrhythmic drugs (IC-AADs) effectively reduced premature ventricular contractions (PVCs) and improved heart function in patients with PVC-induced cardiomyopathy. This study found IC-AADs to be safe and effective in this patient group.
Area of Science:
- Cardiology
- Electrophysiology
- Pharmacology
Background:
- Class IC antiarrhythmic drugs (IC-AADs) effectively suppress premature ventricular contractions (PVCs).
- However, IC-AADs are associated with increased mortality in post-myocardial infarction patients with PVCs and left ventricular dysfunction.
- The safety of IC-AADs for treating premature ventricular contraction-induced cardiomyopathy (PVC-CM) is not established.
Purpose of the Study:
- To determine the safety and efficacy of IC-AADs in patients suspected of having PVC-CM.
Main Methods:
- Retrospective review of electronic medical records at the Hospital of the University of Pennsylvania.
- Identification of patients suspected of PVC-CM treated with flecainide or propafenone.
- Review of clinical, electrocardiographic, and imaging data.
Main Results:
- Twenty patients with suspected PVC-CM received IC-AADs, with a mean PVC burden reduction from 36.2% to 10.0% (P <.001).
- Mean left ventricular ejection fraction (LVEF) improved significantly from 37.4% to 49.0% (P <.001).
- No sustained ventricular arrhythmias or sudden cardiac deaths occurred during an average follow-up of 3.8 years.
Conclusions:
- IC-AADs effectively suppressed PVCs and improved LVEF in the majority of patients with suspected PVC-CM.
- No adverse events were observed in this small cohort, suggesting potential safety and efficacy.
Background:
Class IC antiarrhythmic drugs (IC-AADs) can effectively suppress premature ventricular contractions (PVCs). However, IC-AADs increase mortality in patients with PVCs and left ventricular dysfunction after myocardial infarction. Whether IC-AADs can be safely used to treat premature ventricular contraction-induced cardiomyopathy (PVC-CM) remains to be established.
Objective:
The purpose of this study was to determine the safety and efficacy of IC-AADs in patients suspected of having PVC-CM.
Methods:
The electronic medical records at the Hospital of the University of Pennsylvania were screened to identify all patients suspected of having PVC-CM treated with flecainide or propafenone. Clinical, electrocardiographic, and imaging studies were reviewed.
Results:
Twenty patients suspected of having PVC-CM were treated with IC-AADs. Patients had undergone an average of 1.3 ± 0.2 previous unsuccessful ablations. Six had an implantable or wearable defibrillator. With IC-AAD treatment, mean PVC burden decreased from 36.2% ± 3.5% to 10.0% ± 2.4% (P <.001). Mean left ventricular ejection fraction (LVEF) increased from 37.4% ± 2.0% to 49.0% ± 1.9% (P <.001). Seven patients with myocardial delayed enhancement on cardiac magnetic resonance imaging (all <5% of the total myocardium) experienced similar improvement in LVEF (from 36.8% ± 4.3% before IC-AAD to 51.7% ± 3.7% afterward; P <.01). Over an average 3.8 ± 0.9 treatment-years, no sustained ventricular arrhythmias or sudden cardiac deaths occurred.
Conclusion:
In patients suspected of having PVC-CM, IC-AADs effectively suppressed PVCs, leading to LVEF recovery in the majority. No adverse events occurred in this small cohort.
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