Case Presentation:
A 70-year-old man with a remote history of ischemic cardiomyopathy presented to the hospital with worsening shortness of breath. His review of systems was remarkable for orthopnea. His past medical history was significant for hypertension and hyperlipidemia. His home medications were carvedilol, aspirin, lisinopril and simvastatin. Diagnostic studies including cardiac enzymes and chest x-ray were unremarkable. Surface electrocardiogram showed multiple premature ventricular contractions (PVCs) consistent with non-sustained ventricular tachycardia (NSVTs). With amiodarone infusion, his symptoms improved and the frequency of NSVTs decreased. Transthoracic echocardiogram revealed left ventricular ejection fraction (LVEF) of 20-30%. Left heart catheterization demonstrated non-obstructive coronary artery disease. Cardiac electrophysiology was consulted for further management of frequent PVCs. On 24-hour Holter monitor, patient was found to have frequent runs of monomorphic ventricular tachycardia with total PVC burden of 64%. Because of worsening symptoms, an electrophysiology study was scheduled. On the electrophysiology study, posteromedial papillary muscle was found to be the source of PVCs/NSVT and thus, this site was ablated. Post ablation, patient’s symptoms improved remarkably. Three months later, a follow-up echocardiogram showed an improved LVEF of 50%. This significant improvement of LVEF post ablation supported the diagnosis of ventricular tachycardia induced cardiomyopathy.
Discussion:
Ventricular Tachycardia (VT) induced cardiomyopathy is a rare cause of LV dysfunction. Premature ventricular contraction is usually asymptomatic but with increased frequency of PVCs, patients may develop signs and symptoms of heart failure. A definitive diagnosis is difficult in patients with prior history of ischemic cardiomyopathy as the symptoms may be attributed to underlying Coronary Artery Disease (CAD).
Patients with frequent PVCs/NSVT and symptoms suggestive of heart failure should undergo continuous cardiac monitoring to assess the burden of PVCs. Patients with a high burden of PVCs should undergo further electrophysiology study for ablation of the PVC focus. Post ablation, majority of these patients show significant improvement in symptoms. A follow-up echocardiogram should be done to assess the LVEF.
Conclusions:
VT induced cardiomyopathy is a curable cause of systolic congestive heart failure. It should be considered in patients presenting with symptoms of heart failure and a high burden of PVCs. The diagnosis of VT induced cardiomyopathy can be challenging and hospitalists should have a high index of suspicion to diagnose this condition. When suspected, an aggressive approach is warranted to treat this potentially reversible arrhythmia with ablation.