Case Presentation: A 76-year-old male with past medical history of atrial fibrillation s/p ablation, recent pacemaker placement, heart failure with preserved ejection fraction (HFpEF), type 2 diabetes, leukemia, and colon cancer presented to the emergency department for weakness and dyspnea on exertion. Patient appeared volume overloaded with bilateral lower extremity edema with labs remarkable for B-type natriuretic peptide of 40,856 pg/ml. EKG demonstrated a paced rhythm and prolonged QT interval. His symptoms were thought to be due to heart failure exacerbation. Echocardiogram was obtained and demonstrated a left ventricular ejection fraction (LVEF) of 30-35%, significantly reduced compared to his LVEF of 55% two weeks prior. Due to concerns for ischemia, stress test was obtained and was unremarkable. Interrogation of the pacemaker demonstrated right ventricular pacing 98% of the time. After discussing with electrophysiology, the patient was diagnosed with pacemaker induced cardiomyopathy (PICM). EKG and telemetry showed widening of the QRS greater than 200ms indicating right ventricular dyssynchrony. Patient was upgraded to a biventricular pacemaker due to the high dependence on the right ventricular pacing and resultant heart failure.
Discussion: Despite being a common complication of pacemaker implantation, PICM due to right ventricular pacing is not a common differential when patients present in acute heart failure. The incidence of PICM varies between 10 to 26% as there is variation in the definition, population, and follow-up period. A decrease in LVEF>10% resulting in LVEF< 50% is an acceptable definition of PICM, however, other studies suggest a decrease in LVEF >5% with symptoms of heart failure is also a criterion. Right ventricular pacemakers use a non-physiologic pathway for ventricular activation leading to disproportionate electrical activation and delayed depolarization of the left ventricular segments, causing structural remodeling. Over time, this can lead to decreased LV function. Studies suggest that remodeling can take effect immediately, however, not all patients are affected equally. The ability to identify high risk patients is difficult to assess, but risk factors include: male sex, prolonged paced QRS, baseline LV dysfunction, high ventricular pacing burden, and high myocardial scar score. Diagnostic modalities are evolving as the paced QRS duration is an imperfect marker in identifying dyssynchrony. A novel diagnostic tool is ultra-high-frequency ECG mapping which visualizes ventricular depolarization patterns and allows clinicians to quantify the location of dyssynchrony. Biventricular pacing is the mainstay treatment for PICM and constitutes 23-28% of all biventricular pacemakers. However, the use of biventricular pacing for bradycardia is controversial and is not recommended over right ventricular pacing. PICM is a complication that requires increased awareness and standardization of diagnostic and treatment methods.
Conclusions: Pacemaker implantation is a Class I recommendation for symptomatic bradycardia according to the ACC/AHA guidelines. Given the routine use of pacemakers, PICM should remain a differential for patients in acute heart failure. This case demonstrates the importance of further research for risk stratification, and diagnostic and treatment modalities for patients who develop left ventricular failure secondary to right ventricular dyssynchrony.