Abstract | April 5, 2022
A Diagnostic dilemma – Bradycardia with Premature Ventricular Contraction
- This case highlights the need for considering an exhaustive list of a differential workup for subtle symptoms like dizziness and lightheadedness in the older population which can be missed. Especially in the case with concomitant bradycardia other possible differentials should not be overlooked and a careful decision has to be made regarding beta-blocker therapy influencing the outcome of both conditions- Bradycardia and PVCs.
- A study done by Billet, Sophie et al evaluated the association of mechanical bradycardia and PVCs. It was hypothesized some PVCs do not generate enough ejection volume or pressure to allow the opening of the aortic valve and detectable aortic pressure (mechanical systole), leading to concealed mechanical bradycardia.
- A similar case has been reported by Gupta, Puneet et al bradycardia induced PVCs and the patient was managed on metoprolol and mexiletine who remained symptomatic and further managed with ablation and elective permanent pacemaker placement. It was suggested EP study could be helpful with overdrive suppression.
Introduction: Premature ventricular contractions (PVCs) is a common arrhythmia resulting from enhanced ectopic nodal automaticity in foci of sub-pulmonic valvular pacemaker cells, re-entry circuit involving Purkinje fibers, and induced by toxins like digoxin or reperfusion after myocardial infarction. PVCs are usually diagnosed incidentally on EKG. PVCs are more frequent in patients with underlying heart disease, hypertension, hypokalemia, hypomagnesemia, males, and African-American patients. PVCs associated with underlying heart disease or reversible causes need treatment. In absence of underlying structural heart disease or inability to identify the possible trigger, treatment involves betablocker therapy. But a diagnostic dilemma was faced when we encountered a case of bradycardia with PVCs.
Case presentation and diagnosis: A 59-year-old African- American female presented with dizziness and lightheadedness for around 1 month. There was no positional or diurnal association of episode. She also had a history of hypertension, hyperlipidemia, and occasional snoring during nighttime. Her primary care physician also noted that she had some bradycardia. Her symptoms were initially attributed to bradycardia possibly secondary to metoprolol tartrate 25 mg twice daily, which was discontinued but further resulted in worsening of her symptoms. She was subsequently admitted for further evaluation and management. She underwent a pharmacological stress test with regadenoson in July 2019 which was normal. Her EKG showed sinus rhythm with PVCs-unifocal with a right bundle branch block/superior axis morphology likely originating from a focus around the Left Ventricle (LV) apex and not ischemic. She also had concomitant underlying baseline bradycardia. Her echocardiogram showed normal LV with preserved ejection, mild pulmonary hypertension with RVSP of 43 mmHg. The patient underwent a stress test which showed fair exercise capacity for age and accelerated chronotropic response to exercise. There was no evidence of stress-induced ischemia.
Management: It was both a diagnostic and therapeutic dilemma to manage bradycardia and symptomatic PVCs. It was decided to initiate therapy with metoprolol succinate (MS) 25 mg daily with monitoring of her ventricular rate at home and flecainide 50 mg twice daily. The patient was discharged with outpatient follow-up and was doing fairly well after discharge but later on again developed symptoms of dizziness and lightheadedness. She continued to have skipped beats though improved since discharge. The MS was reduced to 12.5 mg daily. It was decided to consider telemetry for evaluation and possible EP and ablation if PVCs burden continues to remain high.