Case Presentation:
A 29‐year‐old presented with sudden onset of chest pressure associated with palpitations, dizziness, and shortness of breath. EMS found her obtunded and hypotensive. A wide‐complex QRS tachycardia was observed, leading to defibrillation. Her past medical history included hypertension and hyperlipidemia. She denied any prescription, over the counter, or diet medications. The family history did not include any significant cardiac events. Initial EKG demonstrated a wide complex, monomorphic tachycardia at a rate of 260. After stabilization, a repeat EKG demonstrated a heart rate of 60 with a short PR and the presence of delta waves. Cardiac enzymes were negative. An echocardiogram demonstrated a right ventricular mid‐to‐distal wall that appeared thinned, akinetic, and echodense. There was also a cavity at the level of the tricuspid annulus adjacent to the lateral wall, consistent with right ventricular dysplasia. EP evaluation demonstrated an incessant wide‐complex depolarization consistent with anterograde conduction over a right‐sided accessory bypass Tract. The patient was diagnosed with WPW arising from her ARVD predisposing her to a wide complex SVT. An ICD was placed. She remained stable during her hospitalization and she was discharged home with medical management including propafenone and atenolol.
Discussion:
Arrhythmias are commonly encountered by hospitalists. Although wide‐complex tachycardias are frequently ascribed to VT, it is important to consider supraventricular loci with aberrant conduction, which can be treated with nodal agents. However, the hospitalist must ensure that the source of aberrancy is not due to WPW, as nodal agents may accelerate the ventricular response due to increased conduction over the accessory pathway.
Conclusions:
An important cause of wide‐complex ventricular arrhythmias is ARVD, which has a prevalence of 1:1000. The diagnosis is suspected by careful inspection of the echocardiogram, with a subsequent cardiac biopsy for confirmation. Approximately 30% of cases of ARVD are familial. Presentation is common between the ages of 10 and 50 years, with either sudden cardiac death or symptomatic arrhythmia. The pretest probability increases in the absence of known coronary disease. Most commonly the arrhythmia is ventricular in origin; however, as in our case, a supraventricular locus occurs in 25% of cases. Diagnostic criteria for AVRD include family history, electrocardiographic findings, and struclural/histologic abnormalities. The long term treatment consists of limited activity and placement of an ICD, which is the only therapy effective at the prevention of sudden cardiac death in patients with sustained ventricular arrhythmias. Ablation and antiarrhythmic medications may reduce the frequency of arrhythmias if an ICD placement is con Vindicated or refused. Because patients remain at high risk for sudden cardiac death, neither should be used as sole therapy.
Author Disclosure:
R. Drennan, none; K. Cartwright, none.