ong-lasting tachyarrhythmia can result in wall motion abnormality, which is reversible if the culprit arrhythmia is treated. 1-3 Frequent isolated premature ventricular complexes (PVCs) in the absence of tachycardia can cause left ventricular (LV) dysfunction, 4,5 but this phenomenon has rarely been documented. We report resolution of apparent dilated cardiomyopathy (DCM) in a patient after the focal source of PVCs was eliminated by radiofrequency catheter ablation (RF-CA).
Case ReportA 53-year-old man presented with palpitations and exertional fatigue, but without clinical or laboratory evidence of ischemic heart disease. He was diagnosed by echocardiography as having DCM with fractional shortening (FS) of the left ventricle of 25%. All 4 chambers were dilated: LV diastolic diameter 65 mm, LV systolic diameter 49 mm, and left atrial diameter 46 mm. The chest X-ray showed mild cardiomegaly (cardio thoracic ratio) (CTR) 54%, and the serum brain natrinvetic peptide (BNP) level was mildly elevated to 54 pg/ml. The electrocardiogram (ECG) did not record any abnormal findings other than frequent PVCs. Repeated Holter recordings revealed about 50,000 isolated or couplet PVCs in a 24-h period, the majority with a uniform left bundle branch block (LBBB) pattern and inferior-axis morphology. PVCs bigeminy appeared constantly throughout the day. During an exercise test, the number of PVCs decreased with the loading of exercise and increased again after the test. Tl-myocardial scintigraphy showed a mildly decreased uptake in the apicoanteroseptal wall. Cardiac magnetic resonance imaging did not show evidence of infiltration of fatty tissue.