title: Suppression of frequent premature ventricular contractions and improvement of left ventricular function in patients with presumed idiopathic dilated cardiomyopathy.
abstract: OBJECTIVE
  To examine the hypothesis that suppression of frequent premature ventricular contractions may be associated with improvement in left ventricular function in patients with presumed idiopathic dilated cardiomyopathy.
  
  
  METHODS
  We conducted a retrospective case study and statistical analysis of the effect of cardiac medical therapy on outcome.
  
  
  METHODS
  The study population consisted of 14 patients with more than 20,000 premature ventricular contractions in 24 hours recorded by Holter monitoring and associated left ventricular dysfunction (ejection fraction, 40% or less). Clinical characteristics, number of premature ventricular contractions per hour on 24-hour ambulatory Holter monitoring, and ejection fraction based on transthoracic echocardiography were compared before and after cardiac therapeutic intervention.
  
  
  RESULTS
  Of the 14 patients, 10 had presumed idiopathic dilated cardiomyopathy, and 4 had ischemic heart disease. Of the overall study group, seven had received additional cardiac medical therapy after the index evaluation, including four patients who had amiodarone therapy. A significant reduction (75% or more from baseline) in premature ventricular contractions after medical therapeutic intervention was observed in five patients at the first follow-up examination. The mean interval to the first follow-up examination was 6 +/- 3 months. Of the five patients, four had significant improvement in clinical functional status and the ejection fraction. The mean ejection fraction of these five patients increased from 27 +/- 10% at baseline to 49 +/- 17% after medical therapy (P = 0.04).
  
  
  CONCLUSIONS
  The suppression of frequent premature ventricular contractions may be associated with improvement of left ventricular function in patients with presumed idiopathic dilated cardiomyopathy.
authors.affiliation: Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic Rochester, Minnesota 55905, USA.
authors.forename: D F
authors.initials: DF
authors.lastname: Duffee
authors.forename: W K
authors.initials: WK
authors.lastname: Shen
authors.forename: H C
authors.initials: HC
authors.lastname: Smith
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000368:Aged; D000638:Amiodarone / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D002312:Cardiomyopathy, Hypertrophic / Q000150:complications* / Q000000981:diagnostic imaging / Q000503:physiopathology*; D004452:Echocardiography; D015716:Electrocardiography, Ambulatory; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D013318:Stroke Volume / Q000187:drug effects; D016896:Treatment Outcome; D016277:Ventricular Function, Left / Q000187:drug effects; D018879:Ventricular Premature Complexes / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology*
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000889:Anti-Arrhythmia Agents; D000638:Amiodarone