title: Characteristics of premature ventricular complexes as correlates of reduced left ventricular systolic function: study of the burden, duration, coupling interval, morphology and site of origin of PVCs.
abstract: BACKGROUND
  Frequent premature ventricular complexes (PVCs) can cause a decline in left ventricular ejection fraction (LVEF). We investigated whether the site of origin and other PVC characteristics are associated with LVEF.
  
  
  METHODS
  We retrospectively studied 70 consecutive patients (mean age 42 ± 17 years, 40 [57%] female) with no other cause of cardiomyopathy undergoing ablation of PVCs. We analyzed the association of a reduced LVEF, defined by LVEF <50% on echocardiography, with features of PVCs obtained from electrocardiography, 24- or 48-hour Holter monitor and electrophysiology study.
  
  
  RESULTS
  Patients with reduced LVEF (n = 17) as compared to normal LVEF (n = 53) had an increased burden of PVCs (29.3 ± 14.6% vs 16.7 ± 13.7%, P = 0.004), higher prevalence of nonsustained ventricular tachycardia (VT) [13 (76%) vs 21 (40%), P = 0.01], longer PVC duration (154.3 ± 22.9 vs 145.6 ± 20.8 ms, P = 0.03) and higher prevalence of multiform PVCs [15 (88%) vs 31 (58%), P = 0.04]. There was no significant difference in prevalence of sustained VT, QRS duration of normally conducted complexes, PVC coupling interval, or delay in PVC intrinsicoid deflection. Patients with fascicular PVCs (n = 5) had higher mean LVEF compared to others (66.2 ± 4.0% vs 53.0 ± 10.0%, P = 0.002). There was no association of LVEF with other PVC foci or with left-bundle versus right-bundle branch block morphologies. The threshold burden of PVCs associated with reduced LVEF was lower for right as compared to left ventricular PVCs.
  
  
  CONCLUSIONS
  In addition to the PVC burden, other characteristics like a longer PVC duration, presence of nonsustained VT, multiform PVCs and right ventricular PVCs might be associated with cardiomyopathy.
authors.affiliation: Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota 55905, USA.
authors.forename: Freddy
authors.initials: F
authors.lastname: Del Carpio Munoz
authors.forename: Faisal F
authors.initials: FF
authors.lastname: Syed
authors.forename: Amit
authors.initials: A
authors.lastname: Noheria
authors.forename: Yong-Mei
authors.initials: YM
authors.lastname: Cha
authors.forename: Paul A
authors.initials: PA
authors.lastname: Friedman
authors.forename: Stephen C
authors.initials: SC
authors.lastname: Hammill
authors.forename: Thomas M
authors.initials: TM
authors.lastname: Munger
authors.forename: K L
authors.initials: KL
authors.lastname: Venkatachalam
authors.forename: Win-Kuang
authors.initials: WK
authors.lastname: Shen
authors.forename: Douglas L
authors.initials: DL
authors.lastname: Packer
authors.forename: Samuel J
authors.initials: SJ
authors.lastname: Asirvatham
mesh_terms: D000328:Adult; D017281:Cost of Illness; D004562:Electrocardiography / Q000379:methods; D056966:Excitation Contraction Coupling / Q000502:physiology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D013599:Systole / Q000502:physiology; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000473:pathology* / Q000503:physiopathology*; D016277:Ventricular Function, Left / Q000502:physiology; D018879:Ventricular Premature Complexes / Q000473:pathology* / Q000503:physiopathology*