title: High prevalence of cardiac parvovirus B19 infection in patients with isolated left ventricular diastolic dysfunction.
abstract: BACKGROUND
  The etiology of left ventricular (LV) isolated diastolic dysfunction often remains unclear. In the present study, we report a strong association between parvovirus B19 (PVB19) genomes and isolated LV diastolic dysfunction.
  
  
  RESULTS
  In 70 patients (mean+/-SD age, 43+/-11 years) admitted with exertional dyspnea and/or reduced exercise tolerance despite preserved LV systolic contractility (ejection fraction=68%), isolated diastolic dysfunction was clinically suspected. Patients with classic risk factors for diastolic dysfunction such as hypertension, coronary heart disease, diabetes mellitus, or pulmonary disease had been excluded. Diastolic function was assessed by echocardiography and LV and RV catheterization. Endomyocardial biopsies (EMBs) were analyzed for the presence of storage or infiltrative diseases or myocarditis, including molecular screening for cardiotropic virus genomes. In a substudy of 24 patients who reported atypical angina, coronary endothelial function was additionally investigated with a coronary Doppler flow-wire technique. In 37 of 70 patients (53%), isolated diastolic dysfunction was confirmed as the cause of their clinical symptoms. No evidence for cardiac storage or infiltrative diseases was found in these cases, but in 35 of 37 of these patients (95%), cardiotropic virus genomes were detected in EMBs (P<0.001). PVB19 was the most frequent pathogen in 31 of 37 patients (84%). In a subgroup of 10 patients with diastolic dysfunction and coexisting endothelial dysfunction, all 10 (100%) were PVB19 positive.
  
  
  CONCLUSIONS
  PVB19 genomes were predominant in patients with unexplained, isolated diastolic dysfunction. A strong association with the incidence of endothelial dysfunction was obvious, consistent with the hypothesis that PVB19-induced endothelial dysfunction may be a possible pathomechanism underlying diastolic dysfunction.
authors.affiliation: Department of Cardiology and Pneumology, Charité-University Medicine Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12200 Berlin, Germany. ctschoepe@yahoo.com
authors.forename: C
authors.initials: C
authors.lastname: Tschöpe
authors.forename: C-T
authors.initials: CT
authors.lastname: Bock
authors.forename: M
authors.initials: M
authors.lastname: Kasner
authors.forename: M
authors.initials: M
authors.lastname: Noutsias
authors.forename: D
authors.initials: D
authors.lastname: Westermann
authors.forename: P-L
authors.initials: PL
authors.lastname: Schwimmbeck
authors.forename: M
authors.initials: M
authors.lastname: Pauschinger
authors.forename: W-C
authors.initials: WC
authors.lastname: Poller
authors.forename: U
authors.initials: U
authors.lastname: Kühl
authors.forename: R
authors.initials: R
authors.lastname: Kandolf
authors.forename: H-P
authors.initials: HP
authors.lastname: Schultheiss
mesh_terms: D000328:Adult; D001706:Biopsy; D017023:Coronary Angiography; D003971:Diastole; D004727:Endothelium / Q000473:pathology / Q000821:virology; D005260:Female; D016679:Genome, Viral; D006321:Heart / Q000503:physiopathology / Q000821:virology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010322:Parvoviridae Infections / Q000150:complications*; D016732:Parvovirus B19, Human / Q000235:genetics; D015995:Prevalence; D018487:Ventricular Dysfunction, Left / Q000453:epidemiology / Q000209:etiology / Q000821:virology*