title: Losartan-dependent regression of myocardial fibrosis is associated with reduction of left ventricular chamber stiffness in hypertensive patients.
abstract: BACKGROUND
  This study was designed to investigate whether myocardial collagen content is related to myocardial stiffness in patients with essential hypertension.
  
  
  RESULTS
  The study was performed in 34 patients with hypertensive heart disease. Nineteen of these patients were also evaluated after 12 months of treatment with losartan. Transvenous endomyocardial biopsies of the interventricular septum were performed to quantify collagen volume fraction (CVF). Left ventricular (LV) chamber stiffness (K(LV)) was determined from the deceleration time of the early mitral filling wave as measured by Doppler echocardiography. Histological analysis at baseline revealed the presence of 2 subgroups of patients: 8 with severe fibrosis and 26 with nonsevere fibrosis. Values of CVF and K(LV) were significantly higher in the 2 subgroups of hypertensives than in normotensives. In addition, compared with patients with nonsevere fibrosis, patients with severe fibrosis exhibited significantly increased values of CVF and K(LV). After treatment, CVF and K(LV) decreased significantly in patients with severe fibrosis (n=7). None of these parameters changed significantly after treatment in patients with nonsevere fibrosis (n=12). CVF was directly correlated with K(LV) (r=0.415, P<0.02) in all hypertensives.
  
  
  CONCLUSIONS
  These findings show a strong association between myocardial collagen content and LV chamber stiffness in patients with essential hypertension. Our results also suggest that the ability of losartan to induce regression of severe myocardial fibrosis is associated with diminution of myocardial stiffness in hypertensive patients.
authors.affiliation: Division of Cardiovascular Pathophysiology, School of Medicine, University Clinic, University of Navarra, Pamplona, Spain. jadimar@unav.es
authors.forename: Javier
authors.initials: J
authors.lastname: Díez
authors.forename: Ramón
authors.initials: R
authors.lastname: Querejeta
authors.forename: Begoña
authors.initials: B
authors.lastname: López
authors.forename: Arantxa
authors.initials: A
authors.lastname: González
authors.forename: Mariano
authors.initials: M
authors.lastname: Larman
authors.forename: José L
authors.initials: JL
authors.lastname: Martínez Ubago
mesh_terms: D000328:Adult; D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D001706:Biopsy; D001794:Blood Pressure / Q000187:drug effects; D016000:Cluster Analysis; D003094:Collagen / Q000032:analysis / Q000378:metabolism; D015150:Echocardiography, Doppler; D004719:Endomyocardial Fibrosis / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D005260:Female; D006334:Heart Function Tests; D006801:Humans; D006973:Hypertension / Q000145:classification / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D019808:Losartan / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D010446:Peptide Fragments / Q000097:blood; D011347:Procollagen / Q000097:blood; D012016:Reference Values; D012074:Remission Induction; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology
chemical_list: D000959:Antihypertensive Agents; D015415:Biomarkers; D010446:Peptide Fragments; D011347:Procollagen; C042813:procollagen type I carboxy terminal peptide; D003094:Collagen; D019808:Losartan