title: Usefulness of serum carboxy-terminal propeptide of procollagen type I in assessment of the cardioreparative ability of antihypertensive treatment in hypertensive patients.
abstract: BACKGROUND
  We investigated whether serum concentration of carboxy-terminal propeptide of procollagen type I (PIP), a marker of collagen type I synthesis, can be used to assess the ability of antihypertensive treatment to regress myocardial fibrosis in hypertensive patients.
  
  
  RESULTS
  The study was performed in 37 patients with essential hypertension and hypertensive heart disease. After randomization, 21 patients were assigned to losartan and 16 patients to amlodipine treatment. At baseline and after 12 months, right septal endomyocardial biopsies were performed to quantify collagen volume fraction (CVF) on picrosirius red-stained sections with an automated image-analysis system. Serum PIP was measured by specific radioimmunoassay. Nineteen patients in the losartan group and 11 in the amlodipine group finished the study. Time-course changes in blood pressure during treatment were similar in the 2 groups of patients. In losartan-treated patients, CVF decreased from 5.65+/-2.03% to 3.96+/-1.46% (P<0.01) and PIP from 127+/-30 to 99+/-26 microgram/L (P<0.01). Neither CVF or PIP changed significantly in amlodipine-treated patients. CVF was directly correlated with PIP (r=0.44, P<0.001) in all hypertensives before and after treatment.
  
  
  CONCLUSIONS
  These findings suggest that the ability of antihypertensive treatment to regress fibrosis in hypertensives with biopsy-proven myocardial fibrosis is independent of its antihypertensive efficacy. Our data also suggest that blockade of the angiotensin II type 1 receptor is associated with inhibition of collagen type I synthesis and regression of myocardial fibrosis in hypertensives. Thus, determination of serum PIP may be useful to assess the cardioreparative properties of antihypertensive treatment in hypertensives.
authors.affiliation: Division of Cardiovascular Pathophysiology, School of Medicine, University of Navarra, Pamplona, Spain.
authors.forename: B
authors.initials: B
authors.lastname: López
authors.forename: R
authors.initials: R
authors.lastname: Querejeta
authors.forename: N
authors.initials: N
authors.lastname: Varo
authors.forename: A
authors.initials: A
authors.lastname: González
authors.forename: M
authors.initials: M
authors.lastname: Larman
authors.forename: J L
authors.initials: JL
authors.lastname: Martínez Ubago
authors.forename: J
authors.initials: J
authors.lastname: Díez
mesh_terms: D000328:Adult; D000368:Aged; D017311:Amlodipine / Q000627:therapeutic use; D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001706:Biopsy; D001794:Blood Pressure / Q000187:drug effects; D003094:Collagen / Q000378:metabolism; D004719:Endomyocardial Fibrosis / Q000188:drug therapy / Q000209:etiology / Q000473:pathology; D005260:Female; D006321:Heart / Q000187:drug effects*; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000150:complications / Q000188:drug therapy*; D019808:Losartan / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D010349:Patient Compliance; D010446:Peptide Fragments / Q000097:blood*; D011237:Predictive Value of Tests; D011347:Procollagen / Q000097:blood*; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D012074:Remission Induction; D016896:Treatment Outcome; D016277:Ventricular Function, Left / Q000187:drug effects; D044465:White People
chemical_list: D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents; D010446:Peptide Fragments; D011347:Procollagen; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; C042813:procollagen type I carboxy terminal peptide; D017311:Amlodipine; D003094:Collagen; D019808:Losartan