title: Impact of blockade of histamine H2 receptors on chronic heart failure revealed by retrospective and prospective randomized studies.
abstract: OBJECTIVE
  The goal of this work was to determine whether the blockade of histamine H2 receptors is beneficial for the pathophysiology of chronic heart failure (CHF).
  
  
  BACKGROUND
  Because CHF is one of the major life-threatening diseases, we need to find a novel effective therapy. Intriguingly, our previous study, which predicts the involvement of histamine in CHF, suggests that we should test this hypothesis in patients with CHF.
  
  
  METHODS
  We selected 159 patients who received famotidine among symptomatic CHF patients for the retrospective study. We blindly selected age- and gender-matched CHF patients receiving drugs for gastritis other than histamine H2 receptor blockers as a control group. For the prospective study, 50 symptomatic CHF patients were randomly divided into 2 groups. One group received famotidine of 30 mg/day for 6 months, and the other group received teprenone.
  
  
  RESULTS
  In the retrospective study, famotidine of 20 to 40 mg decreased both left ventricular end-diastolic and end-systolic lengths (LVDd and LVDs, respectively) and the plasma B-type natriuretic peptide (BNP) levels (182 +/- 21 vs. 259 +/- 25 pg/ml, p < 0.05) with unaltered fractional shortening (FS). In a randomized, open-label study, compared with teprenone, famotidine of 30 mg prospectively decreased both New York Heart Association functional class (p < 0.05) and plasma BNP levels (183 +/- 26 pg/ml vs. 285 +/- 41 pg/ml, p < 0.05); this corresponded to decreasing both LVDd (57 +/- 2 mm vs. 64 +/- 2 mm, p < 0.05) and LVDs (47 +/- 2 mm vs. 55 +/- 2 mm, p < 0.05) with unaltered FS (15 +/- 1% vs. 17 +/- 1%). The frequency of readmission because of worsening of CHF was lower in the famotidine group (4% and 24%, p < 0.05). On the other hand, teprenone had no effects on CHF.
  
  
  CONCLUSIONS
  Famotidine improved both cardiac symptoms and ventricular remodeling associated with CHF. Histamine H2 receptor blockers may have therapeutic benefits for CHF.
authors.affiliation: Cardiovascular Division, National Cardiovascular Center, Suita City, Osaka Pref, Japan.
authors.forename: Jiyoong
authors.initials: J
authors.lastname: Kim
authors.forename: Akiko
authors.initials: A
authors.lastname: Ogai
authors.forename: Satoshi
authors.initials: S
authors.lastname: Nakatani
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Hashimura
authors.forename: Hideaki
authors.initials: H
authors.lastname: Kanzaki
authors.forename: Kazuo
authors.initials: K
authors.lastname: Komamura
authors.forename: Masanori
authors.initials: M
authors.lastname: Asakura
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Asanuma
authors.forename: Soichiro
authors.initials: S
authors.lastname: Kitamura
authors.forename: Hitonobu
authors.initials: H
authors.lastname: Tomoike
authors.forename: Masafumi
authors.initials: M
authors.lastname: Kitakaze
mesh_terms: D000368:Aged; D002303:Cardiac Output, Low / Q000188:drug therapy* / Q000503:physiopathology*; D002908:Chronic Disease; D015738:Famotidine / Q000627:therapeutic use*; D005260:Female; D005764:Gastroesophageal Reflux / Q000188:drug therapy; D006635:Histamine H2 Antagonists / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D011446:Prospective Studies; D011970:Receptors, Histamine H2 / Q000502:physiology; D012189:Retrospective Studies; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy
chemical_list: D006635:Histamine H2 Antagonists; D011970:Receptors, Histamine H2; D015738:Famotidine