title: The long-acting Ca2+-channel blocker azelnidipine prevents left ventricular remodeling after myocardial infarction.
abstract: Long-acting Ca(2+)-channel blockers have been reported to be effective in treating ischemic heart disease. However, their effects on cardiac remodeling after myocardial infarction (MI) are still unclear. We performed this study to examine the effect of azelnidipine on left ventricular (LV) remodeling, including systolic and diastolic dysfunction, in rats with MI. MI was induced by ligation of the left anterior descending artery. The rats were then separated into 3 groups: a sham-operated group (n = 9), untreated MI group (n = 10), and azelnidipine-treated MI group (n = 10). Four weeks after MI, hemodynamic measurements and Doppler echocardiographic assessment were performed. LV weight and LV end-diastolic dimension were significantly higher in the untreated MI group than in the sham-operated group. Azelnidipine significantly prevented the increases in these parameters. Azelnidipine also improved the ejection fraction (42 +/- 3%, P<0.05) and the E wave to A wave ratio (3.2 +/- 0.5, P<0.05), compared with the untreated MI group (31 +/- 3% and 5.3 +/- 0.8, respectively). In conclusion, azelnidipine can prevent LV remodeling and improve systolic and diastolic function after MI. Administration of long-acting Ca(2+)-channel blockers after MI is an effective strategy for treating MI.
authors.affiliation: Department of Internal Medicine and Cardiology, Osaka City University Medical School, Asahimachi, Osaka, Japan. ndaisuke@med.osaka-cu.ac.jp
authors.forename: Daisuke
authors.initials: D
authors.lastname: Nishiya
authors.forename: Soichiro
authors.initials: S
authors.lastname: Enomoto
authors.forename: Takashi
authors.initials: T
authors.lastname: Omura
authors.forename: Ryo
authors.initials: R
authors.lastname: Matsumoto
authors.forename: Takanori
authors.initials: T
authors.lastname: Kusuyama
authors.forename: Yasukatsu
authors.initials: Y
authors.lastname: Izumi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Iwao
authors.forename: Kazuhide
authors.initials: K
authors.lastname: Takeuchi
authors.forename: Minoru
authors.initials: M
authors.lastname: Yoshiyama
mesh_terms: D000818:Animals; D001383:Azetidinecarboxylic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D015152:Blotting, Northern; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D018932:Chemokine CCL2 / Q000235:genetics; D024042:Collagen Type I / Q000235:genetics; D024061:Collagen Type III / Q000235:genetics; D004095:Dihydropyridines / Q000494:pharmacology*; D004452:Echocardiography; D015870:Gene Expression / Q000187:drug effects; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000235:genetics; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D020097:Natriuretic Peptide, Brain / Q000235:genetics; D009929:Organ Size / Q000187:drug effects; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D016277:Ventricular Function, Left / Q000187:drug effects; D020257:Ventricular Remodeling / Q000187:drug effects*
chemical_list: D002121:Calcium Channel Blockers; D018932:Chemokine CCL2; D024042:Collagen Type I; D024061:Collagen Type III; D004095:Dihydropyridines; D017395:Plasminogen Activator Inhibitor 1; D012333:RNA, Messenger; D020097:Natriuretic Peptide, Brain; D001383:Azetidinecarboxylic Acid; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases; C061679:azelnidipine