title: Effects of two inhibitors of renin-angiotensin system on attenuation of postoperative remodeling after left ventricular aneurysm repair in rats.
abstract: We reported that the initial beneficial effects of left ventricular repair (LVR) surgery for LV aneurysm after myocardial infarction (MI) did not persist because of postoperative LV remodeling in a rat model. The renin-angiotensin system (RAS) plays an important role in postinfarction LV remodeling. Inhibition of RAS may be useful to preserve LV function by preventing remodeling. We studied the effects of two inhibitors of RAS in an attempt to improve the operative results of LVR. LV aneurysms were created in rats after ligating the left anterior descending artery. These rats underwent LVR by plicating the LV aneurysm and were treated by three methods: no treatment, treatment with angiotensin-converting enzyme inhibitor (ACE-I) (lisinopril 10 mg/kg per day), and treatment with angiotensin II receptor blocker (ARB) (candesartan 5 mg/kg per day). One week after LVR, echocardiography revealed smaller LV size and better LV motion than before surgery. Four weeks after LVR, LV size returned to the preoperative value in the untreated group, but not as much in the treated groups. Cardiac catheterization revealed lower LV end-diastolic pressure and higher E-max in the treated groups. There was no difference between ACE-I and ARB groups except for systolic blood pressure. LVR decreased LV size and improved systolic function only in the early phase. Adjuvant therapy of ACE-I or ARB-attenuated LV remodeling and maintained LV function at the same level after LVR. This probably indicates that tissue RAS is associated with postoperative remodeling. Concomitant use of RAS inhibitors may make LVR a longer-lasting procedure for LV aneurysm.
authors.affiliation: Department of Cardiovascular Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
authors.forename: Takuya
authors.initials: T
authors.lastname: Nomoto
authors.forename: Takeshi
authors.initials: T
authors.lastname: Nishina
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Tsuneyoshi
authors.forename: Senri
authors.initials: S
authors.lastname: Miwa
authors.forename: Kazunobu
authors.initials: K
authors.lastname: Nishimura
authors.forename: Masashi
authors.initials: M
authors.lastname: Komeda
mesh_terms: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001562:Benzimidazoles / Q000494:pharmacology; D001713:Biphenyl Compounds; D006328:Cardiac Catheterization; D006322:Heart Aneurysm / Q000209:etiology / Q000601:surgery*; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology / Q000601:surgery; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D017706:Lisinopril / Q000494:pharmacology; D008297:Male; D009203:Myocardial Infarction / Q000150:complications / Q000503:physiopathology; D009929:Organ Size; D051381:Rats; D017207:Rats, Sprague-Dawley; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000502:physiology; D013777:Tetrazoles / Q000494:pharmacology; D016277:Ventricular Function, Left / Q000502:physiology; D020257:Ventricular Remodeling / Q000187:drug effects* / Q000502:physiology
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D001562:Benzimidazoles; D001713:Biphenyl Compounds; D013777:Tetrazoles; D017706:Lisinopril; C081643:candesartan