title: Effects of angiotensin-converting enzyme inhibition on changes in left ventricular myocardial creatine kinase system after myocardial infarction: their relation to ventricular remodeling and function.
abstract: We assessed the effects of angiotensin-converting enzyme (ACE) inhibition on changes in the myocardial intracellular creatine kinase (CK) system in relation to left ventricular (LV) remodeling and function in heart failure after myocardial infarction (MI) in rats. We compared the findings at 4 weeks after MI to those at 12 weeks after MI. LV weight and chamber size were significantly increased and percent fractional shortening (%FS) was decreased in untreated MI rats compared with normal control animals both at 4 and 12 weeks after MI. Animals with MI and treated with the ACE inhibitor temocapril showed significantly reduced LV weight and chamber size and increased %FS compared with untreated MI rats at 12 weeks after MI, but not at 4 weeks after MI. At 4 weeks after MI, no significant changes were found in the total creatine and relative distribution of each CK isoenzyme in either the temocapril-treated or untreated animals with MI compared with the normal controls. In contrast, at 12 weeks after MI, untreated MI rats showed significant reductions in the total creatine and mitochondrial and MM-CK fractions and increases in the MB- and BB-CK fractions compared with the controls. The alterations in the mitochondrial and MB-CK fractions were significantly attenuated after 12 weeks of ACE inhibition. Thus, LV myocardial energy metabolism is progressively impaired and its alteration is not related to the magnitude of geometric changes and LV dysfunction after MI. Most of the beneficial effects of ACE inhibition were observed at 12 weeks after MI. Our results may provide an insight into the therapeutic strategy of ACE inhibition in chronic heart failure after MI.
authors.affiliation: Department of Laboratory Medicine, Shinshu University Hospital, Matsumoto, Japan.
authors.forename: Eiji
authors.initials: E
authors.lastname: Hironaka
authors.forename: Minoru
authors.initials: M
authors.lastname: Hongo
authors.forename: Masako
authors.initials: M
authors.lastname: Azegami
authors.forename: Setsuko
authors.initials: S
authors.lastname: Yanagisawa
authors.forename: Mafumi
authors.initials: M
authors.lastname: Owa
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Hayama
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D003402:Creatine Kinase / Q000378:metabolism*; D052279:Creatine Kinase, MB Form; D005260:Female; D006333:Heart Failure / Q000201:enzymology / Q000209:etiology / Q000503:physiopathology*; D007527:Isoenzymes / Q000378:metabolism*; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D009206:Myocardium / Q000201:enzymology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling / Q000187:drug effects*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D007527:Isoenzymes; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form