title: Aging might increase myocardial ischemia / reperfusion-induced apoptosis in humans and rats.
abstract: Previous studies indicated aging results in the significant cardiac function decreasing and myocardial apoptosis increasing in normal humans or rats. Additionally, animal experiments demonstrated aging increased myocardial ischemia / reperfusion (MI/R)-induced apoptosis. However, whether more myocardial apoptosis happen in the old acute myocardial infarction (AMI) patients is unclear. Reperfusion injury-induced apoptosis is an important cause of heart failure. This study determined the effect of aging upon myocardial apoptosis and cardiac function in patients suffering AMI. All enrolled AMI patients received percutaneous coronary intervention therapy. Volunteers and AMI patients were assigned to four groups: adult (age <65, n = 24) volunteers, elderly (age ≥65, n = 21) volunteers, adult (age <65, n = 29) AMI patients, and elderly (age ≥65, n = 36) AMI patients. Blood samples were obtained from all study participants. Plasma apoptotic markers (soluble form of Fas, tumor necrosis factor alpha, and interleukin 6) levels were determined. Cardiac function was evaluated with echocardiogram and Killip class. Due to lack of a direct apoptotic assay method in live human subjects, an additional animal experiment was performed. Both young (2 months) and old (24 months) rats were subjected to 30-min myocardial ischemia and 3 (for TUNEL/caspase activity apoptotic assay) or 24-h (for cardiac function determination) reperfusion. Compared to adult patients, the elderly patients manifested decreased cardiac function and increased plasma apoptotic marker levels significantly. The animal experiment results (cardiac function and plasma apoptotic markers assays) were consistent with the human result data. Animal TUNEL staining and caspase activity measurement revealed a higher myocardial apoptotic ratio in the older rat group. Aging exacerbated MI/R injury in humans and rats. Differential myocardial apoptosis may play a vital role in mediating the observed effects.
authors.affiliation: Department of Gerontology, Beijing Chaoyang Hospital-Affiliate of Capital Medical University, China.
authors.forename: Miaobing
authors.initials: M
authors.lastname: Liu
authors.forename: Ping
authors.initials: P
authors.lastname: Zhang
authors.forename: Mulei
authors.initials: M
authors.lastname: Chen
authors.forename: Wuning
authors.initials: W
authors.lastname: Zhang
authors.forename: Liping
authors.initials: L
authors.lastname: Yu
authors.forename: Xin-Chun
authors.initials: XC
authors.lastname: Yang
authors.forename: Qian
authors.initials: Q
authors.lastname: Fan
mesh_terms: D000328:Adult; D000368:Aged; D000375:Aging / Q000097:blood / Q000473:pathology*; D015906:Angioplasty, Balloon, Coronary; D000818:Animals; D017209:Apoptosis; D015415:Biomarkers / Q000097:blood; D017023:Coronary Angiography; D004195:Disease Models, Animal; D018450:Disease Progression; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D020287:In Situ Nick-End Labeling; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000175:diagnosis / Q000209:etiology* / Q000628:therapy; D015428:Myocardial Reperfusion Injury / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D011379:Prognosis; D051381:Rats; D017207:Rats, Sprague-Dawley; D013318:Stroke Volume; D019210:Troponin I / Q000097:blood
chemical_list: D015415:Biomarkers; D019210:Troponin I