title: Dyslipidemias have a detrimental effect on left ventricular systolic function in patients with a first acute myocardial infarction.
abstract: Several large-scale clinical trials have shown that lipid-lowering interventions are associated with reduced coronary events and mortality. However, whether dyslipidemias have a detrimental effect on the evolution of myocardial infarction (MI) is still unknown. To examine whether dyslipidemias can aggravate myocardial vulnerability following MI, 165 patients with a first MI were studied. All patients underwent measurements of serum lipid profiles 1 week and 3 months after MI, a radionuclide ventriculographic study, and a coronary angiographic study. The patients were divided into 3 groups according to their 3-month serum cholesterol levels (group 1, <200 mg/dl; group 2, 200 to 240 mg/dl; group 3, >240 mg/dl). Groups 1, 2, and 3 consisted of 66, 59, and 40 patients, respectively. Group 3 had a higher Gensini score than groups 1 and 2, although this was not statistically significant (p = 0.13). The postinfarct left ventricular ejection fraction (LVEF) was highest in group 1 (53 +/- 13%), at mid level in group 2 (43 +/- 14%), and lowest in group 3 (35 +/- 11%) (p < 0.0001). A significant negative correlation between 3-month low-density lipoprotein (LDL) cholesterol (r = -0.55, p < 0.0001) and the postinfarct LVEF was found. The product of peak creatine kinase (CK(MAX)) and time to CK(MAX) (p = 0.001), and patency of the infarct-related artery (p = 0.009), rather than variables of coronary atherosclerosis, were also independent predictors of the postinfarct LVEF. Increases in 1-week LDL cholesterol and decreases in 1-week high-density lipoprotein cholesterol were associated with a higher CK(MAX) and a lower patency rate of the infarct-related artery, respectively. This study revealed that dyslipidemias per se, especially LDL cholesterol, had a detrimental effect on the postinfarct LVEF; this effect might be independent of the atherogenic properties of dyslipidemias.
authors.affiliation: Department of Internal Medicine (Cardiology), National Taiwan University Hospital, Taipei, Republic of China.
authors.forename: T D
authors.initials: TD
authors.lastname: Wang
authors.forename: C C
authors.initials: CC
authors.lastname: Wu
authors.forename: W J
authors.initials: WJ
authors.lastname: Chen
authors.forename: C M
authors.initials: CM
authors.lastname: Lee
authors.forename: M F
authors.initials: MF
authors.lastname: Chen
authors.forename: C S
authors.initials: CS
authors.lastname: Liau
authors.forename: F C
authors.initials: FC
authors.lastname: Sung
authors.forename: Y T
authors.initials: YT
authors.lastname: Lee
mesh_terms: D000368:Aged; D008078:Cholesterol, LDL / Q000097:blood; D017023:Coronary Angiography; D003402:Creatine Kinase / Q000097:blood; D005260:Female; D015637:Gated Blood-Pool Imaging; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications / Q000503:physiopathology*; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D013318:Stroke Volume; D013599:Systole; D014654:Vascular Patency; D016277:Ventricular Function, Left
chemical_list: D008078:Cholesterol, LDL; D003402:Creatine Kinase