Upregulation of cholesterol synthesis after acute myocardial infarction -: is cholesterol a positive acute phase reactant?

被引:59
作者
Pfohl, M [1 ]
Schreiber, I [1 ]
Liebich, HM [1 ]
Häring, HU [1 ]
Hoffmeister, HM [1 ]
机构
[1] Univ Tubingen, Med Klin & Poliklin, D-72076 Tubingen, Germany
关键词
myocardial infarction; acute phase response; cholesterol synthesis; lathosterol;
D O I
10.1016/S0021-9150(98)00242-1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Acute myocardial infarction is associated with profound alterations in the plasma lipoprotein profile. The mechanism of these alterations is not clear, and both cholesterol biosynthesis up- and downregulation could possibly be a consequence of acute myocardial infarction. We determined plasma lipids, lipoproteins, apolipoproteins, and lathosterol-which is regarded as an estimate of whole body cholesterol biosynthesis in humans-concentrations in 34 patients (age 68 +/- 10 years, 24 male, 10 female) admitted to our hospital with acute MI and with onset of symptoms within the last 12 h. Samples were taken immediately after admission to the hospital, and 1, 2, and 10 days after admission. On the first day after admission there was a decrease in total cholesterol (C) by 14.1% (P = 0.01), in LDL-C by 14.4% (P = 0.03), in HDL-C by 9.3% (NS), and in triglycerides by 19.5% (NS). Apolipoprotein B100 was reduced by 18.3% (P = 0.008), and apolipoprotein AI by 12.3% (NS). The lathosterol/cholesterol ratio was increased by 23.1% after 1 day, and by 28.7% after 2 days (P = 0.05). After 10 days, all variables except the apolipoproteins had essentially returned to baseline values. In conclusion, the changes in the plasma lipid profile after acute myocardial infarction are associated with a profound increase of whole body cholesterol biosynthesis as judged by the lathosterol/cholesterol ratio. These changes may possibly enhance the delivery of cholesterol to cells involved in tissue repair mechanisms after acute myocardial infarction. (C) 1999 Elsevier Science Inland Ltd. All rights reserved.
引用
收藏
页码:389 / 393
页数:5
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