LIPID AND LIPOPROTEIN LEVELS REMAIN STABLE IN ACUTE ISCHEMIC STROKE -THE NORTHERN MANHATTAN STROKE STUDY

Serum lipoproteins including lipoprotein(a), Lp(a), are emerging as po ssible biological markers for cerebrovascular disease. Existing data o n Lp(a) and serum lipids levels following acute ischemic stroke (AIS) are however equivocal. To determine whether serum Lp(a) and other lipi d levels obtained within 24 h of acute ischemic stroke onset changed o ver the ensuing 4 weeks and whether these levels are related to an acu te phase response, acquired nutritional deficiency, and neurovascular data, we conducted repeated measurement analyses among 19 subjects (me an age 65.0 +/- 12.1 years; 32% women) presenting with AIS (evaluated within 9.7 +/- 12.7 h). Eleven of the subjects had a moderate-to-sever e stroke, defined by NIH stroke severity scale, and seven patients had a large cerebral infarction. Seven serial measurements of Lp(a), tota l cholesterol, high density lipoprotein cholesterol, low density lipop rotein cholesterol, and other lipoproteins, major acute phase reactant s and albumin levels were collected for each subject over 4 weeks. The mean initial levels, (mg/dl), of total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, Lp(a), apolipoproteins A-I and B were: 225 +/- 57.6, 154 +/- 56.0, 40 +/- 10.4, 181 +/- 93.7, 52 +/- 28.6, 1 30 +/- 24.6, and 141 +/- 46.1, respectively. There were no significant changes in mean serum lipid, apolipoprotein or Lp(a) levels over the 4-week study period, analyzed by a random effects model to test for ti me trend. In addition, there were no significant changes in establishe d acute phase or nutritional markers (C-reactive protein, alpha l-glyc oprotein, haptoglobin or serum albumin). Our findings suggest that ser um lipid, apolipoprotein and Lp(a) levels remain stable following AIS, consistent with the absence of acute phase response or nutritional de ficiency. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.