(Stroke. 1995;26:1841-1848.)
© 1995 American Heart Association, Inc.
Articles |
From the Institute for Medical Biochemistry, Karl-Franzens Universität Graz (G.J., W.P., Q.C., J.G.) and Hospital Barmherzige Brüder Eggenberg (P.K.), Graz, Austria; Organon Teknika/Biotechnology Research Institute, Rockville, Md (W.C.T.-P., P.F.M., B.T.B., J.H.R.); and Organon Teknika Corporation, Durham, NC (A.G.S.).
Correspondence to Dr G. Jürgens, Institute for Medical Biochemistry, Karl-Franzens Universität Graz, Harrachg 21, A-8010 Graz, Austria. E-mail juergens@bkfug.kfunigraz.ac.at.
Background and Purpose Serum lipoprotein(a) [Lp(a)] levels are genetically determined and considered to be an independent risk factor for atherosclerosis. The aim of this study was to provide a complete analysis of Lp(a) serum levels, apolipoprotein(a) phenotypes, and other lipid parameters for different forms of severity of symptomatic ischemic cerebrovascular disorders as well as for different stages of carotid atherosclerosis.
Methods Lp(a) concentration, apolipoprotein(a) phenotype, triglyceride, low-density lipoprotein, high-density lipoprotein, and total cholesterol levels of blind-coded specimens as well as degree of carotid artery stenosis were assessed in a consecutive series of patients with ischemic cerebrovascular disease. We evaluated 265 male (34%) and female (66%) patients (mean age, 51±7.4 years) with transient ischemic attack (55.8%), prolonged reversible ischemic neurological deficits (28.3%), and cerebral infarction (15.9%) as well as 288 male (30%) and female (70%) control subjects (mean age, 51±7.1 years). All subjects were white.
Results Lp(a), total, and low-density lipoprotein
cholesterol were statistically significantly elevated in
all patients compared with control subjects. Lp(a) correlated with the
severity of symptomatic cerebrovascular disease and the
degree of carotid stenosis. Logistic regression
analysis revealed Lp(a) as the best single marker for the
presence of cerebrovascular disease (P<.001) followed by
high-density lipoprotein cholesterol
(P=.003) and triglycerides (P=.049).
With a cutoff of 20 mg/dL of Lp(a), the odds ratio for a subject to
have had ischemic stroke with elevated Lp(a) was 20.3 and 23.7
depending on the method of the Lp(a) estimation, whereas the odds ratio
when the sonography score was >0 was 15.4. The investigation of the
distribution of the apo(a) phenotypes revealed that 16.73% of
the control subjects had major isoforms
580 kD molecular weight (B,
F, S1, S2) versus 42.65% of the patients' group (P<.001).
These isoforms were also present in 14.71% of all individuals with
a sonography score of 0 but in 52.30% of all individuals with a
sonography score >0 (P<.001).
Conclusions This case-control study shows that an elevated Lp(a) level is the primary factor associated with the presence of ischemic cerebrovascular disease and that the increased portion of the smaller-molecular-weight apo(a) isoforms in patients and individuals with a sonography score >0 points toward an inherited predisposition for this disease.
Key Words: apolipoproteins cerebrovascular disorders lipoproteins risk factors
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