Lipoprotein(a) Serum Concentration and Apolipoprotein(a) Phenotype Correlate With Severity and Presence of Ischemic Cerebrovascular Disease

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 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 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.