**5. Stroke**

**Chol TAG VLDL LDL1,2 LDL3-7 LDL HDL Score**

±0.60 ±0.39 ±0.16 ±0.37 ±0.004 ±0.52 ±0.32 ±18.5

**±1.21 ±1.05 ±0.37 ±0.51 ±0.28 ±0.96 ±0.31 ± 4.5**

**Control 4.27 1.17 0.61 1.28 0.04 2.30 1.34 35.8**

**LEAD 5.29 2.21 0.96 1.58 0.39 3.11 1.21 7.2**

**«...............................................p<0.0001.................................»**

**Chol TAG VLDL LDL1,2 LDL3-7 LDL HDL Score**

±0.95 ±0.51 ±0.26 ±0.54 ±0.03 ±0.82 ±0.29 ± 6.5

±1.28 ±1.18 ±0.39 ±0.50 ±0.34 ±0.99 ±0.32 ± 4.0

±1.21 ±1.05 ±0.37 ±0.51 ±0.28 ±0.96 ±0.31 ± 4.5

p<0.01 p<0.001 p<0.05 p< 0.0001 p< 0.0001

**Table 7.** Serum concentration of lipids, lipoproteins, and SAAR-score in LEAD-patients vs. control group

LEAD 5.37 1.81 0.86 1.82 0.10 3.18 1.33 17.4

LEAD 5.28 2.31 0.98 1.52 0.46 3.09 1.18 4.6

**LEAD 5.29 2.21 0.96 1.58 0.39 3.11 1.21 7.2**

**Table 8.** Serum concentration of lipids, lipoproteins, and SAAR-score in lower extremity arterial disease

proteins in serum in the subgroup of patients with an atherogenic lipoprotein profile.

In 80% of patients (Table 8), LEAD was associated with an atherogenic lipoprotein phenotype. An increased concentration of small dense LDL (LDL3-7 subgroups) in the LEAD-patients with an atherogenic lipoprotein profile, compared to the results from the LEAD-patients with a nonatherogenic lipoprotein profile (p<0.0001), confirms the predominance of atherogenic lipo‐

Atherogenic 80% vs. non-atherogenic 20% in lower extremity arterial disease

(mmol/l SD)

(total number n=150)

100 Lipoproteins - From Bench to Bedside

(total number n= 100) Control vs. LEAD

(mmol/l±SD)

(non-atherogenic profile n= 20)

(atherogenic profile n= 80)

(total number n=100)

Non-atherogenic vs. atherogenic

Stroke (Fig. 6) is the leading cause of mortality and of long-term morbidity in the populations of developed industrialized countries in the world. The atherogenic serum lipoproteins in high concentrations create an atherogenic lipoprotein profile, which plays a key role in the acute onset of cardiovascular and cerebrovascular events, that is, stroke [54,55]. Cerebral stroke attack remains a frequent medical problem and is the third most frequent cause of mortality all over the world. It represents a heterogeneous group of diseases with more than 150 known causes. In 25–39% of strokes, the cause leading to the acute cerebrovascular event cannot usually be definitively explained [4].

**Figure 6.** Patient survived an ischemic stroke with combined atherogenic hyperlipoproteinemia high concentration of VLDL, VLDL remnants and atherogenic small dense LDL, i.e. LDL 3, 4 subfractions. SAAR score: 2.4\*Reference ranges derived from 125 serum samples that met the NCEP ATPIII guidelines for desirable lipid status\*\*LDL-C comprised of the sum of cholesterol in Md bands C through A as well as all the subfractions

Dyslipidemia represents a risk factor for the development of cardiovascular disease, and thus dyslipidemia has been classified as an atherogenic phenomenon. The goal of the treatment of hyperlipoproteinemia, that is, of dyslipidemia, is to reduce the lipid concentration in serum to established target values of lipids (cholesterol and triglycerides), but the primary goal is to reduce the atherogenic potential of serum lipids [9, 21, 53]. Dyslipoproteinemia is also the key phenomenon in the pathogenesis of the onset of atherosclerotic alterations in brain vessels [64]. Accompanied by high cholesterol levels – a classic risk factor for the development of cardio‐ vascular diseases – an increased concentration of triglycerides in the blood serum can also play an important role in atherogenesis [3,58].

There are several studies that have provided evidence for the relation between carotid artery stenosis and an ischemic cerebral event [55]. However, the causal inter-relation between dyslipidemia and stroke has not been explained sufficiently [3, 4, 63]. Relapsing ischemic strokes account for one-fourth of all strokes in a year and are a strong evidence for a failure of secondary prevention [10]. This hard reality leads rightly so to the idea of optimal stroke prevention through the selection of individuals, who are at risk of stroke [13]. The aim of this pilot study was to identify the atherogenic lipoproteins and determine the lipoprotein profile in subjects who had suffered an ischemic cerebrovascular event, that is, stroke.
