**5.2. Methods**

See methods published in the section "Arterial hypertension (AH)."

A blood sample from the antecubital vein was obtained throughout the 24 hours after the onset of cerebrovascular event.

### **5.3. Results**

The results of lipid parameters presented in Table 9 confirm a highly significantly increased concentration of analyzed lipid and lipoprotein parameters (p<0.0001) in people who survive a stroke, compared to control values, and also a low value on the SAAR, which is generally low (< 10.8) in an atherogenic lipoprotein phenotype.

In Table 10, an atherogenic lipoprotein phenotype was identified in 85.5 % of the patients who survive a cerebral ischemic stroke. The increased concentration of small dense LDL (LDL3-7


**Table 9.** Serum concentration of lipids, lipoproteins, and SAAR-score in stroke patients vs. control group.

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

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

The study included 55 patients, 23 men, with an average age of 64 years ± 13 years, and 32 women, average age 74 years ± 13 years, who survived an ischemic cerebrovascular event, that is, a large-artery atherosclerosis subtype of stroke. To determine the subtype of ischemic stroke, the original TOAST (Trial of ORG 10172 in Acute Stroke Treatment) [1] criteria were used. The diagnosis of subtype was based on the risk factor profiles, clinical features, and results of diagnostic tests, including CT scan/MRI, vascular imaging (carotid duplex, transcranial Doppler), EEG – electroencephalography, echocardiography (transesophageal/ transthoracic), assessment of prothrombotic syndromes [1,30], activated partial thromboplastin time (aPTT),

A blood sample from the antecubital vein was obtained throughout the 24 hours after the onset

The results of lipid parameters presented in Table 9 confirm a highly significantly increased concentration of analyzed lipid and lipoprotein parameters (p<0.0001) in people who survive a stroke, compared to control values, and also a low value on the SAAR, which is generally

In Table 10, an atherogenic lipoprotein phenotype was identified in 85.5 % of the patients who survive a cerebral ischemic stroke. The increased concentration of small dense LDL (LDL3-7

in subjects who had suffered an ischemic cerebrovascular event, that is, stroke.

See methods published in the section "Arterial hypertension (AH)."

low (< 10.8) in an atherogenic lipoprotein phenotype.

an important role in atherogenesis [3,58].

102 Lipoproteins - From Bench to Bedside

and international normalized ratio (INR).

**5.1. Patients**

**5.2. Methods**

**5.3. Results**

of cerebrovascular event.


**Table 10.** Serum concentration of lipids, lipoproteins, and SAAR-score in patients with stroke.

subgroups) in the atherogenic lipoprotein profile of patients with stroke, compared to the results in a non-atherogenic lipoprotein profile, is mild, but significant (p<0.05). The difference in the SAAR between the two subgroups was highly significant (p<0.0001), which also confirmed the overwhelming atherogenic lipoprotein constellation in patients who survived a stroke. The concentration of LDL1 was significantly higher in the subgroup of stroke-patients with a non-atherogenic lipoprotein profile (p<0.0001), however, the difference in the LDL2 lipoprotein subfraction was not significant.
