**4.1. Patients**

In Table 6, an atherogenic lipoprotein phenotype B is present in 81.7% of patients with CHD. An increased concentration of small dense LDL (LDL3-7) in the CHD-patient subgroup with an atherogenic lipoprotein profile, compared to the results of the CHD-patient subgroup with a non-atherogenic lipoprotein profile (p<0.0001), confirms a predominance of atherogenic

Lower extremity arterial disease (LEAD) (Fig. 5) is a common atherogenic disease of the cardiovascular system. Patients with LEAD exhibit normal to high atherogenic dyslipopro‐

\*Reference ranges derived from 125 serum samples that met the NCEP ATPIII guidelines for desirable lipid status

**Figure 5.** Lower extremity arterial disease with combined atherogenic hyperlipoproteinemia with high concentration

\*\*LDL-C comprised of the sum of cholesterol in Md bands C through A as well as all the subfractions

of atherogenic small dense LDL (LDL3,4 subfractions) SAAR score: 1.5

lipoproteins in the serum of patients with CHD.

**4. Lower extremity arterial disease**

teinemia [8, 31, 50 -52, 62].

98 Lipoproteins - From Bench to Bedside

In the clinical study, 100 patients with newly diagnosed lower extremity arterial disease were examined. The study included 55 males and 45 females: the average age of males was 56.0 years ±11 years and the average age of females 52.5 years ± 14 years. The patients had C2a degree, according to the Claudication classification: [proximal type (AP), the first degree (P1) with dyslipidemia]. Patients were ex-smokers.

LEAD was diagnosed according to the history of disease, intermittent claudication, the medical examination, including physical examination (Ratschow's test in the modification according to Linhart, see the Angiological Section of Slovak Medical Chamber) [23, 24, 27, 28] and examination of the ankle-brachial (pressure) index (ABPI) [40, 55, 57].
