**3. Coronary heart disease**

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

**Figure 3.** Arterial hypertension with a borderline hypertriglyceridemia, small dense LDL are present in LDL3, 4 sub‐

**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

±1.10 ±1.07 ±0.34 ±0.55 ±0.25 ±0.91 ±0.34 ± 4.5

**p<0.0001 p< 0.03 p< 0.0001**

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

**AH 5.19 2.28 0.97 1.54 0.35 3.00 1.25 9.2**

**Table 3.** Serum concentration of lipids, lipoproteins, and SAAR-score in AH patients vs.

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

fractions, SAAR score: 0.9

94 Lipoproteins - From Bench to Bedside

(total number n=150)

(total number n= 107) **Control vs. AH**

(mmol/l SD)

Coronary heart disease (CHD) (Fig. 4) is a common manifestation of cardiovascular diseases and is frequently associated with lipid and lipoprotein metabolism disorders. Hypercholes‐ terolemia and hypertriglyceridemia, as well as combined hyperlipoproteinemia are regular features that accompany CHD [22,50,51]. Pathophysiologically, the cause of myocardial ischemia is a disproportion, or imbalance, between myocardial oxygen supply and oxygen demand. Ischemia in stable angina is generally due to fixed atheromatous stenosis of one or more coronary arteries as a consequence of impaired lipoprotein metabolism and the formation of lipid atheromas in the coronary arteries [5, 33, 34,49].

However, clinically, stable angina is not the only form of manifestation of coronary heart disease. Stable angina, as an ischemia due to fixed atheromatous stenosis, can turn into a myocardial ischemia due to plaque rupture with thrombosis and spasm of the artery (instable angina). In addition, myocardial necrosis (myocardial infarction), caused by acute occlusion of a coronary artery (due to plaque rupture and thrombosis), can have fatal consequences for disabled persons. It can be supposed that the modified forms of lipoproteins can play an important role in any form of clinical manifestation of coronary heart disease. Recently, clinical studies reported that the atherogenic lipoprotein populations (lipoprotein subfractions), presented in the plasma lipoprotein spectrum in high concentrations, play an important role in the development of atherosclerotic changes in the arterial wall [14, 38, 39].

\*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

**Figure 4.** Coronary heart disease combined with an atherogenic hypercholesterolemia. High concentration of athero‐ genic small dense LDL in LDL 3,4 subfractions SAAR score: 5.1

We distinguish facultative atherogenic very low density lipoproteins, VLDL, and their remnants, intermediate density lipoproteins, IDL, low density lipoproteins, LDL (considered a lipoprotein family with high atherogenicity), and high density lipoproteins, HDL. Modified lipoprotein entities in all these lipoprotein families can play a role in the formation of athero‐ genic lipoproteins, which accelerate the atherogenesis in the artery walls, including in the coronary arteries.

In our study, we focused on the determination of the incidence of an atherogenic lipoprotein phenotype in patients with coronary heart disease – in stable angina patients.
