Part of the book: Lipoproteins
Research focus: Identification of incidence of an atherogenic lipoprotein phenotype B in four representative diagnoses of cardiovascular diseases: a) arterial hypertension, b) coronary heart disease, c) lower extremity arterial disease, d) ischemic stroke Research methods: A clinical study included 366 patients with a diagnosis of arterial hypertension (n=107), coronary heart disease (n= 104), lower extremity arterial disease (n= 100) and ischemic stroke (n= 55). The control group consisted of 150 healthy normotensive and normolipemic volunteers, all non-smokers, without signs of cardiovascular disease. In all tested individuals (or subjects) lipid parameters in serum: cholesterol and triglycerides were analyzed, using the enzymatic CHOD-PAP method, Roche Diagnostics Germany. Lipoproteins in serum lipoprotein spectrum by Lipoprint LDL system were analyzed and an atherogenic and a non-atherogenic lipoprotein profile idetified. The Score of the Anti-Atherogenic Risk (SAAR) was calculated as the ratio between non-atherogenic and atherogenic lipoproteins. Results: More than 80 percent of tested patients with cardovascular diseases have an atherogenic lipoprotein profile, with a high level of strongly atherogenic small dense LDL. The atherogenic profile was found in arterial hypertension 78.5%, in coronary heart disease in 81.7%, in lower extremity arterial disease in 80 %, and in patients who survived an ischemic stroke in 85%. Main conclusion: The atherogenic lipoprotein profile was found to be the overwhelming lipoprotein profile in tested cardiovascular diseases A new phenomenon- atherogenic normolipidemia - as a risk factor for the development of cardiovascular disease, would be established as a new term used in the diagnostics of dyslipoproteinemias
Part of the book: Lipoproteins
Patients (n = 40) with hypercholesterolaemia (29 females), mean age 63 years, without previous lipid lowering treatment, were treated with atorvastatin 40 mg/day for 3 months. Total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), LDL-C subfractions (large LDL-C and small dense LDL-C particles), apolipoprotein A1 (apo A1), apolipoprotein B (apo B), apo B/apo A1 ratio, atherogenic index of plasma (AIP), haematological parameters including mean platelet volume (MPV), and red cell distribution width (RDW) and safety parameters (renal and hepatic function) were measured before and after 12 weeks of atorvastatin treatment. Atorvastatin significantly reduced small dense LDL (sdLDL) fraction 3–7 and apo B. There was a negative correlation of AIP with buoyant LDL 1–2 (r = −0.35; p < 0.05) and positive with small dense LDL 3–7 (r = 0.52, p < 0.001). Administration of atorvastatin 40 mg/day in patients with hypercholesterolaemia caused a shift in small dense LDL subfractions to large, buoyant subfractions. AIP correlated better with small dense LDL than apo B levels. At baseline, a strong correlation between HDL-C, TG, small dense LDL-C, apo B, apo B/apo A1 and AIP with MPV was found. After 12 weeks of treatment with atorvastatin, MPV and RDW values underwent significant modification only in those patients displaying the strongest lipid-lowering effect. Values of MPV and RDW seem to reflect a pro-atherogenic lipoprotein profile mainly represented by the presence of small dense LDL-C. No serious atorvastatin adverse events were noted.
Part of the book: Cholesterol Lowering Therapies and Drugs