Aim. To study the lipid-lowering and pleiotropic vasoprotective effects of atorvastatin depending on the achievement of the target low-density lipoprotein cholesterol (LDL-C) level in patients after ST-segment elevation myocardial infarction (STEMI) within 48-week follow-up period.Material and methods. A total of 125 patients with STEMI, randomized to receive atorvastatin 40 or 80 mg per day for 48 weeks, were examined. On days 7-9, after 24, 48 weeks, we performed biochemical blood tests, echocardiography, as well as assessed the carotid arteries and endothelial function. The subjects were divided into the following groups: high-efficiency therapy (HET) — 41 patients who reached target LDL-C at control visits; moderate-efficiency therapy (MET) — 35 patients who achieved target LDL-C at one visit; low-efficiency therapy effective (LET) — 49 people who did not reach the target LDL-C. Differences were considered significant at p<0,05.Results. A decrease in detection rate of an elevated brain natriuretic peptide was found in HET group from 41,5 to 17% (p<0,01) and in MET group from 48,6 to 23% (p<0,01), while no changes in the LET were revealed. The glomerular filtration rate in the LET group decreased by 8% (p<0,01). In the HET group, a decrease in arterial elastance by 9,4%, intima-media thickness by 9,9%, a decrease in the frequency of a negative response and an increase in a positive response (p<0,05) were revealed.Conclusion. The results demonstrate the importance of achieving target LDL-C for the most favorable dynamics of brain natriuretic peptide, structural and functional characteristics of the arterial system.
Aim. To study the vasoprotective effects of atorvastatin depending on the achievement of the target level of low-density lipoprotein cholesterol (LDL-C) in patients with ST-segment elevation myocardial infarction (STEMI) within 48 weeks of follow-up.
Materials and methods. Included were 112 STEMI patients who received atorvastatin 204080 mg. On days 79 from the onset of the disease, after 24 and 48 weeks, ultrasound examination of the carotid arteries with RF technology and applanation tonometry were performed, the lipid profile was determined. The patients were divided into groups: group 1 (n=41) of highly effective therapy (HET) who achieved the target LDL-C after 24 and 48 weeks; group 2 (n=29) in relatively effective therapy (RET) achieving target values at 24th or 48th week; group 3 (n=42) insufficiently effective therapy (IET) did not reach the target LDL-C.
Results. When examining the carotid arteries in the HET group, the intima-media thickness (IMT) decreased by 10.713.1%, the b index by 14.926.3% after 2448 weeks. In the RET group, the IMT regression was 10.413.3%; b index 23.9% by the 48th week. In the IET group, the b index decreased by the 48th week by 14.3%. According to applanation tonometry in the HET group, the central pressure did not change. In the RET group, systolic pressure in the aorta increased by 1015.7% after 2448 weeks, pulse pressure by 33.9% by the end of observation. With IET, the increase was 8.66.8 and 19.825.9%, respectively. The odds ratio of developing endpoints in the RET group was 4.7 (95% CI 1.226.4; p=0.02), in the IET group 3.9 (95% CI 1.124.8; p=0.03) compared with HET.
Conclusion. The most pronounced vasoprotective effect and a decrease in cardiovascular risk are associated with the achievement of the target LDL-C throughout the entire treatment period.
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