Background. In order to provide personalized medicine and improve cardiovascular outcomes, a method for predicting adverse left ventricular remodeling (ALVR) after ST-segment elevation myocardial infarction (STEMI) is needed. Methods. A total of 125 STEMI patients, mean age 51.2 (95% CI 49.6; 52.7) years were prospectively enrolled. The clinical, laboratory, and instrumental examinations were performed between the 7th and 9th day, and after 24 and 48 weeks, including plasma analysis of brain natriuretic peptide (BNP), transthoracic echocardiography, analysis of left ventricular-arterial coupling, applanation tonometry, ultrasound examination of the common carotid arteries with RF signal amplification. Results. Patients were divided into 2 groups according to echocardiography: “ALVR” (n = 63)—end-diastolic volume index (EDVI) >20% and/or end-systolic volume index (ESVI) >15% after 24 weeks compared with initial values; “non-ALVR” (n = 62)—EDVI <20% and ESVI <15%. In the ALVR group, hard endpoints (recurrent myocardial infarction, unstable angina, hospitalization for decompensated heart failure, ventricular arrhythmias, cardiac surgery, cardiovascular death) were detected in 19 people (30%). In the non-ALVR group, hard endpoints were noted in 3 patients (5%). The odds ratio of developing an adverse outcome in ALVR vs. non-ALVR group was 8.5 (95% CI 2.4–30.5) (p = 0.0004). According to the multivariate analysis, the contribution of each of the indicators to the relative risk (RR) of adverse cardiac remodeling: waist circumference, RR = 1.02 (95% CI 1.001–1.05) (p = 0.042), plasma BNP—RR = 1.81 (95% CI 1.05–3.13) (p = 0.033), arterial elastance to left ventricular end-systolic elastance (Ea/Ees)—RR = 1.96 (95% CI 1.11–3.46) (p = 0.020). Conclusion. Determining ALVR status in early stages of the disease can accurately predict and stratify the risk of adverse outcomes in STEMI patients.
Aim. To study conventional risk factors and arterial stiffness parameters to identify non-invasive markers of coronary atherosclerosis in patients with and without history of cardiovascular disease, with premature and physiological vascular aging.Material and methods. The study included 198 patients with coronary artery disease (CAD) and 57 healthy people. The subjects were divided into two cohorts: younger and older than 50 years. Each group included patients with newly diagnosed acute coronary syndrome with/without history of cardiovascular disease (CAD and/or hypertension). Conventional risk factors were analyzed in all subjects. Ultrasound radiofrequency of common carotid arteries (CCA), applanation tonometry, volume sphygmography were performed.Results. Analysis of arterial parameters in individuals <50 years old revealed differences between healthy people and patients with CAD. In the subgroup of patients without a history of cardiovascular disease compared with healthy people, CCA were damaged in 77% (p<0,05), aorta — in 13%, muscular arteries — in 29% (p<0,05); in patients with a history of cardiovascular disease, in 71% (p<0,05), 5% and 34% (p<0,05), respectively. In the older age group of patients with and without history of cardiovascular disease, CCA were damaged in 84% and 94% (p<0,05), aorta — in 92% and 87% (p<0,05), muscular arteries — in 42-44% (p<0,05), respectively. According to the ROC analysis, in patients <50 years old, the area under the curve (AUC) for the intima-media thickness (IMT) was 0,830, the threshold — 622,3 (p=0,000); for the beta stiffness index — 0,850, threshold — 7,01 (p=0,002); for L-/CAVI1 — 0,742, threshold — 7,3 (p=0,000). In patients >50 years of age, AUC for the IMT was 0,948, threshold — 607,5 (p=0,000); for the beta stiffness index — 0,740, threshold — 8,84 (p=0,000); for L-/CAVI1 — 0,861, threshold — 8,4 (p=0,000).Conclusion. Timely identification of atherosclerotic markers using noninvasive techniques can improve the prediction of cardiovascular events. A comprehensive non-invasive examination of the arteries with determination of IMT, beta stiffness index, and L-/CAVI1 will probably identify young people with an unfavorable absolute cardiovascular risk. .
Objective To study the incidence of side effects from muscle tissue during therapy with atorvastatin at various doses in patients with acute ST-segment elevation myocardial infarction (STEMI) during 48 weeks of follow-up. Methods The study included 115 STEMI patients aged 30 to 65 years (mean age 51.7±9.5 years). Patients were randomized to atorvastatin treatment groups. Group 1 included 59 people who took atorvastatin 80 mg / day; group 2 - 56 patients who received moderate doses of atorvastatin. The compared persons were matched by age, sex, and anthropometric data. Initially on the 7–9th days, after 24 and 48 weeks of follow-up, the CPK-MB serum level was analyzed. Muscle damage was assessed after 5–6, 24, 48 weeks of follow-up according to the development of the following symptoms: pain, fatigue, muscle weakness, decreased physical activity - on a 10-point scale. Results The CPK-MB level in the 1st group initialy was 701.5 [95% CI 391; 1012] U / L, after 24 weeks - 162.8 [95% CI 130.2; 195.4] U / L (p<0.001), after 48 weeks - 205.6 [95% CI 134.8; 276.4] U / L (p<0.001). In group 2, the dynamics of CPK-MB: on days 7–9 - 522.7 [95% CI 115.8; 755.1 U / L, after 24 weeks - 141.4 [95% CI 122.6; 160.3] U / L (p=0.0004), after 48 weeks - 150.5 [95% CI 123.9; 177.1] U / L (p=0.0003). A detailed analysis in four patients of the 1st group revealed an increase in CPK-MB >4 upper limit of normal (ULN) after 48 weeks of follow-up (6.8%). Moreover, symptoms of muscle damage against the background of pathological CPK-MB values were observed only in two people (3.4%). In patients of the 2nd group after 24–48 weeks of therapy with atorvastatin, there was no increase in CPK-MB >4 ULN. In addition, there were no cases of drug withdrawal in any of the groups due to an increase in CPK-MB>10 ULN. Clinical symptoms of muscle damage after 5–6th, 24th and/or 48th weeks of follow-up were diagnosed in the 1st group in 41 patients (69.5%), in the 2nd group - in 31 people (55%) (p=0.11). Conclusion In STEMI patients on the background of 48-week therapy with atorvastatin, no serious adverse effects on the muscle tissue were revealed, which testifies in favor of the safety of high-dose statin therapy. The incidence of myalgia did not depend on the dose of the drug. FUNDunding Acknowledgement Type of funding sources: None.
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.
Objective. To study the dynamics of quality of life, exercise tolerance, parameters of central and peripheral blood pressure, adverse cardiovascular events depending on the achievement and maintenance of the target level (TL) of low-density lipoprotein cholesterol (LDL) against the background of 48-week high-dose therapy with atorvastatin.Design and methods. In total, 141 patients with acute myocardial infarction with ST-segment elevation were included. Within 48 weeks patients received atorvastatin 40–80 mg/day. A comprehensive examination was performed on days 7–9, after 24 and 48 weeks. After 192 weeks the endpoints were assessed.Results. The study was completed by 125 people (88,7 %). The patients were divided into groups: “А” (n = 41) — with achieved TL of LDL after 24 and 48 weeks; “PA” (n = 35) — partially achieved TL of LDL — on one of two visits; “NA” (n = 49) — not achieved TL. According to the Minnesota questionnaire, the symptoms of chronic heart failure increased in the groups “PA” (+53,5 %; p = 0,009) and “NA” (+75 %; p = 0,001). During applanation tonometry in the “PA” group, the number of people with elevated pulse pressure in the aorta increased. In the “NA” group, an increase in cases of normal and elevated central aortic systolic, pulse pressure was diagnosed. After 192 weeks the frequency of endpoints in the “PA” and “NA” groups was 38,1 % vs 17,1 % in the “А” group (p = 0,017); the odds ratio was 3,0 (95 % confidence interval 1,2–7,5).Conclusions. Our study demonstrated the most favorable clinical profile and prognosis in patients who achieved and maintained LDL for 48 weeks treatment.
Objective: To study the correlations between the parameters of the left ventricular-arterial coupling (LVAC) and the parameters of local arterial stiffness in patients after STEMI 6 months after revascularization. Design and method: 125 patients (mean age 51.2 ± 8.8 years) after STEMI were included in the study. The diagnosis was confirmed by biomarkers of myocardial necrosis, ECG, coronary angiography. Echocardiography was performed at the 7–9th day and 6 months after STEMI (MyLab, Esaote, Italy), followed by calculation of LVAC indices: arterial elastance (Ea), left ventricular elastance (Ees), LVAC index (Ea/Ees). The study of the right and left common carotid arteries (CCA) was carried out on a MyLab ultrasound scanner (Esaote, Italy) using high-frequency RF signal technology. The following parameters were recorded: QIMT - intima-media thickness, DC - lateral distensibility coefficient, stiffness index β, loc Psys - local SBP, locPdia - local DBP, locPWV - local pulse wave velocity, AP - amplification pressure. Results: In the study of the correlation of LVAC indices with the CCA rigidity parameters recorded on 7–9th day from the STEMI, a relationship was revealed only between Ees and LocPsys (r = 0.40; p = 0.01), Ees and LocPdia (r = 0, 26; p = 0.004). After 6 months of follow-up, a closer relationship between the LVAC and the parameters of the local CCA stiffness was diagnosed. The Ea indicator correlated with DC (r = -0.23; p = 0.009), PWV (r = 0.21; p = 0.02), LocPsys (r = 0.33; p = 0.0002), LocPdia (r = 0.26; p = 0.004) and AP (r = 0.19; p = 0.03). The Ees indicator was found to be associated with LocPsys (r = 0.38; p = 0.00001), LocPdia (r = 0.27; p = 0.002), AP (r = 0.22; p = 0.01). Conclusions: After 6 months, there was a closer correlation between the LVAC indices and the parameters of local pressure and rigidity. This is probably partly due to the remodeling of the cardiovascular system in the postinfarction period and the inclusion of compensatory-adaptive mechanisms that ensure the contractile function of the heart.
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.
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