Пациент с инфарктом миокарда, фибрилляцией предсердий и высоким геморрагическим риском: обоснованный выбор антикоагулянта для эффективной профилактики ишемических событий

Current clinical practice faces the challenges in selecting optimal drugs and the duration of antithrombotic treatment in patients with acute coronary syndrome with atrial fibrillation. A continuous increase of using non-vitamin K oral anticoagulants (NOAC), dabigatran, rivaroxaban, apixaban, edoxaban, and novel antiplatelet agents, prasugrel and ticagrelor, has complicated the decision-making process in this group of patients. The presented clinical case reports the use of dabigatran as a part of double antithrombotic therapy in an elderly patient with type 2 myocardial infarction, paroxysmal AF and a high risk for hemorrhage. The drug choice and its dosage were chosen using the personalized risk assessment. The presented approach has been early proved by the results of the recent randomized clinical trials and, therefore, may be translated into routine clinical practice.В настоящее время в реальной клинической практике имеются сложности понимания правильности выбора препаратов и продолжительности антитромботического лечения у пациентов с острым коронарным синдромом с фибрилляцией предсердий. С учетом непрерывного роста доли использования не-витамин К-зависимых прямых оральных антикоагулянтов (ПОАК) - даби-гатрана, ривароксабана, апиксабана, эдоксабана и активным использованием «новых» антиагрегантов (прасугрель и тикагрелор) принятие решений у этих пациентов стало еще более сложным. Представленный для обсуждения клинический случай демонстрирует применение дабигатрана в составе «двойной» антитромботической терапии у пожилой пациентки с инфарктом миокарда 2 типа с пароксизмальной формой ФП и высоким риском кровотечений. Обсужден выбор препарата и дозировки с учетом данных персонифицированной комплексной рискометрии. Представленный подход является доказанным по результатам ранее проведенных рандомизированных клинических исследований и может быть транслирован в широкую клиническую практику

КЛИНИЧЕСКОЕ НАБЛЮДЕНИЕ ПАЦИЕНТА С СЕМЕЙНОЙ ГЕТЕРОЗИГОТНОЙ ГИПЕРХОЛЕСТЕРИНЕМИЕЙ

The article presents the clinical case of a patient with heterozygous family hypercholesterolemia with a retro-spective review of the disease progression. The patient with severe lipid metabolism disorder was referred to the Center of Lipid Disorders at the Kemerovo Regional Clinical Cardiac Dispensary n. a. Academician L.S. Barbarash. The patient underwent selective screening according to the Dutch diagnostic criteria comprising of hypercho lesterolemia phenotype, personal and family history, as well as genetic factors. For patient N. the total cumulative score by the Dutch criteria was 30. The diagnosis of familial hypercholesterolemia (CGS) was confirmed. The patient was given maximum tolerated doses of statins. However, the statin therapy was switched to combined lipidlowering therapy due to its low effectiveness.В статье представлено клиническое наблюдение пациентки с семейной гетерозиготной гиперхолестеринемией с ретроспективным анализом динамики развития данного заболевания. Пациентка с тяжелым нарушением липидного обмена обратилась в липидный центр Кемеровского областного клинического кардиологического диспансера имени академика Л.С. Барбараша, в котором ей проводилась диагностика и коррекция нарушений липидного обмена. Проведена оценка по Голландским диагностическим критериям, в основе которых лежат фенотипические проявления гиперхолестеринемии, собственный и семейный анамнез, а также генетические факторы. Для пациентки В. общая суммарная оценка по голландским критериям со-ставила 30 баллов, что делает диагноз семейной гиперхолестеринемии (СГХС) в данном клиническом случае определенным. Пациентке были назначены максимально переносимые дозы статинов. Однако ввиду их низкой эффективности лечение было скорректировано в пользу комбинированной гиполипидемической терапии

Biomarkers of myocardial fibrosis and their genetic regulation in patients with heart failure

Currently, the development of chronic heart failure (CHF) is considered from the perspective of pathological structural remodeling of myocardium and fibrosis. Despite the widespread use of molecular genetic markers in clinical practice, only a small number of them are used to evaluate remodeling processes, as well as to predict potential complications associated with heart failure (HF). In addition, the relationship between many biomarkers with instrumental and histological confirmation of myocardial fibrosis has not yet been determined. Myocardial fibrosis remains quite debatable and controversial subject, which actualizes the further study of this direction. The discovery of pathogenetic and diagnostic markers of myocardial fibrosis could contribute to the development of targeted therapy. Of particular interest is the search for possible pathogenetic markers, since this is relevant for clinical practice

Participation of the C-terminal propeptide procollagen type I in the formation of cardiofibrosis in patients with myocardial infarction with preserved left ventricular ejection fraction

Aim. To study the dynamics of procollagen type I carboxy-terminal propeptide (PICP) with an assessment of potential associations with cardiac fibrosis (CF) and diastolic dysfunction (DD) of the left ventricle (LV) during the hospitalization and one year after ST segment elevation myocardial infarction (STEMI).Material and methods. The study included 120 patients with STEMI. There were following inclusion criteria: diagnosis of STEMI (2015 European Society of Cardiology guidelines); Killip £III acute heart failure (AHF); signed informed consent; patient age >18 years old. There were following exclusion criteria: STEMI due to percutaneous coronary intervention or coronary artery bypass grafting; Killip IV AHF; patient age >80 years; clinically significant comorbidities; death of the patient during the first day of hospitalization. On the 1st, 12th day of the disease and after a year all patients underwent echocardiography and the PICP concentration was determined. One year after myocardial infarction, contrast-enhanced cardiac magnetic resonance imaging was performed to assess CF. In the analyzed group of patients, on day 1 of STEMI, mean values of LV ejection fraction (EF) in the range of 40-49% were observed in 3 (2,5%) patients, LVEF <40% — in 31 (26%), LVEF ≥50% — in 86 (71,7%). The final analysis was performed on a sample of patients with preserved LVEF (n=86) (71,7%).Results. On the first day of myocardial infarction, signs of DD were noted in 25 (29,1%) patients, while after 1 year, their number increased by 9 (10%) and amounted to 34 (39,5%) patients. In 15 (17,6%) people, worsening of myocardial systolic dysfunction was noted. Patients with a CF ³16% had the highest PICP expression on the first day of the disease. CF ≥16% one year after STEMI with preserved EF is associated with PICP concentration on day 1 of the disease. In addition, multidirectional correlations were revealed between the CF ≥16% and parameters of LV diastolic function (e’, mean pulmonary artery pressure, E/e’).Conclusion. Determination of the PICP concentration on the 1st day of myocardial infarction will allow early identification of patients at risk of CF one year after STEMI with preserved EF

Predictors of myocardial fibrosis and loss of epicardial adipose tissue volume in the long-term period after myocardial infarction

Aim. To assess the changes of biochemical markers in hospitalization, the relationship with the severity of myocardial fibrosis and the epicardial adipose tissue (EAT) thickness one year after myocardial infarction (MI).Material and methods. A total of 88 patients (65 men and 23 women) with MI were examined. The percentage of cicatricial changes in the myocardium and the EAT thickness were measured using the magnetic resonance imaging (MRI) one year after MI. In the hospitalization (days 1 and 12) and 1 year after MI, the concentrations of N-terminal pro-brain natriuretic peptide (NT-proBNP), stimulating growth factor (ST2), interleukin-33 (IL-33) and type I collagen (COL-1). The data were analyzed using descriptive statistics, correlation and ROC analysis, and logistic regression (Statistica 9.0).Results. One year after MI, cicatricial changes were detected in 68 (77%) patients: 27 people had myocardial fibrosis <5%, 22 patients — 5-15%, and 19 patients >15%. We established that myocardial fibrosis after MI is associated with unfavorable medical history, a complicated course during in-hospital period and higher concentrations of ST2, NT-proBNP, COL-1 compared with patients without myocardial fibrosis. High levels of ST2, NT-proBNP increase the risk of myocardial fibrosis by 1,2 and 1,8 times after hospitalization, respectively. In patients with myocardial fibrosis >15%, IL-33 level was significantly lower in the 1st day of MI. It was found that the EAT thickness increases with fibrosis of 5-15%. An increase in the left (LV) and right ventricular (RV) EAT thickness by 1,33 times and 1,34 times, respectively, increases the risk of myocardial fibrosis (LV EAT thickness, mm (OR 1,33; 95% CI (1,08-1,4), AUC 0,75; RV EAT thickness, mm (OR 1,34; 95% CI (1,15-1,43), AUC 0,79). In patients with myocardial fibrosis >15%, EAT thickness decreases and correlates with NT-proBNP increase in the acute period and a one year after MI.Conclusion. The development of myocardial fibrosis one year after MI is associated with an increase in ST2, NT-proBNP, COL-1, both in the hospitalization and 1 year after MI. The decrease in IL-33 concentration during hospitalization with MI is accompanied by the development of fibrosis >15% of the myocardium

Rivaroxaban with or without aspirin in stable cardiovascular disease

BACKGROUND: We evaluated whether rivaroxaban alone or in combination with aspirin would be more effective than aspirin alone for secondary cardiovascular prevention. METHODS: In this double-blind trial, we randomly assigned 27,395 participants with stable atherosclerotic vascular disease to receive rivaroxaban (2.5 mg twice daily) plus aspirin (100 mg once daily), rivaroxaban (5 mg twice daily), or aspirin (100 mg once daily). The primary outcome was a composite of cardiovascular death, stroke, or myocardial infarction. The study was stopped for superiority of the rivaroxaban-plus-aspirin group after a mean follow-up of 23 months. RESULTS: The primary outcome occurred in fewer patients in the rivaroxaban-plus-aspirin group than in the aspirin-alone group (379 patients [4.1%] vs. 496 patients [5.4%]; hazard ratio, 0.76; 95% confidence interval [CI], 0.66 to 0.86; P<0.001; z=−4.126), but major bleeding events occurred in more patients in the rivaroxaban-plus-aspirin group (288 patients [3.1%] vs. 170 patients [1.9%]; hazard ratio, 1.70; 95% CI, 1.40 to 2.05; P<0.001). There was no significant difference in intracranial or fatal bleeding between these two groups. There were 313 deaths (3.4%) in the rivaroxaban-plus-aspirin group as compared with 378 (4.1%) in the aspirin-alone group (hazard ratio, 0.82; 95% CI, 0.71 to 0.96; P=0.01; threshold P value for significance, 0.0025). The primary outcome did not occur in significantly fewer patients in the rivaroxaban-alone group than in the aspirin-alone group, but major bleeding events occurred in more patients in the rivaroxaban-alone group. CONCLUSIONS: Among patients with stable atherosclerotic vascular disease, those assigned to rivaroxaban (2.5 mg twice daily) plus aspirin had better cardiovascular outcomes and more major bleeding events than those assigned to aspirin alone. Rivaroxaban (5 mg twice daily) alone did not result in better cardiovascular outcomes than aspirin alone and resulted in more major bleeding events