Аim. To study the efficacy, tolerability and safety of using a fixed dose combination of an ACE inhibitor lisinopril with a prolonged-action diuretic indapamide in patients with degree 1-2 hypertension.Material and methods. Patients (n = 32) with uncontrolled 1-2 degrees hypertension, moderate or high cardiovascular risk, without severe comorbid diseases, who were prescribed a fixed dose combination of lisinopril (5, 10 or 20 mg) and indapamide (1.5 mg) were included in the observational study. All patients had home monitoring of blood pressure and diuresis, as well as assessment of subjective tolerance of treatment and registration of adverse events within 3 months of observation. Assessment of changes in circadian fluctuations in blood pressure and diuresis, the frequency of achieving the target blood pressure at the outpatient stage, as well as the subjective tolerance of treatment and adverse events during a three-month follow-up.Results. Target blood pressure was achieved in 44.5% of patients taking the fixed dose combination of lisinopril 5 mg + prolonged-acting indapamide1.5 mg; 76.9% – in patients taking the combination of lisinopril 10 mg + indapamide 1.5 mg; 78,6% – in patients taking the combination of lisinopril 20 mg + indapamide 1.5 mg. The achieved antihypertensive effect was characterized by daily circadian stability, accompanied by an improvement in the initially impaired day and night diuretic profile (increase in the share of daytime diuresis by 29.6% and 22.3% with a decrease in the share of nighttime diuresis by 35% and 49% when using a combination with lisinopril 5 and 10 mg, respectively). The treatment was well tolerated by patients and did not cause the development of serious adverse events. Reported adverse events (non-intense dry cough, headache, general weakness) were transient and did not require correction or withdrawal of treatment.Conclusion. The fixed dose combination of the ACE inhibitor lisinopril (5, 10 or 20 mg) and the long-acting thiazide-like diuretic indapamide (1.5 mg) had good antihypertensive efficacy with improved circadian blood pressure and diuresis profiles, acceptable tolerance and safety of treatment, as well as a simple choice of doses of the drug components.
Среди факторов, способствующих декомпенсации и прогрессированию хронической сердечной недостаточ-ности (ХСН), важное клиническое значение имеет со-путствующая митральная регургитация (МР). Функцио-нальная полноценность митрального клапана зависит от координированного взаимодействия атриовентрику-лярного кольца, створок клапана, хорд, папиллярных мышц, левого предсердия и левого желудочка (ЛЖ). Это взаимодействие определяют как «клапанно-желудоч-ковый комплекс». Нормальная геометрия ЛЖ, функцио-нирование папиллярных мышц и хорд способствует нор-мальному соприкосновению створок и предотвращает воз-никновение обратного тока крови во время систолы же-лудочков. Дисфункция одного или более компонентов дан-ного комплекса может приводить к развитию МР [1]. Ос-новными причинами являются ишемическая болезнь сердца (с развитием ишемической МР), дилатационная кардиомиопатия (с развитием функциональной МР), ревматическое поражение клапанов, инфекционный эн-Mitral regurgitation (MR) is one of the factors contributory to chronic heart failure (CHF) decompensation and progress, that is why it has great clinical importance. Functional competence of mitral valve depends on coordinated interaction of such structures as atrioventricular ring, valve leaflets, chords, papillary muscles, left atrium and left ventricle (LV). This interaction is known as "valve-ventricular complex". Normal LV geometry, papillary muscles and chords correct functioning ensure adequate leaflets contiguity and prevent regurgitation during ventricle systole. Dysfunction of one or more components can lead to MR development [1]. Main reasons of such dysfunction are: ischemic heart disease (with ischemic MR development), dilated cardiomyopathy (with functional MR development), rheumatic valve lesion, infective endocarditis, myxomatous change (in congenital diseases with dysplasia and damage of mitral valve connective tissue) and some other states.Different lesions of mitral valve apparatus lead to MR development. MR can be registered with normal leafs move- Aim. To evaluate chronic heart failure (CHF) course, functional and structural heart changes in patients with functional mitral regurgitation (MR) of various degrees. Material and methods. A total of 104 outpatients (60-85 y. o.) with CHF of functional class II-IV by NYHA and functional MR of I-II degrees and MR of III-IV degrees were included into the study groups. Results: Patients in both groups were comparable in sex, age, CHF duration, body mass index, systolic and diastolic blood pressure, clinical state by the clinical state scale, quality of life, anxious and depressive status. The majority of patients with MR III had significant left ventricle (LV) systolic dysfunction (p=0,029), severe CHF course (p=0,034), received furosemide (p=0.004) and digoxin (p=0,004). They had significant increase in end-diastolic dimension (p<0,001), end-systolic dimension (p<0,001), left atrium (p=0,004), end-diastolic volume (p<0,001), end-systolic volume (p<0,001), pulmonary artery pressure (p<0,001), decrease in LV rel...
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