scholarly journals THE CARDIAC MYOSIN ACTIVATOR, OMECAMTIV MECARBIL, IMPROVES LEFT VENTRICULAR MYOCARDIAL DEFORMATION IN CHRONIC HEART FAILURE (COSMIC-HF)

2017 ◽  
Vol 69 (11) ◽  
pp. 858 ◽  
Author(s):  
Tor Biering-Sorensen ◽  
John Teerlink ◽  
G. Michael Felker ◽  
John McMurray ◽  
Fady Malik ◽  
...  
2020 ◽  
Vol 13 (12) ◽  
Author(s):  
Tor Biering-Sørensen ◽  
Masatoshi Minamisawa ◽  
Brian Claggett ◽  
Jiankang Liu ◽  
G. Michael Felker ◽  
...  

2019 ◽  
Vol 14 (6) ◽  
pp. 870-878 ◽  
Author(s):  
D. S. Novikova ◽  
H. V. Udachkina ◽  
I. G. Kirillova ◽  
T. V. Popkova

Rheumatoid arthritis (RA) is characterized by a twofold increase in morbidity and mortality due to chronic heart failure (CHF). At the same time, the prevalence of CHF among RA patients is significantly underestimated. The aim of the review was to analyze the results of the main studies on the features of the clinical presentation of heart failure (HF) in RA patients, the role of visualization techniques and biomarkers in the diagnosis of HF and preclinical dysfunction of the myocardium. HF in patients with RA is characterized by a predominance of HF with a preserved left ventricular ejection fraction (LVEF). The use of clinical diagnostic criteria in RA patients can lead to both over- or underdiagnosis of CHF. Systolic dysfunction estimated by LVEF is rare in RA and does not reflect the real frequency of myocardial dysfunction. Echocardiography (ECHO-CG) with tissue Doppler echocardiography (TDE) and visualization of myocardial deformation, magnetic resonance imaging (MRI) of the heart in RA patients revealed a high frequency of HF with preserved ejection fraction, left ventricular remodeling and hypertrophy, pre-clinical systolic and diastolic dysfunction. Determination of natriuretic peptides is useful for verifying the diagnosis of HF and estimating the prognosis in this cohort, despite the possible decrease in the sensitivity and specificity of these indicators in RA patients. The review discusses the advantages of MRI of the heart, including quantitative T1 and T2 regimens, in the diagnosis of myocarditis, myocardial fibrosis, and myocardial perfusion disorders in RA patients. In order to verify the diagnosis of heart failure and detect pre-clinical myocardial dysfunction in RA patients, the determination of natriuretic peptides concentration should become part of the routine examination, beginning with the debut of the disease, along with the collection of a cardiological history, physical examination, ECHO-CT with TDE, and visualization of myocardial deformation. Evaluation of the quantitative characteristics of tissue according to MRI of the heart could improve the diagnosis of myocardial damage.


2021 ◽  
Author(s):  
Johannes Kersten ◽  
Carsten Hackenbroch ◽  
Paula Gann ◽  
Anna-Sophie Hoestermann ◽  
Peter Bernhardt

Abstract Background: Myocardial deformation parameters have been shown to yield early detection of pathological changes in chronic heart failure (CHF). Aim of our study was to evaluate myocardial deformation changes under optimal medical therapy (OMT) in CHF patients.Methods: CHF patients were examined longitudinally with two cardiac magnetic resonance imaging (CMR) examinations at a median time interval of 140 days. Left and right ventricular volumes were quantified, and deformation analysis was performed using feature tracking, respectively.Results: 57 patients were included into the study. There was a high rate of OMT with a prescription of beta blockers in 98.2% and ACE-inhibitors/Angiotensin receptor blockers in 93.0%. In the total cohort, there were indications of positive remodeling with a significant improvement in left ventricular (LV) ejection fraction (38.9% ± 11.6 vs. 43.0% ± 12.7, p=0.009), LV enddiastolic volume indexed (92.1ml/m2 ± 23.5 vs. 87.2ml/m2 ± 21.2, p=0.007), LV mass (140.3g ± 35.7 vs. 128.0g ± 34.4, p=0.001) and right ventricular global longitudinal strain (RV GLS) (-18.1% ± 5.1 vs. -20.3% ± 4.5, p<0.001) during follow-up. Discussion: Patients with CHF and OMT show positive reverse remodeling with improvement of LV volumes and function and RV GLS. This has a potential impact on the surveillance of this patient group, which should be further investigated in larger prospective studies.


2020 ◽  
Vol 90 (1-2) ◽  
pp. 49-58 ◽  
Author(s):  
Wang Chunbin ◽  
Wang Han ◽  
Cai Lin

Abstract. Vitamin D deficiency commonly occurs in chronic heart failure. Whether additional vitamin D supplementation can be beneficial to adults with chronic heart failure remains unclear. We conducted a meta-analysis to derive a more precise estimation. PubMed, Embase, and Cochrane databases were searched on September 8, 2016. Seven randomized controlled trials that investigated the effects of vitamin D on cardiovascular outcomes in adults with chronic heart failure, and comprised 592 patients, were included in the analysis. Compared to placebo, vitamin D, at doses ranging from 2,000 IU/day to 50,000 IU/week, could not improve left ventricular ejection fraction (Weighted mean difference, WMD = 3.31, 95% confidence interval, CL = −0.93 to 7.55, P < 0.001, I2 = 92.1%); it also exerts no beneficial effects on the 6 minute walk distance (WMD = 18.84, 95% CL = −24.85 to 62.52, P = 0.276, I2 = 22.4%) and natriuretic peptide (Standardized mean difference, SMD = −0.39, 95% confidence interval CL = −0.48 to 0.69, P < 0.001, I2 = 92.4%). However, a dose-response analysis from two studies demonstrated an improved left ventricular ejection fraction with vitamin D at a dose of 4,000 IU/day (WMD = 6.58, 95% confidence interval CL = −4.04 to 9.13, P = 0.134, I2 = 55.4%). The results showed that high dose vitamin D treatment could potentially benefit adults with chronic heart failure, but more randomized controlled trials are required to confirm this result.


Author(s):  
С.А. Крыжановский ◽  
И.Б. Цорин ◽  
Е.О. Ионова ◽  
В.Н. Столярук ◽  
М.Б. Вититнова ◽  
...  

Цель исследования - разработка трансляционной модели хронической сердечной недостаточности (ХСН) у крыс, позволяющей, с одной стороны, изучить тонкие механизмы, лежащие в основе данной патологии, а с другой стороны, выявить новые биомишени для поиска и изучения механизма действия инновационных лекарственных средств. Методика. Использован комплекс эхокардиографических, морфологических, биохимических и молекулярно-биологических исследований, позволяющий оценивать и дифференцировать этапы формирования ХСН. Результаты. Динамические эхокардиографические исследования показали, что ХСН формируется через 90 дней после воспроизведения переднего трансмурального инфаркта миокарда. К этому времени у животных основной группы отмечается статистически значимое по сравнению со 2-ми сут. после воспроизведения экспериментального инфаркта миокарда снижение ФВ левого желудочка сердца (соответственно 55,9 ± 1,4 и 63,9 ± 1,6%, р = 0,0008). Снижение насосной функции сердца (на 13% по сравнению со 2-ми сут. после операции и на ~40% по сравнению с интактными животными) сопровождается увеличением КСР и КДР (соответственно с 2,49 ± 0,08 до 3,91 ± 0,17 мм, р = 0,0002, и с 3,56 ± 0,11 до 5,20 ± 0,19 мм, р = 0,0001), то есть к этому сроку развивается сердечная недостаточность. Результаты эхокардиографических исследований подтверждены данными морфометрии миокарда, продемонстрировавшими дилатацию правого и левого желудочков сердца. Параллельно проведенные гистологические исследования свидетельствуют о наличии патогномоничных для данной патологии изменений миокарда (постинфарктный кардиосклероз, компенсаторная гипертрофия кардиомиоцитов, очаги исчезновения поперечной исчерченности мышечных волокон и т.д.) и признаков венозного застоя в легких и печени. Биохимические исследования выявили значимое увеличение концентрации в плазме крови биохимического маркера ХСН - мозгового натрийуретического пептида. Данные молекулярно-биологических исследований позволяют говорить о наличии гиперактивности ренин-ангиотензин-альдостероновой и симпатоадреналовой систем, играющих ключевую роль в патогенезе ХСН. Заключение. Разработана трансляционная модель ХСН у крыс, воспроизводящая основные клинико-диагностические критерии этого заболевания. Показано наличие корреляции между морфометрическими, гистологическими, биохимическими и молекулярными маркерами прогрессирующей ХСН и эхокардиографическими диагностическими признаками, что позволяет использовать неинвазивный метод эхокардиографии, характеризующий состояние внутрисердечной гемодинамики, в качестве основного критерия оценки наличия/отсутствия данной патологии. Aim. Development of a translational model for chronic heart failure (CHF) in rats to identify new biotargets for finding and studying mechanisms of innovative drug effect in this disease. Methods. A set of echocardiographic, morphological, biochemical, and molecular methods was used to evaluate and differentiate stages of CHF development. Results. Dynamic echocardiographic studies showed that CHF developed in 90 days after anterior transmural myocardial infarction. By that time, left ventricular ejection fraction was significantly decreased in animals of the main group compared with rats studied on day 2 after experimental myocardial infarction (55.9 ± 1.4% vs . 63.9 ± 1.6%, respectively, p<0.0008). The decrease in heart’s pumping function (by 13% compared with day 2 after infarction and by approximately 40% compared to intact animals) was associated with increased ESD and EDD (from 2.49 ± 0.08 to 3.91 ± 0.17 mm, p = 0.0002, and from 3.56 ± 0.11 to 5.20 ± 0.19 mm, respectively, p = 0.0001); therefore, heart failure developed by that time. The results of echocardiographic studies were confirmed by myocardial morphometry, which demonstrated dilatation of both right and left ventricles. Paralleled histological studies indicated presence of the changes pathognomonic for this myocardial pathology (postinfarction cardiosclerosis, compensatory hypertrophy of cardiomyocytes, foci of disappeared transverse striation of muscle fibers, etc.) and signs of venous congestion in lungs and liver. Biochemical studies demonstrated a significant increase in plasma concentration of brain natriuretic peptide, a biochemical marker of CHF. Results of molecular studies suggested hyperactivity of the renin-angiotensin-aldosterone and sympathoadrenal systems, which play a key role in the pathogenesis of CHF. Conclusions. A translational model of CHF in rats was developed, which reproduced major clinical and diagnostic criteria for this disease. Morphometric, histological, biochemical, and molecular markers for progressive CHF were correlated with echocardiographic diagnostic signs, which allows using this echocardiographic, noninvasive method characterizing the intracardiac hemodynamics as a major criterion for the presence / absence of this pathology.


Sign in / Sign up

Export Citation Format

Share Document