scholarly journals High-sensitivity C-reactive protein in chronic heart failure: patient characteristics, phenotypes, and mode of death

2019 ◽  
Vol 116 (1) ◽  
pp. 91-100 ◽  
Author(s):  
Pierpaolo Pellicori ◽  
Jufen Zhang ◽  
Joe Cuthbert ◽  
Alessia Urbinati ◽  
Parin Shah ◽  
...  

Abstract Aims Plasma concentrations of high-sensitivity C-reactive protein (hsCRP) are often raised in chronic heart failure (CHF) and might indicate inflammatory processes that could be a therapeutic target. We aimed to study the associations between hsCRP, mode and cause of death in patients with CHF. Methods and results We enrolled 4423 patients referred to a heart failure clinic serving a local population. CHF was defined as relevant symptoms or signs with either a reduced left ventricular ejection fraction <40% or raised plasma concentrations of amino-terminal pro-B type natriuretic peptide (NT-proBNP >125 pg/mL). The median [interquartile range (IQR)] plasma hsCRP for patients diagnosed with CHF (n = 3756) was 3.9 (1.6–8.5) mg/L and 2.7 (1.3–5.1) mg/L for those who were not (n = 667; P < 0.001). Patients with hsCRP ≥10 mg/L (N = 809; 22%) were older and more congested than those with hsCRP <2 mg/L (N = 1117, 30%). During a median follow-up of 53 (IQR 28–93) months, 1784 (48%) patients with CHF died. Higher plasma hsCRP was associated with greater mortality, independent of age, symptom severity, creatinine, and NT-proBNP. Comparing a hsCRP ≥10 mg/L to <2 mg/L, the hazard ratio for all-cause mortality was 2.49 (95% confidence interval 2.19–2.84; P < 0.001), for cardiovascular (CV) mortality was 2.26 (1.91–2.68; P < 0.001), and for non-CV mortality was 2.96 (2.40–3.65; P < 0.001). Conclusion In patients with CHF, a raised plasma hsCRP is associated with more congestion and a worse prognosis. The proportion of deaths that are non-CV also increases with higher hsCRP.

2021 ◽  
Vol 102 (4) ◽  
pp. 510-517
Author(s):  
E V Khazova ◽  
O V Bulashova

The discussion continues about the role of systemic inflammation in the pathogenesis of cardiovascular diseases of ischemic etiology. This article reviews the information on the role of C-reactive protein in patients with atherosclerosis and heart failure in risk stratification for adverse cardiovascular events, including assessment of factors affecting the basal level of highly sensitive C-reactive protein. Research data (MRFIT, MONICA) have demonstrated a relationship between an increased level of C-reactive protein and the development of coronary heart disease. An increase in the serum level of highly sensitive C-reactive protein is observed in arterial hypertension, dyslipidemia, type 2 diabetes mellitus and insulin resistance, which indicates the involvement of systemic inflammation in these disorders. Currently, the assessment of highly sensitive C-reactive protein is used to determine the risk of developing myocardial infarction and stroke. It has been proven that heart failure patients have a high level of highly sensitive C-reactive protein compared with patients without heart failure. The level of C-reactive protein is referred to as modifiable risk factors for cardiovascular diseases of ischemic origin, since lifestyle changes or taking drugs such as statins, non-steroidal anti-inflammatory drugs, glucocorticoids, etc. reduce the level of highly sensitive C-reactive protein. In patients with heart failure with different left ventricular ejection fraction values, it was found that the regression of the inflammatory response is accompanied by an improvement in prognosis, which confirms the hypothesis of inflammation as a response to stress, which has negative consequences for the cardiovascular system.


2019 ◽  
Vol 26 (5) ◽  
pp. 33-43 ◽  
Author(s):  
L. G. Voronkov ◽  
К. V. Voitsekhovska ◽  
S. V. Fedkiv ◽  
T. I. Gavrilenko ◽  
V. I. Koval

The aim – to identify prognostic factors for the development of adverse cardiovascular events (death and hospitalization) in patients with chronic heart failure (CHF) and left ventricular ejection fraction (LVEF) ≤ 35 % after long-term observation. Materials and methods. 120 stable patients with CHF, aged 18–75, II–IV functional classes according to NYHA, with LVEF ≤ 35 % were examined. Using multiple logistic regression according to the Cox method, we analyzed independent factors that affect the long-term prognosis of patients with heart failure. Results and discussion. During the observation period, out of 120 patients, 61 patients reached combined critical point (CCР). In the univariate regression model, predictors of CCР reaching were NYHA functional class, weigh loss of ≥ 6 % over the past 6 months, systolic and diastolic blood pressure, patient’s history of myocardial infarction, angina pectoris, anemia, number of hospitalizations over the past year and parameters reflecting the functional state of the patient (6-minute walk distance, number of extensions of the lower limb). The risk of CCP developing is significantly higher in patients with lower body mass index, shoulder circumference of a tense and unstressed arm, hip, thickness of the skin-fat fold over biceps and triceps, estimated percentage of body fat. Рredictors CCP reaching are higher levels of uric acid and C-reactive protein. Echocardiographic predictors of CCP onset were LVEF, size of the left atrium, TAPSE score, as well as its ratio to systolic pressure in the pulmonary artery, index of final diastolic pressure in the left ventricle. Also, the risk of CCP reaching is greater at lower values of the flow-dependent vasodilator response. Independent predictors of CCP onset were the circumference of the shoulder of an unstressed arm, the level of C-reactive protein in the blood, and the rate of flow-dependent vasodilator response. When analyzing the indices in 77 patients, who underwent densitometry, it was revealed that the E/E´ index, the index of muscle tissue of the extremities, the index of fat mass, and the ratio of fat mass to growth affect CCP reaching. In a multivariate analysis, taking into account densitometry indices, independent predictors of CCP onset were the size of the left atrium, the index of muscle mass of the extremities, the rate of flow-dependent vasodilator response and the presence of myocardial infarction in anamnesis. Conclusions. Independent predictors of CCP reaching in patients with CHF and LVEF ≤ 35 % are myocardial infarction in anamnesis, lower arm circumference of the arm, limb muscle mass index, flow-dependent vasodilator response, higher levels of C-reactive protein, sizes of the left atrium.


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.


2018 ◽  
Vol 0 (3) ◽  
pp. 36-40
Author(s):  
L. G. Voronkov ◽  
G. E. Dudnik ◽  
A. V. Liashenko ◽  
T. I. Gavrilenko ◽  
L. S. Mkhitaryan ◽  
...  

Author(s):  
Anna Chuda ◽  
Maciej Banach ◽  
Marek Maciejewski ◽  
Agata Bielecka-Dabrowa

AbstractHeart failure (HF) is the only cardiovascular disease with an ever increasing incidence. HF, through reduced functional capacity, frequent exacerbations of disease, and repeated hospitalizations, results in poorer quality of life, decreased work productivity, and significantly increased costs of the public health system. The main challenge in the treatment of HF is the availability of reliable prognostic models that would allow patients and doctors to develop realistic expectations about the prognosis and to choose the appropriate therapy and monitoring method. At this moment, there is a lack of universal parameters or scales on the basis of which we could easily capture the moment of deterioration of HF patients’ condition. Hence, it is crucial to identify such factors which at the same time will be widely available, cheap, and easy to use. We can find many studies showing different predictors of unfavorable outcome in HF patients: thorough assessment with echocardiography imaging, exercise testing (e.g., 6-min walk test, cardiopulmonary exercise testing), and biomarkers (e.g., N-terminal pro-brain type natriuretic peptide, high-sensitivity troponin T, galectin-3, high-sensitivity C-reactive protein). Some of them are very promising, but more research is needed to create a specific panel on the basis of which we will be able to assess HF patients. At this moment despite identification of many markers of adverse outcomes, clinical decision-making in HF is still predominantly based on a few basic parameters, such as the presence of HF symptoms (NYHA class), left ventricular ejection fraction, and QRS complex duration and morphology.


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