Endothelial dysfunction and C‐reactive protein predict the incidence of heart failure in hypertensive patients

Abstract Introduction Pulmonary endarterectomy leads to a decrease in systemic inflammation and improvement in endothelial function in patients with chronic thromboembolic pulmonary hypertension (CTEPH). Balloon pulmonary angioplasty (BPA) improves pulmonary hemodynamics in patients with inoperable CTEPH. Aim To assess changes in systemic inflammation and endothelial dysfunction after a single BPA session and after completion of the treatment. Methods We enrolled consecutive, inoperable CTEPH patients who underwent BPA. Interleukin 6, 10 (IL-6, IL-10), and C-reactive protein (hsCRP) constituted markers of systemic inflammation. Endothelin-1 (ET-1) served as a marker of endothelial dysfunction. Serum concentration of selected markers was assessed in every patient before, 24 hours after the first BPA session and 6 months after completion of the BPA treatment. Age- and sex-matched healthy subjects served as a control group. Results We recruited 20 patients with inoperable CTEPH (6 males [30%]), aged 67 [61–74] years in New York Heart Association class III (n=19 [95%]) and II (n=1 [5%]). BPA treatment was completed with a median of 5 [2–8] BPA sessions per patient. Before starting the treatment CTEPH patients, as compared to controls (n=10), had raised serum level of IL-6 (3.82 [2.75 - 6.03] vs. 2.64 [0.88 - 4.75] pg/ml; p=0.04), hsCRP (2.47 [0.93 - 4.27] vs. 1.23 [0.48–3.21] ng/ml; p=0.02) and ET-1 (2.68 [2.24 - 3.64] vs. 1.47 [1.4 - 1.82] pg/ml; p=0.004). There was no difference in IL-10 level. 24 hours after a BPA session we observed an increased level of IL-6, IL-10 and hsCRP. (Tab.) 6 months after completion of the BPA treatment there was a reduced level of IL-6, hsCRP and ET-1 (Tab.) Table 1. Changes (Δ) in serum concentration of analyzed markers 24 hours after a single BPA session and at 6-months assessment after completion of the BPA treatment (n=20) Initial Δ at 24 hours after single BPA p Δ at 6-months follow-up p ET-1 [pg/ml] 2.68 [2.24; 3.64] −0.2 [−0.5; 0.23] 0.21 −0.47 [−0.96; 0.05] 0.004 IL-6 [pg/ml] 3.82 [2.75; 6.03] 3.67 [1.41; 7.16] 0.008 −0.82 [−3.11; 0.54] 0.04 IL-10 [pg/ml] 0.53 [0.44; 0.58] 0.32 [0.21; 0.87] 0.006 −0.11 [−0.33; 0.14] 0.94 hsCRP [ng/ml] 2.47 [0.93; 4.27] 5.4 [3.96; 10.59] 0.008 −0.36 [−0.94; 0.16] 0.02 ET-1, endothelin 1; hsCRP, C-reactive protein; IL-6, interleukin 6; IL-10, interleukin 10. Conclusions Patients with inoperable CTEPH, as compared to healthy controls, exhibit an increased systemic inflammation and endothelial dysfunction, which both improve after completion of the BPA treatment. At short-term follow-up after single BPA session there is an increase in systemic inflammatory response.

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Relationships between high-sensitive C-reactive protein and markers of arterial stiffness in hypertensive patients. Differences by sex

BMC Cardiovascular Disorders ◽

10.1186/1471-2261-12-37 ◽

2012 ◽

Vol 12 (1) ◽

Cited By ~ 17

Author(s):

Manuel A Gomez-Marcos ◽

Jose I Recio-Rodríguez ◽

Maria C Patino-Alonso ◽

Cristina Agudo-Conde ◽

Leticia Gomez-Sanchez ◽

...

Keyword(s):

Arterial Stiffness ◽

C Reactive Protein ◽

Hypertensive Patients ◽

Reactive Protein

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The role of systemic inflammation in heart failure

Kazan medical journal ◽

10.17816/kmj2021-510 ◽

2021 ◽

Vol 102 (4) ◽

pp. 510-517

Author(s):

E V Khazova ◽

O V Bulashova

Keyword(s):

Heart Failure ◽

Cardiovascular Diseases ◽

Systemic Inflammation ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

C Reactive Protein ◽

Ventricular Ejection Fraction ◽

Reactive Protein ◽

Highly Sensitive

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.

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Amelioration of C - Reactive Protein and Lectin Like Oxidised Low Density Lipoprotein Receptor Complex Induced Endothelial Dysfunction by Oligomeric Proanthocyanidins.

10.21203/rs.3.rs-770001/v1 ◽

2021 ◽

Author(s):

Sankar Jamuna ◽

Rathinavel Ashokkumar ◽

Niranjali Devaraj Sivasithamparam

Keyword(s):

Nitric Oxide ◽

Endothelial Cells ◽

Endothelial Dysfunction ◽

Capillary Tube ◽

Morphological Changes ◽

Protein Docking ◽

Pcr Analysis ◽

Inhibitory Mechanism ◽

C Reactive Protein ◽

Reactive Protein

Abstract C-reactive protein (CRP) is a well established biochemical marker for atherosclerosis. Inflammation induced by CRP promotes endothelial dysfunction. Modification of LDL inside the artery wall favors the elevation of this acute phase protein. The mechanism of OxLDL+CRP complex is unrevealed so far. Hence, this mechanism was considered as the important factor to trigger the monocyte to macrophages differentiation which in leads to foam cells formation. Hence this key event should be targeted and focused on how this complex (OxLDL+CRP) proceeds to endothelial dysfunction. OPC is a well known cardioprotective flavon-3-ols. The present study is challenged between the protective roles of OPC against the deleterious effect of this complex (OxLDL+CRP) on endothelial cells. Monolayer of Endothelial cells were incubated with THP-1 monocytes for 48 h supplemented with OxLDL (10mg/ml) + CRP (10 mg/ml) complex and treated with OPC (100mg/ml). Morphological changes, cell migration assay and capillary tube forming assay was carried out. Myeleoperoxidase levels were estimated to determine the adhesion of monocytes onto EC monolayer. RT-PCR analysis of L-Selectin was done. The quantification of NO levels and analysis of mRNA expressions of eNOS is to determine the nitric oxide demand caused due to OxLDL+CRP complex. LOX-1, scavenger receptor levels were analysed by mRNA expression. Proinflammatory markers such as IL-6, MCP-1 and IL-1b were studied. Accumulation of ROS levels were measured fluorimetrically using DCF-DA. Spectrophotometric analysis of Sirius red dye binding collagen levels was observed. Mitochondrial membrane potential was determined by JC-1 dye and cell cycle analysis was done by FACS analysis. Protein –Protein docking was carried out between CRP and LOX-1. This docked protein complex were again docked with OPC and atrovastatin to show the inhibitory mechanism of CRP binding with LOX-1. OPC showed a promising inhibitory mechanism against OxLDL+CRP complex. To emphasis the results OPC treated group showed decreased levels of proinflammatory markers, LOX-1 and L-Selectin levels. Endothelial nitric oxide levels were increased upon OPC treatment and reduction in the ROS levels. Endothelial cells apoptosis was prevented by OPC. Docking studies showed that in the absence of ligands (OPC) binding of CRP and LOX-1 was greater and vice versa in the presence of ligands. To conclude, OxLDL + CRP complex inhibitory effects of OPC could maintain the normal homeostasis.

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Long-term clinical prognosis predictors in patients with chronic heart failure and reduced left ventricular ejection fraction

Ukrainian Journal of Cardiology ◽

10.31928/10.31928/1608-635x-2019.5.3342 ◽

2019 ◽

Vol 26 (5) ◽

pp. 33-43 ◽

Cited By ~ 1

Author(s):

L. G. Voronkov ◽

К. V. Voitsekhovska ◽

S. V. Fedkiv ◽

T. I. Gavrilenko ◽

V. I. Koval

Keyword(s):

Myocardial Infarction ◽

Heart Failure ◽

Left Atrium ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

C Reactive Protein ◽

Ventricular Ejection Fraction ◽

Reactive Protein ◽

Vasodilator Response

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.

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