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  • Author: Luminița Animarie Vida-Simiti x
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Alexandra Florina Cocoi, Dana Pop, Mihai Cocoi, Adela Mihaela Serban and Luminita Animarie Vida-Simiti

Abstract

Inflammation of the venous wall is involved in thrombogenesis, thrombus resolution, wall remodeling and the post-thrombotic syndrome. Different mechanisms are involved in both arterial and venous thrombosis and patients with atherothrombosis hold a higher risk of venous thrombosis. Although inflammation may represent the connection between arterial and venous thrombosis, it is not yet sure if it is the cause or consequence of venous thrombosis. Consequently, the relationships between inflammation markers as indicators of the inflammatory process and clinical venous thromboembolism need to be investigatd. For example, inflammation mediators such as the pro-inflammatory cytokines interleukin 8 (IL-8), IL-6, monocyte chemotactic protein 1 (MCP-1), C Reactive Protein (CRP), vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), matrix metalloproteinases and tumor necrosis factor alpha (TNF alpha) are all involved in thrombogenesis. Studies of venous thromboembolism on animal models proved that there are specific phases of the inflammatory process in venous thromboembolism and thrombus resolution. Knowing the molecular and immunologic mechanisms, identifying and understanding the inflammation markers which are relevant for venous thrombosis, can help to target specific pathways and to develop future therapies of this disease

Open access

Cerasela Mihaela Goidescu, Florin Petru Anton, Daniel Corneliu Leucuța, Petru Adrian Mircea and Luminița Animarie Vida-Simiti

Abstract

Background: Apelin is a potent endogenous inotropic peptide with a major role in counteracting the aldosterone and angiotensin II and their negative effects on the cardiovascular system. The exact role of apelin in the patho-physiology of this disease is not well understood. We aimed to investigate the possible associations of apelin-13 with clinical and paraclinical characteristics in HF patients as well as studying its dynamics during the course of the heart failure.

Method: We performed a prospective observational cohort single-center study. We compared the baseline serum levels of apelin-13 and NT-proBNP level in 53 heart failure patients (acute heart failure, chronic compensated heart failure and chronic decompensated heart failure). We divided the patients according to the apelin-13 level: above and below the median, and we analyzed the relationship between serum apelin-13 and the clinical, echocardiographic, electrocardiographic and biological parameters. Twenty patients were followed-up (after an average time interval of 9 months), investigating the same parameters.

Results: The median of apelin-13 was 495pg/mL (IQR 276-845pg/mL). We found strong, negative correlation between the serum levels of apelin-13 and NT-proBNP (Spearman rho= −0.83, p<0.001). For the reassessed patients the median apelin level was significantly higher at follow-up (460 pg/mL, IQR 342-871 pg/mL) as compared with the baseline level (395 pg/mL, IQR 270-603 pg/mL), p=0.019, and maintained the negative correlation with NT-proBNP level (Spearman’s rho −0.7, p<0.001. The Low Apelin-13 group have higher NT-proBNP levels and also contains all the patients in NYHA IV class heart failure, 71% of the acute HF patients, and 7 of 8 patients who died before follow-up.

Conclusion: Apelin-13 was negatively correlated with NT-proBNP. The Low Apelin-13 group contained the majority of the patients with a negative outcome (death before follow-up), most of the patients who presented with acute HF and all the patients in NYHA IV class.