Publications by authors named "Habib Haybar"

44 Publications

COVID-19: imbalance of multiple systems during infection and importance of therapeutic choice and dosing of cardiac and anti-coagulant therapies.

Mol Biol Rep 2021 Apr 10. Epub 2021 Apr 10.

Golestan Hospital Clinical Research Development Unit, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

The renin-angiotensin-aldosterone system and its metabolites play an important role in homeostasis of body, especially the cardiovascular system. In this study, we discuss the imbalance of multiple systems during the infection and the importance of therapeutic choice, dosing, and laboratory monitoring of cardiac and anti-coagulant therapies in COVID-19 patients. The crosstalk between angiotensin, kinin-kallikrein system, as well as inflammatory and coagulation systems plays an essential role in COVID-19. Cardiac complications and coagulopathies imply the crosstalks between the mentioned systems. We believe that the blockage of bradykinin can be a good option in the management of COVID-19 and CVD in patients and that supportive treatment of respiratory and cardiologic complications is needed in COVID-19 patients. Ninety-one percent of COVID-19 patients who were admitted to hospital with a prolonged aPTT were positive for lupus anticoagulant, which increases the risk of thrombosis and prolonged aPTT. Therefore, the question that is posed at this juncture is whether it is safe to use the prophylactic dose of heparin particularly in those with elevated D-dimer levels. It should be noted that timing is of high importance in anti-coagulant therapy; therefore, we should consider the level of D-dimer, fibrinogen, drug-drug interactions, and risk factors during thromboprophylaxis administration. Fibrinogen is an independent predictor of resistance to heparin and should be considered before thromboprophylaxis. Alteplase and Futhan might be a good choice to assess the condition of heparin resistance. Finally, the treatment option, dosing, and laboratory monitoring of anticoagulant therapy are critical decisions in COVID-19 patients.
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http://dx.doi.org/10.1007/s11033-021-06333-wDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8035598PMC
April 2021

[Informatori biologici per ischemia miocardica silente: approccio diagnostico e prognostico.]

Recenti Prog Med 2020 Jul-Aug;111(7):415-425

Physiology Research Center and Department of Physiology, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Riassunto. L'ischemia miocardica silente (SMI) è un aspetto dello spettro della cardiopatia ischemica che varia dalla malattia coronarica asintomatica all'angina grave. Considerando il progressivo aumento della prevalenza di SMI e l'inaffidabilità di test diagnostici comuni, l'identificazione di biomarcatori SMI benefici è molto critica per una diagnosi rapida e un trattamento efficace della malattia. La presente revisione ha lo scopo di analizzare l'efficienza clinica di biomarcatori ben applicati e nuovi per la diagnosi e la previsione dei risultati dei pazienti con SMI. Questi biomarcatori includono cTnT, cTnI, hs-cTnT, hs-cTnI, hsCRP, NT-proBNP, sST2, GDF-15, Lp-PLA2, recettori della superficie cellulare, citochine antinfiammatorie, OPG, leptina, colesterolo totale, HDL, LDL, lipoproteine (a), omocisteina, albuminuria, microalbuminuria e miRNA circolanti. Nel database PubMed sono stati cercati rapporti scientifici (articoli originali) usando i termini "biomarcatori", "ischemia miocardica silenziosa", "biomarcatori cardiaci", "infiammatori", "marcatori", "stress ossidativo". Una migliore comprensione di vari biomarcatori SMI fornisce una migliore comprensione della sua varia patofisiologia e aspetto asintomatico, nonché dell'uso clinico di routine di questi biomarcatori.
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http://dx.doi.org/10.1701/3407.33924DOI Listing
July 2020

Cardiomyopathy in Thalassemia: Quick Review from Cellular Aspects to Diagnosis and Current Treatments.

Lab Med 2020 Mar;51(2):143-150

Child Growth & Development Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.

Background: Cardiomyopathic manifestations induced by continuous blood transfusion are the leading cause of death among patients with thalassemia major (TM). Despite introduction of chelation therapy, heart failure after cardiomyopathic manifestations is still a major threat to patients.

Methods: We performed a search of relevant English-language literature, retrieving publications from the PubMed database and the Google Scholar search engine (2005-2018). We used "thalassemia major", "cardiomyopathy", "iron overload", "cardiac magnetic resonance T2" "chelation therapy", and "iron burden" as keywords.

Results: The results of the studies we found suggest that cardiac hepcidin is a major regulator of iron homeostasis in cardiac tissue. Unlike previous assumptions, the heart appears to have a limited regeneration capability, originating from a small population of hypoxic cardiomyocytes.

Conclusions: Oxygen levels determine cardiomyocyte gene-expression patterns. Upregulation of cardiac hepcidin in hypoxia preserves cardiomyocytes from forming out of reactive oxygen species catalyzed by free cellular iron in cardiomyocytes. Using the limited regeneration capacity of cardiac cells and gaining further understanding of the cellular aspects of cardiomyopathic manifestations may help health care professionals to develop new therapeutic strategies.
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http://dx.doi.org/10.1093/labmed/lmz052DOI Listing
March 2020

Expression of Blood Cells Associated CD Markers and Cardiovascular Diseases: Clinical Applications in Prognosis.

Lab Med 2020 Mar;51(2):122-142

Thalassemia and Hemoglobinopathy Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background: Cardiovascular diseases (CVDs) are a major cause of mortality worldwide. The results of various studies have shown that abnormality in the frequency and function of blood cells can be involved in CVD complications. In this review, we have focused on abnormalities in the expression of the CD (cluster of differentiation) markers of blood cells to assess the association of these abnormalities with CVD prognosis.

Methods: We identified the relevant literature through a PubMed search (1990-2018) of English-language articles using the terms "Cardiovascular diseases", "CD markers", "leukocytes", "platelets", and "endothelial cells".

Results: There is a variety of mechanisms for the effect of CD-marker expressions on CVDs prognosis, ranging from proinflammatory processes to dysfunctional effects in blood cells.

Conclusion: Considering the possible effects of CD-marker expression on CVDs prognosis, particularly prognosis of acute myocardial infarction and atherosclerosis, long-term studies in large cohorts are required to identify the prognostic value of CD markers and to target them with appropriate therapeutic agents.
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http://dx.doi.org/10.1093/labmed/lmz049DOI Listing
March 2020

Platelets in In-stent Restenosis: From Fundamental Role to Possible Prognostic Application.

Curr Cardiol Rev 2020 ;16(4):285-291

Thalassemia & Hemoglobinopathy Research center, Health research institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background: Introduction of new generations of stents has decreased the percentage of patients experiencing in-stent restenosis (ISR) following the implantation of stent. However, a large number of patients are still afflicted with this phenomenon, which necessitates further study of ISR pathophysiology.

Methods: Relevant English literature was searched up to 2018 and retrieved form the PubMed database and Google Scholar search engine. The following keywords were used: "In-stent restenosis", "Platelet", "Chemokine", "Inflammation", "Vascular smooth muscle cell" and "Neointima".

Results: Previous studies have shown that ISR is a pathophysiologic response to damage of the artery wall after its elongation and separation of the atherosclerotic plaque. Development of neointimal hyperplasia (NIH) following this pathophysiologic response is a function of inflammation caused by platelets, monocytes, macrophages, and lymphocytes, as well as rapid migration and proliferation of generally quiescent cells in the median layer of the artery wall.

Conclusion: After damage to the artery wall, platelets play an essential role in the incidence of NIH by contributing to inflammation and migration of vascular smooth muscle cells and extracellular matrix remodeling, especially via secretion of different chemokines; therefore, developing therapeutic strategies for platelet inhibition in a controlled manner could be the basis of preventive treatments in the near future. In this study, for the first time, we hypothesize that evaluation of platelet activity profile in patients before and after stent implantation may determine the prognosis and likelihood of ISR.
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http://dx.doi.org/10.2174/1573403X15666190620141129DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7903513PMC
February 2021

Evaluation of complete blood count parameters in cardiovascular diseases: An early indicator of prognosis?

Exp Mol Pathol 2019 10 11;110:104267. Epub 2019 Jun 11.

Thalassemia & Hemoglobinopathy Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Electronic address:

Background: Studies have been conducted to evaluate the correlation between complete blood count (CBC) indices and cardiovascular diseases (CVDs). Considering the dispersion of these studies as well as reports on prognostic value of CBC parameters in CVDs, we have summarized these findings as a review article for the first time.

Methods: Relevant English language literature was searched and retrieved from Google Scholar search engine and PubMed database (1996-2018). We used "Complete blood count", "Cardiovascular disease", "Red cell distribution width", and "Mean platelet volume" as keywords.

Results: Numerous studies indicated that red cell distribution width (RDW) is an independent prognostic biomarker in relation to CVD diseases. MPV is another considerable prognostic biomarker for CVDs. Elevations of inflammatory markers such as neutrophil to lymphocyte ratio (NLR) in CVD patients (especially in myocardial infarction and heart failure) can be considered as a factor of poor prognosis.

Conclusions: RDW can be used as a valuable independent biomarker to investigate the prognosis of patients with heart failure (HF), atherosclerosis, myocardial infarction (MI), and other CVDs. Rapid and stable increase in MPV makes it a reliable prognostic/diagnostic parameter in CVDs such as MI and unstable angina. Among different inflammatory markers the evaluation of total white blood cell count, NLR, monocyte to high-density lipoprotein ratio (MHR) and platelet to lymphocyte ratio (PLR) may have a high value in predicting the prognosis of different CVDs including MI, HF and atherosclerosis in patients.
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http://dx.doi.org/10.1016/j.yexmp.2019.104267DOI Listing
October 2019

Development and Usability Evaluation of Web-Based Telerehabilitation Platform for Patients After Myocardial Infarction.

Stud Health Technol Inform 2019 ;261:68-74

Musculoskeletah research center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Introduction: Cardiac rehabilitation (CR) is a multidisciplinary intervention that improves quality of life and reduces the risk of recurrent heart attack. Unlike all known benefits for CR, the patient participation in CR is low. Telerehabilitation has the potential to improve lifestyle and helps patients having long-term compliance with clinician advice. The objective of this study was the development of a web-based cardiac telerehabilitation platform to engage the post-myocardial infarction (MI) patients in self-management of disease.

Method: Development process of creating and evaluating a telerehabilitation platform included four phases: (1) need assessment, (2) design the prototype, (3) implement the cardiac telerehabilitation platform, (4) usability evaluation.

Result: Cardiac telerehabilitation platform consists of an Android-based application for patients and web-based dashboard for rehabilitation mentors. The modules of the application are daily self-assessment, weekly self-assessment, educational content, stress and sleep improvement skills, medication reminder, online chat, prescribed diet, prescribed physical activity and rehabilitation records. The self-assessment modules allow users to enter the data such as physical activity, diet, blood pressure, heart rate, and body weight. The patient data entries are interpreted in the system knowledge base and colored symbol feedbacks display for patients and mentors. In the dashboard, the mentors review the patient data entries and set the rehabilitation plan for next week. In a beta test of usability evaluation, the mean of SUS score for patients was 75.16, for clinicians was 73.33 and for medical informatics specialist was 72.33. These results showed that the usability of our system was at an acceptable level.

Conclusion: The cardiac telerehabilitation platform is a convenient tool for post-MI patients who cannot attend at outpatient cardiac rehabilitation centers for any reason.
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September 2019

Involvement of circulating inflammatory factors in prognosis and risk of cardiovascular disease.

J Mol Cell Cardiol 2019 07 15;132:110-119. Epub 2019 May 15.

Thalassemia & Hemoglobinopathy Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Electronic address:

Cardiovascular disease (CVD) is an inflammatory disease that different factors play a crucial role in the development of clinical outcome of this disease. Inflammation could have effects on initiation, progression, and clinical complications of CVD. Previous studies have indicated that delineating the underlying mechanisms of inflammatory factors involved in this disease should be considerably beneficial both as predictive markers and targets for advancement of appropriate therapeutic approaches in offsetting development and progression of cardiovascular complications. Mechanisms of inflammatory factors involved in CVD combined with the development of atherosclerosis, reperfusion injury, and myocardial infarction caused by changes in processes such as endothelial cells function and hemostasis can contribute to the development of clinical outcome in CVD. Therefore, it can be stated that recognition of inflammatory mechanisms involved in this disease can be a promising tool for evaluation of prognosis in CVD patients. In this article, our goal is to evaluate the possible role of changes in the expressions of inflammatory factors in CVD as well as their relationship with prognosis of this disease.
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http://dx.doi.org/10.1016/j.yjmcc.2019.05.010DOI Listing
July 2019

Strategies to inhibit arsenic trioxide-induced cardiotoxicity in acute promyelocytic leukemia.

J Cell Physiol 2019 Feb 15. Epub 2019 Feb 15.

Thalassemia and Hemoglobinopathy Research Center, Research Institute of Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Objective: Arsenic trioxide (ATO) is a drug commonly used for the treatment of acute promyelocytic leukemia (APL). Although ATO has been shown to cause significant improvement in patients, it is associated with serious side effects, which sometimes lead to the patient's death. In this review paper, we examine the reports of ATO-induced cardiotoxicity in APL patients and evaluate the strategies to reduce the incidence of such toxicity.

Methods: The key search terms were "arsenic trioxide," "acute promyelocytic leukemia," "cardiotoxicity," "molecular pathway," and "biomarker."

Results: Studies have indicated the involvement of several molecular pathways in ATO-induced cardiotoxicity. These pathways increase the production of reactive oxygen species by interfering with intracellular calcium homeostasis as well as impairing the transfer of calcium into endoplasmic reticulum and mitochondria. On the other hand, increasing or decreasing expressions of some microRNAs (miRs) have been shown to play a role in cardiotoxicity.

Conclusion: Finally, it can be stated that given the essential role of molecular pathways in cardiotoxicity and considering the fact these pathways impair the regulation of miRs expression, identification of molecular pathways involved in ATO-induced cardiotoxicity aimed at targeting miRs could be a new therapeutic strategy to prevent cardiotoxicity.
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http://dx.doi.org/10.1002/jcp.28292DOI Listing
February 2019

Relationship Between Level of Heart Type Fatty Acid Binding Protein (Before and after Procedures) with Acute Renal Failure after PCI in Patients Under PCI.

Cardiovasc Hematol Disord Drug Targets 2020 ;20(1):41-46

Atheroclerosis Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background & Objective: Acute renal failure (AKI) is one of the most important complications of PCI. Due to delay in creatinine increase, we need specific factors to detect AKI earlier. The aim of this study is to evaluate the valuable factors by focusing on HFAB-P that can be predictive for AKI after Percutaneous Coronary Intervention (PCI).

Methods: This prospective study was performed on 95 patients (55 males and 44 females aged between 49-78 years) under PCI in Golestan and Imam Khomeini hospitals in Ahvaz. Patients were divided into three groups based on the development of AKI after the procedure: no AKI, severe AKI (doubling of serum creatinine or needing dialysis) and any type of AKI (increased creatinine ≥ 0/3 mg/dl or a 50% increase in the means of 1/5 times serum creatinine). The demographic and clinical characteristics of the patients, the medical history and the results of the HFABP marker, GFR, and creatinine before and after PCI were evaluated for all patients.

Results: The progenies showed 6 patients with severe AKI, 17 patients with any type of AKI, and 72 patients without AKI. Diabetes (P = 0.003), hypertension (P = 0.027), gender of patients (P = 0.025) and hospital admission days (P <0.001) were significantly different among the groups. Patients' age and positive troponin were significantly higher in patients with AKI. HFABP was the only factor that had significant changes before and after PCI (P <0.001). The cut-off value of HFABP was 4.69 with 95.6% sensitivity and 84.7% specificity. It has a good negative predictive value of 98.39% which suggests it to be a good test for the AKI prediction. Glomerular Filtration Rate (GFR) and creatinine (Cr) were significantly different after PCI (P <0.001).

Conclusion: HFABP can be considered as a predictor for AKI after PCI. Moreover, our study suggests that evaluating several parameters such as Cr and GFR before and after PCI can predict the AKI development after PCI.
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http://dx.doi.org/10.2174/1871529X19666190206153012DOI Listing
March 2021

Evaluation of cardiac rehabilitation on functional capacity in depressed and nondepressed patients after angioplasty.

J Family Med Prim Care 2018 Nov-Dec;7(6):1304-1308

Department of Psychiatry, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background: About 50% of the annual deaths in the developed countries are as a result of coronary artery disease. Several studies have shown the role of cardiac rehabilitation (CR) in improving cardiovascular indices including functional capacity, reducing depression, and mortality rates in cardiovascular patients. One of the psychological problems observed in cardiovascular patients is depression. Depression is one of the most important barriers to the treatment of heart attack, because it leads to denial of the disease and reduces the patient's motivation to continue treatment.

Objectives: There are controversy information about the relationship between the effects of CR on these cases after angioplasty. The aim of this study was to evaluate the effect of CR on functional capacity in depressed and nondepressed patients after angioplasty in patients referred to Imam Khomeini, Ahvaz.

Methods: This descriptive epidemiological study was performed on 54 patients referred for angioplasty. Functional capacity and depression score before and after participation in the 2-month CR program were evaluated in two groups of depressed and nondepressed patients. Data were analyzed by SPSS software, and the significance level was considered as < 0.05.

Results: The results of this study showed that in both the groups, the functional capacity after CR was significantly increased compared with the previous period ( < 0.001). Also in depressed patients, there was a significant decrease in depression scores ( < 0.001).

Conclusion: Our findings showed improvement of functional capacity index following angioplasty, suggesting that patients participating in CR can be recommended by therapists. In addition, the results of this study showed that the participation in the CR program greatly affects the improvement of functional capacity and reduction in depression in patients undergoing angioplasty.
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http://dx.doi.org/10.4103/jfmpc.jfmpc_306_18DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6293924PMC
January 2019

Effect of gemfibrozil on cardiotoxicity induced by doxorubicin in male experimental rats.

Biomed Pharmacother 2019 Jan 6;109:530-535. Epub 2018 Nov 6.

Physiology-Pharmacology Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran; Department of Physiology and Pharmacology, Rafsanjan University of Medical Sciences, Rafsanjan, Iran. Electronic address:

Cardiotoxicity is an adverse effect of the anticancer drug doxorubicin (DOX). Gemfibrozil (GEM) is a lipid-lowering drug with a number of biological properties such as anti-inflammatory and antioxidant activities. Therefore, we decided to investigate the effect of GEM on DOX-induced cardiotoxicity in rats. Twenty-eight adult male Wistar rats were divided into four experimental groups as follows: Group I received normal saline (2 ml/kg) orally for 14 days, group II received DOX (2.5 mg/kg; in six injections; accumulative dose: 15 mg/kg) intraperitonially for 14 days, group III received DOX + GEM (100 mg/kg) orally for 14 days concomitantly with DOX administration, and group IV received GEM orally for 14 days. Lipid panel, various biochemical biomarkers, and histological observations were evaluated in serum and heart samples. According to our results, DOX significantly increased the levels of lipid panel (triglycerides, total cholesterol, and low-density lipoproteins cholesterol) as well as markers of cardiac dysfunction (Aspartate aminotransferase, Creatine kinase-muscle/brain, Lactate dehydrogenase and Cardiac Troponin I). Moreover, DOX significantly increased malondialdehyde and nitric oxide levels in cardiac tissue. Furthermore, administration of DOX reduced the level of glutathione as well as the superoxide dismutase, catalase, and Glutathione peroxidase activities. DOX-treated rats showed significantly higher tumor necrosis factor-α and interleukin-1β. GEM administration significantly attenuated the lipid panel and biochemical biomarkers in DOX-treated rats. Our results were confirmed by histopathological evaluations of the heart. Based on our findings, GEM is a promising cardioprotective agent in patients treated with DOX through mitigative effects on biochemical markers and oxidative stress indices.
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http://dx.doi.org/10.1016/j.biopha.2018.10.101DOI Listing
January 2019

Wnt/β-catenin in ischemic myocardium: interactions and signaling pathways as a therapeutic target.

Heart Fail Rev 2019 05;24(3):411-419

Department of biochemistry and hematology, faculty of medicine, Semnan University of Medical Sciences, Semnan, Iran.

Cardiovascular disease (CVD) is still a factor of mortality in the whole world. Through canonical and noncanonical pathways and with different receptors, the Wnt/β-catenin signaling pathway plays an essential role in response to heart injuries. Wnt regulates the mobilization and proliferation of cells in endothelium and epicardium in an infarcted heart. Therefore, with its profibrotic effects as well as its antagonism with other proteins, Wnt/β-catenin signaling pathway leads to beneficial effects on fibrosis and cardiac remodeling in myocardium. In addition, Wnt increases the proliferation and differentiation of cardiac progenitors in an ischemic heart. Complex interactions and dual activity of Wnt, the changes in its expression, and mutations that can change its activity during heart development have an adverse effect on cardiac myocardium after injury. However, targeting the Wnt in myocardium with cellular and molecular pathways can be suggested to improve and repair ischemic heart. Given these challenges, in this review article, we deal with the role of Wnt/β-catenin signaling pathway as well as its interactions with other cells and molecules in an ischemic myocardium.
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http://dx.doi.org/10.1007/s10741-018-9759-zDOI Listing
May 2019

T-bet transcription factor in cardiovascular disease: Attenuation or inflammation factor?

J Cell Physiol 2019 06 7;234(6):7915-7922. Epub 2018 Dec 7.

Thalassemia and Hemoglobinopathy Research Center, Research Institute of Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

T-bet is a major transcription factor increasing inflammatory responses in the immune system. Recently, it has been shown that this factor leads to inflammation in cardiovascular disease (CVD). In this study, we examine the dual role of T-bet in inducing and suppressing inflammatory reactions as well as angiogenesis induction due to inflammatory cytokines in CVD. Relevant literature was identified by a Pubmed search (1992-2018) of English-language papers using the terms "T-bet," "Cardiovascular disease," "Immune response," and "Angiogenesis." Although T-bet causes differentiation of Th1 cells and activation of immune cells such as NK and DC, it suppresses inflammatory responses and replaces damaged vessels with new ones by activating regulatory T-cells and stimulating angiogenesis. It can be stated that T-bet acts as double-edged sword. Therefore, the identification of pathways that can increase the function of T-bet in activating Tregs and inducing angiogenesis might be used as a new therapeutic option in future investigations.
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http://dx.doi.org/10.1002/jcp.27935DOI Listing
June 2019

Diagnostic Value of HLA Typing in Pathogenesis of Cardiomyopathy.

Cardiovasc Hematol Disord Drug Targets 2019 ;19(2):132-138

Thalassemia and Hemoglobinopathy Research Center, Research Institute of Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Development of cardiomyopathy (CM) is dependent upon several factors. However, the reaction of the immune response against myocardial tissue due to microbial and viral infections plays an important role in this disease. Therefore, the purpose of this study is to investigate the relationship between HLAs and their pathogenic mechanisms in the incidence of CM. Relevant literature was identified by a PubMed search (1989-2017) of English-language papers using the terms "Cardiomyopathy", "Human leukocyte antigen or HLA", "immune response", and "polymorphism". If CM patients are afflicted with viral and microbial infections, HLA class II molecules, which are not expressed on myocardial tissue in normal conditions, are mainly expressed on it. As a result, these HLAs present self- antigens and provoke autoimmune responses against myocardial tissue. On the other hand, the occurrence of polymorphism as well as disrupted expression of miRNAs can affect HLA expression, leading to hypertrophy and fibrosis of cardiac muscle. Finally, it is inferred that the expression evaluation of HLAs as well as identification of polymorphisms in their coding genes can be effective diagnostic factors in the detection of people susceptible to CM.
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http://dx.doi.org/10.2174/1871529X19666181205151340DOI Listing
July 2020

Endothelial Cells: From Dysfunction Mechanism to Pharmacological Effect in Cardiovascular Disease.

Cardiovasc Toxicol 2019 02;19(1):13-22

Thalassemia and Hemoglobinopathy Research Center, Research Institute of Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Endothelial cells (ECs) are the innermost layer of blood vessels that play important roles in homeostasis and vascular function. However, recent evidence suggests that the onset of inflammation and the production of reactive oxygen species impair the function of ECs and are a main factor in the development of cardiovascular disease (CVD). In this study, we investigated the effects of inflammatory markers, oxidative stress, and treatment on ECs in CVD patients. This review article is based on the material obtained from PubMed up to 2018. The key search terms used were "Cardiovascular Disease," "Endothelial Cell Dysfunction," "Inflammation," "Treatment," and "Oxidative Stress." The generation of reactive oxygen species (ROS) as well as reduced nitric oxide (NO) production by ECs impairs the function of blood vessels. Therefore, treatment of CVD patients leads to the expression of transcription factors activating anti-oxidant mechanisms and NO production. In contrast, NO production by inflammatory agents can cause ECs repair due to differentiation of endothelial progenitor cells (EPCs). Therefore, identifying the molecular pathways leading to the differentiation of EPCs through mediation of factors induced by inflammatory factors can be effective in regenerative medicine for ECs repair.
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http://dx.doi.org/10.1007/s12012-018-9493-8DOI Listing
February 2019

Pentraxin Level is the Key to Determine Primary Percutaneous Coronary Intervention (PCI) or Fibrinolysis.

Cardiovasc Hematol Disord Drug Targets 2019 ;19(2):160-168

Golestan Hospital Clinical Research Development Unit, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Aims: To examine if pentraxin can help identify patients benefitting most from primary Percutaneous Coronary Intervention (PCI) vs. fibrinolysis.

Methods: Patients with acute ST-Elevation Myocardial Infarction (STEMI) were consecutively recruited from a community center without PCI and a tertiary center with PCI facilities. Left ventricular ejection fraction (LVEF) was determined echocardiographically at baseline and 5 days after the index admission; the difference between two measurements was considered as the magnitude of improvement. We used regression models to test the hypothesis that the magnitude of the advantage of PCI over fibrinolysis in preserving LVEF 5 days after STEMI is modified by pentraxin 3 (PTX3).

Results: The functional advantage (LVEF) of the PCI over fibrinolysis has been determined by PTX3. LVEF was attenuated and even reversed as PTX3 level increased. The primary PCI of the participants with less than 7 ng.ml-1 PTX3 level, achieved a clinically significant increase in the LVEF as compared to fibrinolysis. At lower levels of PTX3, PCI shows a conspicuous advantage over fibrinolysis in terms of the probability of developing an LVEF <40%.

Conclusion: We demonstrated not only the functional advantage of PCI over fibrinolysis performed within the recommended time frames but also the relative advantage of its relevance to the baseline PTX3 levels. PTX3 can play a role in determining the choice of best therapy. More than 75% of patients with STEMI who have PTX3 levels ≤7 ng.ml-1 imply the need of PCI.
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http://dx.doi.org/10.2174/1871529X19666181120161810DOI Listing
July 2020

Clonal hematopoiesis: Genes and underlying mechanisms in cardiovascular disease development.

J Cell Physiol 2019 06 11;234(6):8396-8401. Epub 2018 Nov 11.

Research Center of Thalassemia and Hemoglobinopathy, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

The clonal hematopoiesis when occurring without hematologic abnormalities is defined as clonal hematopoiesis of indeterminate potential (CHIP). Aging causes accumulation of somatic mutations, and hematopoietic stem cells (HSCs) can develop clonal expansion of different lineages by these mutations. CHIP has a correlation with cancer and cardiovascular disease (CVD) through acquired mutations in genes. DNMT3A, TET2, ASXL1, and JAK2 genes as well as other genes are the most common somatic mutations causing CHIP and CVD in an older age. Other factors such as cholesterol level, laboratory tests and indexes also affect CVD. In addition, mutations in adenosine triphosphate-binding cassette transporters and also chronic stress in nervous system can result in HSCs proliferation and CVD. However, laboratory tests and indexes are not sensitive for CVD diagnosis. But the therapeutic interventions can be helpful to prevent CVD cases by targeting somatic mutations, chemokine receptors, and growth factors in HSCs. Also, new drugs can control CVD by targeting of cells and their signaling pathways in HSCs. Therefore, more investigations are needed and more questions should be answered for the relationship between CHIP and CVD as a challenging issue in future.
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http://dx.doi.org/10.1002/jcp.27752DOI Listing
June 2019

Protective role of heat shock transcription factor 1 in heart failure: A diagnostic approach.

J Cell Physiol 2019 06 30;234(6):7764-7770. Epub 2018 Oct 30.

Thalassemia and Hemoglobinopathy Research Center, Research Institute of Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Objective: Nonexpression or expression inhibition of protective factors has been determined in the occurrence of heart failure (HF). Heat shock transcription factor 1 (HSF1) is among such factors, which reduces the incidence of HF by controlling cardiac hypertrophy and fibrosis. In this study, molecular mechanisms for nonexpression of HSF1 in HF patients have been investigated.

Materials And Methods: This review paper is based on the material obtained via PubMed search of 1996-2018. The key search terms were "heart failure," "heat shock transcription factor 1," "hypertrophy", "fibrosis," and "apoptosis."

Results: Although factors such as janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) and heat shock proteins (HSPs) may respectively increase and decrease susceptibility to HF, in some circumstances, these factors may unexpectedly prevent HF progression.

Conclusion: Finally, identification of molecular pathways expressed by various factors could be used to design appropriate treatments or to employ strategies inducing the expression of HSF1 to prevent HF.
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http://dx.doi.org/10.1002/jcp.27639DOI Listing
June 2019

Strategies to increase cardioprotection through cardioprotective chemokines in chemotherapy-induced cardiotoxicity.

Int J Cardiol 2018 Oct 19;269:276-282. Epub 2018 Jul 19.

Golestan Hospital Clinical Research Development Unit, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background: Cardiotoxicity is one of the most important side effects of chemotherapy and its management save myocardium from injury and its consequences.

Aim: In this review we discuss cardioprotective chemokines and cardioprotective mechanisms and pathways that induce cardioprotection through cardioprotective chemokines.

Method: We searched English literature articles in Google scholar and PubMed from "1990 to 2018" through using the terms "Cardioprotection; Cardioprotective Chemokine; Chemotherapy Induced Cardiotoxicity; Cardiomyocytes; Cytokine".

Discussion: The routine cardioprotective strategies during chemotherapy such as angiotensin-converting enzyme inhibitors and β-blockers have cardioprotective effects. Cardioprotective mechanisms and strategies can offer the oncologist several methods to protect the cardiac system through using efficient cardioprotective agents. Chemokines such as SDF-1a, IL-6,IL-8,IL-12 and G-CSF are cardioprotective chemokines. Accelerating the cardioprotection through inducing cardioprotective chemokines production can be useful in chemotherapy.

Conclusion: Stimulating the production of cardioprotective chemokines through the pathways which induce the production of cardioprotective chemokines can work strongly beside the β-blockers and ACE inhibitors. The ambiguous point in cardioprotective pathways is that JAK2/STAT3 pathway which is linked to IL-6 production pathway, which induce intracellular adhesion molecule-1 in the area of the ischemia in myocardium and this process is not benefit in cardioprotection however IL-6 induce cardiomyocytes regeneration so it enhance our dull vision about IL-6. Finally there are several choices which can increase cardioprotection during the chemotherapy and if we overcome the boundaries in confirming the efficiency of cardioprotective chemokines and the activation of them through using several mechanisms we will break through the difficulties over chemotherapy-induced cardiotoxicity.
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http://dx.doi.org/10.1016/j.ijcard.2018.07.087DOI Listing
October 2018

The effects of Melissa officinalis (lemon balm) in chronic stable angina on serum biomarkers of oxidative stress, inflammation and lipid profile.

Asia Pac J Clin Nutr 2018;27(4):785-791

Department of Nutrition sciences, School of Para-medicine, Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background And Objectives: Coronary artery disease (CAD) is a major cause of death worldwide. Chronic stable angina (CSA) is the primary sign of CAD. Oxidative stress and inflammation play a substantial role in pathogenesis and progression of CAD. The aim of this study was to investigate the effects of oral administration of powdered Melissa officinalis (MO) on biomarkers of oxidative stress, inflammation, and lipid profile in patients with CSA.

Methods And Study Design: A randomized, double-blind, placebo-controlled clinical trial was performed in 80 patients with CSA. The subjects were randomly assigned to obtaineither oral MO 3 g/d (n=40) or placebo (n=40) for eight weeks. Anthropometric indices, biomarkers of oxidative stress, inflammation, and lipid profile were evaluated at baseline and post-intervention.

Results: The mean serum concentrations of triglycerides, total-cholesterol, LDL-cholesterol, and malondialdehyde (MDA), and high sensitive C-Reactive Protein (hs-CRP) were lower in the intervention group compared with placebo (p<0.01) post intervention. Moreover, the mean serum concentration of paraxonase 1 (PNO1) and HDL-c were higher (p<0.001) in the intervention group compared with the control group.

Conclusion: Oral MO supplementation improves the lipid profile, MDA, hs-CRP, and PNO1 in patients with CSA.
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http://dx.doi.org/10.6133/apjcn.022018.01DOI Listing
September 2019

Metformin one in a Million Efficient Medicines for Rheumatoid Arthritis Complications: Inflammation, Osteoblastogenesis, Cardiovascular Disease, Malignancies.

Curr Rheumatol Rev 2019 ;15(2):116-122

Golestan Hospital Clinical Research Development Unit, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background: Rheumatoid arthritis is a widespread autoimmune disease and inflammation and bone destruction are two main issues in rheumatoid arthritis.

Objective: To discussing metformin effects on rheumatoid arthritis complications.

Methods: We conducted a narrative literature search including clinical trials, experimental studies on laboratory animals and cell lines. Our search covered Medline, PubMed and Google Scholar databases from 1999 until 2018. We used the terms" Metformin; Rheumatoid arthritis; Cardiovascular disease; Cancer; Osteoblastogenesis.

Discussion: Inflammatory pro-cytokines such as Interlukin-6 play important roles in T. helper 17 cell lineage differentiation. Interlukin-6 and Tumor Necrosis Factor-α activate Janus kinase receptors signal through signaling transducer and activator of transcription signaling pathway which plays important role in inflammation, bone destruction and cancer in rheumatoid arthritis patients. Interlukin-6 and Tumor Necrosis Factor-α synergistically activate signaling transducer and activator of transcription and Nuclear Factor-kβ pathways and both cytokines increase the chance of cancer development in rheumatoid arthritis patients. Metformin is AMPK activators that can suppress mTOR, STAT3 and HIF-1 so AMPK activation plays important role in suppressing inflammation and osteoclastogenesis and decreasing cancer.

Conclusion: Metformin effect on AMPK and mTOR pathways gives the capability to change Treg/Th17 balance and decrease Th17 differentiation and inflammation, osteoclastogenesis and cancers in RA patients. Metformin can be useful in protecting bones especially in first stages of RA and it can decrease inflammation, CVD and cancer in RA patients so Metformin beside DAMARs can be useful in increasing RA patients' life quality with less harm and cost.
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http://dx.doi.org/10.2174/1573397114666180717145745DOI Listing
August 2019

The effects of Melissa officinalis supplementation on depression, anxiety, stress, and sleep disorder in patients with chronic stable angina.

Clin Nutr ESPEN 2018 08 19;26:47-52. Epub 2018 May 19.

Department of Nutrition Sciences, School of Para-medicine, Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Electronic address:

Background: Despite advances in the treatment of cardiovascular diseases in recent decades, patients experience high levels of depression, anxiety, stress, and insomnia. Since the calming effect of Melissa officinalis (MO) has been known, this study aimed to determine the effects of MO supplementation on depression, anxiety, stress, and sleep disturbances in patients with chronic stable angina (CSA).

Methods: In this double-blind placebo-controlled clinical trial, 80 patients with CSA were divided randomly into two groups (taking 3 g MO supplement or placebo daily for 8 weeks). The shortened 21-item version of the depression, anxiety and stress scale (DASS-21) test and Pittsburgh sleep quality index were done before and after the intervention.

Results: At the end of the study, the intervention group receiving MO capsules had a significant reduction in scores of depression, anxiety, stress, and total sleep disturbance, compared with the placebo group (P < 0.05).

Conclusions: The results showed that 8-week supplementation with 3 g MO can decrease depression, anxiety, stress, and sleep disorder in patients with CSA.
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http://dx.doi.org/10.1016/j.clnesp.2018.04.015DOI Listing
August 2018

Mutations and Common Polymorphisms in ADAMTS13 and vWF Genes Responsible for Increasing Risk of Thrombosis.

Cardiovasc Hematol Disord Drug Targets 2018 ;18(3):176-181

Research Center of Thalassemia & Hemoglobinopathy, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background And Objective: ADAMTS13 (A Disintegrin-like and Metalloproteases with Thrombospondin type-1 repeats, member-13) plays an important role in vascular hemostasis by cleaving the von Willebrand Factor (vWF). ADAMTS13 and vWF are involved in the development of ischemic heart disease. In this review paper, we examine the effects of Single Nucleotide Polymorphisms (SNPs) and mutations in the vWF and ADAMTS13 genes and their contribution to the development of thrombosis.

Methods: Relevant English-language literature was searched and retrieved from PubMed search engine (2001-2017). The following keywords were used: "ADAMTS13", "vWF", "Polymorphism", and Thrombosis".

Results: SNPs in the ADAMTS13 and vWF genes cause genetic variability and affect the plasma levels of these genes. Moreover, environmental (such as age, smoking, hypertension) and genetic factors (like ABO blood groups) play a role in the development of different polymorphisms in ADAMTS13 and vWF genes.

Conclusion: The increased or decreased activity of these two genes as a result of genetic changes and the development of thrombosis are a challenging and contradictory matter, and the study of genetic variability in ADAMTS13 and vWF genes may be helpful in the diagnosis of thrombotic disorders.
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http://dx.doi.org/10.2174/1871529X18666180419102214DOI Listing
June 2019

Platelet Activation Polymorphisms in Ischemia.

Cardiovasc Hematol Disord Drug Targets 2018 ;18(2):153-161

Research Center of Thalassemia & Hemoglobinopathy, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background: Ischemia is a multifactorial disorder in which several genetic and environmental factors are involved. Platelets are the major causative agents of this disease because their elevated activity and aggregation would increase the risk of atherosclerosis and thrombosis, as well as ischemia. A number of polymorphisms in platelet receptors can increase the risk of ischemia and single-nucleotide polymorphisms (SNPs) have been detected in platelets. In addition, polymorphisms in other genes have been shown to cause platelet adhesion and aggregation that plays a role in ischemia. Patients respond differently to anti-platelet drugs which are used to treat patients with ischemia. Polymorphisms affect patients' responses to anti-platelet drugs, for instance, by increasing platelet activity and causing resistance of platelets to these drugs. Diagnosis of these polymorphisms can greatly contribute to better prediction of prognosis and response to treatment of patients, leading to more effective therapeutic strategies and a proper approach to ischemia.

Conclusion: In this review, we have evaluated the role of polymorphisms involved in platelet activation and development of ischemia.
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http://dx.doi.org/10.2174/1871529X18666180326121239DOI Listing
March 2019

The severity of coronary artery disease was not associated with non-alcoholic fatty liver disease in a series of 264 non-diabetic patients who underwent coronary angiography.

Rom J Intern Med 2018 Sep;56(3):167-172

Non-Communicable Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.

Background: It is now suggested an association between non-alcoholic fatty liver disease (NAFLD) and the occurrence of coronary artery disease even in non-diabetic patients. We will determine the rate of NAFLD and its main determinants in non-diabetic patients undergoing coronary angiography.

Methods: This cross-sectional study was accomplished on 264 patients who were candidates for coronary angiography during the year 2016. Coronary angiography has been done to depict the presence or absence of coronary involvement, and the severity of coronary artery disease by determining the number of vessels involved and also the SYNTAX score. During 48 hours after coronary angiography, the patients underwent abdominal ultrasonography for detection of NAFLD.

Results: The overall prevalence of NAFLD in the patients was 72.3%. The prevalence of NAFLD in those with and without coronary involvement was 71.9% and 73.1% respectively, with no notable difference (p = 0.837). The mean SYNTAX score in the patients with and without NAFLD was 22.32 ± 11.10 and 21.75 ± 10.71 respectively with no difference (p = 0.702). According to the multivariable regression models, the presence of NAFLD could not predict the likelihood of coronary artery disease (OR = 0.879, p = 0.669) or its severity assessed by the SYNTAX score (beta = 0.046, p = 0.456). NAFLD grade was also not a determinant for coronary artery disease (OR = 1.139, p = 0.178) or its severity (beta = 0.058, p = 0.165).

Conclusion: It seems that the presence and grade of NAFLD may not be correlated with atherosclerotic involvement of coronary arteries and its severity in non-diabetic patients. Future large studies and trials could elucidate the independent role of fatty liver in nondiabetic non-alcoholic patients.
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http://dx.doi.org/10.2478/rjim-2018-0009DOI Listing
September 2018

What Genetics Tells us about Cardiovascular Disease in Diabetic Patients?

Cardiovasc Hematol Disord Drug Targets 2018 ;18(2):147-152

Golestan Hospital Clinical Research Development Unit, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background: Long-term diabetes causes other disease development such as cardiovascular diseases (CVD).

Objective: Genetics can help us to predict cardiovascular diseases in diabetic patients.

Method And Search Strategy: We searched PubMed and Google scholar for the terms: Cardiovascular disease, Diabetes, Polymorphism, Genetics from 2000 to 2017, and then included the relevant studies in our study.

Discussion: Essential role of inheritance in multifactorial disease is obviously clear, however, varies by disease and by other factors such as age of disease onset and subtype of disease. CVD is a multifactorial disease which can develop in diabetes patients as a result of increase in oxidative stress. It may also increase expression of pro-inflammatory factors and induce apoptosis in cardiomyocytes.

Conclusion: Predictive polymorphisms are risk estimators for CVD incidence in diabetes patients. SNPs such as 894G>T in NOS3 gene, V16 in MnSOD gene, Rs3918188 in NOS3 gene and Rs11614913 in MiR-196a2 increase the risk of CVD in diabetic patients are precious polymorphisms for CVD prediction in diabetic population. CDKN2B, MTHFR and ACE genes have polymorphisms which increase the risk of diabetes and other polymorphisms on these genes increase the risk of CVD, we suggest these genes are valuable to study and find out if there are any polymorphisms that predict CVD susceptibility in diabetic patients.
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http://dx.doi.org/10.2174/1871529X18666180212114305DOI Listing
March 2019

Cardiovascular Events: A Challenge in JAK2-positive Myeloproliferative Neoplasms.

Cardiovasc Hematol Disord Drug Targets 2017 ;17(3):161-166

Thalassemia & Hemoglobinopathy Research Center, Research Institute of Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background: Myeloproliferative neoplasms (MPNs) are chronic blood disorders caused by clonal expansion in one or more myeloid lineages and include essential thrombocythemia (ET), polycythemia vera (PV), primary myelofibrosis (PMF) and chronic myeloid leukemia (CML). Cardiovascular events are a main challenge for patients with MPN and can lead to their death.

Objective: JAK2V617F mutation is observed in Philadelphia-negative MPNs such as ET and PV, increasing the risk of cardiovascular complications in these patients. JAK2 mutation can affect cardiac arteries and veins in ET and PV, which results in thrombosis, ischemia and other cardiovascular events. JAK/STAT signaling pathway plays an important role in heart diseases. In this review, we will survey the cardiovascular events in JAK2-positive MPN patients.

Method: Relevant English-language literature were searched and retrieved from PubMed search engine (1995-2017). The following keywords were used: "Cardiovascular Events", "JAK2" and "Myeloproliferative Neoplasms". Forty three articles were selected by using the key words.

Results: JAK2 phosphorylates the signal transducers and activators of transcription (STAT). Various factors like angiotensin II (ANG II) and cardiotrophin-1 (CT-1) can bind their receptors on myocytes and increase the expression of angiotensinogen (Ao) gene by binding of STAT proteins to these factors in myocytes, causing different cardiovascular complications through autocrine mechanisms.

Conclusion: JAK2 mutation is observed in patients with thrombosis, ischemia and other cardiovascular complications having abnormal increase in cell count even without definite clinical diagnosis of MPN. Therefore, identification of this mutation in these patients contributes to definite diagnosis of cardiovascular events. Also, cardiovascular complications in MPN patients can be prevented by targeting the factors involved in JAK/STAT signaling pathway.
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http://dx.doi.org/10.2174/1871529X17666171030122345DOI Listing
March 2019

Evaluation of pentraxin-3 level and its related factors in patients undergoing primary percutaneous coronary intervention.

ARYA Atheroscler 2017 Mar;13(2):73-78

Student of Medicine, Student Research Committee, Department of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background: Inflammation has an important role in the development and progression of atherosclerosis, and acute phase proteins such as pentraxin-3 (PTX3) can be deployed in determining the prognosis of coronary artery disease (CAD). So the purpose of this paper was to evaluate the PTX3 level and its related factors in patients undergoing primary percutaneous coronary intervention (PCI).

Methods: In this cross-sectional study, the PTX3 levels were determined for 100 patients with ST-elevation myocardial infarction referred to the Modarres Hospital, Tehran, Iran. Checklist included demographic data [age, gender, history of myocardial infarction (MI)] and characteristics of heart disease (type of MI, culprit, and pre-dilation). PTX3 was measured for all patients before PCI.

Results: In this study, the mean age of the participants was 58.7 (11.4). Global registry of acute coronary events (GRACE) score was higher in the group with abnormal PTX3 levels (P = 0.008). The number of the involved vessels (P = 0.005), MI type (P = 0.05), and the need for PCI all had a significant relation with abnormal PTX3 levels. The increased levels of PTX3 received higher Killip class, lower ejection fraction, and higher GRACE score. The group with abnormal PTX3 had a significant difference in platelet counts (P = 0.018) in comparison with the group with normal level of PTX3.

Conclusion: Currently, the biomarkers are highly important in the field of cardiovascular diseases. The diagnostic and prognostic importance of PTX3 as a new marker has been underscored in recent studies. Differentiating between high-risk patients with acute cardiac infarction and low-risk ones through their clinical signs is difficult.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5628854PMC
March 2017

Interesting Correlation Between the Circulating Pentraxin 3 and Cardiac Rehabilitation Program Outcomes in Coronary Artery Bypass Grafting Patients.

Cardiol Res 2016 Apr 4;7(2):59-65. Epub 2016 May 4.

Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background: Pentraxin 3 (PTX3) is an inflammatory mediator, reaches to the high levels after ischemic heart diseases (IHD) and could be a helpful tool to predict cardiac rehabilitation (CR) outcomes. The aim of this study was to investigate the possibility of the circulating levels of PTX3 in prediction of CR outcomes in patients with IHD who had undergone coronary artery bypass grafting (CABG).

Methods: One hundred patients who had undergone CABG were included in this study. The CR plan was started 6 weeks after CABG and then PTX3 level, high-sensitivity C-reactive protein (hs-CRP), ejection fraction (EF) and metabolic equivalent (MET) were assessed before and after the CR program. Finally, all gathered data were analyzed using SPSS version 22.

Results: After a 3-month course of CR program, EF, MET, PTX3 and hs-CRP values changed. Statistically significant changes were observed in EF, MET and PTX3 values (P < 0.05) after the CR program and no statistically significant changes were seen in hs-CRP value (P = 0.546) at the end of CR program. Correlations between EF levels and MET with pre-PTX3 levels were also assessed and most changes were observed in the group with pre-PTX3 level more than 0.40 ng/dL.

Conclusion: Our study showed that a regular sufficient CR program based on exercises in IHD patients after CABG increases EF and MET levels, particularly in those patients with pre-PTX3 levels more than 0.40 ng/dL.
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http://dx.doi.org/10.14740/cr462wDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5295543PMC
April 2016