Plasma thrombin-activatable fi brinolysis inhibitor levels and Thr325Ile polymorphism as a risk marker of myocardial infarction in Egyptian patients

Kamal, Hanan; Ahmed, Abeer; Fawzy, Manal S.; Mohamed, Faten A.; El-Baz, Amani A.

doi:10.1080/ac.66.4.2126597

Cited by 15 publications

(14 citation statements)

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“…From the above analysis, we conclude that the rs3742264 G>A and rs1926447 C>T polymorphisms can affect the expression and activation of TAFI, which inhibits fibrinolysis and promotes thrombus formation, thereby participating in the progression of CCVDs. In accordance with our analysis, Kamal et al (2011) reported that the Thr/Ile and Ile/Ile genotypes of rs1926447 were more frequent in myocardial infarction patients than in the control group, indicating the association between the CPB2 gene polymorphism and the risk of myocardial infarction. Moreover, Biswas et al (2009) revealed a strong connection between the rs3742264 polymorphism and the development of pediatric stroke.…”

Section: Discussionsupporting

confidence: 76%

“…An additional study was removed owing to a lack of data integrity. Ultimately, we obtained nine case-control research papers published between 2003 and 2013 that were of moderate-to-high quality (Zorio et al, 2003;Leebeek et al, 2005;Xu et al, 2008;Biswas et al, 2009;Si, 2010;Kamal et al, 2011;Shi et al, 2011;Sun et al, 2011;Tokgoz et al, 2013). The demographic information, baseline characteristics, and other features, and the methodological quality of the extracted studies are presented in Tables 1 and 2.…”

Section: Selection Of Eligible Studiesmentioning

confidence: 99%

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Meta-analysis of TAFI polymorphisms and risk of cardiovascular and cerebrovascular diseases

et al. 2016

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ABSTRACT. Cardiovascular and cerebrovascular diseases (CCVDs) are common and have high rates of morbidity, mortality, and recurrence. Thrombin-activatable fibrinolysis inhibitor (TAFI) is also known as carboxypeptidase B2 and is encoded by the CPB2 gene; CPB2 polymorphisms have been explored in a variety of studies, but their correlation to the risk of CCVDs remains ambiguous. We examined the hypothesized associations between CPB2 mutations and CCVDs in a general population. We searched, Embase, the Cumulative Index to Nursing and Allied Health Literature, the Science Citation Index, and several Chinese databases without applying any language restrictions. Nine case-control studies were analyzed in the current meta-analysis, and odds ratios (ORs) with their 95% confidence intervals were calculated. The pooled ORs indicated that the CPB2 rs3742264 G>A polymorphism was associated with an increased risk of CCVDs in the allele model (all P values < 0.05). A similar result for the CPB2 rs1926447 C>T polymorphism and CCVDs risk was detected in the allele model (P < 0.05). Ethnicity subgroup analysis implied that the rs3742264 G>A polymorphism was more likely to lead to the development of cerebrovascular disease in Asians (all P values < 0.05), whereas rs1926447 C>T was associated with cardiovascular disease among Africans (all P values < 0.05). These data suggest that the polymorphisms investigated, especially rs3742264 G>A and rs1926447 C>T, have a modest effect on susceptibility to CCVDs.

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Section: Discussionsupporting

confidence: 76%

Section: Selection Of Eligible Studiesmentioning

confidence: 99%

Meta-analysis of TAFI polymorphisms and risk of cardiovascular and cerebrovascular diseases

et al. 2016

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“…7 Some studies have shown that increased TAFIa is a risk factor for ischemic stroke, acute myocardial infarction, and venous thrombosis. [8][9][10] Although not all thrombotic disorders will cause activation of TAFI. Coagulation activation in a baboon model of low-dose E. coli induces sepsis not accompanied by activated TAFI, while continuous TAFI activation up to 8 hours, is seen in coagulation activation seen by high-dose E. coli.…”

Section: Introductionmentioning

confidence: 99%

Thrombin-Activatable Fibrinolysis Inhibitor Is Activated in an Instant Blood-Mediated Inflammatory Reaction After Intraportal Islet Transplant

Wang

Zhang²,

Cong³

et al. 2014

Exp Clin Transplant

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Objectives: Activated thrombin-activatable fibrinolysis inhibitor is a coagulation factor in some thrombotic diseases. However, available data on whether thrombin-activatable fibrinolysis inhibitor is activated in islet transplant are limited. In this study, changes of plasma-activated thrombinactivatable fibrinolysis inhibitor levels in instant blood-mediated inflammatory reaction after islet transplant were assessed. Materials and Methods: Plasma concentrations of thrombin-antithrombin complex, D-dimer, C-peptide, and activated thrombin-activatable fibrinolysis inhibitor were assessed at 0 minutes, 30 minutes, 1 hour, 6 hours, 12 hours, and 24 hours after an intraportal islet transplant using rats via an enzymelinked immunosorbent assay, or solid-phase, 2-site chemiluminescent immunometric assay. We recovered the liver at 1 hour after the transplant for histologic examination. Results: Thrombin-antithrombin complex, C-peptide, and activated thrombin-activatable fibrinolysis inhibitor levels increased immediately after we stopped islet infusion, and their peak levels occurred at 1 hour after islet infusion. D-dimer levels increased continually after islet infusion was stopped, and peaked 24 hours after infusion. Histologic examination of the liver 1 hour after islet infusion revealed frequent portal venous thrombi, with entrapped islets. The entrapped islets showed a disrupted morphology. Conclusions:Activated thrombin-activatable fibrinolysis inhibitor was generated and peaked 1 hour after islet transplant according with activating coagulation, indicating that thrombin-activatable fibrinolysis inhibitor is activated and accumulated at levels in instant blood-mediated inflammatory reaction was sufficient to affect fibrinolysis.

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“…Cardiovascular risk factors were recorded as described previously [28]. Hypertension was defined if the patient was receiving anti-hypertensive drugs or blood pressure exceeded 140/90 mmHg in repeated measurements.…”

Section: Methodsmentioning

confidence: 99%

Atherosclerotic and thrombotic genetic and environmental determinants in Egyptian coronary artery disease patients: a pilot study

Fawzy

Toraih

Aly

et al. 2017

BMC Cardiovasc Disord

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BackgroundCoronary artery disease (CAD) is the leading cause of morbidity and mortality worldwide. Multiple genetic variants in combination with various environmental risk factors have been implicated. This study aimed to investigate the association of twelve thrombotic and atherosclerotic gene variants in combination with other environmental risk factors with CAD risk in a preliminary sample of Egyptian CAD patients.MethodsTwenty three consecutive CAD patients undergoing diagnostic coronary angiography and 34 unrelated controls, have been enrolled in the study. Genotyping was based on polymerase chain reaction and reverse multiplex hybridization. Five genetic association models were tested. Data distribution and variance homogeneity have been checked by Shapiro-Wilk test and Levene test, respectively; then the appropriate comparison test was applied. Spearman’s rank correlation coefficient was used for correlation analysis and logistic regression has been performed to adjust for significant risk factors. Clustering the study participants according to gene-gene and gene-environment interaction has been done by Detrended Correspondence Analysis (DCA).ResultsThe univariate analysis indicated that the five variants; rs1800595 (FVR2; factor 5), rs1801133 (MTHFR; 5,10-methylenetetrahydrofolate reductase), rs5918 (HPA-1; human platelet antigen 1), rs1799752 (ACE; angiotensin-converting enzyme), and rs7412 and rs429358 (ApoE; apolipoprotein E) were significantly associated with CAD susceptibility under different genetic models. Multivariate analysis revealed clustering of the study population into three patient groups (P) and one control group. FVR2 was the most variant associated with CAD patients, combined with the factor V Leiden (FVL) variant in P1 cluster and with both ACE and MTHFR 667C > T in P2. Whereas, P3 was mostly affected by both MTHFR 667C > T and FXIII (factor 13) V89L mutations. When combined with traditional risk factors, P1 was mostly affected by dyslipidemia, smoking and hypertension, while P2 was mostly affected by their fasting blood sugar levels and ApoE variant.ConclusionsTaken together, these preliminary results could have predictive value to be applied in refining a risk profile for our CAD patients, in order to implement early preventive interventions including specific antithrombotic therapy. Further large scale and follow-up studies are highly recommended to confirm the study findings.Electronic supplementary materialThe online version of this article (doi:10.1186/s12872-016-0456-3) contains supplementary material, which is available to authorized users.

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Plasma thrombin-activatable fi brinolysis inhibitor levels and Thr325Ile polymorphism as a risk marker of myocardial infarction in Egyptian patients

Abstract: TAFI Thr325Ile and its respective plasma protein level could have a contribution to MI risk in the Egyptian population.This could be helpful in refining a risk profile for coronary heart disease (CHD) patients.

Cited by 15 publications

References 0 publications

Meta-analysis of TAFI polymorphisms and risk of cardiovascular and cerebrovascular diseases

Meta-analysis of TAFI polymorphisms and risk of cardiovascular and cerebrovascular diseases

Thrombin-Activatable Fibrinolysis Inhibitor Is Activated in an Instant Blood-Mediated Inflammatory Reaction After Intraportal Islet Transplant

Atherosclerotic and thrombotic genetic and environmental determinants in Egyptian coronary artery disease patients: a pilot study

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