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Association of factor V Leiden R506Q, FXIIIVal34Leu, and MTHFR C677T polymorphisms with acute myocardial infarction



Acute myocardial infarction (AMI) is a leading cause of death and morbidity around the world. Although the association between thrombophilia and AMI is well-established, controversial data are present on the association between thrombophilic polymorphisms and AMI. The aim of this study was to investigate the association of three thrombophilic polymorphisms including factor V Leiden (FVL), MTHFRC677T (methylenetetrahydrofolate reductase), and Coagulation factor XIIIVal34Leu with AMI in East of Iran.


There were no statistically significant differences between the patients and control groups in terms of the distributions of allelic and genotypic frequencies of FVL and FXIIIVal34Leu polymorphisms (P-value > 0.05). Subjects who carried CT genotype of MTHFR C677T polymorphism were at a 2.03-fold higher risk for AMI (P-value: 0.02, OR 1.76, 95% CI 1.07–2.75). Furthermore, patients with MTHFR 677CT (P-value < 0.001, β = - 0.90, 95% CI − 1.33, − 047) or 677CC (P-value < 0.001, β = - 1.04, 95% CI − 1.47, − 0.61) genotypes showed significantly Lower creatinine levels compared with patients having the MTHFR 677TT. No association was observed between the other remaining polymorphisms and AMI (P-value > 0.05).


Our findings showed that MTHFRC677T polymorphism could contribute to AMI susceptibility and increase creatinine levels in east Iran population. This was the first study to examine the association of these three polymorphisms with AMI in east Iran.


AMI is one of the leading causes of death in both developed and developing countries. According to data from the World Health Organization, 17.9 million people die from cardiovascular diseases worldwide each year, accounting for 31% of all deaths. The cause of 85% of these deaths is either AMI or stroke [1, 2]. AMI occurs when plaque that has built up in the walls of coronary arteries erodes or ruptures, resulting in a transient, partial, or complete occlusion of the arteries [3]. Although the exact association of risk factors for AMI has not been established, a growing number of studies have shown that age, race, ethnicity, alcohol use, blood pressure abnormalities, diabetes, obesity, and an unhealthy lifestyle increase the risk of AMI. A genetic predisposition is now recognized as a significant risk factor for atherosclerosis, leading to coronary artery disease, myocardial ischemia, and AMI [4]. Several mutations such as factor V Leiden (FVL) [5], MTHFRC677T [6], and FXIIIVal34Leu [7] polymorphisms have been identified as inherent risk factors for thrombosis.

The R506Q polymorphism increases FVL resistance to degradation by activating protein C and accentuating thromboembolic risk [8, 9]. Coagulation factorXIIIVal34Leu polymorphism influences the balance between thrombus formation and dissolution [5]. This polymorphism can play a protective role against myocardial infarction, but the results of studies on this topic have been contradictory [10, 11]. The MTHFRC677T polymorphism is associated with a reduction in the catalytic activity of the enzyme, which in turn could lead to total homocysteine accumulation and endothelial dysfunction, both of which are two well-known risk factors for coronary artery disease [12, 13]. Despite numerous studies examining the relationship between these polymorphisms and the susceptibility to AMI, the results of these studies have been contradictory. Thus, further studies are needed to provide a clear picture of this association. Moreover, to the best of our knowledge, no study has yet been conducted on this very topic in Iran. Therefore, we conducted this study to investigate the association of the FVL, FXIIIVal34Leu, and MTHFRC677T polymorphisms with susceptibility to AMI.


Study population

In this case–control study, we collected 300 participants including 150 AMI patients and 150 ethnically matched healthy volunteers from the Iranian population. The AMI patients included in this study were patients with AMI admitted to Razi Hospital of Birjand, Iran in 2019–2021 who did not receive any intervention medication. All cases were selected based on the criteria of the world health organization [14]. Inclusion criteria for AMI patients were age between 18 and 65 years and positive angiography with 50% or more stenosis of at least one coronary artery. Angiography was carried out and evaluated by experienced cardiologists who were blinded to patients’ genotype. Clinical electrocardiography (ECG) and cardiac enzyme findings were used to make the diagnosis of AMI. Non-inclusion criteria for all participants including patients and healthy controls were: history of previous angiography, heart failure, history of a coagulation disease, deep vein thrombosis, hepatic dysfunction, renal dysfunction, advanced cancer, history of thyroid disease and consumption of related medication, organ inflammation, pregnancy, and lactation.

Concentrations of total cholesterol (Chol), high density lipoprotein (HDL), low density lipoprotein (LDL), triglycerides (TG), and fasting blood sugar (FBS), were measured using an automatic analyzer (BT-4500, Biotecnica, Italy). After informed consent was obtained, venous blood sample was collected from all participants. The study protocol was evaluated and approved by the Ethics Committee of Birjand University of Medical Sciences (Ref. ID: IR.BUMS.REC.1399.264).

DNA isolation and SNP selection and genotyping

Blood samples were stored at − 20 °C until use. Genomic DNA for PCR was extracted from peripheral blood by DNA extraction kit. Genotype determination was performed using tetra-primer amplification refractory mutation system-polymerase chain reaction (T-ARMS-PCR) assay. Primer sequences and fragment sizes are shown in Table 1. All primers used in this research were designed by a web primer design program (Primer1) [15]. Amplification was done in Eppendorf thermal cycler (Germany). Following amplification, PCR products were separated by 2% agarose gel electrophoresis using a 100 bp ladder. Bands of PCR products were visualized under UV transilluminator. Sequencing was performed to confirm the genotypes initially identified by the T-ARMS-PCR. The final T-ARMS-PCR was conducted with a total volume of 20 μl containing 50 ng of template DNA, 1 μL of each inner primer, 0.25 μL of each outer primer (each primer has a concentration of 10 μM), and 10 μL of 1X PCR Master mix (amplicon, Denmark). PCR amplification conditions are shown in Table 2.

Table 1 Primers used in the T-ARMS-PCR for genotyping of FVL G1691A, MTHFRC677T, and FXIIIval34leu gene polymorphisms
Table 2 PCR procedure for T-ARMS-PCR genotyping of FVL G1691A, MTHFR C677T, and FXIIIval34leu polymorphisms

Statistical analysis

The data were analysed using SPSS version 16.0. The mean and standard deviation (SD) of normally distributed data were calculated, and the Student’s t test was used to compare groups. To compare genotype distribution and allele frequency between groups, the χ2-test was used. The allele and genotype frequencies in various patient subgroups were analysed using Fisher’s exact test. The Chi-square was used to assess the Hardy–Weinberg equilibrium in the control group. The association between polymorphisms and risk of AMI was assessed by logistic regression. Data that were not normally distributed were expressed as medians, and the Mann–Whitney U test was used to compare patients. Multiple groups were compared using Kruskal–Wallis tests. The χ2-test was used to compare patients’ categorical data, which were expressed as percentages. Odds Ratio (OR) along with 95% Confidence Interval (CI) were estimated in order to assess the risk of the association between AMI and the studied gene polymorphisms and Linear regression was used for estimate of gene polymorphisms on clinical characteristics. Statistical significance was defined as P < 0.05.


Study group characteristics

This study enlisted the participation of 300 Iranian subjects comprising 150 individuals with primary MI (men = 77; women = 73) and 150 healthy individuals (male = 75; female = 75). The demographic and clinical characteristics of AMI patients and the control group are shown in Table 3. The mean age of the AMI patients and the controls was 57.94 ± 7.72 and 47.06 ± 8.70, respectively (P < 0.001). In addition, 50% of the control group (n = 75) and 51.3% of the case group (n = 77) were male and there was no significant difference in the distribution of sex between the two groups (P = 0.53). Unlike HDL which was lower in AMI patients, total and LDL cholesterol, creatinine, and FBS concentrations were higher in these patients compared with the controls (P < 0.001). Diabetes, dyslipidemia, and smoking were all more common in the AMI group than in the control group (P < 0.001).

Table 3 Baseline characteristics of the individuals included in the study

Genotyping data

All the studied polymorphisms in the control group followed Hardy–Weinberg equilibrium (HWE) (P > 0.05). Table 4 summarizes the genotypic and allelic frequencies of the FVL, MTHFRC677T and FXIIIVal34leu polymorphisms. There were no statistically significant differences between the patients and control groups in the distribution of allelic and genotypic frequencies of FVL, and FXIIIVal34leu polymorphisms (P > 0.05). However, there was a significant association between CT genotype of MTHFRC677T polymorphism and AMI (OR 1.76, 95% CI 1.07–2.75, P = 0.02).

Table 4 Genotypic and allelic frequencies of FactorVG1691A, MTHFRC677T and Factor XIII V34L polymorphisms in AMI patients and control group

Association of genotypes with clinical characteristics

No association was observed between clinical characteristics and FVL and FXIIIval34leu polymorphisms. The association between MTHFRC677T polymorphism and clinical characteristics of AMI patients is shown in Table 5. According to our findings, patients with the TT genotype of MTHFR polymorphism had higher creatinine levels (2.07 ± 0.19 mg/dl; P < 0.001).

Table 5 The associations between clinical characteristics and genotypes for MTHFR C677T polymorphism in AMI patients


Although there was no significant association between FVL and FXIIIVal34Leu polymorphisms and AMI. A meaningful relationship was found between CT genotype of MTHFR polymorphism and AMI. Furthermore, higher creatinine levels were observed in patients with the MTHFR677TT genotype.

Factor V is a blood protein that aids in the conversion of prothrombin to thrombin by acting as a cofactor. After clot formation, activated protein C, a natural anticoagulant, cleaves and inactivates FVa. The FVL polymorphism makes factor V resistant to APC inactivation so it will remain active for a longer period and facilitate increased thrombin production, resulting in an increased risk of thrombosis. We found no association between FVL and occurrence of AMI, which is in line with Msalati et al. who reported that the FVL mutation is not significantly associated with MI [16]. Similarly, FVL has not been linked to myocardial infarction or stroke in prospective cohort studies [17,18,19]. In addition, Mahmoodi et al. found no association between FVL and increased risk of subsequent atherothrombotic events and mortality in high-risk participants with coronary heart disease [20]. In contrast to these studies, some previous studies reported the association of FVL with MI [5, 21]. Therefore, the association between FVL and AMI is still a controversial topic. It is worthy of note that in the present study as in the study by Ezzat et al. [21], one myocardial infarction patient had the mutated homozygous genotype AA (0.7%).

Mechanical stabilization of fibrin clots and the protection of newly formed fibrin from fibrinolysis are two main hemostatic functions of coagulation FXIII [22]. The FXIIIVal34Leu polymorphism has been reported to increase the activation rate of this coagulation factor by thrombin that affects the clot structure [23]. According to research findings, individuals with the 34Leu allele have clots with thinner fibrin fibers [24]. The effect of this polymorphism may vary depending on the plasma levels of fibrinogen and thrombin in different populations [25]. In our study, there were no differences between AMI patients and healthy groups in the prevalence of the FXIII genotypes, which is consistent with some previously published research [26, 27]. In contrast, some studies have shown a protective role of this polymorphism against thrombosis [28]. By the same token, a meta-analysis of the published data revealed that the Leu34 allele provides moderate but significant protection [29]. Ethnicity has been reported as a major driver behind Val34Leu frequencies around the world [30, 31].

One of the interesting findings from our study was the association of CT genotype in MTHFRC677T polymorphism with the risk of AMI. As indicated by the results of previously published studies, the common C677T (rs1801133) single nucleotide polymorphism is associated with lower MTHFR enzyme activity and plasma homocysteine concentration [32]. For instance, Kang et al. reported that the mean total plasma homocysteine level in patients with MTHFRC677T polymorphism was significantly higher than the normal value [33]. It has also been proved that hyperhomocysteinemia is associated with endothelial dysfunction [34]. Although the exact mechanism of homocysteine toxicity is unknown, it is believed that homocysteine causes atherosclerosis by negatively affecting the vascular endothelium [35]. Unfortunately, the present study did not measure plasma homocysteine levels. Most importantly, however, we found that patients with the MTHFR677TT genotype have higher levels of creatinine. Since homocysteine is crucial for the formation of creatine and creatinine, the increase in serum creatinine can be a reflection of high levels of serum homocysteine [36].

Given the differences in sample sizes, ethnicity, and geographical conditions, the frequency of FVL, MTHFRC677T, and FXIIIVal34Leupolymorphisms in this population differs from that of other populations.

The main study limitation is small sample size of study population, which prevented further examination of the studied gene polymorphisms in relation to the clinical characteristics of the patients. We believe that more research involving a larger number of people will yield more conclusive results. Furthermore, the two study groups in the present study were not age-matched due to the time constraints and our limitation in patient selection. Finally, AMI patients had more cardiovascular risk factors (Table 3), which naturally made them more at risk of developing AMI.


To the best of our knowledge, this was the first study to examine the association of these three mutations with AMI in east Iran. These results may imply the effects of MTHFR C677T polymorphism and higher mean serum creatinine levels in the pathogenesis of AMI. Therefore, screening of these parameters might be used for clinical risk assessment.

Availability of data and materials

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.



Body mass index




Fasting blood sugar


Factor V Leiden


High-density lipoprotein


Low-density lipoprotein


Methylenetetrahydrofolate reductase


Tetra primer-amplification refractory mutation system-polymerase chain reaction






  1. Damar İH, Eroz R (2020) The association of hereditary prothrombotic risk factors with ST-elevation myocardial infarction. Medeniyet Med J 35(4):295.

    Article  Google Scholar 

  2. Shen G-Q, Li L, Rao S, Abdullah KG, Ban JM, Lee B-S et al (2008) Four SNPs on chromosome 9p21 in a South Korean population implicate a genetic locus that confers high cross-race risk for development of coronary artery disease. Arterioscler Thromb Vasc Biol 28(2):360–365.

    CAS  Article  PubMed  Google Scholar 

  3. Huang DL, Chen QF, Wang W, Huang Z, Li T, Li J et al (2018) Association of rs1333040 SNPs with susceptibility, risk factors, and clinical characteristics of acute myocardial infarction patients in a Chinese Han population. Int J Clin Exp Pathol 11(2):727–738

    PubMed  PubMed Central  Google Scholar 

  4. Wilson PW (1994) Established risk factors and coronary artery disease: the Framingham Study. Am J Hypertens 7(7Pt2):7S-12S.

    CAS  Article  PubMed  Google Scholar 

  5. Amara A, Mrad M, Sayeh A, Haggui A, Lahideb D, Fekih-Mrissa N et al (2018) Association of FV G1691A polymorphism but not A4070G with coronary artery disease. Clin Appl Thromb Hemost 24(2):330–337

    CAS  Article  Google Scholar 

  6. Li M-N, Wang H-J, Zhang N-R, Xuan L, Shi X-J, Zhou T et al (2017) MTHFR C677T gene polymorphism and the severity of coronary lesions in acute coronary syndrome. Medicine.

    Article  PubMed  PubMed Central  Google Scholar 

  7. Balogh L, Katona É, Mezei ZA, Kállai J, Gindele R, Édes I et al (2018) Effect of factor XIII levels and polymorphisms on the risk of myocardial infarction in young patients. Mol Cell Biochem 448(1):199–209.

    CAS  Article  PubMed  Google Scholar 

  8. They-They TP, Hamzi K, Moutawafik MT, Bellayou H, El Messal M, Nadifi S (2010) Prevalence of angiotensin-converting enzyme, methylenetetrahydrofolate reductase, Factor V Leiden, prothrombin and apolipoprotein E gene polymorphisms in Morocco. Ann Hum Biol 37(6):767–777.

    Article  PubMed  Google Scholar 

  9. Asghar M, Kabita S, Kalla L, Murry B, Saraswathy KN (2013) Prevalence of MTHFR, Factor V, ACE and APOE gene polymorphisms among Muslims of Manipur, India. Ann Hum Biol 40(1):83–87.

    Article  PubMed  Google Scholar 

  10. Kohler H, Ariëns R, Whitaker P, Grant P (1998) A common coding polymorphism in the FXIII A-subunit gene (FXIIIVal34Leu) affects cross-linking activity. Thromb Haemost 80(10):704–704

    CAS  PubMed  Google Scholar 

  11. Shafey M, Anderson JL, Scarvelis D, Doucette SP, Gagnon F, Wells PS (2007) Factor XIII Val34Leu variant and the risk of myocardial infarction. Thrombosis Haemostasis 97(04):635–641.

    CAS  Article  PubMed  Google Scholar 

  12. Liew S-C, Gupta ED (2015) Methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism: epidemiology, metabolism and the associated diseases. Eur J Med Genet 58(1):1–10.

    Article  PubMed  Google Scholar 

  13. Xuan C, Bai X-Y, Gao G, Yang Q, He G-W (2011) Association between polymorphism of methylenetetrahydrofolate reductase (MTHFR) C677T and risk of myocardial infarction: a meta-analysis for 8,140 cases and 10,522 controls. Arch Med Res 42(8):677–685.

    CAS  Article  PubMed  Google Scholar 

  14. Antman E, Bassand J-P, Klein W, Ohman M, Lopez Sendon JL, Rydén L et al (2000) Myocardial infarction redefined—a consensus document of the Joint European Society of Cardiology/American College of Cardiology committee for the redefinition of myocardial infarction: the Joint European Society of Cardiology/American College of Cardiology Committee. J Am Coll Cardiol 36(3):959–969

    Article  Google Scholar 

  15. Collins A, Ke X (2012) Primer1: primer design web service for tetra-primer ARMS-PCR. Open Bioinform J.

    Article  Google Scholar 

  16. Msalati A, Bashein A, Ghrew M, Khalil I, Sedaa K, Ali A et al (2021) Association of venous thromboembolism and myocardial infarction with Factor V Leiden and Factor II gene mutations among Libyan patients. Libyan J Med 16(1):1857525.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  17. Cushman M, Rosendaal FR, Psaty BM, Cook EF, Valliere J, Kuller LH et al (1998) Factor V Leiden is not a risk factor for arterial vascular disease in the elderly: results from the Cardiovascular Health Study. Thromb Haemost 79(05):912–915

    CAS  Article  Google Scholar 

  18. Juul K, Tybjærg-Hansen A, Steffensen R, Kofoed S, Jensen G, Nordestgaad BG (2002) Factor V Leiden: the copenhagen city heart study and 2 meta-analyses. Blood J Am Soc Hematol 100(1):3–10.

    CAS  Article  Google Scholar 

  19. Ridker PM, Hennekens CH, Lindpaintner K, Stampfer MJ, Eisenberg PR, Miletich JP (1995) Mutation in the gene coding for coagulation factor V and the risk of myocardial infarction, stroke, and venous thrombosis in apparently healthy men. N Engl J Med 332(14):912–917

    CAS  Article  Google Scholar 

  20. Mahmoodi BK, Tragante V, Kleber ME, Holmes MV, Schmidt AF, McCubrey RO et al (2020) Association of factor V Leiden with subsequent atherothrombotic events: a GENIUS-CHD study of individual participant data. Circulation 142(6):546–555.

    Article  PubMed  PubMed Central  Google Scholar 

  21. Ezzat H, Attia FA, Mokhtar A, El-Tokhy HM, Alalfy MN, Elkhouly NY (2014) Prevalence of thrombophilic gene polymorphisms (FVLG1691A and MTHFRC677T) in patients with myocardial infarction. Egypt J Med Hum Genet 15(2):113–123.

    Article  Google Scholar 

  22. Bagoly Z, Koncz Z, Hársfalvi J, Muszbek L (2012) Factor XIII, clot structure, thrombosis. Thromb Res 129(3):382–387.

    CAS  Article  PubMed  Google Scholar 

  23. Wartiovaara U, Mikkola H, Szôke G, Haramura G, Kárpáti L, Balogh I et al (2000) Effect of Val34Leu polymorphism on the activation of the coagulation factor XIII-A. Thromb Haemost 84(10):595–600

    CAS  Article  Google Scholar 

  24. Lim BC, Ariëns RA, Carter AM, Weisel JW, Grant PJ (2003) Genetic regulation of fibrin structure and function: complex gene-environment interactions may modulate vascular risk. Lancet 361(9367):1424–1431.

    CAS  Article  PubMed  Google Scholar 

  25. Gdl R, Tàssies D, Espinosa G, Monteagudo J, Bové A, Plaza J et al (2009) Factor XIII-A subunit Val34Leu polymorphism is associated with the risk of thrombosis in patients with antiphospholipid antibodies and high fibrinogen levels. Thromb Haemost 101(02):312–316

    Article  Google Scholar 

  26. Amin HA-KA, Kotb-El-Sayed MI, Hashish AA, Mohamed FM, Aziz HFA, Leheta OF (2013) Correlation of FXIII Val34Leu polymorphism with decreased risk of myocardial infarction in Egypt. J Adv Med Med Res.

    Article  Google Scholar 

  27. Vishwajeet V, Jamwal M, Sharma P, Das R, Ahluwalia J, Dogra RK et al (2018) Coagulation F13A1 V34L, fibrinogen and homocysteine versus conventional risk factors in the pathogenesis of MI in young persons. Acta Cardiol 73(4):328–334.

    Article  PubMed  Google Scholar 

  28. Chen F, Qiao Q, Xu P, Fan B, Chen Z (2013) Effect of Factor XIII-A Val34Leu polymorphism on myocardial infarction risk: a meta-analysis. Clin Appl Thromb Hemost 20(8):783–792.

    CAS  Article  PubMed  Google Scholar 

  29. Vokó Z, Bereczky Z, Katona E, Adany R, Muszbek L (2007) Factor XIII Val34Leu variant protects against coronary artery disease. Thrombos Haemost 97(03):458–463.

    CAS  Article  Google Scholar 

  30. Attié-Castro FA, Zago MA, Lavinha J, Elion J, Rodriguez-Delfin L, Guerreiro JF et al (2000) Ethnic heterogeneity of the factor XIII Val34Leu polymorphism. Thrombos Haemost 84(10):601–603.

    Article  Google Scholar 

  31. Sajjadi SM, Khosravi A, Pakravesh J, Soheili Z, Samiei H, Mohammadi S et al (2016) Factor XIII Val34Leu polymorphism and risk of recurrent pregnancy loss in Iranian population: a case control study. Front Biol 11(6):471–475

    CAS  Article  Google Scholar 

  32. Dayakar S, Goud KI, Reddy TPK, Rao SP, Sesikeran SB, Sadhnani M (2011) Sequence variation of the methylene tetrahydrofolate reductase gene (677C> T and 1298 A> C) and traditional risk factors in a South Indian population. Genet Test Mol Biomark 15(11):765–769.

    CAS  Article  Google Scholar 

  33. Kang S-S, Wong P, Susmano A, Sora J, Norusis M, Ruggie N (1991) Thermolabile methylenetetrahydrofolate reductase: an inherited risk factor for coronary artery disease. Am J Hum Genet 48(3):536–545

    CAS  PubMed  PubMed Central  Google Scholar 

  34. Lai WKC, Kan MY (2015) Homocysteine-induced endothelial dysfunction. Ann Nutr Metabol 67(1):1–12.

    CAS  Article  Google Scholar 

  35. McCully KS (2015) Homocysteine and the pathogenesis of atherosclerosis. Expert Rev Clin Pharmacol 8(2):211–219.

    CAS  Article  PubMed  Google Scholar 

  36. Xu B, Kong X, Xu R, Song Y, Liu L, Zhou Z et al (2017) (2017) Homocysteine and all-cause mortality in hypertensive adults without pre-existing cardiovascular conditions: Effect modification by MTHFRC677T polymorphism. Medicine 96(8):e5862-e.

    CAS  Article  Google Scholar 

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The authors express their thanks to Cardiovascular Diseases Research Center, and also Cellular and molecular research center, Birjand University of Medical Sciences, Birjand, Iran. They would also like to express their gratitude to everyone who kindly assisted them with this investigation.


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Authors and Affiliations



AG performed the experiments, and wrote the manuscript. AR and NM performed the experiments. GAS and KD collected the studied samples, critical revision of the manuscript. FS analysed the data. NA designed the study, physical examination of the patients, revised the manuscript. SMS designed the study, revised the manuscript, and supervised the project. All authors read and approved the final manuscript.

Corresponding authors

Correspondence to Nahid Azdaki or Seyed Mehdi Sajjadi.

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The study protocol was evaluated and approved by the Ethics committee of Birjand University of medical sciences (Ref. ID: IR.BUMS.REC.1399.264).

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After informed consent was obtained, venous blood sample was collected from all participants.

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The authors declare that they have no competing interests.

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Golestani, A., Rahimi, A., Moridi, N. et al. Association of factor V Leiden R506Q, FXIIIVal34Leu, and MTHFR C677T polymorphisms with acute myocardial infarction. Egypt J Med Hum Genet 23, 118 (2022).

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  • Acute myocardial infarction
  • Factor V Leiden
  • Methylenetetrahydrofolate reductase
  • Factor XIII
  • PCR