Plasminogen activator inhibitor-1 4G/5G-polymorphism and factor V Q506 mutation are not associated with myocardial infarction in young men

Junker, Ralf; Heinrich, J.; Schulte, Helmut; Tataru, Mira-Christine; Köhler, S. Eleonore; Schönfeld, R; Nowak-Göttl, U.; Assmann, G.

doi:10.1097/00001721-199810000-00005

Cited by 28 publications

(19 citation statements)

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“…The Copenhagen City Heart Study together with the 5 largest studies previously published 18,20,22,32,53 largely account for this conclusion, contributing approximately 60% to the overall result of the meta-analysis. All 6 studies demonstrate statistically insignificant odds ratios above 1.0 (range, 1.03-1.40).…”

Section: Factor V Leiden and Arterial Thrombosismentioning

confidence: 88%

Factor V Leiden: The Copenhagen City Heart Study and 2 meta-analyses

Juul

Tybjærg‐Hansen²,

Steffensen³

et al. 2002

Blood

181

101

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Section: Factor V Leiden and Arterial Thrombosismentioning

confidence: 88%

Factor V Leiden: The Copenhagen City Heart Study and 2 meta-analyses

Juul

Tybjærg‐Hansen²,

Steffensen³

et al. 2002

Blood

181

101

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“…[5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] From those, 12 studies were excluded because no solid diagnostic criteria for myocardial infarction were used, [17][18][19][20] there was inadequate delineation of cases, 21,22 or there was an inadequate spectrum of cases, [11][12][13][14][15][16] leaving a total of 6 studies in the analysis.…”

Section: Factor V Leiden Mutationmentioning

confidence: 99%

“…[5][6][7][8][9][10] Eight studies that investigated patients with myocardial infarction before the age of 55 years were initially identified. [11][12][13][14][15][16] From those, 2 were excluded because of an inadequate spectrum of cases. 21,22 Addition of the remaining 6 studies made the association stronger and significant (OR 1.29, 95% CI 1.03 to 1.61, Pϭ0.02).…”

Section: Factor V Leiden Mutationmentioning

confidence: 99%

“…21,22 Addition of the remaining 6 studies made the association stronger and significant (OR 1.29, 95% CI 1.03 to 1.61, Pϭ0.02). [11][12][13][14][15][16] All tests for heterogeneity were nonsignificant.…”

Section: Factor V Leiden Mutationmentioning

confidence: 99%

“…13,15,[35][36][37][38][39][40][41][42][43][44][45][46][47][48][49][50] From those, 11 studies were excluded because they did not use solid diagnostic criteria for myocardial infarction [43][44][45][46][47][48][49] or because of inadequate delineation of cases 15,50 or an inadequate spectrum of cases, 13,42 leaving 7 studies in the analysis. The qualifying 7 studies described a total of 2813 patients and 3358 controls from 8 distinct populations.…”

Section: Pai-1 4g/5g Polymorphismmentioning

confidence: 99%

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Genetic Variation in Coagulation and Fibrinolytic Proteins and Their Relation With Acute Myocardial Infarction

et al. 2001

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Background-It is pathophysiologically conceivable that genetic variations in coagulation and fibrinolytic proteins are associated with the risk of myocardial infarction. Methods and Results-We performed a literature search to identify published case-control studies correlating the factor V Leiden or prothrombin G20210A mutations or fibrinogen GϪ455A or plasminogen activator inhibitor-1 (PAI-1) 4G/5G polymorphisms with the risk of myocardial infarction. Studies were included only if they used solid diagnostic criteria and complied with published methodological criteria. A common OR with corresponding 95% CI was calculated for the risk of myocardial infarction in a fixed-effect model according to Mantel-Haenszel. The factor V Leiden and prothrombin G20201A mutations did not significantly correlate with myocardial infarction (OR 1.26, 95% CI 0.94 to 1.67, Pϭ0.12 and OR 0.89, 95% CI 0.59 to 1.35, Pϭ0.6, respectively). Inclusion of the studies that investigated young patients (Ͻ55 years) made the association significant for factor V Leiden (OR 1.29, 95% CI 1.03 to 1.61, Pϭ0.02). Homozygosity for the fibrinogen Ϫ455A allele was significantly associated with a decreased risk of myocardial infarction (OR 0.66, 95% CI 0.44 to 0.99, Pϭ0.04), whereas the PAI-1 4G4G genotype was significantly associated with increased risk (OR 1.20, 95% CI 1.04 to 1.39, Pϭ0.04). Conclusions-Associations between these genetic variations and myocardial infarction were weak or absent. In the absence of clinical implications, our results indicate that screening of patients with myocardial infarction for these genetic variations is not warranted. Key Words: myocardial infarction Ⅲ genetics Ⅲ coagulation T hrombosis, triggered by atherosclerotic plaque rupture, is generally accepted as the most common pathogenetic pathway of acute myocardial infarction. 1 In recent years, several genetic variations in coagulation and fibrinolytic proteins have been described, and numerous case-control studies have sought to correlate these genetic variations with the risk of myocardial infarction. However, clear relationships have not been established, possibly owing to lack of statistical power of the individual studies or their heterogeneity in terms of methodological design, outcome definition, or selection of cases and controls. We hypothesized that a meta-analysis could provide stronger evidence in favor of the hypothesis that genetic variations in coagulation or fibrinolytic proteins are associated with the risk of myocardial infarction. We limited our analysis to 4 genetic variations that are common and on which sufficient published data were available, ie, the factor V Leiden and prothrombin G20210A mutations and the fibrinogen ␤-chain GϪ455A and plasminogen activator inhibitor-1 (PAI-1) 4G/5G polymorphisms. Methods Literature SearchWe identified all case-control studies correlating the factor V Leiden mutation, the prothrombin G20210A mutation, the fibrinogen ␤-chain GϪ455A polymorphism, or the PAI-1 4G/5G polymorphism with myocardial infarction. The lit...

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