Effects of Changes in Smoking and Other Characteristics on Clotting Factors and the Risk of Ischaemic Heart Disease

Meade, T. W.; Imeson, John; Stirling, Yvonne

doi:10.1016/s0140-6736(87)92556-6

Cited by 426 publications

(193 citation statements)

References 15 publications

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“…Our patient had no previous history of chest pain, and experienced chest pain at 14 : 00 when spontaneous coronary spasm was not likely to occur. However, he experienced chest pain during smoking which was associated with coronary spasm, platelet aggregation and blood coagulability (14,15). Thus, we thought that such adverse effects of smoking caused thrombus formation under the existence of myocar- dial bridging.…”

Section: Discussionmentioning

confidence: 99%

Acute Myocardial Infarction Associated with Myocardial Bridging in a Young Adult

et al. 2004

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A 28-year-old man was admitted because of chest pain. Emergency coronary angiography showed a massive thrombus in the proximal segment and another occlusive thrombus in the distal segment of the left anterior descending artery. He was treated with thrombolytic therapy. Repeat coronary angiography showed disappearance of the thrombi in the proximal and distal segments and obvious myocardial bridging in the mid segment. Intravascular ultrasound revealed an atherosclerotic plaque in the segment immediately proximal to the myocardial bridging, but did not reveal any plaque within or distal to the site. He was discharged 12 days later.

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Section: Discussionmentioning

confidence: 99%

Acute Myocardial Infarction Associated with Myocardial Bridging in a Young Adult

et al. 2004

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“…However, prospective data indicate that smoking cessation results in a decrease of »15 mg/100 mL in plasma fibrinogen after a 6-year follow-up. 20 Accordingly, it can be assumed that the difference in fibrinogen levels between smokers and nonsmokers was reduced slightly. Our data support this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Genetic variation at the beta-fibrinogen locus in relation to plasma fibrinogen concentrations and risk of myocardial infarction. The ECTIM Study.

Scarabin

Bara

Ricard

et al. 1993

Arterioscler Thromb

121

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Increased plasma fibrinogen concentration is a major cardiovascular risk factor. Conflicting results on genetic variations in plasma fibrinogen levels have been reported. Furthermore, whether flbrinogen genotype is associated with the risk of ischemic heart disease has not been studied so far. An HaelU restriction fragment length polymorphism of the ^-fibrinogen gene was used in a case-control study to investigate the genetic variation at this locus in relation to plasma fibrinogen concentrations and the risk of myocardial infarction (MI). Five hundred thirty-three male patients aged 27-66 years and 648 control subjects were recruited from four World Health Organization MONICA centers in Northern Ireland and in France. The absence of the HaeWl cutting site (H2 allele) was associated with a significant rise in fibrinogen concentrations in both patients and control subjects. The effect of the HaelU polymorphism on plasma fibrinogen levels did not significantly differ between centers. Fibrinogen levels were higher in smokers than in nonsmokers. The difference between the two groups was larger in subjects with the genotype H2H2 than in those with either genotype H1H1 or H1H2, regardless of the case-control status. However, there was no significant interaction between smoking status and genotype in their effects on fibrinogen levels. HaelU genotype accounted for «1% of the total variance in fibrinogen levels, whereas smoking and age together explained 7% and 5% in control subjects and patients, respectively. The frequency of the H2 allele was 0.21 in control subjects and 0.19 in patients. The relative risk estimate of MI associated with the presence of the H2 allele was 0.89 (95% confidence interval, 0.69-1.13). The results were consistent with respect to the centers. Multiple regression analysis showed that smoking and raised plasma fibrinogen made independent contributions to the increase in MI risk. There was no significant interaction between HaelU genotype and the effect of smoking on MI risk. These data provide further evidence for a role of the genetic variation at the /3-fibrinogen locus in the determination of plasma fibrinogen concentrations. However, this study failed to detect an association between this genetic variation and MI risk. Further investigations are needed to assess the relative contribution of genetic and environmental determinants of plasma fibrinogen to the prediction of atherothrombotic diseases.

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“…Further studies would be needed to determine whether these changes have any therapeutic relevance to thrombotic disease. No studies have been performed on the effect of smoking on fibrin clot architecture, but smoking increases fibrinogen levels, 107 and this is likely to influence fibrin characteristics.…”

Section: Lifestyle Factors-diet and Smokingmentioning

confidence: 99%

Genetic and Environmental Determinants of Fibrin Structure and Function

Scott

Ariëns

Grant

2004

ATVB

137

129

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Abstract-The formation of a fibrin clot is one of the key events in atherothrombotic vascular disease. The structure of the fibrin clot and the genetic and environmental factors that modify it have effects on its biological function. Alterations in fibrin structure and function have implications for the clinical presentation of vascular disease. This review briefly describes the key features involved in the formation of a fibrin clot, its typical structure, and function. This is followed by a review of the current literature on genetic and environmental influences on fibrin structure/function and the relationship to clinical disease. Key Words: fibrin Ⅲ hemostatis Ⅲ genetic Ⅲ environment Ⅲ atherothrombosis D iseases associated with the development of thrombosis are a major cause of morbidity and mortality in the developed world. Atherothrombotic vascular disorders develop over many decades and involve the interaction of classic atherogenic risk factors such as diabetes, hyperlipidemia, and hypertension with abnormalities of the inflammatory and hemostatic systems. Arterial disease develops in a high-pressure, high-flow system, with lipid deposition and smooth muscle hyperplasia occurring to form an atherosclerotic plaque. 1 Subsequently, the plaque becomes unstable and ruptures exposing a prothrombotic lipid core activating the clotting cascade and leading to the development of a platelet-rich fibrin blood clot and arterial thrombotic occlusion. The extent of this process determines clinical outcome, ranging from no clinically noticeable event to acute coronary artery syndromes including myocardial infarction (MI), cerebrovascular and peripheral vascular disease, or sudden death. The Formation of a Fibrin ClotFibrin is the major protein constituent of the blood clot and is formed from fibrinogen, a glycoprotein that circulates largely inactively, in the blood stream. Fibrinogen consists of 6 polypeptide chains (A␣, B␤, ␥) 2 held together by disulphide bonds in a molecule with bilateral symmetry (Figure 1). The molecule consists of 3 main structural regions, 2,3 including a central region (E), which contains fibrinopeptides A and B and the amino acid termini of all 6 polypeptide chains, 2 distal regions (D) connected to the E region by 2 ␣-helical coiled segments and the D regions containing the carboxyl termini of the B␤ and ␥ chains, and those of the A␣ chain, which extend to form relatively flexible ␣C-domains, each ending in a globular domain. 2,3 In situations of tissue injury and inflammation, thrombin is generated after cleavage of prothrombin by the Xase complex. Thrombin subsequently binds to fibrinogen and cleaves the amino termini of the fibrinogen A␣ and B␤ chains at region E. This results in the release of fibrinopeptides A and B from fibrinogen, producing fibrin and initiating fibrin clot formation. Release of fibrinopeptide A by thrombin is fast and exposes a polymerization site on the E region of fibrin. 4,5 This combines with a complementary binding site on the ␥ chain in the D region of an adjac...

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Effects of Changes in Smoking and Other Characteristics on Clotting Factors and the Risk of Ischaemic Heart Disease

Cited by 426 publications

References 15 publications

Acute Myocardial Infarction Associated with Myocardial Bridging in a Young Adult

Acute Myocardial Infarction Associated with Myocardial Bridging in a Young Adult

Genetic variation at the beta-fibrinogen locus in relation to plasma fibrinogen concentrations and risk of myocardial infarction. The ECTIM Study.

Genetic and Environmental Determinants of Fibrin Structure and Function

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