Factor VII hyperactivity in acute myocardial thrombosis. A relation to the coagulation activation

Sousa, João de; Azevedo, Jader Cunha de; Soria, Claudine; Barros, Fernando de; Ribeiro, C; Parreira, F; Caen, Jacques P.

doi:10.1016/0049-3848(88)90060-6

Cited by 49 publications

(7 citation statements)

References 18 publications

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“…Together with the association between raised factor VII activity and increased cardiovascular mortality in prospective studies [3,4], these findings suggest that the raised levels of factor VII activities may have contributed, at least in part, to the increased prevalence of macrovascular disease in the Type II diabetic patients. On the other hand, the presence of coronary heart disease in Type II diabetic patients, even if minimal, can itself contribute to elevated levels of VIIc via the rupture of atheromatous plaques and release of tissue factor, leading to activation of the coagulation system [28]. The increase in patients with retinopathy and neuropathy was not unexpected and may not imply any causal relationship as macrovascular and various microvascular complications often coexist in the same patient with diabetes.…”

Section: Discussionmentioning

confidence: 79%

Genetic influence of the R/Q353 genotype on factor VII activity is overwhelmed by environmental factors in Chinese patients with Type II (non-insulin-dependent) diabetes mellitus

Lam

Bourke

et al. 1998

Diabetologia

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Diabetes mellitus is associated with a two to threefold increase in cardiovascular mortality [1]. The mechanism whereby diabetes increases cardiovascular risk is probably multifactorial. Recent studies suggest that this may in part be attributed to an increase in thrombotic tendency [2] including an increase in circulating level of factor VII, a key enzyme in the initiation of coagulation. A positive correlation between increased factor VII activity and cardiovascular mortality has been shown in the Northwick Park Heart Study [3]. A similar trend Diabetologia (1998) In both diabetic and control subjects the allele frequencies of the R (M1) and Q (M2) alleles were 0.96 and 0.04; the corresponding reported frequencies in Caucasians being 0.90 and 0.10: VIIc were 21 % lower in Chinese control subjects and Type I diabetic patients with R/Q, compared with R/R subjects (p < 0.001 and p < 0.05). The corresponding difference was 4 % for Type II diabetc patients (p = NS). Type II diabetic patients had higher mean VIIc levels than control subjects and Type I diabetic patients (p < 0.01); they were also older, and had higher serum creatinine and triglyceride (all p < 0.01). They also had higher VIIc levels than an age-matched older control group (p < 0.01; n = 182) in whom the genotype effect was clearly seen. On stepwise linear regression analysis, the significant independent determinants of VIIc were serum triglyceride (contributing 20 % and 25 % to variance in control subjects and diabetic patients), the R/Q353 genotype (contributing to 12 % of the variance in control subjects but only 1 % in diabetic patients), age and total cholesterol in all subjects, and in the diabetic patients female sex, urinary albumin excretion rate and serum creatinine. VIIc was higher in diabetic patients with macroangiopathy and retinopathy (both p < 0.0001). We conclude that compared with Caucasians, the Q allele frequency is significantly lower in these Chinese subjects. Plasma VIIc is determined by both genetic and environmental influences such that in Chinese Type II diabetic patients, the effect of environmental factors predominates, almost negating the influence of the R/Q353 genotype. High VIIc may contribute to the increased cardiovascular risk in Type II diabetic patients. [Diabetologia (1998) 41: 760±766]

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Section: Discussionmentioning

confidence: 79%

Genetic influence of the R/Q353 genotype on factor VII activity is overwhelmed by environmental factors in Chinese patients with Type II (non-insulin-dependent) diabetes mellitus

Lam

Bourke

et al. 1998

Diabetologia

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“…Elevated plasma fVII coagulant activity (fVII:C) or elevated levels of circulating fVIIa have also been described with angina pectoris, transient ischemic attacks, diabetes, uremia, and peripheral vascular disease (Broadhurst et al ., 1990; Carvalho de Sousa et al ., 1988; Cortellaro et al ., 1992; Hoffman et al ., 1988; Hoffman et al ., 1989; Kario et al ., 1993; Kario et al ., 1994; Kario et al ., 1995; Orlando et al ., 1987; Suzuki et al ., 1991). In contrast, some studies have failed to find a relationship between fVII levels and thrombotic disease (Hultin, 1991; Grant, 2003).…”

Section: Tf:viia In Diseasementioning

confidence: 99%

How it all starts: Initiation of the clotting cascade

Smith

Travers

Morrissey

2015

Critical Reviews in Biochemistry and Molecular Biology

333

307

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The plasma coagulation system in mammalian blood consists of a cascade of enzyme activation events in which serine proteases activate the proteins (proenzymes and procofactors) in the next step of the cascade via limited proteolysis. The ultimate outcome is the polymerization of fibrin and the activation of platelets, leading to a blood clot. This process is protective, as it prevents excessive blood loss following injury (normal hemostasis). Unfortunately, the blood clotting system can also lead to unwanted blood clots inside blood vessels (pathologic thrombosis), which is a leading cause of disability and death in the developed world. There are two main mechanisms for triggering the blood clotting, termed the tissue factor pathway and the contact pathway. Only one of these pathways (the tissue factor pathway) functions in normal hemostasis. Both pathways, however, are thought to contribute to thrombosis. An emerging concept is that the contact pathway functions in host pathogen-defenses. This review focuses on how the initiation phase of the blood clotting cascade is regulated in both pathways, with a discussion of the contributions of these pathways to hemostasis versus thrombosis.

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“…Although the aggregation of platelets on the arterial plaque rupture site may develop into ACS, the aggregation of platelets, sometime may also block the pericardial artery that might result in the cardiac cells death which appeared as dark patchy areas of infarcts developed due to the death of heart cells that ultimately could lead to acute myocardial infarction (AMI), which when massive, could result in the death of the victims9. Although >90% of the cases of AMI are the consequence of the development of the thrombus due to platelet aggregation10, severe anemia, coronary artery spasm are also known to cause AMI11.…”

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confidence: 99%

Dermcidin isoform-2 induced nullification of the effect of acetyl salicylic acid in platelet aggregation in acute myocardial infarction

Bank

Jana

Maiti

et al. 2014

Sci Rep

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The aggregation of platelets on the plaque rupture site on the coronary artery is reported to cause both acute coronary syndromes (ACS) and acute myocardial infarction (AMI). While the inhibition of platelet aggregation by acetyl salicylic acid was reported to produce beneficial effects in ACS, it failed to do in AMI. The concentration of a stress induced protein (dermcidin isoform-2) was much higher in AMI than that in ACS. Incubation of normal platelet rich plasma (PRP) with dermcidin showed one high affinity (Kd = 40 nM) and one low affinity binding sites (Kd = 333 nM). When normal PRP was incubated with 0.4 μM dermcidin, the platelets became resistant to the inhibitory effect of aspirin similar to that in the case of AMI. Incubation of PRP from AMI with dermcidin antibody restored the sensitivity of the platelets to the aspirin effect. Incubation of AMI PRP pretreated with 15 μM aspirin, a stimulator of the NO synthesis, resulted in the increased production of NO in the platelets that removed the bound dermcidin by 40% from the high affinity binding sites of AMI platelets. When the same AMI PRP was retreated with 10 μM aspirin, the aggregation of platelets was completely inhibited by NO synthesis.

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Factor VII hyperactivity in acute myocardial thrombosis. A relation to the coagulation activation

Cited by 49 publications

References 18 publications

Genetic influence of the R/Q353 genotype on factor VII activity is overwhelmed by environmental factors in Chinese patients with Type II (non-insulin-dependent) diabetes mellitus

Genetic influence of the R/Q353 genotype on factor VII activity is overwhelmed by environmental factors in Chinese patients with Type II (non-insulin-dependent) diabetes mellitus

How it all starts: Initiation of the clotting cascade

Dermcidin isoform-2 induced nullification of the effect of acetyl salicylic acid in platelet aggregation in acute myocardial infarction

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