The complex between tPA and PAI-1: risk factor for myocardial infarction as studied in the SHEEP project

Nordenhem, Arvid; Leander, Karin; Hallqvist, Johan; Fairé, Ulf dé; Sten-Linder, Margareta; Wiman, Björn

doi:10.1016/j.thromres.2004.12.007

Cited by 50 publications

(34 citation statements)

References 102 publications

(97 reference statements)

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“…Furthermore, the free radicals contained in cigarette smoke react with NO, which also leads to a lowering of its availability. It is noteworthy that the expression of other molecules with known vasodilatation effects, such as tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) have also been shown to be altered by cigarette smoke 71 . Interestingly, impairment of vasodilation in smokers has been demonstrated to be partially reversed by administration of vitamin C (known to have anti oxidative properties), which suggests that it is mainly due to the oxidative stress 72 .…”

Section: Effect Of Cigarette Smoking On the Endotheliummentioning

confidence: 99%

SASH1, a new potential link between smoking and atherosclerosis

et al. 2015

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Section: Effect Of Cigarette Smoking On the Endotheliummentioning

confidence: 99%

SASH1, a new potential link between smoking and atherosclerosis

et al. 2015

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“…Others have investigated tPA/ PAI complex levels and shown these to be a risk factor for MI. 61 This may be related to the correlation between tPA/ PAI levels and PAI-1 activity, 62 and therefore measuring tPA/PAI-1 complex may offer a more accurate marker of vascular disease.…”

Section: Coagulation Proteins Involved In Fibrinolysismentioning

confidence: 99%

Review article: Coagulation and fibrinolysis in diabetes

Alzahrani

Ajjan

2010

Diabetes and Vascular Disease Research

207

188

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Atherothrombotic complications are the main cause of mortality in subjects with diabetes. Premature atherosclerosis, increased platelet reactivity and activation of coagulation factors with associated hypofibrinolysis all contribute to increased cardiovascular risk in this population. Blood clot formation represents the last step in the atherothrombotic process, and the structure of the fibrin network has a role in determining predisposition to cardiovascular disease. In this review, we discuss alterations in coagulation factor plasma levels and/or activity in diabetes and clarify their role in predisposition to cardiovascular events. The effect of diabetes on fibrin network structure/fibrinolysis is reviewed and potential mechanisms that modify clot properties are discussed. Finally, modulation of clotting potential by the various therapeutic agents used in diabetes is examined. Understanding the mechanisms by which diabetes influences the coagulation pathway will help to develop more effective treatment strategies to reduce thrombotic events in subjects with this condition. KeywordsAtherothrombosis, clot structure, coagulation factors, coronary artery disease, diabetes, fibrinogen Clot formation and lysisFibrin clot formation, leading to vessel occlusion, represents the final step in the atherothrombotic process and involves multiple interactions between coagulation factors and platelets.6 Rupture or fissuring in atherosclerotic plaques exposes a prothrombotic core that comes into contact with platelets and coagulation factors. Initially, platelets adhere to the site of the break and become partially activated. Factor VII (FVII) binds to exposed tissue factor (TF) and forms a complex, which subsequently activates FIX and FX, resulting in FV activation. Activated FX and FV cleave prothrombin to generate limited amounts of thrombin, enough to maintain platelet activation but insufficient to sustain thrombus formation. Platelet stimulation by thrombin and exposed collagen results in full activation and degranulation, followed by FV release and activation by both FXa and thrombin. Thrombin also activates FVIII and this can form an active complex with FIXa, further enhancing the coagulation process. Subsequently, enough Diabetes and thrombosis riskCardiovascular disease (CVD) remains the main cause of morbidity and mortality in individuals with diabetes. Up to 80% of diabetes subjects die as a result of cardiovascular complications, and the risk of atherothrombotic events in this population is similar to non-diabetic individuals with a history of ischaemic heart disease (IHD).1 Moreover, the prognosis in these individuals following an event remains poor, despite major advances in treatment.2 Increased atherothrombosis risk is even evident in the pre-diabetes stage, as subjects with insulin resistance and normoglycaemia are at risk of cardiovascular events secondary to clustering of risk factors. 3The underlying mechanisms for increased thrombosis risk in diabetes are complex and involve multiple pathways. S...

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“…223,[230][231][232] In a recent prospective nested case-control study of 2246 Swedish patients with a first AMI matched for age and sex, elevated levels of PAI-1 were significantly associated with a 2-fold increased risk of AMI in both men and women. 233 A few studies have shown that premenopausal women have lower plasma PAI-1 levels than postmenopausal women. 234 In addition, postmenopausal women receiving hormone replacement therapy have lower plasma PAI-1 levels than those not receiving such therapy.…”

Section: Plasminogen Activator Inhibitor Type-1mentioning

confidence: 99%

A comprehensive view of sex-specific issues related to cardiovascular disease

Pilote¹,

Dasgupta²,

Guru³

et al. 2007

Canadian Medical Association Journal

374

256

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A comprehensive view of sex-specific issues related to cardiovascular disease Cardiovascular disease (CVD) is the leading cause of mortality in women. In fact, CVD is responsible for a third of all deaths of women worldwide and half of all deaths of women over 50 years of age in developing countries. The prevalence of CVD risk factor precursors is increasing in children. Retrospective analyses suggest that there are some clinically relevant differences between women and men in terms of prevalence, presentation, management and outcomes of the disease, but little is known about why CVD affects women and men differently. For instance, women with diabetes have a significantly higher CVD mortality rate than men with diabetes. Similarly, women with atrial fibrillation are at greater risk of stroke than men with atrial fibrillation. Historically, women have been underrepresented in clinical trials. The lack of good trial evidence concerning sex-specific outcomes has led to assumptions about CVD treatment in women, which in turn may have resulted in inadequate diagnoses and suboptimal management, greatly affecting outcomes. This knowledge gap may also explain why cardiovascular health in women is not improving as fast as that of men. Over the last decades, mortality rates in men have steadily declined, while those in women remained stable. It is also becoming increasingly evident that gender differences in cultural, behavioural, psychosocial and socioeconomic status are responsible, to various degrees, for the observed differences between women and men. However, the interaction between sex-and gender-related factors and CVD outcomes in women remains largely unknown. CMAJ 2007;176(6):S1-44 Although cardiovascular disease (CVD) is common, significant sex-related differences in its epidemiology have only recently been appreciated. The objective of this section is to demonstrate that there are sex-specific differences in the prevalence, complications and burden of CVD in terms of mortality, hospital admissions and quality of life. Abstract Search strategyA MEDLINE search was conducted using the MeSH terms "cardiovascular disease" OR "atrial fibrillation" OR "congestive heart failure." A second search used the terms "prevalence" OR "incidence" OR "mortality" and the final search combined the results of the first 2 searches and added the terms "gender" OR "sex." Articles identified in this manner were retrieved and their reference lists searched for additional relevant articles. The search was limited to English-language publications, but no other restrictions were applied. Other data sources included Web sites of the World Health Organization, the Canadian Institute for Health Information and the National Centre for Health Statistics. Thirty-three original studies were reviewed. Studies were included if they were cohort studies, case-control studies or nested cohort studies that examined the incidence, prevalence or mortality of CVD, congestive heart failure or atrial fibrillation. The studies had to include data on both ...

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The complex between tPA and PAI-1: risk factor for myocardial infarction as studied in the SHEEP project

Cited by 50 publications

References 102 publications

SASH1, a new potential link between smoking and atherosclerosis

SASH1, a new potential link between smoking and atherosclerosis

Review article: Coagulation and fibrinolysis in diabetes

A comprehensive view of sex-specific issues related to cardiovascular disease

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