Elevated fibrinogen and plasminogen activator inhibitor (PAI‐1) in hypertension are related to metabolic risk factors for cardiovascular disease

Landin, Kerstin; Tengborn, Lilian; Smith, Ulf

doi:10.1111/j.1365-2796.1990.tb00157.x

Cited by 309 publications

(138 citation statements)

References 21 publications

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“…A significant correlation among hypertensives between PAI-1 and the level was noted between absolute levels of vWF and both of both insulin and lipoprotein and a negative systolic and diastolic BP among patients with either relationship with the rate of glucose disposal have controlled or uncontrolled hypertension in the been shown. 59,62,73 In a study of non-obese hypertenabsence of vascular disease or risk factors. This, sive men, treatment with metformin lowered BP and coupled with the finding that concurrent vascular tended to increase the fibrinolytic activity of the disease or risk factors were not associated with any subjects.…”

Section: Red Cell Aggregationmentioning

confidence: 99%

The role of rheological and haemostatic factors in hypertension

Lee

1997

J Hum Hypertens

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Research into the pathogenesis of hypertension has, in tors are known to be involved in thrombogenesis, their potential role in the pathogenesis of patients with hyperthe past, tended to concentrate on changes in vascular geometry, cardiac output and blood volume. However, tension has received increasing attention. The purposes of this review are to update previous reviews and to patients with hypertension are known to be at an increased risk of both coronary heart disease and ceresummarise the relationship between hypertension, its complications and treatment and a range of haemorheobrovascular disease; complications which are thrombotic in origin. Since rheological and haemostatic faclogical factors.

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Section: Red Cell Aggregationmentioning

confidence: 99%

The role of rheological and haemostatic factors in hypertension

Lee

1997

J Hum Hypertens

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“…[12][13][14][15] The metabolic background of this strong relationship between fibrinogen levels and cardiovascular risk has not been fully elucidated, although a number of studies showed significant associations between fibrinogen and several other cardiovascular and hemostatic variables. [16][17][18][19][20][21][22][23] Unfortunately, measurements for fibrinogen were poorly standardized for some time, thereby limiting its wide adoption in the clinical setting. Currently accepted assays for fibrinogen are widely available and have acceptable coefficients of variation.…”

mentioning

confidence: 99%

Body fat and C-reactive protein levels in healthy non-obese men

Bo¹,

Raspo²,

Morra³

et al. 2004

Nutrition, Metabolism and Cardiovascular Diseases

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Previous studies have demonstrated that circulating levels of C-reactive protein (CRP), a marker of cardiovascular risk, are strictly related to body fatness. Elevated fibrinogen levels are also predictive of future cardiovascular events. The metabolic background of this relationship and the predictors of fibrinogen levels have not been well established. We aimed to evaluate whether fibrinogen levels are associated with body fat content and distribution and to determine the independent predictors of fibrinogen levels in a sample of healthy, non-obese, nonsmoking young adult men. Age, anthropometric measures ( -6), and acute-phase reactants levels (fibrinogen, highly sensitive [hs]-CRP) were determined in 87 healthy nonsmoking, non-obese subjects. Linear regression analysis was used to evaluate the association between body fat, fibrinogen, and metabolic variables, and multiple regression model analysis was used to examine the independent predictors of fibrinogen levels. Eighty-seven (30.5 ؎ 3.5 years) non-obese (mean BMI 24.1 ؎ 3.5) men were studied. Fibrinogen levels were strongly associated with measures of body fat and with metabolic variables. Total body fat (P < .0001) and LDLcholesterol (P < .01) were the independent predictors of fibrinogen levels, accounting for 29.5% and 10.9% of its variance, respectively. Total body fat was the best independent predictor of hs-CRP levels, accounting for 32.5 % of its variance. We conclude that in healthy, non-obese subjects, body fat content is the main predictor of fibrinogen levels, as well of hs-CRP levels. These findings support the speculation that there is a direct mechanism by which adipose tissue might regulate the levels of circulating acute-phase reactants.

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“…[73] These changes suggest impaired fibrinolysis and a procoagulant hemostatic blood profile. Experimental studies indicate that the spontaneous dissolution of a cerebral embolus is significantly lower in hypertensive compared with normotensive rats.…”

Section: Hypertensionmentioning

confidence: 99%

Antithrombotic, procoagulant, and fibrinolytic mechanisms in cerebral circulation: implications for brain injury and protection

Zloković

1997

FOC

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Maintaining a delicate balance among anticoagulant, procoagulant, and fibrinolytic pathways in the cerebral microcirculation is of major importance for normal cerebral blood flow. Under physiological conditions and in the absence of provocative stimuli, the anticoagulant and fibrinolytic pathways prevail over procoagulant mechanisms. Blood clotting is essential to minimize bleeding and to achieve hemostasis; however, excessive clotting contributes to thrombosis and may predispose the brain to infarction and ischemic stroke. Conversely, excessive bleeding due to enhanced anticoagulatory and fibrinolytic mechanisms could predispose the brain to hemorrhagic stroke. Recent studies in the author's laboratory indicate that brain capillary endothelium in vivo produces thrombomodulin (TM), a key cofactor in the TM-protein C system that is of major biological significance to the antithrombotic properties of the blood-brain barrier (BBB). The BBB endothelium also expresses tissue plasminogen activator (tPA), a key protein in fibrinolysis, and its rapid inhibitor, plasminogen activator inhibitor (PAI-1). The procoagulant tissue factor is normally dormant at the BBB. There is a vast body of clinical evidence to document the importance of hemostasis in the pathophysiology of brain injury. In particular, functional changes caused by major stroke risk factors in the TM-protein C, tPA/PAI-1, and tissue factor systems at the BBB may result in large and debilitating infarctions following an ischemic insult. Thus, correcting this hemostatic imbalance could ameliorate drastic CBF reductions at the time of ischemic insult, ultimately resulting in brain protection. Delineation of the molecular mechanisms of BBB-mediated hemostasis will likely contribute to future stroke prevention efforts and brain protection strategies.

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Elevated fibrinogen and plasminogen activator inhibitor (PAI‐1) in hypertension are related to metabolic risk factors for cardiovascular disease

Cited by 309 publications

References 21 publications

The role of rheological and haemostatic factors in hypertension

The role of rheological and haemostatic factors in hypertension

Body fat and C-reactive protein levels in healthy non-obese men

Antithrombotic, procoagulant, and fibrinolytic mechanisms in cerebral circulation: implications for brain injury and protection

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