Longitudinal associations between plasma viscosity and cardiovascular risk factors in a middle-aged French population

doi:10.1016/0021-9150(93)90188-Z

Atherosclerosis

Volume 104, Issues 1–2, December 1993, Pages 173-182

https://doi.org/10.1016/0021-9150(93)90188-Z Get rights and content

Abstract

A recent prospective study has suggested that increased plasma viscosity may be associated with higher risk of coronary heart disease. A longitudinal approach was used to investigate associations between plasma viscosity and conventional risk factors in an apparently healthy French population aged 45–56 years (637 men and 431 women) over a 2-year follow-up period. In univariate analysis, change in plasma viscosity was significantly related to changes in smoking status, systolic and diastolic blood pressure, gamma glutamyl transferase (γGT), body mass index and triglycerides only in men, and to changes in total cholesterol, low-density lipoprotein (LDL) cholesterol and apolipoprotein (apo) B in both sexes. Change in plasma viscosity was also significantly associated with changes in fibrinogen and hemoglobin levels in both sexes. No association was found with age, high-density lipoprotein (HDL) cholesterol or apo A1 in both sexes, or with changes in smoking and menopausal status in women. In multiple stepwise regression analysis, independent determinants of change in plasma viscosity were changes in smoking status, systolic blood pressure, γGT, total cholesterol, fibrinogen and hemoglobin in men, and changes in fibrinogen and apo B in women. These results strengthen the hypothesis that increased plasma viscosity may be one of the mechanisms linking conventional risk factors to the risk of cardiovascular disease and suggest that its decrease may be obtained by appropriate life-style changes.

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Cited by (30)

Plasma viscosity and related cardiovascular risk factors in a Spanish Mediterranean population
2007, Thrombosis Research
Plasma viscosity (PV) constitutes an independent important predictor of initial and recurrent cardiac events and mortality. It has been suggested that there is a geographical variation in PV values related to coronary event rates. Little information exists regarding PV in Spain. Therefore, our objective was to determine PV in a large sample of randomly selected subjects from the Spanish population and to study which demographic or cardiovascular risk factors (CVRF) influence levels of PV in this population.
1277 subjects (503 males, 774 females) aged 43 ± 14 years (range: 20–70) were randomly selected from an Eastern Spanish population. These subjects were free of cardiovascular diseases and other major diseases. PV was measured at 37 °C by means of the Fresenius GmbH plasma viscosimeter. In addition, total cholesterol, triglycerides, glucose and fibrinogen were measured.
In the crude analysis, no differences in PV were observed regarding gender (males: 1.235 ± 0.061 cP; females: 1.236 ± 0.059 cP, P = 0.952). Women older than 50 years showed higher PV:1.248 ± 0.057 cP than those aged less than 50 years: 1.232 ±0.059 cP, P = 0.001. No differences in PV by age groups were observed in men (P = 0.842). Furthermore, we evaluated the prevalence of the following CVRF: hypercholesterolemia, hypertriglyceridemia, hypertension, diabetes, tobacco smoking, obesity, and high fibrinogen levels. Prevalence of these factors was: 28%, 4.3%, 8%, 2.3%, 33%, 8.8% and 15% respectively. As some of these CVRF were correlated with PV levels, we carried out a multivariate analysis to adjust PV levels for the potential confounding effect of each one of these factors. After multivariate adjustment, PV was positively associated with high fibrinogen (> 320 mg/dL) levels in both men and women (P < 0.001). In addition, in women, but not in men, PV levels were independently associated with obesity (P < 0.001) and hypertriglyceridemia (P = 0.01). After the multivariate adjustment, the association between PV and age older than 50 in women did not remain statistically significant, revealing a confusing effect of the CVRF in the crude analysis.
Haemorrhoeology and cardiology. Processes, mechanisms, roles in cardiovascular disorders
2005, EMC - Cardiologie-Angeiologie
Il revient à AL. Copley (1910-1992) d’avoir compris que le sang et la paroi des vaisseaux constituaient un organe unique, en ce sens que l’influence du contenu sur le contenant, objet de l’hémorhéologie, est déterminante. Sous l’effet de la pression motrice, le flux sanguin se dispose en lames concentriques (flux laminaire), développant une friction entre elles, ou shear stress, plus accentuée à la paroi, fortement « cisaillée », qu’au centre du vaisseau, où les lames sont moins individualisées. Les hématies épousent les lames en se déformant longitudinalement, rendant le sang fluide (viscosité basse). Dans tous les secteurs vasculaires où la pression diminue et le shear stress est faible, le sang est plus visqueux du fait de l’apparition de gros agrégats de globules rouges proportionnels au taux du fibrinogène (phénomène de thyxotropie, agrégation érythrocytaire), déréglant et diminuant le cisaillement de la paroi. Cet aspect biphasique du shear stress est caractéristique de la réactivité du flux sanguin vis-à-vis du vaisseau. L’exploration de la viscosité se fait par la viscosité plasmatique et du sang total et surtout par la mesure du temps et des seuils de l’agrégation des hématies. La mécanotransduction du shear stress s’effectue par des récepteurs membranaires endothéliaux (cavéolis, canaux ioniques, intégrines), puis par les systèmes des mitogen activated protein (MAP)-kinases, enfin par des facteurs de transcription qui activent des zones spécifiques des promoteurs géniques. Aujourd’hui, plus de 10 000 gènes sont connus pour être influencés par le shear. Au niveau des artères, le cisaillement assure la production du NO (oxyde nitrique), agent vasodilatateur et de la désactivation plaquettaire. La friction de la paroi endothéliale est souvent affaiblie, sous l’effet du flux pulsé et dans des zones situées aux embranchements. La sécrétion de NO est alors faible et les fonctions, sous-régulées par le shear stress, sont libérées, surtout l’adhésion-migration des leucocytes. Au niveau veineux, la variation des cisaillements est encore plus variable, en particulier au niveau des valvules. La microcirculation fonctionne en unités fonctionnelles comportant un versant artériel précapillaire vasoactif, des capillaires dont le diamètre moyen est inférieur à celui des hématies et un versant veinulaire postcapillaire, à débit faible, où les shears stress sont bas. Les cellules endothéliales à ce niveau sont très actives pour l’adhésion-migration leucocytaire, l’inflammation et l’hémostase. L’athérosclérose a comme point de départ les zones où les monocytes-macrophages pénètrent dans la paroi et véhiculent une grande partie des lipoprotéines constituant la plaque. L’hyperagrégation des hématies, consécutive aux facteurs de risque qui augmentent le fibrinogène, accentue les variations du shear à la paroi, ce qui active le récepteur des low density lipoproteins (LDL), accélère la formation des plaques et les étend aux gros troncs. Une fois formée, la plaque athéroscléreuse sténosante est soumise à des cisaillements en amont, activant les plaquettes, et ménage en aval des zones stagnantes où adhèrent et migrent les leucocytes. L’infarctus du myocarde est lié à la fracture d’une plaque coronaire, mais sa taille est corrélée aux facteurs rhéologiques (fibrinogène, viscosité). L’artériopathie des membres inférieurs développe largement de tels troubles rhéologiques, actifs aussi sur l’ischémie. L’hémodilution est proposée dans les épisode aigus, surtout l’accident vasculaire cérébral. La restauration du débit (pontage), la lutte contre les facteurs de risque, la contention élastique et les traitements vasoactifs réduisent l’influence des troubles rhéologiques dans les maladies vasculaires.
The discovery that the blood and the vessel wall constitute a single organ, i.e., that the content definitely influences the container - which is the main object of the haemorrheology - is attributable to A.L. Copley (1910-1992). Due to driving forces, blood flow organizes itself as concentric layers (laminar flow) shearing over each other. Such a shear stress is stronger at the wall level than in the middle of the vessel, where layers are less distinct. Red cells deform and take the shape of layers, allowing blood to become fluid (low viscosity). In vascular areas with decreased pressure, thus lower shear stress, blood becomes more viscous due to the presence of huge red cell aggregates, in relation to fibrinogen level (thyxotropy, red cell aggregation), changing and decreasing the shearing at the wall level. Such a two-phase behaviour of the shear stress characterizes the blood flow reactivity toward the wall. As viscosity measurement consists of plasma and blood viscosity, time and threshold of erythrocyte aggregation appear more accurate determinants. The shear stress mechanotransduction involves endothelial membrane receptors (caveoli, ion channels, integrins), then MAP-kinases systems, and finally transcription factors able to bind specific areas in gene promoters. Over 10 000 shear-sensitive genes have been identified to date. In arteries the shear stress induces NO, which is vasoactive and inhibits platelets. The shearing power at the wall level or at branching zones is often poor, due to pulsations and picks, where subsequently NO production is low and shear-down-regulated functions can occur, mainly leukocyte adhesion and migration. In veins changes in shear are more frequent, particularly in valvulae. Microcirculation is implemented as functional units, exhibiting a vasoactive precapillary side, capillaries with diameters lower than those of red cells and a post-capillary venous side with low output and much decreased shear stress. Endothelial cells are here very active for leukocyte adhesion, inflammation and haemostasis as well. Atherosclerosis stems from zones where monocytes-macrophages are able to enter the wall, bearing large amounts of lipoproteins, the main plaque constituent. As risk factors increase fibrinogen, high red cell aggregates change the wall shear stress and then LDL-receptors can be activated allowing plaques to grow up and extend along the arterial trunks. The atherosclerosis plaque is submitted to high shear upwardly, that activates platelets, but exhibits a stagnant zone downward, where leucocytes adhere and migrate. Myocardial infarct is due to the rupture of a coronary plaque, but its size is related to the rheological factors (fibrinogen, viscosity). Occlusive arterial disease largely exhibits such rheological disorders, with subsequent actions on ischemia. Hemodilution is proposed during acute events, mainly in stroke. Flow restoration (bypass), prevention of risk factors, venous contention and venoactive drugs reduce the influence of rheological disorders in vascular diseases.
Social, behavioral, and metabolic determinants of plasma viscosity in the Whitehall II Study
2005, Annals of Epidemiology
Citation Excerpt :
However, in women age was no longer significantly associated with plasma viscosity when menopausal status was included in the analysis, suggesting menopausal status was more important to plasma viscosity that age itself in the age range of this population. This finding disagrees with a previous report that change in menopausal status itself was not related to change in plasma viscosity (31). Our definition of menopausal status included an indicator for HRT use which is associated with plasma viscosity (32, 33) and may explain this finding.
To examine the social, biological, and metabolic associations of plasma viscosity in a large epidemiological study.
Plasma viscosity was measured from 4548 men and 1837 women that took part in the fifth phase of the Whitehall II Study (1997–1999). Employment grade was used as a measure of social position.
A strong inverse relation between employment grade and plasma viscosity was evident (p < 0.0001). This employment grade gradient was apparent overall, and among non-smokers and when participants with poor health were removed from the analyses. Plasma viscosity was associated with a number of biological factors that are themselves socially determined, including fibrinogen (p < 0.001), triglycerides (p < 0.001), fasting insulin (p < 0.001), and height (p < 0.001). Associations with smoking and alcohol intake were apparent in women. In men a U-shaped curve was apparent such that those drinking between 11 and 24 units/week had the lowest plasma viscosity. Alcohol intake, physical activity, and smoking explained 18% of the grade gradient in men and 40% in women while the biological factors examined accounted for 35% in men and 40% in women.
There is a grade gradient in plasma viscosity which was not fully explained by health related behaviors or measured risk factors for CHD. These data suggest that additional factors that contribute to the rheological properties of plasma may contribute to the explanation for social inequalities in cardiovascular disease.
Clinical hemorheology. Concept, pathophysiology and role in vascular diseases
2004, EMC - Cardiologie-Angeiologie
Il revient à A.L. Copley (1910–1992) d’avoir compris que le sang et la paroi des vaisseaux constituaient un organe unique, en ce sens que l’influence du contenu sur le contenant, objet de l’hémorhéologie, est déterminante. Sous l’effet de la pression motrice, le flux sanguin se dispose en lames concentriques (flux laminaire), développant une friction entre elles, ou shear stress, accentuée à la paroi fortement « cisaillée ». Au centre du vaisseau, où les lames sont moins individualisées, les hématies épousent les lames en se déformant longitudinalement rendant le sang fluide (viscosité basse). Dans tous les secteurs vasculaires où la pression diminue et le shear stress est faible, le sang est plus visqueux du fait de l’apparition de gros agrégats de globules rouges proportionnels au taux du fibrinogène (phénomène de thyxotropie, agrégation érythrocytaire), déréglant et diminuant le cisaillement de la paroi. Cet aspect biphasique du shear stress est caractéristique de la réactivité du flux sanguin vis-à-vis du vaisseau. L’exploration de la viscosité se fait par la viscosité plasmatique et du sang total et surtout la mesure du temps et des seuils de l’agrégation des hématies. La mécanotransduction du shear stress s’effectue par des récepteurs membranaires endothéliaux (caveoli, canaux ioniques, intégrines), puis par les systèmes des mitogen activated protein (MAP-kinases), enfin par des facteurs de transcription qui activent des zones spécifiques des promoteurs géniques. Aujourd’hui plus de 10 000 gènes sont connus pour être influencés par le shear. Au niveau des artères, le cisaillement assure la production du NO (oxyde nitrique), agent vasodilatateur et de la désactivation plaquettaire. La friction de la paroi endothéliale est souvent affaiblie, sous l’effet du flux pulsé et dans des zones situées aux embranchements. La sécrétion de NO est alors faible et les fonctions, sous-régulées par le shear stress, sont libérées, surtout l’adhésion-migration des leucocytes. Au niveau veineux la variation des cisaillements est encore plus variable, en particulier au niveau des valvules. La microcirculation fonctionne en unités fonctionnelles comportant un versant artériel précapillaire vasoactif, des capillaires dont le diamètre moyen est inférieur à celui des hématies et un versant veinulaire postcapillaire, à débit faible, où les shears stress sont bas. Les cellules endothéliales à ce niveau sont très actives pour l’adhésion-migration leucocytaire, l’inflammation et l’hémostase. L’athérosclérose a, comme point de départ, les zones où les monocytes macrophages pénètrent dans la paroi et véhiculent une grande partie des lipoprotéines constituant la plaque. L’hyperagrégation des hématies, consécutive aux facteurs de risque qui augmentent le fibrinogène, accentue les variations du shear à la paroi, ce qui active le récepteur des low density lipoprotein (LDL), accélère la formation des plaques et les étend aux gros troncs. L’artériopathie des membres inférieurs développe largement de tels troubles rhéologiques, actifs aussi sur l’ischémie. Il en est de même au cours du diabète, où s’ajoute l’effet des pics d’hyperglycémie, de la viscosité de l’HbA1C et des hématies glycatées, le tout étant actif sur la rétinopathie. Les accidents vasculaires cérébraux ischémiques sont accompagnés d’hyperagrégation des hématies influençant le pronostic, surtout chez les personnes âgées. L’accident vasculaire cérébral (AVC) lacunaire de Binswanger présente une forte hyperviscosité. Les troubles hémorhéologiques sont aggravants au cours de l’occlusion veineuse de la rétine, de la surdité brusque, des formes secondaires de la maladie de Raynaud. Ils sont déterminants au cours de l’insuffisance veineuse chronique, où ils contribuent à la croissance de la varice et à la genèse de l’ulcère, en facilitant l’adhésion-migration des leucocytes. L’hémodilution est proposée dans les épisodes aigus, surtout l’AVC. La restauration du débit (pontage), la lutte contre les facteurs de risque, la contention élastique et les traitements vasoactifs réduisent l’influence des troubles rhéologiques dans les maladies vasculaires.
The discovery that the blood and the vessel wall constitute a single organ, i.e, that the content definitely influences the container - which is the main object of the hoemorheology - is attributable to A.L. Copley (1910-1992). Due to driving forces, blood flow organizes itself as concentric layers (laminar flow) shearing over each other. Such a shear stress is stronger at the wall level than in the middle of the vessel, where layers are less distinct. Red cells deform and take the shape of layers, allowing blood to become fluid (low viscosity). In vascular areas with decreased pressure, thus lower shear stress, blood becomes more viscous due to the presence of huge red cell aggregates, in relation to fibrinogen level (thyxotropy, red cell aggregation), changing and decreasing the shearing at the wall level. Such a two-phase behaviour of the shear stress characterizes the blood flow reactivity toward the wall. As viscosity measurement consists of plasma and blood viscosity, time and threshold of erythrocyte aggregation appear more accurate determinants. The shear stress mechanotransduction involves endothelial membrane receptors (caveoli, ion channels, integrins), then MAP-kinases systems, and finally transcription factors able to bind specific areas in gene promoters. Over 10,000 shear-sensitive genes have been identified to date. In arteries the shear stress induces NO, which is vasoactive and inhibits platelets. The shearing power at the wall level or at branching zones is often poor, due to pulsations and picks, where subsequently NO production is low and shear-down-regulated functions can occur, mainly leukocyte adhesion and migration. In veins changes in shear are more frequent, particularly in valvulae. Microcirculation is implemented as functional units, exhibiting a vasoactive precapillary side, capillaries with diameters lower than those of red cells and a post capillary venous side with low output and very decreased shear stress. Endothelial cells are here very active for leukocyte adhesion, inflammation and haemostasis as well. Atherosclerosis stems from zones where monocytes-macrophages are able to enter the wall, bearing large amounts of lipoproteins, the main plaque constituent. As risk factors increase fibrinogen, high red cell aggregates change the wall shear stress and then LDL-receptors can be activated allowing plaques to grow up and extend along the arterial trunks. The occlusive arterial disease largely exhibits such rheological disorders, with subsequent actions on ischemia. The same is observed in diabetes, along with the addition of hyperglycemia picks, viscous HbA1c et glycation of red cells, adding worsened effect on retinopathy. Ischemic cerebral vascular accidents also exhibit high red cell aggregation making prognostic worse, mainly in elderly. Patients with lacunar CVA of Binswanger use to show a strong hyperviscosity. Haemorrhoeological disorders also worsen retinal vein occlusion, hearing loss, secondary forms of Raynaud’s disease. In chronic venous disease, they appear as contributory factors to the development of varicosities and ulcer genesis, for their facilitating action upon adhesion migration of leukocytes. Hemodilution is proposed during acute events, mainly in CVA. Flow restoration (bypass), prevention of risk factors, venous contention and venoactive drugs, are the opposing treatments of rheological disorders in vascular diseases.
The role of whole blood viscosity in premature coronary artery disease in women
2002, Atherosclerosis
Background: Impaired hemorheology has been demonstrated in atherosclerotic disease and has shown a relationship with classical risk factors. Blood viscosity (η), being the ratio of shear stress over shear rate, is an important parameter of hemorheology. In women with premature coronary artery disease (CAD), the underlying risk factors are a matter of debate and the role of whole blood viscosity in its pathogenesis has not been documented. Aim: To investigate the association of whole blood viscosity with premature CAD in women, with complaints suggestive of angina pectoris. Methods: Eighty-eight women (mean age 53 years) were divided into two groups, those with a high likelihood of CAD (LIKELI+) and those with a low likelihood of CAD (LIKELI−), based on medical history and technical investigations. Assessment of risk factors comprised smoking, diabetes mellitus, arterial hypertension, left ventricular hypertrophy (LVH), systolic and diastolic blood pressures, total low-density lipoprotein (LDL)- and high-density lipoprotein (HDL)-cholesterol, triglycerides, body mass index, menopause, hormone replacement therapy, uric acid and creatinine, and predicted 10-year cardiovascular risk according to the Framingham study was calculated. Whole blood viscosity was determined at 37 °C using a rotational cone-and-plate viscosimeter. Results: Baseline characteristics did not differ significantly between the groups except for antiplatelet therapy (P=0.001), prevalence of diabetes mellitus (P=0.002), predicted 10-year cardiovascular risk (P=0.007), essential hypertension (P=0.02), LVH (P=0.03) and smoking habits (P=0.04). LIKELI+ women had a significantly higher whole blood viscosity at all shear rates compared with LIKELI− women (P<0.05). All blood viscosities measured from 25 to 125 s⁻¹ were highly significantly (P<0.0001) correlated with $η_{250s^{−1}}$ . Univariate correlates with $η_{250s^{−1}}$ comprised triglycerides (P=0.006) and haematocrit (P=0.026). Binary logistic multivariate regression analysis for high likelihood of CAD revealed that only presence of arterial hypertension (P<0.0001) was predictive. Multiple regression analysis demonstrated that haematocrit (P=0.001) and likelihood of CAD (P=0.01) were the only significant determinants of $η_{250s^{−1}}$ . Conclusion: In this study, blood viscosity did not appear as an independent risk factor for the prediction of premature CAD in women. Viscosity may act as a marker of CAD or of classical risk factors.
Gender differences in wall shear - Mediated brachial artery vasoconstriction and vasodilation
2001, Journal of the American College of Cardiology
Citation Excerpt :
Because shear stress is dependent on both shear rate and fluid viscosity, an increase or decrease in either should cause parallel changes in arterial reactivity. The expected lower blood viscosity in women (31)may still induce lower shear stress, without changing the main results observed in the study. A final limitation of our study was the lack of provocative endothelium-independent vasodilation and constriction, because gender differences of the sensitivity of the vascular smooth muscle are another possible mechanism of shear-induced release of vasoactive substances.
OBJECTIVES
We sought to investigate wall shear rate (WSR) and brachial artery diameter (BAD) changes simultaneously and to determine whether any gender differences exist in arterial reactivity.
BACKGROUND
Wall shear rate/stress and arterial reactivity are rarely assessed at the same time. Furthermore, flow-mediated vasoconstriction has received less attention than flow-mediated vasodilation in humans.
METHODS
A new noninvasive evaluation of WSR in the brachial artery, using multigated, pulsed Doppler velocimeter and a double-transducer probe moved and fixed by a robotic system, was developed.
RESULTS
The validity of the system was tested in vitro with calibrated tubes and showed a high correlation (r = 0.98, p < 0.001). In 10 men and 10 women of similar age, induction of low and high shear rates by forearm occlusion produced significant vasoconstriction and vasodilation, respectively. The time lag for maximal BAD changes was 3 min for vasoconstriction and 1 min for vasodilation. A greater half-time for vasodilation (96 ± 6 for men and 86 ± 12 s for women) than for shear rate (31 ± 5 s for men and 34 ± 4 s for women) was observed after discontinuation of occlusion. Relative BAD was correlated with WSR changes, showing a significantly higher slope in women than in men (p < 0.01). Moreover, a larger normalized arterial diameter per shear rate was observed for vasoconstriction (p < 0.01) and vasodilation (p < 0.01) in women than in men.
CONCLUSIONS
Shear-mediated arterial vasodilation and vasoconstriction were more pronounced in women than in men, suggesting different gender-related sensitivity in the regulation of large-artery vascular tone.

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Research paperLongitudinal associations between plasma viscosity and cardiovascular risk factors in a middle-aged French population

Abstract

Lancet

J. Clin. Epidemiol.

Atherosclerosis

Lancet

Atherosclerosis

Lancet

Lancet

Atherosclerosis

Blood viscosity and cardiovascular disease

Thromb. Haemost.

Relation between extent of coronary artery disease and blood viscosity

Br. Med. J.

Fibrinogen as a risk factor for stroke and myocardial infarction

J. Engl. J. Med.

Plasma fibrinogen: A major coronary risk factor

J.R. Coll. Gen Pract.

Fibrinogen and risk of cardiovascular disease, The Framingham Study

J. Am. Med. Assoc.

Fibrinogen and arterial disease: The next stages

Fibrinogen, viscosity and white blood cell count are major risk factors for ischemic heart disease, The Caerphilly and Speedwell Collaborative Heart Disease Studies

Circulation

Epidemiological study on factor VII, factor VIII and fibrinogen in an industrial population — II Baseline data on the relation to blood pressure, blood glucose, uric acid, and lipid fractions

Thromb. Haemost.

Plasma fibrinogen and ischemic heart disease risk factors

Arterioscler. Thromb.

Menopause-related changes in lipoproteins and some other cardiovascular risk factors

Int. J. Epidemiol.

Gerinnungsphysiologische schnell-Methode zur bestimmung des Fibrinogens

Acta Haematol.

Research paper
Longitudinal associations between plasma viscosity and cardiovascular risk factors in a middle-aged French population