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      Altered Blood Rheology in Obstructive Sleep Apnea as a Mediator of Cardiovascular Risk


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          Background: Cardiovascular complications are common in patients with obstructive sleep apnea (OSA). Blood rheology is a major determent of coagulation and an established risk factor for cardiovascular events. Since nocturnal hypoxemia could influence parameters of blood rheology, we hypothesized that OSA alters blood rheology independent of other cardiovascular risk factors. Methods: One hundred and ten consecutive patients admitted to the sleep laboratory were included. The association of plasma fibrinogen and viscosity (as parameters of blood rheology) with OSA was evaluated. Results: One hundred and ten patients aged 61.4 ± 10.1 years (body mass index 28.4 ± 4.1 kg/m<sup>2</sup>) were included. OSA was confirmed in 63 patients (57.2%) with an apnea-hypopnea index (AHI) of 28.7 ± 14.9 events/hour. Patients with OSA showed higher levels of plasma viscosity (1.36 ± 0.09 vs. 1.31 ± 0.08 mPas, p = 0.005). Nevertheless, hypertensive apneics have even higher levels of plasma viscosity than nonapneics (1.38 ± 0.091 vs. 1.32 ± 0.028 mPas, p = 0.018). Similar results were found in patients with coronary artery disease, where OSA was associated with elevated plasma viscosity (1.36 ± 0.076 vs. 1.31 ± 0.081 mPas, p = 0.007). Plasma fibrinogen was correlated with nocturnal minimal oxygen saturation (r = –0275, p = 0.0036) and AHI (r = 0.297, p = 0.001). OSA was associated with higher plasma fibrinogen (353 ± 83 vs. 317 ± 62 mg/dl, p = 0.015). These differences persist with control for cardiovascular risk factors. Conclusions: Patients with OSA have elevated morning fibrinogen levels and a higher plasma viscosity, which correlate positively with indices of sleep apnea severity. These changes in blood rheology are independent of cardiovascular risk factors, and therefore, might be specific mechanisms of OSA. This supports the pathophysiological concept that sleep apnea is a cardiovascular risk factor.

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          Most cited references 8

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          Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group.

          Increased levels of certain hemostatic factors may play a part in the development of acute coronary syndromes and may be associated with an increased risk of coronary events in patients with angina pectoris. We conducted a prospective multicenter study of 3043 patients with angina pectoris who underwent coronary angiography and were followed for two years. Base-line measurements included the concentrations of selected hemostatic factors indicative of a thrombophilic state or endothelial injury. The results were analyzed in relation to the subsequent incidence of myocardial infarction or sudden coronary death. After adjustment for the extent of coronary artery disease and other risk factors, an increased incidence of myocardial infarction or sudden death was associated with higher base-line concentrations of fibrinogen (mean +/- SD, 3.28 +/- 0.74 g per liter in patients who subsequently had coronary events, as compared with 3.00 +/- 0.71 g per liter in those who did not; P = 0.01), von Willebrand factor antigen (138 +/- 49 percent vs. 125 +/- 49 percent, P = 0.05), and tissue plasminogen activator (t-PA) antigen (11.9 +/- 4.7 ng per milliliter vs. 10.0 +/- 4.2 ng per milliliter, P = 0.02). The concentration of C-reactive protein was also directly correlated with the incidence of coronary events (P = 0.05), except when we adjusted for the fibrinogen concentration. In patients with high serum cholesterol levels, the risk of coronary events rose with increasing levels of fibrinogen and C-reactive protein, but the risk remained low even given high serum cholesterol levels in the presence of low fibrinogen concentrations. In patients with angina pectoris, the levels of fibrinogen, von Willebrand factor antigen, and t-PA antigen are independent predictors of subsequent acute coronary syndromes. In addition, low fibrinogen concentrations characterize patients at low risk for coronary events despite increased serum cholesterol levels. Our data are consistent with a pathogenetic role of impaired fibrinolysis, endothelial-cell injury, and inflammatory activity in the progression of coronary artery disease.
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            Elevated C-reactive protein in patients with obstructive sleep apnea.

            Obstructive sleep apnea (OSA) has been increasingly linked to cardiovascular and cerebrovascular disease. Inflammatory processes associated with OSA may contribute to cardiovascular morbidity in these patients. We tested the hypothesis that OSA patients have increased plasma C-reactive protein (CRP). We studied 22 patients (18 males and 4 females) with newly diagnosed OSA, who were free of other diseases, had never been treated for OSA, and were taking no medications. We compared CRP measurements in these patients to measurements obtained in 20 control subjects (15 males and 5 females) who were matched for age and body mass index, and in whom occult OSA was excluded. Plasma CRP levels were significantly higher in patients with OSA than in controls (median [range] 0.33 [0.09 to 2.73] versus 0.09 [0.02 to 0.9] mg/dL, P<0.0003). In multivariate analysis, CRP levels were independently associated with OSA severity (F=6.8, P=0.032). OSA is associated with elevated levels of CRP, a marker of inflammation and of cardiovascular risk. The severity of OSA is proportional to the CRP level.
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              The possible role of hemorheology in atherothrombogenesis.

              Conventional risk factors predict only about 30-50% of incidental cases in cardiovascular diseases, which are still the leading cause of death in western societies. During the last decade, the importance of thrombosis as an essential mechanism in acute myocardial infarction (AMI) and stroke has been established. The introduction of thrombolysis has led to an impressive reduction in AMI case fatality and possibly also to a substantial amelioration of its prognosis. Evidence from experimental, clinical and epidemiological studies suggest, that several hemostatic and hemorheological factors (e.g., fibrinogen, Factor VII, plasma viscosity, hematocrit, red blood cell aggregation, total white cell count) might not only play an important role in the evolution of acute thrombotic events, but may also take part in the pathophysiology of atherosclerosis. An increasing number of studies reports altered hemostatic and hemorheological parameters to be associated with smoking, hyperlipoproteinemia, and high blood pressure, as well as with adverse dietary habits and other life-style factors. To date, their way of interaction with the atherosclerotic process is poorly understood. Hemorheological or hemostatic mechanisms that might promote thromboatherogenesis include the predisposition to thrombosis via a hypercoagulable state, the enhancement of atherosclerosis by fibrinogen and its metabolites, and finally the reduction of blood flow through various rheological effects (e.g., increase in plasma viscosity and red cell aggregation, or leukocyte activation). Future research should focus in more detail on the interrelationship between accepted risk factors and the hemostatic system as well as hemorheological parameters. Deeper insight into the mechanisms involved might lead to new preventive strategies as well as to therapeutic procedures in the management of atherosclerosis and associated thrombotic events.

                Author and article information

                S. Karger AG
                August 2005
                24 August 2005
                : 104
                : 2
                : 92-96
                Department of Cardiology, Pneumology and Angiology, Division of Internal Medicine, Heinrich Heine University, Düsseldorf, Germany
                86729 Cardiology 2005;104:92–96
                © 2005 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 1, References: 19, Pages: 5
                General Cardiology


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