Increased erythrocyte adhesiveness and aggregation in obstructive sleep apnea syndrome.

BACKGROUND: Obstructive sleep apnea (OSA) is associated with an increased incidence of stroke and myocardial infarction as well as increased prothrombotic and inflammatory processes. Although erythrocyte adhesiveness/aggregation is known to be elevated in cardiovascular diseases, it has never been evaluated in OSA. The aim of this study was to examine the possible association of OSA and erythrocyte adhesiveness/aggregation. METHODS: The study was conducted in the Sleep Laboratory of a tertiary university-affiliated medical center in 79 patients (age 57.1+/-12.9 years) with a diagnosis of OSA (apnea hypopnea index 41.2+/-25.9). Findings were compared with data on 1079 controls without clinical symptoms of OSA, matched for sex, age, and body mass index. Overnight polysomnography and blood sampling for erythrocyte sedimentation rate, levels of fibrinogen, high-sensitivity C-reactive protein, and erythrocyte adhesion/aggregation test consisting of measures of erythrocyte percentage and vacuum range on image analysis. RESULTS: The study group had significantly higher values than controls of all three markers of inflammation (p<0.001 for erythrocyte sedimentation rate and fibrinogen; p=0.037 for C-reactive protein). Erythrocyte percentage was significantly lower in the sleep apnea group (84.05+/-15.97 vs. 90.79+/-11.23%, p<0.001), and vacuum range was significantly higher (8.22+/-7.98 vs. 4.63+/-4.05 microm, p<0.001), indicating stronger erythrocyte adhesion/aggregation. Both these factors were significantly correlated with erythrocyte sedimentation rate and to hs-CRP (percentage: r=-0.630; 0.258, p=0.005; 0.031; vacuum range: r=0.494; -0.328, p=0.001; 0.005 respectively). CONCLUSION: OSA is associated with increased erythrocyte aggregation/adhesion, which is correlated with an increase in inflammation markers. These findings might help explain the increased cardiovascular morbidity in OSA.

Pregnancy-induced hypertension is associated with elevation of aggregability of red blood cells.

In order to differentiate between the contributions of cellular and plasmatic factors to the elevated aggregation in pregnancy-induced hypertension (PIH), we determined RBC aggregation in autologous plasma and in plasma-free medium. The aggregation was determined as a function of shear stress, to evaluate the strength of the intercellular interaction. These procedures were applied to RBC from PIH women (n=20), normotensive pregnant (NTP) women (n=15), and non-pregnant (control) women (n=15). The average aggregate size (AAS) in plasma for PIH, NTP and control RBC was 38.7+/-3.2, 28.4+/-3.0, and 11.5+/-2.2 (P<0.05, between the three groups), respectively. For the same groups, the aggregation in plasma-free standard medium was 17.3+/-2.0, 12.0+/-1.2 and 10.0+/-1.6 (P<0.05 between PIH and the other two groups), respectively. The contribution of plasma to the elevated aggregation was 75% and 88% for PIH and NTP respectively. Tau(S50), the shear stress required to singly disperse 50% of the RBC population, in plasma and in standard medium, was about the same for PIH and NTP, and both were markedly higher than that for control RBC. These findings suggest that the increased aggregation of RBC from women with PIH, over those at of NTP women, may be due largely to changes in cellular factors and the increased aggregability has the potential to affect blood flow mainly in low-flow states such as in the placental intervillous space.