SUMMARY BackgroundTemporal changes in the incidence of cause-specific gastrointestinal (GI) complications may be one of the factors underlying changing medical practice patterns.

Stiffness of aortic walls has been shown to be a marker of coronary and cerebrovascular diseases in patients with myocardial infarction or stroke. However, its value for predicting preclinical atherosclerosis has not been demonstrated. Therefore, this study tested the association of aortic wall stiffness and coronary and extracoronary atherosclerosis in the absence of clinical cardiovascular disease. In 190 asymptomatic men at cardiovascular risk, carotid-to-femoral pulse wave velocity (PWV) was measured mechanographically and the compliance of the aorta (C), as well as the intrinsic compliance (Ci), was deduced after correction for the effect of blood pressure. Also determined noninvasively were 1) the degree of coronary calcium deposit coded as grade 0, 1, 2, or 3 using ultrafast computed tomography; 2) the extent of extracoronary plaque detected by B-mode echography at three different sites (carotid, abdominal aorta, and femoral) coded as 0, 1, 2, or 3 diseased sites; and 3) the estimated Framingham coronary risk. The grade of coronary calcium was not associated with any aortic elastic parameter. The number of extracoronary diseased sites was not associated with PWV and C but correlated negatively with Ci before but not after age adjustment. The coronary risk correlated positively with PWV and negatively with C before but not after age adjustment and was not associated with Ci. In symptom-free subjects aortic stiffening does not predict the presence of coronary and extracoronary atheroma and therefore cannot be considered as a useful surrogate marker of early atherosclerosis.

Recent studies have suggested that rheological mechanisms may be involved in the pathogenesis of ischemic syndromes in hyperlipidemias. We investigated the association between erythrocyte aggregation and components of lipoproteins in the blood of 60 normotensive, hypercholesterolemic men aged 45±8 years. The rheological parameters assessed were aggregation index (AI) and disaggregation shear rate threshold (yt) as determined by laser reflectometry, plasma fibrinogen, total serum protein, and hematocrit. The lipoprotein variables included total cholesterol, triglycerides, highdensity lipoprotein (HDL) cholesterol and its subfractions HDL 2 cholesterol and HDL3 cholesterol, apolipoprotein (apo) B, apoA-I, HDL particles containing apoA-I without apoA-II (LpA-I), and HDL particles containing both apoA-I and apoA-II (LpA-I/A-II). Covariables considered for possible confounding effects were age, body mass index, and smoking behavior. Fibrinogen, total serum protein, and both aggregation parameters (AI and yt) were elevated in this hypercholesterolemic population. Univariate analysis showed that both T he fluidity of blood plays an important role in the physiological behavior of the circulation, and its alteration might promote cardiovascular complications in situations associated with low-flow states. 1In this condition red blood cells (RBCs) aggregate due to the increase in the bridging force of high-molecularweight plasma proteins.12 Among these proteins, some are considered to be cardiovascular risk markers (eg, lipoproteins, fibrinogen) and are associated with increased plasma and whole-blood viscosity.313 Associations between rheology and components of lipoproteins in human blood are reported. Studies in patients with various forms of hyperlipoproteinemia show a concentration-dependent increase in plasma viscosity for lowdensity lipoprotein cholesterol (LDL-C) and chylomicrons and hence, for total triglycerides. 9 ' 10 These earlier studies are in line with the positive linear correlation of plasma viscosity with total cholesterol and apolipoprotein (apo) A-II and apoB observed in a recent study. 11Moreover, both blood viscosity 11 and erythrocyte aggregation 12 are negatively related to high-density lipoprotein cholesterol (HDL-C) concentration, which is known to be inversely correlated with coronary heart disease risk. 14 Furthermore, HDL may also be separated according to apolipoprotein composition, leading to at least two species of particles: LpA-I, which contains apoA-I without apoA-II, and LpA-I/A-II, which contains both apoA-I and apoA-II. 15 These heterogeneous HDL subfractions seem to have distinct metabolic roles, but the specific effect of one or another particle on the atherosclerotic process remains unclear. 1621 In the present study we investigated the relation of lipoprotein components, and especially HDL subfractions, to the aggregation and disaggregation of RBCs in a population of asymptomatic, hypercholesterolemic, normotriglyceridemic, normotensive subjects. Methods Selection of Su...