Abstract-Pulse pressure (PP), a marker of arterial stiffness, predicts cardiovascular risk. We aimed to determine whether augmentation pressure (AP) derived from the aortic pressure waveform predicts major adverse cardiovascular events (MACE) and death independently of PP in patients with established coronary artery disease (CAD). We prospectively followed-up 297 males undergoing coronary angiography for 1186Ϯ424 days. Ascending aortic pressure tracings obtained during catheterization were used to calculate AP (difference between the second and the first systolic peak). Augmentation index (AIx) was defined as AP as a percentage of PP. We evaluated whether AP and AIx can predict the risk of MACE (unstable angina, acute myocardial infarction, coronary revascularization, stroke, or death) and death using Cox regression. All models evaluating AP included PP to assess whether AP adds to the information already provided by PP. Both AP and AIx significantly predicted MACE.
We determined the prevalence of antibodies to the hepatitis C virus (anti-HCV) in 90 patients and 37 staff members of two hemodialysis units utilizing a recently developed anti-HCV recombinant based assay. Eleven patients (12%) were anti-HCV(+). Of these, eight (73%) had antibodies to the hepatitis B core antigen (anti-HBc) indicating prior hepatitis B infection; one patient was hepatitis B surface antigen (HBsAg)(+). All staff members were anti-HCV(-), although seven (19%) of them were anti-HBc(+). Alanine aminotransferase elevations were present at the time of the study in four anti-HCV(-) patients and in only one anti-HCV(+) patient. All anti-HCV(+) (mean 59 +/- 74; range 3 to 269 units) and 85% of anti-HCV(-) patients (mean 16 +/- 27; range 0 to 204 units) had received multiple blood transfusions (P = 0.348). Among 50 patients tested for human immunodeficiency virus (HIV), 43% of anti-HCV(+) as compared to only 7% anti-HCV(-) were positive (P = 0.003). There was a history of intravenous drug abuse (IVDA) in eight (72%) of the anti-HCV(+) patients and in only seven (9%) of the anti-HCV(-) group (P = 0.00001). The results of this serologic survey suggests that anti-HCV positivity is prevalent, although much less than anti-HBc, among our dialysis patients, whereas it was not detected among staff members. The prevalence rate of anti-HCV was statistically significantly higher among anti-HIV(+) and IVDA patients but not in multi-transfused patients.
Complement activation during exposure of plasma to cuprophan has been postulated to cause leukopenia and hypoxia in hemodialysis patients. To determine if hypoxia is related to leukopenia and if complement activation leads to a depletion of functional complement components, we dialyzed four patients three times sequentially against each of four types of membranes: cuprophan, regenerated cellulose, cellulose acetate, and polyacrilonitrile. Within 20 min there was a marked leukopenia with cuprophan from 5541 +/- 376 to 1216 +/- 94 (P less than 0.001) and with regenerated cellulose from 5541 +/- 411 to 1533 +/- 203 (P less than 0.001). With cellulose acetate, the change from 5558 +/- 400 to 3783 +/- 341 (P less than 0.001) was less dramatic, and with polyacrilonitrile the fall from 5591 +/- 381 to 464 +/- 401 (P less than 0.02) was minimal. After 2 and 4 hours of dialysis, a rebound leukocytosis was seen with cuprophan, regenerated cellulose, and cellulose acetate, but not with polyacrilonitrile. Transient thrombocytopenia occurred with cuprophan and regenerated cellulose. In spite of the variable degree of leukopenia, all membranes induced a similar and significant hypoxia, which was progressive throughout dialysis, even during the rebound leukocytosis. After 4 hours, the mean PO2 ranged from 91 to 93 mm Hg with all membranes. Functional hemolytic titers of whole complement, C3, C5, and C4 were normal prior to hemodialysis and failed to decrease after 4 hours with any membrane. It is concluded that hemodialysis leukopenia is membrane-dependent and is not the cause of hypoxia. In addition, hemodialysis complement activation does not lead to functional complement depletion and is of no clinical significance.
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