Search

Background Tranexamic acid reduces blood loss and transfusion requirements in cardiac surgery but may increase the risk of coronary graft thrombosis. We previously reported the 30-day results of a trial evaluating tranexamic acid for coronary artery surgery. Here we report the 1-year clinical outcomes. Methods Using a factorial design, we randomly assigned patients undergoing coronary artery surgery to receive aspirin or placebo and tranexamic acid or placebo. The results of the tranexamic acid comparison are reported here. The primary 1-year outcome was death or severe disability, the latter defined as living with a modified Katz activities of daily living score of less than 8. Secondary outcomes included a composite of myocardial infarction, stroke, and death from any cause through to 1 year after surgery. Results The rate of death or disability at 1 year was 3.8% in the tranexamic acid group and 4.4% in the placebo group (relative risk, 0.85; 95% confidence interval, 0.64-1.13; P = .27), and this did not significantly differ according to aspirin exposure at the time of surgery (interaction P = .073). The composite rate of myocardial infarction, stroke, and death up to 1 year after surgery was 14.3% in the tranexamic acid group and 16.4% in the placebo group (relative risk, 0.87; 95% CI, 0.76-1.00; P = .053). Conclusions In this trial of patients having coronary artery surgery, tranexamic acid did not affect death or severe disability through to 1 year after surgery. Further work should be done to explore possible beneficial effects on late cardiovascular events.

Studies in explanted hearts from patients supported with a left ventricular assist device (LVAD) suggest that no or a less pronounced reverse remodeling process occurs in the right ventricle (RV) during LVAD support. The intermediate-term functional changes in RV function in patients with refractory heart failure (HF) supported with a continuous LVAD are not well characterized.Serial transthoracic echocardiograms and simultaneous measurements of biochemical surrogates of disease severity and organ perfusion were obtained in 20 patients (aged 57 +/- 17 years) with refractory HF before and after implantation of a continuous-flow LVAD (VentrAssist, Ventracor Ltd, Chatswood, Australia).After a median (interquartile range) follow-up of 140 days (34-367 days), RV diameter was reduced (36 +/- 7 vs 33 +/- 4 mm; p = 0.04), as was right atrial area (27 +/- 5 vs 24 +/- 6 cm(2); p = .04). There was a trend toward a reduction in tricuspid annulus plane systolic excursion (14 +/- 6 vs 13 +/- 5 mm; p = .05). RV fractional area change (26% +/- 13% vs 27% +/- 10%; p = .53) and global RV dysfunction graded visually using a scale from 0 (absent) to 3 (severe dysfunction) did not change from pre-implant to follow-up (2 [1-2] vs 1.5 [0.5-2]; p = .18). The degree of global RV dysfunction at follow-up was closely related to the degree of RV dysfunction at the pre-implant study (r = 0.69; p = .001). Changes in global RV dysfunction were inversely related to changes in glomerular filtration rate (r = -0.49; p = .03).During continuous-flow LVAD support, pre-existing RV dysfunction does not worsen in the intermediate term.

In the present study, peripheral blood mononuclear cells (PBMCs) were obtained from HIV+ subjects as well as cardiac transplant recipients, and the presence of A- and B-type Epstein-Barr virus (EBV) was determined using the polymerase chain reaction (PCR). Of the HIV+ patients studied, 24% were found to be infected with A-type EBV, 27% with B-type EBV, and 39% with both A and B virus types. Analysis of PBMCs from cardiac transplant recipients revealed that 39% were infected with A-type EBV, 33% with B-type EBV, and 28% with both EBV types. These results demonstrate a higher prevalence of infection with B-type EBV in HIV+ patients, than had been found previously by an analysis of spontaneously generated lymphoblastoid cell lines. The data indicated that it is not HIV per se which is responsible for the high incidence of B-type EBV in HIV+ individuals.