Persons with atrial fibrillation are at increased risk of thromboembolic stroke; long-term antithrombotic therapy (warfarin sodium or aspirin) reduces this risk. Balanced against this benefit is the risk of antithrombotic-associated upper gastrointestinal (GI) tract bleeding complications. Thus, many physicians are reluctant to prescribe antithrombotic therapy to older patients with atrial fibrillation whom they deem at increased risk of major upper GI tract hemorrhage. Using Markov decision analytic modeling, this study determined how factors that increase the risk of major upper GI tract hemorrhage should influence the choice of antithrombotic therapy in older patients with atrial fibrillation. For 65-year-old patients with average risks of stroke and upper GI tract bleeding, warfarin therapy was associated with 12.2 quality-adjusted life-years (QALYs) per patient; aspirin therapy, 10.8 QALYs; and no antithrombotic therapy, 10.1 QALYs. For persons with significantly higher risks of upper GI tract bleeding and/or lower risks of stroke, warfarin was no longer clearly the optimal antithrombotic therapy (eg, for 80-year-old persons with a baseline risk of stroke of 4.3% per year and concurrently taking a conventional nonsteroidal anti-inflammatory drug: warfarin, 7.44 QALYs; aspirin, 7.39 QALYs; and no treatment, 7.21 QALYs). Thus, for older patients with atrial fibrillation and factors that place them at higher than average risk of upper GI tract bleeding, the optimal choice of antithrombotic therapy to prevent stroke can vary according to the magnitude of these risks. Clinicians can use the treatment recommendations of this study to provide rational stroke prevention therapy for older patients with atrial fibrillation.
Soumerai and colleagues report the results of an observational study regarding the use of thrombolytic agents in a large community population of patients with acute myocardial infarction. The findings suggest that thrombolytic use is associated with reduced mortality among eligible patients younger than 80 years, but increased mortality among the very old, even among those without relative or absolute contraindications to therapy. A substantial proportion of thrombolytic recipients in the study (38%) had relative and absolute contraindications to treatment, and this was strongly associated with an increased risk of mortality.
Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) stimulate bone formation in vitro and in rodents. Recent data from separate studies suggest that statins used in the treatment of hypercholesterolemia decrease fracture risk and increase bone mineral density (BMD). Current statin use and BMD were evaluated in 573 women (aged 50-95 years) with incident fracture and in a random sample of 802 women (aged 50-94 years) without incident fracture, drawn from the same community. There were 16 statin users in the fracture group and 53 in the nonfracture group. Unadjusted odds ratio (OR) for fracture associated with statin use was 0.40 (95% confidence interval [CI], 0.23-0.71). Adjusting for BMD at the femoral neck, spine, and whole body increased the OR to 0.45 (95% CI, 0.25-0.80), 0.42 (95% CI, 0.24-0.75), and 0.43 (95% CI, 0.24-0.78), respectively; adjusting for the potential confounders age, weight, dietary calcium intake, alcohol consumption, smoking, activity levels, and exposure to hormone replacement therapy, glucocorticoids, or calcium and/or vitamin D supplements had no effect on the OR. Statin use was associated with a 3% greater age- and weight-adjusted BMD at the femoral neck (P = .08), and BMD tended to be greater but did not achieve statistical significance at the spine and whole body. Results suggest that increases in BMD associated with statin use are small and may be insufficient to account for the observed 60% reduction in fracture risk. Unless confounded by unrecognized factors, statin use is associated with substantial protection against fracture, but the mechanisms of action remain unclear.
In This Issue of Archives of Internal Medicine. Arch Intern Med. 2002;162(5):505. doi:10.1001/archinte.162.5.505