Low-dose aspirin and rupture of abdominal aortic aneurysm.

OBJECTIVE: The use of low-dose aspirin (acetylsalicylic acid [ASA]) has been suggested to attenuate growth of abdominal aortic aneurysms (AAAs), yet solid clinical evidence of this hypothesis is still missing. This study aimed to investigate whether preadmission ASA use influenced the risk of presenting with rupture of AAA (rAAA) on hospital admission and subsequent 30-day case fatality. METHODS: There were 4010 patients with an incident diagnosis of rAAA and 4010 age- and sex-matched AAA patients identified in the Danish National Registry of Patients. Data on comorbidity, concomitant drug use, primary health care utilization, socioeconomic status, and vital status were obtained from nationwide health care and administrative registries. RESULTS: Preadmission ASA use was identified for 1815 (45.3%) rAAA patients and 2111 (52.6%) AAA patients, corresponding to a crude odds ratio for rAAA in ASA users of 0.72 (95% confidence interval [CI], 0.66-0.79) compared with nonusers. However, after adjustment for possible confounders, no association between ASA use and the risk of rAAA was found (adjusted odds ratio, 0.97; 95% CI, 0.86-1.08). The aggregated 30-day rAAA case-fatality rate for users of ASA was 66.0% compared with 56.9% for nonusers, corresponding to an adjusted mortality rate ratio of 1.16 (95% CI, 1.06-1.27). CONCLUSIONS: Preadmission ASA use is not associated with an altered risk of AAA rupture but seems to be associated with a worse prognosis after rupture of AAA.

Risk factors for mortality and ischemic heart disease in patients with long-term type 1 diabetes.

AIMS: The purpose of this study is to evaluate the effect of glycemic regulation, dyslipidemia, and renal dysfunction on mortality (all-cause and cardiovascular) and ischemic heart disease (IHD) in a long-term follow-up of a population-based cohort of Danish type 1 diabetic patients with at least 20 years of diabetes. METHODS: A population-based cohort of type 1 diabetic patients was identified as of July 1, 1973 (n=727). In 1993 to 1996, the cohort was reassessed and baseline data were collected from blood and urine samples in 389 patients. Mean (glycemic regulation and lipids) and highest values (creatinine and albuminuria) of the baseline period were used to predict mortality and IHD between baseline and 2006. Data of mortality and morbidity were provided by the Danish Civil Registration System, the Danish Causes of Death Registry, and the Danish National Patient Registry. RESULTS: At the follow-up in 2006, 256 patients (65.8%) were still alive. In a statistical model adjusted for age, sex and duration of diabetes, the following parameters were related to all-cause mortality and cardiovascular mortality: glycemic regulation, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (inversely), total cholesterol, creatinine, and macroalbuminuria. Furthermore, all markers except macroalbuminuria were associated with IHD. Microalbuminuria at baseline was not related to any of the endpoints. CONCLUSIONS: Glycemic regulation, dyslipidemia, and renal dysfunction were all related to mortality and IHD in a 13-year follow-up of long-term Danish type 1 diabetic patients. These results underscore the better outcome for tightly regulated type 1 diabetic patients, even in long-term survivors.