Levels of Lipoprotein (a) in patients with coronary artery disease with and without inflammatory rheumatic disease: a cross-sectional study.

OBJECTIVES: Patients with various inflammatory rheumatic diseases (IRDs) have increased risk of atherothrombotic disease. Lipoprotein (a) (Lp(a)) is a risk factor for atherosclerosis but its role in IRD with accompanying coronary artery disease (CAD) is still unclear. We aimed to examine if serum Lp(a) levels differed between CAD patients with and without accompanying IRD. DESIGN: A cross-sectional observational, patient-based cohort study. SETTING: Referred centre for coronary artery bypass grafting in the South Eastern part of Norway. PARTICIPANTS: 67 CAD patients with IRD (CAD/IRD) and 52 CAD patients without IRD (CAD/non-IRD). All patients were Caucasians, aged >18 years, without any clinically significant infection or malignancy. METHODS: Lp(a) levels in serum were analysed by particle enhanced immunoturbidimetric assay, and Lp(a) levels were related to clinical and biochemical characteristics of the patient population. RESULTS: We found no differences in serum levels of Lp(a) between CAD patients with and without IRD. In general, we found that Lp(a) correlated poorly with clinical and biochemical parameters including C reactive protein with the same pattern in the CAD/non-IRD and CAD/IRD groups. CONCLUSIONS: Our data do not support a link between inflammation and Lp(a) levels in CAD and in general Lp(a) levels were not correlated with other risk factors for cardiovascular disease.

Early coagulopathy in patients with ruptured abdominal aortic aneurysm.

Ruptured abdominal aortic aneurysm (AAA) is associated with a high mortality despite surgical management. Earlier reports indicate that a major cause of immediate intraoperative death in patients with ruptured AAA is related to hemorrhage due to coagulopathy. Acidosis is, besides hypothermia and hemodilution, a possible cause of coagulopathy. The aim of the present study was to investigate the incidence of coagulopathy and acidosis preoperatively in patients with ruptured AAA in relation to the clinical outcome with special regard to the influence of shock. For this purpose, 95 consecutive patients who underwent surgery for AAA (43 ruptured with shock, 12 ruptured without shock, and 40 nonruptured) were included. Coagulopathy was defined as prothrombin time (international normalized ratio [INR]) ≥1.5 and acidosis was defined as base deficit ≥6 mmol/L. Mortality and postoperative complications were recorded. The present study shows a state of acidosis at the start of surgery in 30 of 55 patients with ruptured AAA. However, only in 7 of 55 patients with ruptured AAA a state of preoperative coagulopathy was demonstrated. Furthermore, in our patients with shock due to ruptured AAA only 2 of 12 deaths were due to coagulopathy and bleeding. Indeed, our results show a relatively high incidence of thrombosis-related causes of death in patients with ruptured AAA, indicating a relation to an activated coagulation in these patients. These findings indicate that modern emergency management of ruptured AAA has improved in the attempt to prevent fatal coagulopathy.