Bleeding post coronary artery bypass surgery. Clopidogrel--cure or culprit?

BACKGROUND: Clopidogrel, in addition to aspirin, has become a common treatment of acute coronary syndrome and for stent thrombosis prevention, when given before percutaneous transluminal coronary angioplasty. However, some patients turn out to have surgical coronary artery disease and are sent for coronary artery bypass grafting (CABG) where the irreversible effect of aspirin and clopidogrel on platelet function becomes a concern. This study was conducted to evaluate the role of preoperative use of clopidogrel in bleeding complications after CABG. MATERIAL AND METHODS: A total of 462 patients who underwent CABG between 2001 and 2003 were studied as a retrospective cohort. Comparison was made between patients who had taken clopidogrel within 7 days of surgery (n=162), and those who were not exposed to clopidogrel (n=300). Chest tube output and bleeding index (a modified TIMI criteria), were the primary outcomes measured. RESULTS: Our data showed that patients taking clopidogrel within 7 days of surgery have a higher bleeding index than those who were not exposed to the drug (p = 0.024). Similarly, chest tube output was significantly higher in those who were exposed to clopidogrel within 7 days compared to those not taking clopidogrel (p = 0.01). To further dissect this relationship, we divided our population into three categories. We found that patients taking clopidogrel within 3 days prior to CABG (immediate exposure) have a higher bleeding index and TIMI major bleeding than either patients taking the drug between 3 and 7 days (recent exposure) or patients not exposed to clopidogrel at all (p = 0.009 and 0.03 respectively for inter-groups comparison). The same was true for chest tube output (p = 0.05 and 0.01 respectively). CONCLUSION: Clopidogrel increased the risk of post-CABG bleeding if taken within three days prior to surgery but not if taken before that.

Cardiovascular disease in renal allograft recipients is associated with elevated sialic acid or markers of inflammation.

BACKGROUND: Cardiovascular disease (CVD) is more common in patients with renal failure, even after renal transplantation. We wished to examine the relationship between markers of inflammation and CVD in stable renal transplant patients. METHODS: Ninety stable renal transplant outpatients with no recent illnesses or rejection were invited for study. Blood was drawn for a variety of inflammatory markers including total plasma sialic acid (SA) levels. RESULTS: Patients with CVD were significantly older than patients without (54 +/- 12 vs. 42 +/- 14 yr, p < 0.01) and had significantly lower total cholesterol (4.5 +/- 1.6 vs. 5.1 +/- 1.0 mmol/L, p < 0.01). Time from transplantation, present creatinine and blood pressure, smoking history were similar in both groups. Patients with CVD had significantly higher levels of SA (89.2 +/- 22.3 vs. 77.4 +/- 13.9 mg/dL, p = 0.01); fibrinogen [4.6 (2.2-6.7) vs. 3.6(1.9-5.7) g/L; p = 0.05); and C-reactive protein (CRP) [2.2 (1.5-8.0) vs 1.5 (0.7-3.0) microg/dL] than those without CVD. A logistic multiple linear regression analysis of the data with CVD as the dependent variable, and all the other parameters as independent variables, showed significant associations (F = 16.9; p < 0.001) with diastolic blood pressure (beta = 5.6; p = 0.02) and CRP (beta = 4.4; p = 0.04). CONCLUSIONS: This study suggests that inflammation is associated with a higher prevalence of cardiovascular disease in patients with renal allografts. The measurement of sialic acid as a risk factor may be superior to that of CRP in this group as its concentration is independent of renal function.

Cerivastatin monotherapy-induced muscle weakness, rhabdomyolysis and acute renal failure.

Statins are now widely prescribed and without doubt save many lives. However there are rare potentially serious side-effects, including acute renal failure. Patient education and physician vigilence are vital.

Page kidney--a review of the literature.

Page kidney was first described in animal experiments in 1939. In the 1950s and 1960s the human counterpart became evident. In this review we examine the modest literature on this rare but important renal/urological complication, summarize the clinical features, and discuss the best approach to diagnosis and management.