Plasma levels of marine n-3 fatty acids and cardiovascular risk markers in renal transplant recipients.

BACKGROUND/OBJECTIVES: Cardiovascular (CV) disease is the leading cause of death after renal transplantation. Marine n-3 polyunsaturated fatty acids (PUFAs) exert potential cardio-protective metabolic effects and might reduce CV morbidity and mortality in renal transplant recipients (RTRs). SUBJECTS/METHODS: In this cross-sectional study of 1990 Norwegian RTRs, transplanted between 1999 and 2011, associations between plasma phospholipid marine n-3 PUFA levels and various CV risk markers at 10 weeks after transplant were evaluated. RESULTS: Higher plasma marine n-3 PUFA levels were associated with lower resting heart rate (rHR), lower fasting plasma glucose (fPG) levels, lower plasma triglyceride levels and higher plasma high-density lipoprotein (HDL) cholesterol levels. Plasma levels of eicosapentaenoic acid, but not docosahexaenoic acid, showed a positive association with plasma HDL cholesterol levels. Plasma marine n-3 PUFA levels were not associated with plasma low-density lipoprotein cholesterol levels, pulse wave velocity or systolic and diastolic blood pressure. A negative association between plasma marine n-3 PUFA levels and CV mortality was weakened by additional adjustment for plasma triglyceride levels and rHR. The ratio of n-6 to n-3 PUFAs showed similar associations with CV risk markers as absolute plasma marine n-3 PUFA levels. CONCLUSIONS: This is the first study in RTRs showing that marine n-3 PUFAs are negatively associated with rHR and fPG in addition to beneficial effects on plasma HDL cholesterol and triglyceride levels. Especially, effects on autonomic nervous function and triglyceride metabolism might contribute to explain the lower CV mortality risk with higher plasma marine n-3 PUFA levels previously shown in this cohort.

No case of COX-1-related aspirin resistance found in 289 patients with symptoms of stable CHD remitted for coronary angiography.

OBJECTIVE: To assess the prevalence of a lacking aspirin effect on cyclooxygenase-1 (COX-1) ("aspirin resistance") in patients with symptomatic, stable coronary heart disease (CHD) using test methods directly reflecting inhibition of COX-1. MATERIAL AND METHODS: Arachidonic acid (AA)-induced platelet aggregation and plasma thromboxane B2 (TXB2) were determined twice 3 weeks apart - prior to elective coronary angiography - in 289 patients on 75 or 160 mg aspirin daily, all prompted to take aspirin before testing. Subjects who demonstrated lacking any effect of aspirin (>/=20 % AA-induced aggregation) on one or both occasions were later given a third test. Forty-two patients not taking aspirin were used as TXB2 controls. RESULTS: Eleven (3.8 %) had aggregation > or = 20 % in at least one of the two initial tests, but only two on both occasions. During the third test, all 11 patients had aggregation <20 %. The TXB2 distributions in controls and study patients differed markedly (mean 173 versus 19 pg/mL). Taking 45 pg/mL as the TXB2 cut-off level, sensitivity and specificity for detecting subjects taking aspirin were 90 % and 89 %, respectively. The area under the ROC curve was 0.96. CONCLUSION: Repeated AA-induced platelet aggregometry showed that COX-1 could be blocked by low-dose aspirin in all 289 tested patients, suggesting that aspirin resistance is rare in patients with stable CHD.