Omega-3 fatty acids plus rosuvastatin improves endothelial function in South Asians with dyslipidemia.

BACKGROUND: The present study was undertaken to investigate the effect of statins plus omega-3 polyunsaturated fatty acids (PUFAs) on endothelial function and lipid profile in South Asians with dyslipidemia and endothelial dysfunction, a population at high risk for premature coronary artery disease. METHODS: Thirty subjects were randomized to rosuvastatin 10 mg and omega-3-PUFAs 4 g or rosuvastatin 10 mg. After 4 weeks, omega-3-PUFAs were removed from the first group and added to subjects in the second group. All subjects underwent baseline, 4-, and 8-week assessment of endothelial function and lipid profile. RESULTS: Compared to baseline, omega-3-PUFAs plus rosuvastatin improved endothelial-dependent vasodilation (EDV: -1.42% to 11.36%, p = 0.001), and endothelial-independent vasodilation (EIV: 3.4% to 17.37%, p = 0.002). These effects were lost when omega-3-PUFAs were removed (EDV: 11.36% to 0.59%, p = 0.003). In the second group, rosuvastatin alone failed to improve both EDV and EIV compared to baseline. However, adding omega-3-PUFAs to rosuvastatin, significantly improved EDV (-0.66% to 14.73%, p = 0.001) and EIV (11.02% to 24.5%, p = 0.001). Addition of omega-3-PUFAs further improved the lipid profile (triglycerides 139 to 91 mg/dl, p = 0.006, low-density lipoprotein cholesterol 116 to 88 mg/dl, p = 0.014). CONCLUSIONS: Combined therapy with omega-3-PUFAs and rosuvastatin improves endothelial function in South Asian subjects with dyslipidemia and endothelial dysfunction.

Contrast-associated nephropathy.

Contrast-associated nephropathy (CaN) has become a major cause of iatrogenic acute renal failure, especially with the increasing use of radiographic contrast media in both diagnostic and interventional procedures. CaN is the third most common cause of iatrogenic acute renal failure, and is associated with increased morbidity and in-hospital mortality. CaN typically presents as an acute rise in serum creatinine levels, usually within 48 hours after exposure to contrast media. Renal medullary ischemia secondary to contrast-induced vasoconstriction is now believed to be the most likely cause of CaN, although direct renal tubular cytotoxicity does appear to play a role. The occurrence of CaN is directly related to the number of coexisting clinical risk factors. Among the many risk factors, preexisting renal impairment, the presence of diabetes mellitus and the volume of the contrast agent administered are the most important. The most effective means of reducing the incidence of CaN is through prevention, by first identifying the risk factors and then attempting to correct for them before the administration of contrast material. Although the earliest and most well-tested preventive measure, namely intravenous hydration, continues to be the most effective way to prevent CaN, recent studies have provided many new preventive modalities. The growing use of these new agents, such as acetylcysteine, endothelin blockers, and most recently fenoldopam, has increased the options available for the prevention of CaN.