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(Circulation. 2004;110:3617.)
© 2004 American Heart Association, Inc.
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
CHRONIC KIDNEY DISEASE, CARDIOVASCULAR RISK, AND RESPONSE TO ANGIOTENSIN-CONVERTING ENZYME INHIBITION AFTER MYOCARDIAL INFARCTION: THE SURVIVAL AND VENTRICULAR ENLARGEMENT (SAVE) STUDY, by Tokmakova et al.
It is well known that kidney disease portends increased cardiovascular mortality. This increased risk is likely to be largely due to hypertension, dyslipidemia, and anemia associated with kidney disease, but unknown factors contributing to plaque rupture also may play a role. ACE inhibitors have been shown to reduce the risk of myocardial infarction and death in patients with chronic kidney disease but often are not prescribed because of concerns about deterioration in kidney function. The SAVE investigators report, from their randomized study of captopril versus placebo in 2000 patients with ejection fractions <40% after acute myocardial infarction, that heightened cardiovascular risk occurred at a threshold of an estimated glomerular filtration rate (GFR) of 60 mL · min1 · 1.73 m2. Captopril tended to have a larger relative treatment effect and a greater absolute benefit in reducing the risk of cardiovascular events, including myocardial infarction, in patients with lower GFRs. Only 9 patients with GFRs <60 mL · min1 · 1.73 m2 needed to be treated for 31/2 years to reduce 1 cardiovascular event. See p 3667.
IMPAIRED L-ARGININE TRANSPORT AND ENDOTHELIAL FUNCTION IN HYPERTENSIVE AND GENETICALLY PREDISPOSED NORMOTENSIVE SUBJECTS, by Schlaich et al.
Prior studies have demonstrated dysfunction of the vascular endothelium in patients with hypertension, but the underlying mechanisms remain incompletely defined. In this regard, experimental studies have implicated impaired transport of L-arginine into endothelial cells, leading to an intracellular deficiency of the substrate for synthesis of nitric oxide. In this issue of Circulation, Schlaich and colleagues demonstrate impaired uptake of L-arginine in the forearm and into isolated blood monocytes
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