Abstract

In patients with a first anterior ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention, iron deficiency (ID) was associated with larger infarcts, more extensive microvascular obstruction, and higher frequency of adverse left ventricular remodeling as assessed by cardiac magnetic resonance imaging. In mice, an ID diet reduced the activity of the endothelial nitric oxide synthase/solubleguanylate cyclase/protein kinase G pathway in association with oxidative/nitrosative stress andincreased infarct size after transient coronary occlusion. Iron supplementation or administration ofansGCactivator before ischemia prevented the effects of the ID diet in mice. Not only iron excess,butalsoID, may have deleterious effects in the setting of ischemia and reperfusion.

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