| pubmed-article:1451258 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1451258 | lifeskim:mentions | umls-concept:C0030705 | lld:lifeskim |
| pubmed-article:1451258 | lifeskim:mentions | umls-concept:C0014257 | lld:lifeskim |
| pubmed-article:1451258 | lifeskim:mentions | umls-concept:C0008031 | lld:lifeskim |
| pubmed-article:1451258 | lifeskim:mentions | umls-concept:C0205042 | lld:lifeskim |
| pubmed-article:1451258 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
| pubmed-article:1451258 | lifeskim:mentions | umls-concept:C0205307 | lld:lifeskim |
| pubmed-article:1451258 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:1451258 | pubmed:dateCreated | 1993-1-4 | lld:pubmed |
| pubmed-article:1451258 | pubmed:abstractText | A subgroup of patients with chest pain and angiographically normal epicardial coronary arteries have reduced dilator response to metabolic or pharmacological stimuli, but the mechanisms responsible for this reduced dilator response are unknown. In this study, we have investigated whether microvascular endothelial dysfunction is a cause of the observed reduced vasodilator reserve. | lld:pubmed |
| pubmed-article:1451258 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1451258 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1451258 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:1451258 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1451258 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1451258 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1451258 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:1451258 | pubmed:issn | 0009-7322 | lld:pubmed |
| pubmed-article:1451258 | pubmed:author | pubmed-author:EpsteinS ESE | lld:pubmed |
| pubmed-article:1451258 | pubmed:author | pubmed-author:QuyyumiA AAA | lld:pubmed |
| pubmed-article:1451258 | pubmed:author | pubmed-author:CannonR... | lld:pubmed |
| pubmed-article:1451258 | pubmed:author | pubmed-author:PanzaJ AJA | lld:pubmed |
| pubmed-article:1451258 | pubmed:author | pubmed-author:DiodatiJ GJG | lld:pubmed |
| pubmed-article:1451258 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1451258 | pubmed:volume | 86 | lld:pubmed |
| pubmed-article:1451258 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1451258 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1451258 | pubmed:pagination | 1864-71 | lld:pubmed |
| pubmed-article:1451258 | pubmed:dateRevised | 2010-3-24 | lld:pubmed |
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| pubmed-article:1451258 | pubmed:meshHeading | pubmed-meshheading:1451258-... | lld:pubmed |
| pubmed-article:1451258 | pubmed:meshHeading | pubmed-meshheading:1451258-... | lld:pubmed |
| pubmed-article:1451258 | pubmed:meshHeading | pubmed-meshheading:1451258-... | lld:pubmed |
| pubmed-article:1451258 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1451258 | pubmed:articleTitle | Endothelial dysfunction in patients with chest pain and normal coronary arteries. | lld:pubmed |
| pubmed-article:1451258 | pubmed:affiliation | Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. | lld:pubmed |
| pubmed-article:1451258 | pubmed:publicationType | Journal Article | lld:pubmed |
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