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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions |
umls-concept:C0012373,
umls-concept:C0019010,
umls-concept:C0028066,
umls-concept:C0030705,
umls-concept:C0151814,
umls-concept:C0205373,
umls-concept:C0205374,
umls-concept:C0475224,
umls-concept:C0871261,
umls-concept:C1280500,
umls-concept:C1522318,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2911692
|
| pubmed:issue |
1
|
| pubmed:dateCreated |
1990-2-14
|
| pubmed:abstractText |
Diltiazem and nifedipine improve coronary blood flow and reduce peripheral determinants of myocardial oxygen demand through activation of similar but distinct cellular mechanisms. To identify differences during myocardial ischemia, systemic and coronary hemodynamics were measured continuously before and during brief periods of left anterior descending coronary balloon occlusion in 23 patients undergoing single-vessel angioplasty. Data were compared for two matched ischemic periods, one control and one "drug" period. In 13 patients, diltiazem, 10 mg (intravenous bolus with continuous 500 mg/min infusion), was given; in 10 patients, nifedipine, 10 mg sublingual, was given and after 15 minutes, ischemia was reinduced. Both drugs significantly reduced systolic and mean arterial pressure (for diltiazem, 108 +/- 15 to 93 +/- 10 mm Hg; and for nifedipine, 117 +/- 20 to 96 +/- 8 mm Hg, both p less than 0.01). Diltiazem significantly reduced heart rate-pressure product (with heart rate unchanged), while both drugs maintained the resting great vein blood flow (for diltiazem, 97 +/- 25 to 91 +/- 34 ml/min; for nifedipine, 115 +/- 49 to 98 +/- 58 ml/min, p = ns) with reduced arterial pressure. Coronary flow during occlusion was unchanged (for control versus diltiazem, 63 +/- 21 versus 59 +/- 14 ml/min; for nifedipine, 66 +/- 33 versus 73 +/- 38 ml/min, both p = ns). Neither drug improved collateral hemodynamics or resistance index during ischemia. Both diltiazem and nifedipine prolonged the time to ischemic ST segment alteration (for diltiazem, 27 +/- 10 to 40 +/- 16 seconds, p less than 0.05; for nifedipine, 24 +/- 14 to 38 +/- 14 seconds, p = ns) during transient coronary occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jan
|
| pubmed:issn |
0002-8703
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
119
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
47-54
|
| pubmed:dateRevised |
2010-11-18
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| pubmed:meshHeading |
pubmed-meshheading:2296873-Angiography,
pubmed-meshheading:2296873-Balloon Dilation,
pubmed-meshheading:2296873-Collateral Circulation,
pubmed-meshheading:2296873-Coronary Circulation,
pubmed-meshheading:2296873-Coronary Disease,
pubmed-meshheading:2296873-Diltiazem,
pubmed-meshheading:2296873-Electrocardiography,
pubmed-meshheading:2296873-Hemodynamics,
pubmed-meshheading:2296873-Humans,
pubmed-meshheading:2296873-Nifedipine,
pubmed-meshheading:2296873-Vascular Resistance
|
| pubmed:year |
1990
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| pubmed:articleTitle |
Effects of diltiazem and nifedipine on systemic and coronary hemodynamics and ischemic responses during transient coronary artery occlusion in patients.
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| pubmed:affiliation |
Department of Cardiology, St. Louis University School of Medicine, MO.
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| pubmed:publicationType |
Journal Article
|