Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in coronary arterial size due to ergonovine maleate are described and quantitated in 90 patients--18 with typical angina pectoris, 56 with atypical chest pain, nine with variant angina pectoris, and seven heart transplant (allograft) recipients. We observed two angiographic changes in the diameter of coronary arteries: 1) spasm, which was characterized by occlusion or marked (greater than 85%) focal or diffuse vessel narrowing, or 2) relatively mild and diffuse vessel narrowing, which was interpreted as the normal pharmacologic response to the drug. Serial bolus injections of 0.05 mg, 0.10 mg and 0.25 mg of ergonovine maleate produced diffuse narrowing of the diameter of coronary arteries of 10 +/- 1.5%, 16 +/- 1.4% and 20 +/- 1.3% (mean +/- SEM), respectively, in the 72 patients with anginal syndromes who did not develop coronary spasm. The degree of coronary arterial narrowing was the same in heart transplant recipients and in patients with normally innervated hearts who did not develop coronary spasm. We believe the normal pharmacologic response to ergonovine maleate was due to a direct vasoconstrictor action of the drug; this action was independent of neural control extrinsic to the heart.
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PMID:The effects of ergonovine maleate on coronary arterial size. 75 27

M-mode echocardiograms were recorded in 12 patients with Prinzmetal's angina during 29 episodes of transient myocardial ischemia at rest (18 spontaneous and 11 ergonovine-induced). At peak ST segment elevation a regional mechanical impairment was observed in the interventricular septum during 23 episodes of angina and in the posterior wall during six episodes. In the 18 spontaneous episodes the left ventricular ischemic wall, when compared to the basal state, was found to have a significant reduction in motion (-76.3 +/- 9.1%) (mean +/- SEM), in diastolic thickness (-11.7 +/- 2.5%), and in percent systolic thickening (-88.0 +/- 5.6%). Increase in left ventricular end-diastolic diameter (+13.1 +/- 2.1%) and decrease in percent fractional shortening (-38.1 +/- 3.7%) were also observed. When ST segment was back to the isoelectric line, a transient overshoot in regional left ventricular function was observed. In induced episodes statistically significant changes could be detected by M-mode echocardiography even before appearance of ST segment elevation and anginal pain. No significant difference was found in type or degree of mechanical impairment between induced and spontaneous episodes. Therefore, in patients with Prinzmetal's angina: (1) M-mode echocardiography allows detection of mechanical changes due to transient myocardial ischemia; and (2) mechanical impairment occurs earlier than clinical (pain) and electrocardiographic (ST segment elevation) signs of transmural ischemia.
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PMID:Transient changes in left ventricular mechanics during attacks of Prinzmetal's angina: an M-mode echocardiographic study. 669 89

To evaluate whether the flow-mediated vasodilation and coronary flow reserve are impaired or not in patients with vasospastic angina (VA), we measured the changes of epicardial coronary artery diameter and flow reserve in spasm related-left anterior descending coronary artery (LAD). The flow mediated-response of epicardial coronary arteries in 15 VA were compared with 15 controls. Using quantitative coronary angiography, we measured the diameter of proximal (pLAD) and middle segment (mid-LAD) of LAD under baseline conditions, during increased blood flow after distal adenosine injection and after proximal administration of nitroglycerin. An increased fraction of average peak velocity after injection of adenosine was similar in both groups [control 340 (mean)+/-24 (SEM)%; VA 330+/-19%]. Flow-mediated vasodilation was preserved in all controls (pLAD 13.1+/-1.4%; mid-LAD 15.8+/-2.5%) but it was significantly impaired in patients with VA (pLAD -1.0+/-1.8%; mid-LAD 0.1+/-3.5%). The vasodilator response to nitroglycerin was comparable in controls (pLAD 25.8+/-2.8%; mid-LAD 27.2+/-2.8%) and VA (pLAD 26.2+/-5.2%; mid-LAD 26.7+/-3.5%). Coronary flow reserve is preserved in patients with VA. However, the flow-mediated response of spasm related-epicardial coronary artery is impaired. This may play an important role in the pathogenesis of coronary artery spasm.
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PMID:Impaired flow-mediated vasodilation of epicardial coronary artery in vasospastic angina. 988 66