[The ergonovine maleate test during coronarography].
Explore the source record for details and available documents.
Adult↗
SEARCH · Search PubMed
Results for “ERGONOVINE”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Reversible cardiac arrest related to late-onset coronary spasm after a positive ergonovine test.
Explore the source record for details and available documents.
Adult↗
Acute myocardial infarction induced by ergonovine administration for artificially induced abortion.
Acute myocardial infarction after artificially induced abortion is an uncommon event because such patients are usually young females and are not usually subject to atherosclerosis. This report describes two premenopausal females who developed acute myocardial infarction after administration of ergot derivatives which were used following abortion. Coronary arteries in both cases were angiographically normal. Both patients were smokers. We concluded that the ischemic event was caused by coronary vasospasm which was precipitated by the acute administration of ergot derivatives.
Abortion, Induced↗
[Ergonovin in the third stage of labor].
Explore the source record for details and available documents.
Claviceps↗
Angina due to coronary microvascular disease in hypertensive patients without left ventricular hypertrophy.
When angina occurs in patients with hypertension, it is usually attributed to coronary artery disease or left ventricular hypertrophy. To determine the contribution of coronary microvascular abnormalities to angina in patients with hypertension, we evaluated hypertensive patients without coronary artery disease or left ventricular hypertrophy by measuring the coronary responses to rapid atrial pacing before and after administration of ergonovine. We compared 12 hypertensive patients who had pacing-induced angina with 13 normotensive subjects without such angina. The two groups had similar coronary flow (in the great cardiac vein) at rest; however, pacing increased coronary flow less in hypertensive patients with angina than in normotensive subjects (48 vs. 83 percent; P = 0.05). In the hypertensive patients with angina, pacing after ergonovine increased coronary flow by only 32 percent (as compared with 48 percent before ergonovine; P less than 0.05) and decreased coronary resistance by 15 percent (as compared with 28 percent before ergonovine; P less than 0.05), indicating the presence of ergonovine-induced vasoconstriction. In normotensive subjects, in contrast, cardiac pacing after ergonovine increased coronary flow by 112 percent (P less than 0.001), and its effect on coronary resistance was not different from that of pacing before ergonovine. The hypertensive patients with angina had a significant increase in myocardial oxygen extraction during pacing after ergonovine and less of an increase in myocardial lactate consumption - a response consistent with the presence of myocardial ischemia. Thus, angina in hypertensive patients without epicardial coronary disease may be caused by myocardial ischemia, which appears to be due to an abnormally elevated resistance of the coronary microvasculature.
Angina Pectoris↗
Spontaneous coronary artery spasm in variant angina is caused by a local hyperreactivity to a generalized constrictor stimulus.
To assess whether spontaneous coronary artery spasm in patients with variant angina results from local coronary hyperreactivity to a generalized constrictor stimulus or from a stimulus generated only at the site of the hyperreactive segment, the behavior of spastic and nonspastic coronary segments was studied in six patients with variant angina in whom focal coronary spasm developed spontaneously during cardiac catheterization. None of the patients had critical (greater than 50% luminal diameter reduction) organic coronary stenoses. Coronary diameters were measured by computerized quantitative arteriography during control, spontaneous spasm and ergonovine-induced spasm and after intracoronary nitrates were given. During spontaneous spasm, the luminal diameter of spastic and both proximal and distal nonspastic coronary segments was significantly reduced from control values, 64.2%, 13.2% and 14.8%, respectively. Average diameter reduction of unrelated arteries was 12.3%. Ergonovine, which was also administered to four patients, provoked focal spasm at the same site as spontaneous spasm. During intravenous ergonovine, luminal diameter of spastic segments was reduced by 91.5%, that of nonspastic proximal segments by 17.8% and that of nonspastic distal segments by 11.5%. Luminal diameter of unrelated arteries during ergonovine-induced spasm was reduced by 17.7%. Constriction of spastic segments was greater during ergonovine-induced spasm (p less than 0.05), whereas the extent of diameter reduction of nonspastic segments was not significantly different during spontaneous spasm and ergonovine-induced spasm. Intracoronary isosorbide dinitrate dilated spastic and nonspastic coronary segments to a similar extent from control (20.7%, 18% and 16.5%, respectively; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Low prevalence of coronary artery spasm in patients with normal coronary angiograms and unexplained ventricular fibrillation.
AIMS: The aetiology of ventricular fibrillation in patients without identifiable structural heart disease is unknown. Recently, high prevalence of silent ischaemia due to coronary artery spasm has been reported in such patients. However, in at least one report, all patients had non-critical coronary artery lesions. Identification of coronary artery spasm as the underlying aetiology of ventricular fibrillation has important therapeutic implications. METHODS AND RESULTS: We performed ergonovine provocation tests in 18 patients (14 males, and four females; mean age, 36 years) with documented ventricular fibrillation in the absence of identifiable structural heart disease who had undergone aborted sudden death. In group I (n = 7) ergonovine provocation tests were performed at a mean interval of 31 months (range 21-42 months) after the index episode. These patients had already received an implantable cardioverter defibrillator, after failed electrophysiologically guided antiarrhythmic therapy. In group II (n = 11) the ergonovine provocation test was performed prospectively as part of the diagnostic evaluation. All patients were off antiarrhythmic drugs, calcium entry or beta-adrenoceptor blockers at the time of the ergonovine provocation test. Ergonovine was administered intravenously as a bolus injection, beginning with 0.05 mg followed every 3 min by incremental doses up to a cumulative maximum dose of 0.45 mg. Predefined end-points were (1) recording of ischaemic ST segment shifts of > or = 1 mm in at least two corresponding leads of the 12-lead electrocardiogram; (2) induction of ventricular tachycardia or ventricular fibrillation; and (3) administration of a cumulative dose of 0.45 mg. A positive response to ergonovine was seen in only one patient (5%) in group I in whom there developed ST segment elevation without angina and a short burst of rapid ventricular tachycardia. CONCLUSIONS: This study found a low prevalence of coronary artery spasm in patients with aborted sudden death resulting from documented ventricular fibrillation and non-apparent underlying heart disease. All patients had normal coronary angiograms and a negative history for spontaneous episodes of chest pain. The mechanism of arrhythmogenesis in such patients remains largely unknown.
Adult↗
Pathophysiology of coronary artery spasm.
Coronary arterial measurements were made from cineangiograms in patients with positive and negative ergonovine tests. In those with positive tests, normal segments of arteries adjacent to the site of spasm and arteries without spasm showed no greater sensitivity to ergonovine than arteries from control patients (20 +/- 13% constriction vs 17 +/- 12%, NS). In patients with positive and negative ergonovine tests, constriction was measured at lesion sites after ergonovine and compared with values predicted from a geometric theory. The measured constriction was always greater than predicted in patients with a positive ergonovine test, and frequently less than predicted in patients with a negative test. The increased sensitivity of arteries that show localized vasospasm at lesion sites after ergonovine administration is not explained by geometry alone.
Adult↗
Problems related to the detection of myocardial ischemia caused by coronary vasospasm.
We compared the sensitivity of three commonly used provocative tests, exercise, ergonovine and the cold pressor test, in a series of 34 hospitalized patients with well-documented, active variant angina. All tests were performed off medication at the same time of day, usually on 3 consecutive days. Angina was provoked by ergonovine in all 34 patients, by exercise in 17 and by the cold pressor test in only 5 (p less than 0.005). ST elevation developed during the ergonovine test in 32 (94%), during exercise in 10 (29%) and during the cold pressor test in only 3 (9%). With ergonovine one patient had ST depression only and one had no ECG changes. During the cold pressor test two patients had pseudonormalization of abnormally negative T waves and 29 had no ECG changes. Exercise induced T wave pseudonormalization in 4 patients, ST depression in 9 others and no ECG changes in 11. Thus, in patients with active variant angina, the sensitivity of the cold pressor test and exercise are too low to be useful clinically. Other studies suggest that the sensitivity of hyperventilation or provoked alkalosis is higher, but not as high as ergonovine administration. In patients who have become asymptomatic, either with treatment or spontaneously, the sensitivity of all tests decreases markedly. If such patients no longer have coronary spasm, the test is not a 'false negative' but a 'true negative'. Deaths have been reported following ergonovine administration and for this reason the test is not universally accepted.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[Must the medical treatment of vasospastic angina be continued indefinitely?].
A subgroup of 22 patients with Prinzmetal angina and a good clinical response to treatment with calcium inhibitors was studied to determine whether the ergonovine provocation test could help decide when to stop treatment. Before treatment, all patients had ST elevation during the ergonovine test which was performed in the coronary care unit. After 9,4 +/- 4,7 months' treatment, all 22 patients were asymptomatic. Their treatment was discontinued and the ergonovine test repeated. Twelve of the 22 patients had no anginal pain or ST segment changes during the test. Without therapy, none of these 12 patients have experienced recurrence of angina during a follow up period of 4,2 +/- 2,9 months. Angina with ST elevation occurred in 7 patients during the ergonovine test, as observed during their initial provocation tests. In 3 other patients, ergonovine induced ST depression in the leads in which ST elevation had been recorded during their initial tests. Treatment was restarted in these 10 patients with positive tests. There were no complications. Spontaneous remissions of symptoms and negative ergonovine tests may be observed in some patients with Prinzmetal angina. Without treatment this group of patients may remain asymptomatic for several months.
Adult↗
Patterns of coronary artery stenosis vasomotion: observed versus "predicted" stenosis reactivity in patients with chronic stable angina.
BACKGROUND: Patterns of constriction and dilatation of angiographically normal coronary artery segments and coronary stenoses, in response to vasoactive stimuli, remain speculative. METHODS: We compared the vasomotor response of angiographically normal and stenotic coronary segments and assessed the effects of stenosis location and morphology on coronary stenosis vasomotion in 52 patients with chronic stable angina (40 men and 12 women) who underwent intracoronary ergonovine or isosorbide dinitrate administration or both. Changes in coronary diameter in response to nitrate and ergonovine were assessed by computed arteriography. The "predicted" change in stenosis diameter was calculated according to the "geometric theory" (based on the vasomotor response of angiographically normal segments adjacent to the lesion and on stenosis severity). Coronary diameter was assessed at baseline and after nitrate administration in 58 stenoses (34 concentric and 24 eccentric), of which 40 were located proximally and 18 distally, and also after ergonovine administration (23 stenoses: 14 proximal and 9 distal, 14 concentric and 9 eccentric). RESULTS: Significant (> or = 10% lumen diameter change) vasoconstriction was observed after ergonovine administration in 14 of the 23 stenoses (61%), and significant vasodilation was noted after nitrate administration in 29 of 58 stenoses (50%). A larger proportion of distal (89%) and eccentric (89%) compared with proximal (43%) and concentric (43%) stenoses showed a greater than 10% vasoconstriction after ergonovine administration (P < 0.05). Vasodilatation after nitrate administration was also observed in a larger proportion of distal (78%) and eccentric (67%) than in proximal (38%) and concentric (38%) stenoses (P < 0.05). On average, the "observed" changes in coronary diameter in response to nitrate and ergonovine administration were of significantly less magnitude than those "predicted" by the geometric theory in both proximal and distal stenoses and in concentric and eccentric stenoses. In only 17% of stenoses were observed and predicted vasoconstriction similar. CONCLUSIONS: Our results suggest that in patients with chronic stable angina, calculations based on the "geometric theory" cannot predict the actual vasomotor response of a stenosis. Factors other than severity, such as baseline coronary tone, stenosis location, and stenosis morphology, appear to modulate stenosis vasomotion in vivo.
Adult↗
Coronary flow reserve, esophageal motility, and chest pain in patients with angiographically normal coronary arteries.
PURPOSE AND METHODS: To ascertain the relative prevalence of abnormalities of coronary flow reserve and esophageal function in patients with chest pain despite angiographically normal coronary arteries, 87 patients underwent invasive study of coronary flow reserve and, during the same week, esophageal testing. RESULTS: Sixty-three of the 87 patients (72%) demonstrated abnormalities of coronary flow reserve, as evidenced by an increase in coronary resistance during the stress of rapid atrial pacing after administration of ergonovine 0.15 mg intravenously (1.33 +/- 0.36 mm Hg.minute/mL), compared with pacing at the same heart rate before ergonovine administration (1.10 +/- 0.33 mm Hg.minute/mL). This higher coronary vascular resistance occurred in the absence of significant epicardial coronary artery luminal narrowing. Fifty-seven of these 63 patients (90%) with a coronary vasoconstrictor response to ergonovine described their typical chest pain during pacing stress, compared with only six of 24 patients (25%) who demonstrated no coronary flow abnormality (p less than 0.001). After administration of dipyridamole 0.5 to 0.75 mg/kg intravenously to 65 patients, the 48 patients with ergonovine-induced vasoconstriction had a significantly higher minimum coronary resistance, compared with the 17 patients without a coronary vasoconstrictor response to ergonovine (0.65 +/- 0.21 versus 0.47 +/- 0.13 mm Hg.minute/mL, p less than 0.03). Twenty of 87 patients (23%) had abnormal esophageal motility [nutcracker esophagus (11), nonspecific motility disorder (seven), and diffuse esophageal spasm (two)], including 16 of the 63 patients (25%) with abnormal coronary flow reserve. Twenty-four (28%) patients experienced their typical chest pain during motility testing, but only five of these patients met criteria for abnormal esophageal motility. Nine of 75 patients tested (12%) had their typical chest pain during Bernstein testing, and 18 of 38 patients (47%) tested had their typical chest pain provoked by intraesophageal balloon distention. CONCLUSIONS: Seventy-one of 87 patients (82%) with anginal-like chest pain and normal epicardial vessels in our series had a disorder of either coronary flow reserve, esophageal motility, and/or reproduction of typical chest pain during acid infusion. Of interest, chest pain was commonly encountered during cardiac and esophageal testing (85% of patients), regardless of the ability to demonstrate an abnormality of coronary flow reserve or abnormal esophageal function. This suggests that pain experienced by these patients may be a consequence of myocardial ischemia, esophageal dysfunction, abnormal visceral nociception, or a combination of any or all of these entities.
Adult↗
Progression of coronary atherosclerosis: is coronary spasm related to progression?
A total of 239 patients undergoing serial coronary angiography with a concomitant ergonovine provocation test were studied between July 1974 and June 1987. The progression of coronary artery disease was evaluated in relation to risk factors, especially coronary artery spasm. Patients were classified into three groups: 1) new myocardial infarction group (39 patients); 2) progression without infarction group (90 patients); and 3) nonprogression group (110 patients). To assess how risk factors and coronary spasm are related to the occurrence of new myocardial infarction and progression without infarction, 11 variables in the three groups were examined: age, gender, the time interval between the studies, fasting blood sugar, systolic blood pressure, diastolic blood pressure, smoking, serum cholesterol, triglyceride, uric acid and a positive response to the ergonovine provocation test. Multiple regression analysis selected three independent predictors of progression without infarction: cholesterol (p less than 0.01), systolic blood pressure (p less than 0.05) and a positive response to the ergonovine provocation test (p less than 0.001). Multiple regression analysis also selected three independent predictors of the occurrence of new myocardial infarction: fasting blood sugar (p less than 0.01), systolic blood pressure (p less than 0.05) and a positive response to the ergonovine provocation test (p less than 0.001). A positive response to the ergonovine provocation test was the strongest factor for occurrence of both new myocardial infarction and progression without infarction. To evaluate segmental arterial changes, 3,275 coronary artery segments were analyzed in the 239 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac Catheterization↗
Reactivity of eccentric and concentric coronary stenoses in patients with chronic stable angina.
Dynamic coronary stenoses may be the cause of a variable angina threshold and rest angina in patients with chronic stable angina. It has been suggested that eccentric but not concentric coronary artery stenoses have the potential for dynamic changes of caliber in response to vasoactive stimuli. The vasomotor response of eccentric (asymmetric narrowing) and concentric (symmetric narrowing) coronary stenoses to ergonovine (20 micrograms intracoronary or 300 micrograms intravenous) and isosorbide dinitrate (1 mg intracoronary) was studied in 51 patients with chronic stable angina. Diameter of reference segments (angiographically normal segments proximal to the stenoses) and that of eccentric (n = 30) and concentric (n = 35) coronary stenoses that ranged from 50% to 90% luminal diameter reduction were measured by computerized quantitative angiography before and after ergonovine and isosorbide dinitrate. Ergonovine reduced stenosis diameter (by greater than or equal to 10%) in 80% of eccentric stenoses and 42% of concentric stenoses (p less than 0.05). Mean (+/- SEM) diameter reduction with ergonovine was 19 +/- 3% and 9.5 +/- 2% for eccentric and concentric stenoses, respectively (p less than 0.05). Isosorbide dinitrate increased coronary diameter (by greater than or equal to 10%) in 70% of eccentric and 43% of concentric stenoses (p less than 0.05). Mean diameter of eccentric stenoses increased from 1.15 +/- 0.05 to 1.35 +/- 0.06 mm after nitrate (18.6 +/- 2.5%), whereas diameter of concentric stenoses increased from 1.05 +/- 0.05 to 1.14 +/- 0.05 mm (10 +/- 2.5%) (p less than 0.05). Average dilation of reference segments with administration of isosorbide dinitrate and constriction with ergonovine were not significantly different in patients with concentric and eccentric stenoses.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
The hypertensive response to vasopressor agents stimulates the release of thromboxane A2 in hypercholesterolaemic rabbits.
The production of thromboxane A2 (TXA2) and prostacyclin (PGI2) is altered in hypercholesterolaemia. The purpose of this study was to investigate the effect of an acute rise in arterial pressure produced by pressor agents on the release of TXA2 and PGI2 in hypercholesterolaemic rabbits. Hypercholesterolaemia was induced in rabbits by feeding pellet food containing 1% cholesterol for 3 months. Administration of pressor agents (ergonovine 0.5-2.0 mg.kg-1, noradrenaline 5.0-20.0 micrograms.kg-1 and angiotensin-II 0.5-2.0 micrograms.kg-1) increased arterial pressure dose dependently, accompanied by a pressure dependent increase in the plasma concentrations of both TXB2 and 6-keto-PGF1 alpha (stable metabolites of TXA2 and PGI2) in control rabbits, but only of TXB2 in hypercholesterolaemic rabbits. In control rabbits the maximum increase in TXB2 was 51% with ergonovine, 73% with noradrenaline, and 51% with angiotensin-II; and the maximum increase in 6-keto-PGF1 alpha was 48% with ergonovine, 76% with noradrenaline, and 198% with angiotensin-II. In hypercholesterolaemic rabbits the maximum increase in TXB2 was 130% with ergonovine, 144% with noradrenaline, and 128% with angiotensin-II. The pressor induced increase in TXB2 was suppressed when the increase in arterial pressure was counteracted by the concomitant administration of vasodilators (glyceryl trinitrate 40 micrograms.kg-1.min-1 and verapamil 20 micrograms.kg-1.min-1) in both control and hypercholesterolaemic rabbits. Neither TXB2 biosynthesis nor phospholipase A2 activity in platelets was affected by ergonovine, noradrenaline or angiotensin-II in vitro. These results suggested that the acute rise in arterial pressure caused by these pressor agents increased TXA2 release in vivo and that the increase was greater in hypercholesterolaemic than in control rabbits.
6-Ketoprostaglandin F1 alpha↗
Dilatation of epicardial coronary arteries and attenuation of provoked coronary vasoconstriction by nisoldipine.
By using quantitative coronary angiography, this study evaluated the coronary artery dilative action of intravenous nisoldipine and furthermore examined the efficacy of the agent to prevent an ergonovine-provoked increase in the coronary arterial tone. Ten patients suspected of either vasospastic or mixed form of angina pectoris underwent coronary angiography under resting conditions, after 3 micrograms kg-1 of intravenous nisoldipine and finally after a cumulative dose of 0.7 mg of ergonovine maleate. The ergonovine-provocation was performed subsequent to a second intravenous administration of 3 micrograms kg-1 nisoldipine. Coronary artery diameters were measured in angiographically normal, proximal segments by using a computer assisted procedure with automatic contour detection. The following results are given as the mean +/- SEM of the percentage changes in the diameters of 30 coronary artery segments. Nisoldipine produced dilatation of the epicardial coronary arteries with a mean increase in the diameters by 9.5 +/- 1.3% with respect to baseline (P less than 0.01). Subsequent ergonovine-testing caused coronary artery vasoconstriction with a mean diameter decrease of 7.7 +/- 1.3% below baseline (P less than 0.01). Though nisoldipine did not totally block the ergonovine-induced increase in the coronary vasomotor tone, there was a significant attenuation of the coronary constriction compared with patients without any premedication (7.7 +/- 1.3% versus 13.6 +/- 0.6%, P less than 0.01). The ability of nisoldipine to dilate epicardial coronary arteries but also to reduce a provoked coronary artery constriction promises therapeutic effectiveness for both the prevention and release of angina pectoris caused by an increased coronary vasomotor tone.
Adult↗
[Contractile properties of coronary artery bypass conduit--comparison between saphenous vein and internal mammary artery].
This study was designed to examine the response of coronary artery bypass conduit to serotonin, phenylephrine, and ergonovine as provocation agents of vasoconstriction. Saphenous veins (SV) and internal mammary arteries (IMA) were obtained during coronary artery bypass grafting (CABG), and their contractile properties were measured using isometric contraction recording apparatus. Both SV and IMA showed sigmoid contraction curves indicating dose dependence to ergonovine, serotonin, and phenylephrine. The concentration-response relations for phenylephrine showed a similar curve in both SV and IMA, however, those for ergonovine and serotonin showed a leftward shift in SV compared with IMA. Half maximum effective dose for ergonovine and serotonin were less in SV than IMA. From these results, it was suggested that "perioperative spasm" during CABG might occur not only in coronary arteries but also in the graft conduit itself. Graft spasm might be a possible mechanism for occlusion of the bypass graft. In conclusion, greater hyperreactivity of SV compared with IMA in response to ergonovine and serotonin was suggested, so it is concluded that, from this point of view, IMA is more suitable for use in CABG.
Coronary Artery Bypass↗
Angiographic determination of disease-produced alterations of vasomotor tone in large coronary arteries.
Quantitative coronary arteriography was done before and after ergonovine and/or nitroglycerin in 24 patients. After nitroglycerin there was an average 18.6 +/- 3.9% increase in diameter of normal vessels over 2 mm in diameter, and a similar 19.3 +/- 8.7% increase in diameter of the same sized, normal appearing segments in subjects with coronary disease. In individual cases the luminal response to the drug was significantly more variable in "normal" segments of diseased vessels than in entirely normal arteries. Twenty-eight of thirty seven coronary stenoses dilated an average of 18 +/- 10.8% (range 3 to 43%) after nitroglycerin. Unequal dilation of stenosis and normal reference segment caused a 10% or greater change in calculated percent diameter stenosis in 16 lesions. Because they dilated less than would be predicted using a hypothetical geometric model to assess vessel reactivity, most of the lesions could be considered hyporeactive. Ergonovine predictably constricted normal coronary vessels in a relatively uniform fashion. Response of diseased arterial segments was more variable in a limited number of observations. Ergonovine partially antagonized the vasodilating effect of subsequently administered nitroglycerin, and larger than average or intracoronary doses of nitroglycerin had to be used to achieve the same degree of dilation seen with smaller doses in the absence of ergonovine. Disease of large coronary arteries focally alters their vasomotor tone and reactivity as gauged by responsiveness to nitroglycerin and ergonovine. Some implications of this are discussed.
Coronary Angiography↗