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[The local and systemic effects of intracoronary ergonovine in patients with normal and nonspastic coronary arteries. A comparison with the intravenous ergonovine test].

Local and systemic effects of intracoronary (two bolus injections of 25 micrograms at 3-min intervals) ergonovine were determined in 60 patients with angiographic non-spastic normal coronary arteries and were compared with the most usual intravenous ergonovine dose to induce coronary artery spasm (incremental doses of 50, 100 and 200 micrograms at 3-min intervals). The mean diameter of the vessels was reduced by 15% after selective injections (baseline 2.38 +/- 0.7; after intracoronary ergonovine 2.02 +/- 0.6 mm; p less than 0.001) and no significant changes were induced in the heart rate (before 80 +/- 15; after 79 +/- 15 beats/min) and systolic aortic pressure (before 147 +/- 27; after 149 +/- 28 mmHg). Following intravenous administration, the mean coronary diameter decreased by 20% (1.90 +/- 0.6 mm; p less than 0.01 vs intracoronary dose) and the heart rate diminished slightly (76 +/- 12 beats/min; p less than 0.01). Nevertheless, the systolic aortic pressure did increase by 16% (171 +/- 28 mmHg; p less than 0.001). No major complications were observed and the appearance of side effects was minimal. Thus, the intracoronary delivery route, at the applied dosage, induces lesser vasoconstriction than usual intravenous administration, and systemic effects, such as hypertension, are avoided.

Cardiac Catheterization↗
PubMed1976

The response of the human Fallopian tube to ergonovine and methyl-ergonovine in vivo.

Ergonovine maleate (EM) is a powerful stimulant of human tubal motility. It has been therefore thought that EM could interfere with normal ovum transport and serve as a contraceptive. The tube activating effects of EM and methyl EM were evaluated in 14 women and results confirmed that both are powerful stimulants of the human Fallopian tube. EM immediately post coitus significantly reduces the conception rate.

Ergonovine↗
PubMed1986

The mechanism of ergonovine-induced airway smooth muscle contraction.

There have been three articles in the clinical literature of ergonovine maleate-induced bronchospasm. The effect of the alkaloid on isolated canine tracheal smooth muscle was analyzed to investigate the mechanism of ergonovine-induced airway smooth muscle contraction. Both ergonovine and 5-hydroxytryptamine (5HT, serotonin) contracted the smooth muscle preparations with EC50s of 1.35 X 10(-8) mol/L and 5.06 X 10(-7) mol/L, respectively. The maximal contractile response observed with ergonovine was approximately 30% less than that observed with 5HT. Methysergide competitively blocked both ergonovine and 5HT responses with similar calculated pKB values (8.33 against ergonovine and 8.46 against 5HT) and also similar pA2 values determined by Schild plots (8.50 and 8.45, respectively). The relative affinity and efficacy of ergonovine versus 5HT were determined by use of a concentration of the irreversible antagonist, phenoxybenzamine, which partially blocked receptor sites. The calculated affinity of ergonovine was about 16 times higher than that of 5HT. The relative efficacy at EC100 for ergonovine was 0.2, but at EC10 it was 41.9 (5HT efficacy = 1). Ergonovine 10(-9) or 10(-8) mol/L shifted the 5HT dose-response curve to the right without reducing the maximal response, but the shift was nonparallel. Blockade of muscarinic (atropine), alpha 1-adrenergic (prazosin), beta-adrenergic (propranolol), H1 (pyrilamine), or H2 (cimetidine) receptors did not alter ergonovine-induced contraction. These data indicate that ergonovine directly contracts canine tracheal smooth muscle as a result of its combination with 5HT receptors. This effect may result in precipitation of an asthmatic attack in susceptible individuals.

Animals↗
PubMed1989

[The mechanism of ergonovine-induced airway smooth muscle contraction].

There have been three articles in the clinical literature concerning ergonovine maleate-induced bronchospasm. The effect of this alkaloid on isolated canine tracheobronchial smooth muscle was analyzed to investigate the mechanism of ergonovine-induced airway smooth muscle contraction. Both ergonovine and serotonin (5-hydroxytryptamine, 5HT) contracted canine tracheal smooth muscle with EC50 1.4 X 10(-8) M and 5.1 X 10(-7) M, respectively. The maximal contractile response observed with ergonovine was approximately 30% less than that observed with 5HT. In diverse blockers such as methysergide, atropine, prazosin, propranolol, pyrilamine and cimetidine, only methysergide competitively blocked both ergonovine and 5HT responses with a similar calculated dissociation constant (pKB); 8.3 +/- 0.2 against ergonovine and 8.5 +/- 0.2 against 5HT (n = 6, p = 0.9). The relative affinity and efficacy of ergonovine and 5HT were determined by use of a partial irreversible antagonist, phenoxybenzamine. The calculated affinity of ergonovine was about 16 times higher than that of 5HT. The relative efficacy of EC100 for ergonovine was 0.2 but at EC10 it was 41.9 (5HT efficacy = 1). Ergonovine 10(-9) M or 10(-8) M shifted the 5HT dose-response curve to the right without reducing the maximal response, but the shift was nonparallel. Ergonovine and 5HT also contracted canine bronchial smooth muscle in a dose dependent manner with EC50 6.4 X 10(-8) M and 1.8 X 10(-7) M, respectively. The dose-responses curve of these two agonists were competitively blocked by methysergide 10(-6) M. These data indicate that ergonovine directly contracts canine tracheobronchial smooth muscle as a result of its combination with 5HT receptors. This effect may result in the precipitation of an asthmatic attack in susceptible individuals.

Animals↗
PubMed1986

Response of the coronary artery to a small dose of ergonovine in variant angina.

The response of the coronary artery to a small dose (0.01 mg) of ergonovine was observed in nine patients without variant angina and in 10 patients with variant angina. Coronary angiograms were obtained before and after small and larger (routinely used) doses of ergonovine. With the larger dose, all 10 patients with variant angina had total or subtotal spastic occlusion accompanied by angina and ECG changes. Excluding the site of spastic occlusion produced by the larger dose of ergonovine, diameters of proximal, middle, and distal segments in each major coronary artery were measured before and after a small dose of ergonovine. The mean percentage of change in diameter (diameter before - diameter after a small dose of ergonovine)/diameter before a small dose of ergonovine X 100% in patients without variant angina was not significantly different from that in patients with variant angina (5.2 +/- 9.5% vs 7.0 +/- 11.9%, respectively). However, in patients with variant angina, a small dose of ergonovine produced a percentage of change in diameter of 39.8 +/- 15.3% at the site of spastic occlusion included by a larger dose of ergonovine, compared with that of 7.0 +/- 11.9% in the remaining non-spastic coronary arteries (p less than 0.05). These results indicate that patients with variant angina have local segments which respond differently to ergonovine from the remaining segments of coronary arteries. Clinically, this observation might be helpful in determining the angiographic positivity to ergonovine.

Adult↗
PubMed1981

Ergonovine testing to detect spontaneous remissions of variant angina during long-term treatment with calcium antagonist drugs.

A subgroup of 22 patients with variant angina who had responded well to calcium antagonist drugs were studied to determine if ergonovine testing could help assess the need for continued therapy. Before treatment all 22 patients exhibited angina with S-T elevation during ergonovine testing done in the coronary care unit according to a previously described protocol with sequential ergonovine doses of 0.0125, 0.025, 0.05, 0.1, 0.2, 0.3 and 0.4 mg administered at 5 minute intervals. After 9.4 +/- 4.7 (range 1 to 24) months of treatment (nifedipine 7 patients, diltiazem 3, verapamil 8, perhexiline 3, nifedipine and diltiazem 1), all patients were free from anginal attacks. Medication was discontinued and ergonovine testing repeated 24 to 48 hours later (3 weeks for perhexiline). In 12 of the 22 patients, angina or S-T segment shifts did not occur during the second ergonovine test to a maximal dose of 0.4 mg. Treatment was not restarted in these patients and all 12 remain free of variant anginal attacks 4.2 +/- 2.9 (range 1 to 13) months later. In seven patients angina and S-T elevation occurred during the second ergonovine test, in the same electrocardiographic leads as during the test before treatment. In three patients the ergonovine test induced angina with S-T depression in the leads where S-T elevation had occurred during the previous test. Treatment was reinstituted in these 10 patients with a positive test. No complications resulted from ergonovine testing in any patient. We conclude that in many patients with variant angina, symptoms will disappear spontaneously and the ergonovine test will revert to negative. Treatment with calcium antagonist drugs can probably be safely discontinued in some patients with variant angina; ergonovine testing appears to be helpful in identifying such patients. Longer periods of follow-up are required to confirm that symptoms do not recur.

Adult↗
PubMed1996

Ergonovine echocardiography as a screening test for diagnosis of vasospastic angina before coronary angiography.

OBJECTIVES: In patients with chest pain suggestive of variant angina, we performed this prospective study to test the specificity and diagnostic validity of ergonovine echocardiography (detection of regional wall motion abnormality during bedside ergonovine challenge) as a screening procedure before coronary angiography. BACKGROUND: Spasm provocation test outside the catheterization room has generally not been accepted as a safe diagnostic method. METHODS: Ergonovine echocardiography was performed in 80 consecutive patients with chest pain syndrome after confirmation of negative treadmill or normal stress myocardial perfusion scan results using thallium-201. A bolus of ergonovine maleate was injected at 5-min intervals up to a total cumulative dosage of 0.35 mg with echocardiographic monitoring of left ventricular wall motion. A 12-lead electrocardiogram (ECG) was also recorded every 3 min after each ergonovine injection. Positive test results were development of regional wall motion abnormalities or transient ST segment elevation or depression >0.1 mV in any single lead of the 12-lead ECG. Coronary angiography was undertaken within 2 +/- 4 days (mean +/- SD) after ergonovine echocardiography, and the spasm provocation test with acetylcholine or ergonovine was performed in patients with normal angiographic findings or lumen diameter narrowing <70%. RESULTS: On the basis of angiographic criteria, 56 patients had coronary vasospasm; this finding was later ruled out in 19 patients with near-normal angiographic results by a negative response on the spasm provocation test. In the remaining five patients, coronary spasm provocation was not performed because they revealed a high degree of fixed stenosis (lumen diameter narrowing 97 +/- 4%). Ergonovine echocardiography could diagnose coronary vasospasm before angiography, with a sensitivity of 91% (51 of 56 patients, 95% confidence interval [CI] 84% TO 98%) and specificity of 88% (21 of 24 patients, 95% CI 75% to 100%). Of 53 patients showing regional wall motion abnormalities during ergonovine echocardiography, characteristic ST segment elevation in the simultaneously recorded ECG was observed in only 20 (38%). There were no complications, including myocardial infarction or fatal arrhythmia, during the test. CONCLUSIONS: Ergonovine echocardiography before coronary angiography is safe and can be used as a reliable diagnostic screening test for coronary vasospasm in patients with negative treadmill or normal stress myocardial perfusion scan results. These findings suggest that invasive coronary angiography can be avoided in selected patients for the diagnosis of vasospastic angina.

Adult↗
PubMed1983

Provocative ergonovine testing in patients without obstructive coronary disease.

Ergonovine administration during coronary angiography is frequently used to rule out coronary spasm as a cause of chest pain. We performed this study to determine which electrocardiographic variables (other than ST segment elevation with pain) and which chest pain characteristics might be predictive of ergonovine test outcome in patients without obstructive coronary disease. Thirty-one patients had an electrocardiogram recorded during chest pain. Three of four patients (75%) who had an ischemic electrocardiogram with pain had a positive ergonovine test while only 1 of 27 (4%) patients who had a nonischemic electrocardiogram during chest pain had a positive ergonovine test (p less than 0.001) Pain that occurred predominantly at rest was present in five of five patients with positive ergonovine tests but pain occurring predominantly at rest was also present in 76% of patients with negative ergonovine tests (85%). Prompt relief of pain with nitroglycerine was also present in all patients with a positive ergonovine test but was also seen in 58% of patients with a negative test (NS). Association of chest pain with nausea, vomiting, diaphoresis, or radiation to left arm, jaw or neck were similarly poor predictors of ergonovine test outcome. We conclude that ergonovine testing in patients without obstructive coronary disease is of low yield if an electrocardiogram recorded during pain does not show evidence of ischemia. Historical features of the chest pain are not good predictors of test outcome.

Coronary Vasospasm↗
PubMed1984

Prolonged coronary vasoconstrictor effect of ergonovine maleate.

The duration of the coronary artery vasoconstrictor effect of ergonovine maleate is an important clinical parameter that has not been clearly defined. Since ergonovine is generally administered in incremental, cumulative doses and since this agent may have potentially serious toxic effects related to its vasoconstrictor properties, knowledge of duration of this effect is crucial to its safe and efficacious use. We present clinical evidence of ergonovine-induced coronary artery spasm recurring after pharmacologic relief of a first episode of ergonovine-induced spasm. Recurrent spasm occurred 18 minutes after a cumulative dose of 0.15 mg ergonovine and 14 minutes after intravenous nitroglycerin was given to ameliorate the initial spasm. Therefore, clinical monitoring of patients after ergonovine administration should be designed to identify a possibly prolonged duration of vasoconstrictor effect of the drug. Sequential doses of ergonovine at intervals of ten minutes or less should be recognized as having cumulative effect. The duration of action of pharmacologic agents utilized to alleviate ergonovine-induced coronary artery spasm should exceed the potential duration of action of ergonovine in order to minimize the possibility of late spasm.

Cardiac Catheterization↗
PubMed1992

Comparison of coronary responses to intracoronary and intraaortic ergonovine and isosorbide dinitrate in patients with atypical chest pain.

Fifty patients with atypical chest pain were studied to compare coronary responses to intracoronary and intraaortic ergonovine. The diameters of the proximal, middle (1) and (2) (proximal segments of segments 2 and 3 [AHA classification], respectively), and distal segments of the right coronary artery were measured before and after intracoronary ergonovine (4 micrograms/minute over 4 minutes) and isosorbide dinitrate (ISDN) (2 mg) in 24 patients, and before and after intraaortic ergonovine (0.2 mg) and ISDN (5 mg) in 26. Mean vasoconstriction by intracoronary and intraaortic ergonovine were 13 +/- 1.5% and 9 +/- 0.8%, respectively (p < 0.02). Irrespective of the methods of administration, the responses to ergonovine were similar in the 4 segments. Mean vasodilation by intracoronary and intraaortic ISDN, which were used to quantify the degree of basal coronary tone, were 25 +/- 2.2% and 27 +/- 1.5%, respectively (p = not significant [NS]). There were significant negative linear correlations between the responses to ergonovine and ISDN in the middle (2) (r = -0.51; p < 0.05) and distal (r = -0.53; p < 0.01) segments in patients with intracoronary injection, and the proximal (r = -0.41; p < 0.05), middle (1) (r = -0.66; p < 0.01) and middle (2) (r = -0.69; p < 0.01) segments in patients with intraaortic injection. These observations indicate that low-dose administration of intracoronary ergonovine produces sufficient coronary vasoconstriction, similar to or slightly greater than that of intraaortic ergonovine in patients with atypical chest pain, but basal coronary tone may influence the vasoreactivity to ergonovine.

Aorta↗
PubMed1983

Mode of action of ergonovine on isolated porcine coronary artery: the role of Ca2+.

Coronary vasoconstrictor responses to ergonovine were examined in helical coronary arterial strips of young swine. Both ergonovine and serotonin (5-hydroxytryptamine) produced dose-dependent contractions of the strips. The distal region (less than 1.00 mm outer diameter) of the circumflex coronary artery was most sensitive to the responses of serotonin and ergonovine. Methysergide and nifedipine significantly depressed the contractions induced by ergonovine and serotonin. Atropine, propranolol, and the alpha 1 blocker, prazosin, did not antagonize ergonovine-induced contractions. The ergonovine response may depend entirely upon extracellular Ca2+ while the effect of serotonin may be mediated in part through the mobilization of intracellular Ca2+ stores. Increases in 45Ca2+ cellular contents occurred after ergonovine or serotonin and these increases were blocked by methysergide or nifedipine at concentrations which blocked mechanical responses to the agonist. It is concluded that the contractions of the porcine coronary artery produced by ergonovine and serotonin are as follows: (i) regionally sensitive; (ii) blocked by Ca2+ antagonists and therefore may utilize Ca2+ channels similar to those described in other excitable tissues; (iii) blocked by methysergide. These studies indicate that the major mechanism of ergonovine's action in the porcine coronary artery is through the activation of serotonin receptors on coronary arteries which are, in turn, linked to Ca2+ channels. However, this mechanism of action may be different in an intact animal.

Animals↗
PubMed1984

Mechanisms of the ergonovine-induced vasoconstriction in the rabbit main coronary artery.

The mean membrane potential of smooth muscle cells of the rabbit main coronary artery was -60.3 mV and an evoked action potential could be recorded in response to acetylcholine (ACh). Ergonovine or 5-hydroxytryptamine (5-HT) slightly depolarized the membrane and methysergide, a relatively selective antagonist for the 5-HT receptor, had a slight inhibitory action on these depolarizations. 5-HT produced larger contractions than ergonovine, and the concentration-effect relationships obtained for both agents shifted to higher concentrations following pre-equilibration with methysergide. ACh (10(-11)M) slightly hyperpolarized the membrane and relaxed the tissue, and high concentrations of ACh (greater than 10(-8)M) depolarized the membrane, increased the membrane resistance and produced a contraction. ACh but not ergonovine or 5-HT, produced a contraction in Ca-free EGTA-containing solution. Following a 60 min pre-equilibration with indomethacin, the ergonovine-induced contraction was markedly enhanced but the 5-HT- or ACh-induced contractions were not. Removal of the endothelium by rubbing the vascular lumen enhanced the ergonovine- or ACh-induced contractions, but not those to 5-HT. The results obtained can be summarized as follows: ergonovine probably accelerates Ca influx and thereby produces contraction in the rabbit main coronary artery. This contraction is due to activation of the 5-HT receptor as an agonist, but the ergonovine-induced contraction is attenuated due to activation of the endothelium from which inhibitory prostanoid substances may be released. Ergonovine, therefore, may produce greater contractions in coronary arteries with damaged endothelium than in intact tissues.

Acetylcholine↗
PubMed1989

Time-related decrease in sensitivity to ergonovine in patients with variant angina.

Eighteen patients with variant angina, a positive ergonovine test, and a favorable response to calcium antagonists were studied by serial ergonovine tests and Holter monitoring to assess the long-term changes in response to ergonovine and the relationship with the spontaneous activity of the disease. The number of patients with a positive test decreased from 18 of 18 in the acute phase to 12 of 18 (66%) at 3 months, 10 of 17 (59%) at 6 months, and five of 17 (29%) at 12 months. The mean dose level of ergonovine associated with a positive response and the percentage of positive tests with ST segment depression increased progressively during follow-up. The results of the ergonovine test were well correlated with the spontaneous activity of the disease in 94%, 83%, 76%, and 71% of the patients at initial observation and at 3, 6 and 12 months, respectively. Thus in patients with variant angina and a favorable response to calcium antagonists, a time-related decrease in sensitivity to ergonovine develops during follow-up. In most patients the response to ergonovine is well correlated with the spontaneous activity of the disease; thus the ergonovine test may be a useful tool in the assessment of the natural evolution of vasospastic angina.

Adult↗
PubMed1989

Hyperventilation and ergonovine tests in Prinzmetal's variant angina pectoris in men.

Hyperventilation and ergonovine tests were carried out in a group of 30 patients with variant angina to assess the sensitivity of the 2 tests and to correlate the response with spontaneous disease activity. Hyperventilation produced a positive response in 83% (25 of 30) and ergonovine in 93% (28 of 30) of the patients. After hyperventilation 22 of 25 showed ST-segment elevation, 2 ST depression and 1 T-wave pseudonormalization; after ergonovine ST-segment elevation developed in 23 patients, ST depression in 4 and T-wave pseudonormalization in 1. In all cases the electrocardiographic changes occurred in the same leads as during the spontaneous attacks. The incidence of chest pain and ventricular arrhythmias was similar during both tests; spontaneous remission of ischemia, however, was more frequent (48 vs 14%) after hyperventilation than after ergonovine. Acute ischemia developed at a mean of 218 +/- 112 seconds after the end of hyperventilation in 19 of 25 positive tests; at that time double product was not significantly different from basal values. The sensitivity of hyperventilation was similar (95 vs 100%) to ergonovine in the patients with greater than or equal to 1 daily attack, while in those with less than 1 daily attack the sensitivity of hyperventilation decreased to 55% compared to 77% with ergonovine. Thus, in variant angina the sensitivity of both tests correlates with disease activity. Hyperventilation is a safe provocative test with a sensitivity similar to ergonovine in patients with active disease; however, in patients with sporadic attacks hyperventilation has a lower sensitivity than ergonovine and therefore a limited diagnostic value.

Adult↗
PubMed1986

Beta-thromboglobulin release within coronary circulation--a potential role of platelets in ergonovine-induced coronary vasospasm.

The role of platelets in the pathogenesis of acute myocardial ischemia is not yet agreed upon. In this study, the gradient of plasma beta-thromboglobulin concentration between coronary sinus and aorta was used as an indicator of platelet activation within the coronary circulation. Blood samples were drawn before and after injection of ergonovine maleate in patients without fixed coronary stenosis in whom significant coronary spasm was induced by ergonovine (n = 8, Group 1), patients with significant stenosis (greater than or equal to 75%) of the left anterior descending artery and positive ergonovine test (n = 7, Group 2) and patients with significant stenosis of left anterior descending coronary artery and negative ergonovine test (n = 11, Group 3). Fifteen patients with normal coronary arteries who were negative in the ergonovine test served as controls (Group 4). After the ergonovine test, all Group 1 patients revealed a significant increase of beta-thromboglobulin gradient (P less than 0.001), while those in other groups did not. Additionally, the gradient after the ergonovine test of Group 1 patients was larger than those of the other groups (P less than 0.01). All blood samples after the ergonovine test were collected before or at the onset of angina attacks. These results suggest that platelet activation within the coronary circulation has some pathogenic role, probably as an aggravating factor, in coronary artery spasm.

Adult↗
PubMed1983

Ergonovine provocation to assess efficacy of long-term therapy with calcium antagonists in Prinzmetal's variant angina.

In the patient with Prinzmetal's variant angina, the response to therapy with calcium antagonists may be assessed symptomatically, electrocardiographically (that is, by ambulatory electrocardiographic monitoring), or by response to ergonovine provocation. Although some studies have suggested a good relation between anginal frequency and ergonovine responsiveness in these patients, none has compared ambulatory electrocardiographic activity with the results of ergonovine provocation during the long-term administration of calcium antagonists. Therefore, the present study was performed to compare ergonovine responsiveness with both clinical and ambulatory electrocardiographic activity in patients with Prinzmetal's variant angina during long-term therapy with placebo, verapamil, and nifedipine. Accordingly, 27 patients with variant angina (19 men and 8 women, mean age 52 years) received placebo and verapamil for 2 months each, after which 23 of the 27 also received nifedipine for 2 months. All patients kept a diary of chest pains, and all had weekly 24-hour 2-channel ambulatory electrocardiographic (Holter) monitoring, from which episodes of transient S-T segment deviation were quantitated. During the final week of therapy with each agent, ergonovine was administered, beginning at 0.025 mg and incrementally increasing to 0.20 mg. It was discontinued when the patient had chest pain with S-T segment elevation greater than or equal to 0.1 mV or received a total dose of 0.50 mg. Of the 74 tests, 59 were negative; 6 of the negative tests occurred during a treatment period in which the patient had greater than 10 chest pains/week and greater than 25 episodes of S-T segment deviation/week. Of the 15 positive tests, 8 became positive during administration of less than 0.20 mg ergonovine; 5 of the positive tests occurred during a treatment period in which the patient had no chest pain or S-T segment deviation. Thus, in patients with variant angina, disease activity cannot be monitored reliably by ergonovine provocation because some patients have negative ergonovine tests at a time of marked clinical and electrocardiographic activity, whereas others have positive tests at a time of little (or no) disease activity.

Adult↗