Search PubMed⌕ Search

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.

At least 73 records · Page 4Linked to original sources
PubMed1994

Vasomotor response to ergonovine of epicardial and resistance coronary arteries in the nonspastic vascular bed in patients with vasospastic angina.

The hypothesis that a coronary vasomotion disorder may exist in the entire coronary artery tree in patients with vasospastic angina was investigated by examining the coronary responses to atrial pacing (130 beats/min) before and after the administration of ergonovine (16 micrograms) into nonspastic coronary arteries. Seven patients with angiographically normal coronary arteries and focal spasm in the right coronary artery and 7 control patients with atypical chest pain and angiographically normal coronary arteries without spasm were studied. Great cardiac vein flow (GCVF) and left anterior descending coronary artery diameters (CDs) were measured by the thermodilution method and quantitative arteriography, respectively. Although the CDs before ergonovine were similar in the 2 groups, the pacing-induced increased in GCVF before ergonovine administration was smaller in patients with vasospastic angina than in control patients (22 +/- 4% vs 49 +/- 11%, respectively; p < 0.05). After ergonovine administration, pacing both increased GCVF and decreased anterior regional coronary resistance (ACR) to a lesser extent in patients with vasospastic angina than in control patients (GCVF, 16 +/- 4% vs 47 +/- 8%, respectively [p < 0.01]; ACR, -12 +/- 3% vs -29 +/- 3%, respectively [p < 0.01]). The decreases in CDs in patients with vasospastic angina observed after ergonovine administration were greater than those in control patients (-18 +/- 2% vs -9 +/- 2%, respectively; p < 0.05). Thus, not only epicardial, but also resistance coronary arteries are affected by the coronary vasomotion disorder in the nonspastic vascular bed in patients with vasospastic angina.

Adult↗
PubMed2006

Ergonovine test in angina with normal coronary arteries. Is it worth doing it?

BACKGROUND: Patients with angina and normal coronary arteries are often misdiagnosed with having non-cardiac pain. Although vasospasm is a well-known entity, spasm provocation is not routinely done in the majority of hospitals at present. MATERIALS AND METHODS: One hundred and sixty two consecutive patients with thoracic pain and normal coronary arteries were retrospectively studied. The characteristics of pain were analysed. One hundred and sixty one non-invasive tests (with and without imaging) were done to 126 patients before angiography. Increasing doses of ergonovine (from 1 to 30 microg) were injected into the coronary arteries to provoke coronary spasm. The correlation between ergonovine-induced spasm and non-invasive tests was studied. RESULTS: Oppressive thoracic pain suggestive of angina was present in 144 patients. It occurred at rest in 59 patients, only at night in 14, with effort in 40, and it was mixed in 31. Non-oppressive atypical pain was reported by 18 patients. Non-invasive tests were 94 positive, 60 negative and 7 non-diagnostic. Ergonovine test elicited coronary spasm in 85 patients (52.5%). No significant correlation was found between the positivity of a non-invasive test and ergonovine-induced spasm. CONCLUSIONS: More than half of the patients with angina and normal coronary arteries can be diagnosed with vasospastic angina if ergonovine test is performed. Even patients with a negative non-invasive test maybe sent to coronary angiography when vasospastic angina is suspected, in order to have an accurate diagnosis.

Adult↗
PubMedDate not supplied

Values of intravenous ergonovine test with two-dimensional echocardiography for diagnosis of coronary artery spasm.

The purpose of this study was to evaluate the clinical validity of the bedside ergonovine test with digital echocardiography and the side-by-side continuous cineloop display method (ergonovine echocardiography) as a noninvasive diagnostic tool for coronary artery spasm. Bedside ergonovine test was performed in 66 patients who showed coronary vasospasm during coronary angiography including provocation testing (group with variant angina) and 39 patients with normal angiograms and no evidence of coronary artery spasm (group with nonanginal pain). A bolus of ergonovine maleate (0.025 or 0.05 mg) was injected at 5-minute intervals up to total cumulative dosage of 0.35 mg, and 12-lead electrocardiography and two-dimensional echocardiography were recorded every 3 minutes after each injection. Left ventricular wall motion was analyzed with a commercially available quad system. The positive criteria of bedside ergonovine test included reversible ST segment elevation or depression on electrocardiograms (ECG criteria) and reversible regional wall motion abnormalities by echocardiography (Echo criteria). The overall sensitivity and specificity of ECG criteria were 53% (35/66; 95% confidence interval 41% to 65%) and 100%, respectively. By Echo criteria the sensitivity increased to 89% (59/66; 95% confidence interval 81% to 97%), with a specificity of 95% (37/39).(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris, Variant↗
PubMed1996

Hypersensitivity of human coronary segments to ergonovine 6 months after injury by coronary angioplasty: a quantitative angiographic study in consecutive patients undergoing single-vessel angioplasty.

OBJECTIVE: Multiple studies have been designed to analyse restenosis angiographically but few have studied the vasoreactivity of coronary segments subjected to angioplasty a few months before. In the present study we analysed, with use of quantitative angiography, the vasoreactivity of previously dilated segments to graded doses of ergonovine and of isosorbide dinitrate. PATIENTS: Fifty consecutive patients undergoing follow-up angiography 6 months after a single coronary angioplasty procedure were studied. RESULTS: The vasoconstrictor response at dilated segments (-19.3 +/- 3.0%) was significantly greater than at control proximal and distal sites in dilated (-7.3 +/- 1.1%, -11.0 +/- 2.9%) and non-dilated (-9.1 +/- 1.3%, -8.3 +/- 2.2%) vessels for the lowest dose of ergonovine (100 micrograms). The constrictor response to 100 micrograms ergonovine (-20.2 +/- 5.3%) at restenosed segments (> 50% stenosis, n = 18) was similar to that (-18.8 +/- 3.8%) at non-restenosed sites (n = 32). In contrast, the degree of constrictor response was similar in all segments including dilated segments for the highest dose of ergonovine used. All segments dilated significantly after intracoronary injection of isosorbide dinitrate. CONCLUSION: Our results demonstrate hypersensitivity of the dilated site to ergonovine 6 months after angioplasty at both restenosed and non-restenosed sites. This response may reflect partial dysfunction of endothelium that has regenerated after injury or hypersensitivity of vascular smooth muscle cells at the site of arterial injury.

Aged↗
PubMed1991

Coronary reactivity to ergonovine--possible relationship to accelerated coronary arterial disease in cardiac transplant recipients.

Severe coronary artery spasm can occur in orthotopic cardiac transplant recipients. To investigate the possible mechanisms and relevance of coronary spasm to the subsequent development of coronary disease, the response of the coronary arteries to intracoronary ergonovine maleate was studied in 10 patients who had undergone orthotopic cardiac transplantation and were shown to have normal coronary arteries at angiography. Ergonovine in doses of 1, 5 and 10 micrograms was injected into the left coronary artery followed by 2 mg of isosorbide dinitrate. Proximal coronary artery luminal diameters were measured using automated computerized quantitative angiography of the left anterior descending (LAD) and circumflex (LCX) vessels. Five patients (responders) demonstrated a dose response curve to intracoronary ergonovine which was similar to that previously seen in non-transplant patients (mean percentage diameter change +/- SEM, -24.68 +/- 1.93 for LAD, -24.06 +/- 3.91 for LCX). The remaining five patients (non-responders) demonstrated a virtually flat dose response curve significantly different from that of the responders (P = 0.001 for LAD, P = 0.013 for LCX). Angiography after 2 years demonstrated significant coronary disease in four of the five responders to ergonovine. In contrast, the five non-responders to ergonovine continue to have no detectable disease by angiography.

Adult↗
PubMed1994

Influence of inhibition of endothelium-derived nitric oxide formation to effects of vasoconstrictor agents neuropeptide Y, clonidine, and ergonovine on coronary vascular resistance.

To determine whether inhibition of endothelium-derived nitric oxide (EDNO) synthesis enhances the effects of exogenous vasoconstrictor agents on the coronary vasculature, we examined the effects of neuropeptide Y (NPY), clonidine, and ergonovine on coronary vascular resistance (CVR) with and without EDNO inhibitor and compared the results. In 15 anesthetized mongrel dogs, the left circumflex coronary artery (LCX) was perfused with arterial blood from the left common carotid artery through an extracorporeal bypass tube and LCX blood flow was measured with an electromagnetic flowmeter. Nine of the dogs were pretreated with intracoronary NG-nitro-L-arginine methyl ester (L-NAME 300 microM in LCX blood) (L-NAME group) and the other 6 were treated with normal saline (vehicle group). Three doses of NPY (4.3, 43, 430 ng/kg), two doses of clonidine (30 and 300 ng/kg), and one dose of ergonovine (20 micrograms/kg) were infused into LCX. NPY decreased LCX flow and increased CVR dose dependently in both groups, and there was no significant difference in the dose-response relation between the two groups. Clonidine decreased LCX flow and increased CVR in both groups, and there was no difference in the effect between the groups. In contrast, ergonovine decreased LCX flow and increased CVR to a greater degree in the L-NAME group than in the vehicle group (p < 0.01). Thus, inhibition of EDNO synthesis by L-NAME did not result in enhancement of the vasoconstrictor effects of NPY and clonidine, whereas it significantly enhanced the effect of ergonovine, possibly through inhibition of ergonovine-induced EDNO release.

Animals↗
PubMed2000

Modulation of contractions to ergonovine and methylergonovine by nitric oxide and thromboxane A2 in the human coronary artery.

This study explored the modulatory effects of nitric oxide and thromboxane A2 on contractions to ergonovine and methylergonovine in human coronary arteries. To elucidate the different role of nitric oxide synthase in the response to the ergot alkaloids, the serotonin (5-HT) receptors involved in nitric oxide synthase in the response to the ergot alkaloids, the 5-HT receptors involved in nitric oxide release and the contraction of the vascular smooth muscle were characterized with more selective 5-HT-receptor agonists and antagonists. Rings of human coronary arteries from explanted hearts were suspended in organ chambers for isometric tension recording. After testing for contractile (potassium chloride, 60 mM) and endothelial function (substance P, 10(-8) M), respectively, they were exposed to ergot alkaloids or other agonists in the absence or presence of U 46619 (10(-9) M), or nitro-L-arginine (10(-4) M), or both. Ergonovine and methylergonovine were comparable, weak vasoconstrictors in untreated preparations. Contractions to ergonovine were augmented by U 46619, but not by nitro-L-arginine. Contractions to methylergonovine were augmented only by combining U 46619 and nitro-L-arginine. Serotonin and methylergonovine, but not ergonovine, elicited endothelium-dependent, nitric oxide-mediated relaxations. Nonselective 5-HT(1B/1D)-receptor stimulation caused both contractions and relaxations; selective 5-HT1B stimulation caused relaxations only. In the human coronary artery, contractions to ergonovine are not dependent on NO release but are synergistically augmented by thromboxane. Methylergonovine causes similar effects on the vascular smooth muscle, but contractions are inhibited by the release of NO from the endothelium. The 5-HT receptor on the endothelium appears to be different from the receptor on the vascular smooth muscle, which mediates the contractile response to the ergot alkaloids.

Adult↗
PubMed1987

Ergonovine testing in patients with exertional angina.

Injection of ergonovine has been suggested as a diagnostic test in patients with suspicion of a vasospastic component in the pathophysiology of angina pectoris. However, a thorough case history has been considered by others to give the same information regarding the anginal mechanism. Therefore a bedside ergonovine test (0.075-0.675 mg i.v.) was performed in 21 consecutive patients with effort angina in order to study the relation between the outcome of the test and the case history concerning angina at rest. A coronary angiography was performed in all cases and showed significant stenoses in 17 patients and normal coronary arteries in 4. Eight patients had angina only during effort, 11 had angina both during effort and at rest and 2 patients had atypical chest pain. Ten of the 11 patients with concomitant rest angina developed chest pain at the ergonovine test and 9 coexisting ECG changes. However, these effects were about as common among the 8 patients without angina at rest: 7 developed chest pain and 4 also ECG changes. The two patients with atypical chest pain had normal coronary angiograms and in these patients ergonovine provoked the same atypical chest pain but no ECG changes. Thus, a concomitant angina at rest is a common finding among patients with severe effort angina. However, the response to ergonovine was as common in the group with only effort angina as in the group with concomitant rest angina, indicating the limited value of this test in patients with severe angina.

Adult↗
PubMed1987

Induction of coronary artery spasm by a direct local action of ergonovine.

To investigate whether ergonovine acts directly on coronary arteries or via remote neurohumoral reflexes, we administered small titrated increments of intracoronary ergonovine up to a maximum cumulative dose of 50 micrograms to 15 patients. In six patients with variant angina (group 1), ischemic electrocardiographic ST changes, angina, and localized coronary spasm (local coronary diameter reduction of 87.8 +/- 18.9% [mean +/- SD]) followed after 6 to 50 micrograms (mean 20.7) cumulative intracoronary ergonovine. In nine patients with atypical chest pain, normal baseline coronary arteriograms, and no evidence of variant angina (group 2), there was no ischemic ST segment change or localized coronary spasm after 6 to 50 micrograms (mean 31.6) intracoronary ergonovine. Coronary diameter of proximal vessels of patients in group 2 was reduced by 16.2 +/- 6.5% and did not differ from the response of nonspastic vessels of comparable size of group 1 (20.5 +/- 13.8%; p = .7). There was no significant difference in the median effective dose values in the dose-response curves of the spastic and nonspastic segments between groups 1 and 2. Ergonovine causes coronary spasm by a direct local effect, which seems to be caused by localized arterial hyperreactivity rather than supersensitivity. Intracoronary delivery may be safer than intravenous administration because negligible drug recirculation may prevent perpetuation of spasm and selective coronary administration can avoid branches with critical stenoses.

Coronary Vasospasm↗
PubMed1989

Endothelium-dependent inhibition of ergonovine-induced contraction is impaired in porcine coronary arteries with regenerated endothelium.

The inhibitory effects of the endothelium against ergonovine-induced contraction were examined in isolated porcine coronary arteries under normal conditions and after endothelial regeneration. Endothelium-dependent responses were examined in vitro in normal Yorkshire pigs (n = 16) and in pigs that had undergone balloon endothelium removal of the left anterior descending coronary artery (LAD) 4 weeks before the study (n = 10). The presence of a complete endothelial lining was confirmed histologically. In rings from normal arteries contracted with prostaglandin F2 alpha in the presence of indomethacin and ketanserin (a 5-HT2-serotonergic blocker), ergonovine caused endothelium-dependent relaxations. They were attenuated by rauwolscine (an alpha 2-adrenergic blocker), inhibited by methiothepin (a combined 5-HT1- and 5-HT2-serotonergic blocker) or by pertussis toxin (an inhibitor of several G proteins) and abolished by oxyhemoglobin (a selective inactivator of endothelium-derived relaxing factor). In quiescent rings from normal arteries, ergonovine caused contractions that were inhibited by the presence of the endothelium; this endothelium-dependent inhibition was abolished by oxyhemoglobin. The direct contractions were not affected by prazosin (an alpha 1-adrenergic blocker), rauwolscine, 6-hydroxydopamine (an agent causing chemical sympathetectomy), or diphenhydramine (an H1-histaminergic blocker) but were inhibited by ketanserin. In rings with regenerated endothelium contracted with prostaglandin F2 alpha, the endothelium-dependent relaxations to ergonovine were reduced significantly and were not inhibited by pertussis toxin. In quiescent rings with regenerated endothelium, the endothelium-dependent inhibition of ergonovine-induced contraction was less.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Effects of ergonovine-induced vasoconstriction on the genesis of myocardial ischemia during coronary stenosis in dogs.

We developed a canine model with coronary stenosis produced by intraluminal obstruction with a micro-balloon occluder to assess the role of vasomotor tone of a large coronary artery with a preexisting fixed stenosis in the genesis of myocardial ischemia. Hemodynamic and electrocardiographic responses to ergonovine, an agent capable of provoking coronary spasm, were evaluated. In the absence of coronary stenosis, intracoronary infusion of 4 micrograms/min ergonovine had no systemic and coronary hemodynamic effects. Similarly, with various degrees of external obstruction created by a screw-type metal constrictor, ergonovine had little hemodynamic effects. By contrast, with a stenosis greater than 28.4 +/- 5.0 mmHg in pressure gradient, created by intraluminal obstruction which preserved active arterial vasomotion, ergonovine-induced vasoconstriction produced a marked decrease in coronary blood flow and distal coronary pressure, followed by ST-elevation. These deleterious effects of ergonovine on coronary hemodynamics were reversed completely by intracoronary infusion of nitroglycerin. Our results indicate that the effects of normal coronary arterial vasomotor activity on a stenosed vessel can cause myocardial ischemia.

Animals↗
PubMed2001

Long-term outcome of patients with ergonovine induced coronary constriction not associated with ischemic electrocardiographic changes.

OBJECTIVES: This study investigated the long-term outcome of patients with coronary artery constriction induced with ergonovine but not associated with ischemic electrocardiographic changes. METHODS: The ergonovine provocation test was performed in 419 patients with suspected but unproven variant angina. Ergonovine maleate was administered into the coronary arteries at 8 micrograms/min for 5 min during cardiac catheterization. Patients were categorized into three groups according to their response to ergonovine. The positive group contained patients who developed coronary constriction of more than 90% in diameter associated with ischemic electrocardiographic changes and chest pain. The intermediate group contained patients who had coronary constriction of more than 90% but no electrocardiographic changes. The negative group contained patients who had neither significant coronary constriction nor ST segment changes. RESULTS: There were 305 patients, 49, and 65 in the negative, intermediate, and positive groups, respectively. Death occurred in six patients (2%), one (2%), and one (2%) in the negative, intermediate, and positive groups, respectively. Sudden cardiac death occurred in one patient in the negative group. Recurrence of chest pain with effectiveness of sublingual administration of nitroglycerine was observed in 26 patients (9%), 10 (20%), and 11 (17%) in the negative, intermediate, and positive groups, respectively. CONCLUSIONS: Some patients in the intermediate group might show "false negative" response to ergonovine so careful treatment with calcium antagonists should be continued in patients in the intermediate group as well as patients with vasospastic angina.

Coronary Angiography↗
PubMed1985

[Changes in angina threshold induced by administration of ergonovine maleate during pacing in patients with chronic exertional angina].

It is widely accepted that the occurrence of chest pain and/or ST segment elevation during ergonovine testing is a hallmark of abnormal coronary constriction. However, the negativity of this test cannot be considered as an incontrovertible proof of the absence of coronary sensitivity to vasoconstriction. Indeed, it could only indicate that the resulting effect is inadequate to critically reduce coronary blood flow. To test this hypothesis we studied 12 patients with proven coronary artery disease and negative ergonovine test who had complained of chronic exertional angina pectoris and referred variable threshold for the occurrence of pain. They were submitted to atrial pacing (starting from 90 bpm, with 10 bpm increments every 2 min) before (control) and after ergonovine administration (total dose = 0.675 mg). Time, heart rate and rate pressure product were evaluated at the onset of angina and significant ischemia (0.1 mV ST segment depression). After ergonovine, angina was achieved earlier (405 +/- 173 vs 526 +/- 180 sec, p less than 0.005) than during control and at a lower heart rate (116 +/- 15 vs 131 +/- 15 bpm, p less than 0.001) and rate pressure product (15.8 +/- 2.0 vs 18.8 +/- 2.3 X 10(3) U, p less than 0.001). Changes in anginal threshold were widely variable among cases being that the time to onset of pain was dramatically reduced in certain patients but unchanged in one. Similar results were obtained when substituting the ischemic to the anginal threshold. Thus, negativity to ergonovine testing does not imply the absence of coronary constriction which may be revealed when increasing myocardial oxygen demand by atrial pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1979

Predictability of the response to the ergonovine test. Value in the diagnosis of coronary spasm.

Thirty-five patients with atypical chest pain were given ergonovine maleate as a provocative test for coronary spasm. None of the patients had significant coronary atherosclerosis. The patients were divided into two groups based on clinical information available before ergonovine testing. Group 1 patients (n=13) had objective evidence of cardiac disease manifested by episodes of syncope, ventricular tachyarrhythmias, myocardial infarction, or transient ST segment shifts with chest pain. Group 2 patients had chest pain but no objective evidence of cardiac disease. The ergonovine test was positive in 11 of 13 patients in group 1. None of the 22 group 2 patients had a positive response to ergonovine. These data suggest that ergonovine testing does not allow for any more precise recognition of patients with atypical chest pain who have coronary artery spasm than do clinical data alone.

Adult↗
PubMed1978

Selective blockade of dopamine-induced vasodilation by ergonovine maleate in the vasculatures of dogs and rabbits.

In urethane anesthetized rabbits, ergonovine maleate significantly attenuated dopamine-induced systemic hypotension. Initial pressor responses to dopamine were significantly prolonged and potentiated by ergonovine. Mesenteric vasodilation elicited by dopamine in dogs was competitively inhibited by ergonovine at doses of 0.09 and 0.18 mg/kg, i.a. Failure of ergonovine to inhibit vasodilatory responses to acetylcholine or isoproterenol suggested selective blockade. These results confirm existing evidence that ergonovine selectively antagonizes peripheral dopaminergic receptors subserving vasodilation.

Acetylcholine↗
PubMed1980

[The influence of ergonovine on coronary artery diameter and hemodynamics in patients with angina pectoris at rest (author's transl)].

The influence of methyl ergonovine on coronary artery diameter and regional ventricular function was studied in three groups of patients with and without suspected coronary artery spasm. Ten patients with angina at rest in whom spasm was suspected were compared to seven coronary heart disease patients with stable effort angina. Six patients without coronary heart disease served as controls. Ergonovine, an agent known to cause coronary vasoconstriction, was administered in order to identify the possible role of spasm in the various subgroups. The standardized study procedure comprised coronary and left ventricular angiography before and after 0.1 to 0.4 mg ergonovine i.v. as well as after 1.6 mg nitroglycerin sublingually. Following ergonovine provocation, narrowing of the anterior descending branch averaged 22 per cent in the patient group with suspected spasm, 3 per cent in patients with coronary heart disease, and 6 per cent in the control group. The spasm group also displayed regional ventricular hypokinesis and an increase in endsystolic volume. LVEDP increased from 15 +/- 6 to 28 +/- 7 mm Hg (p < 0.0005) mean circumferential fiber shortening (mean Vcf) decreased from 1.6 +/- 0.4 to 1.1 +/- 0.4 circ/s (p < 0.0025), and the velocity of shortening in the anterior apical hemiaxis (Vm3) declined from 1.9 +/- 0.2 to 0.8 +/- 0.4/s (p < 0.0005). These changes were much less evident in the coronary heart disease group. No significant hemodynamic changes were observed in the control group. Patients with angina at rest are much more susceptible to ergonovine-induced coronary artery narrowing than patients with stable exertional angina.

Adult↗
PubMed1994

Evaluation of a dosing method for studying ergonovine effects in cattle.

We evaluated the feasibility of using miniosmotic pumps as a way to continuously treat cattle with a singular ergot alkaloid (ergonovine) of known content, thus mimicking the natural fescue toxicosis disease state, but allowing study of specific alkaloid effects. Dosing animals with increasing amounts of ergonovine via miniosomotic pumps, followed by daily acquisition of plasma samples for high-performance liquid chromatographic determination of the alkaloid, resulted in stepwise increases in plasma ergonovine concentration. However, despite the detectable blood concentration of ergonovine, calves did not have typical clinical signs of ergot alkaloid toxicosis. Similarly, serum prolactin concentration was unaffected by ergonovine in these cattle, implicating some other alkaloid of endophyte-infested fescue as causative of the usual prolactin-suppressive response. The results confirm use of this animal dosing method to study biological effects of singular purified alkaloids of known amount, without bioavailability concerns. Thus, this dosing method will facilitate studies to determine the harmful effects of individual alkaloids found in toxic tall fescue, and ultimately, to alleviate their costly effects in cattle, horses, and other species.

Animals↗
PubMed1988

Biphasic response of coronary arterial diameter to intracoronary ergonovine.

This report presents a case of paradoxical coronary arterial dilation induced by intracoronary ergonovine. When compared with the control angiogram, the right coronary artery obviously dilated with selective, intracoronary administration of cumulative doses of 5 micrograms and 15 micrograms ergonovine without concomitant hemodynamic changes. Additional intracoronary infusion of 35 micrograms ergonovine into the right coronary artery inversely increased vascular tone of the vessel associated with a focal hyperconstriction. Such a biphasic response of arterial diameter to intracoronary ergonovine was also observed in the left coronary artery, but the degree of dilation was much smaller.

Angina Pectoris, Variant↗