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PubMed1982

Variability of electrocardiographic responses to repeated ergonovine provocation in variant angina patients with coronary artery spasm.

We reviewed our experience with serial ergonovine provocative tests for coronary artery spasm (CAS) in ten variant angina patients with angiographically proved CAS. Of the 26 ergonovine tests performed in the ten patients, only four patients exhibited reproducible ECG response to ergonovine. The remaining six patients had variable and unpredictable ECG responses to ergonovine. All patients were in an active phase of their disease. The variability of ST segment directional response to ergonovine is considered to be on the basis of disparate sensitivity of the coronary circulation to intravenous ergonovine. Because of this variable response, the ECG response alone should not be considered as the standard indicator for CAS presence but should be utilized with other hemodynamic and angiographic criteria.

Angiography↗

PubMed1984

Ventricular arrhythmias during ergonovine-induced episodes of variant angina.

Of 95 consecutive patients with active variant angina who underwent ergonovine testing in the coronary care unit while off treatment, 24 (25%) developed serious ventricular arrhythmias: ventricular tachycardia in eight, bigeminy in seven, pairs in five, and frequent ventricular extrasystoles in four. Ergonovine-induced arrhythmias were observed more often in patients with anterior than inferior ST segment elevation (p less than 0.05). ST segment elevation was significantly higher (10.3 +/- 8.1 vs 3.1 +/- 2.1 mm) in patients who developed arrhythmias. All ventricular arrhythmias began within 3 minutes after the onset of ST segment elevation. The intravenous administration of nitroglycerin eliminated arrhythmias in 22 of 24 cases; in only two patients did ventricular arrhythmias develop after the administration of nitroglycerin. Serious ventricular arrhythmias were found during spontaneous variant angina attacks in 14 of 24 patients with ergonovine-induced arrhythmias compared to 16 of 71 patients without ergonovine-induced arrhythmias (p less than 0.001). We conclude that arrhythmias during ergonovine testing are most often caused by ischemia and not reperfusion. Patients with arrhythmias during ergonovine-induced attacks are more likely to have arrhythmias during spontaneous attacks.

Adult↗

PubMed1992

The effect of ergonovine on coronary vasodilatory reserve in patients with angiographically normal coronary arteries.

Ergonovine produces physiologic coronary artery narrowing in many patients without focal coronary spasm. The effect of ergonovine-induced coronary vasoconstriction on coronary vasodilatory reserve is unknown. Therefore we studied 10 patients with atypical chest pain and angiographically normal coronary arteries. The heart rate and blood pressure were recorded continuously and coronary Doppler flow velocity was measured continuously with a 20 MHz Doppler-tipped catheter. Ergonovine caused diffuse narrowing of the vessels in all patients, with a 12% +/- 5% change in diameter of the left anterior descending coronary artery (p less than 0.001). There was a significant change in systolic (17% +/- 12% change; p less than 0.05) and mean arterial pressure (13% +/- 13% change; p less than 0.05), with no significant change in mean coronary flow velocity with ergonovine. Ergonovine also did not attenuate the maximal hyperemic response with papaverine. Thus despite an increase in myocardial demand and a decrease in caliber of conductance coronary vessels, the coronary autoregulatory flow responses were intact after the administration of ergonovine.

Angina Pectoris, Variant↗

PubMed1992

Induction of coronary artery spasm by intracoronary acetylcholine: comparison with intracoronary ergonovine.

To investigate the mechanism of coronary spasm, we compared the action of acetylcholine with that of ergonovine in 11 patients with vasospastic angina (group 1) and in 15 patients with chest pain (group 2). Coronary arteriography was performed immediately after the patients received intracoronary injections of titrated increments of each agent. In the patients in group 1 occlusive or near-occlusive (99% luminal narrowing) coronary spasm associated with angina and ischemic electrocardiographic ST changes was noted in nine of 11 patients receiving acetylcholine and in all 11 patients receiving ergonovine. The region and the degree of the most severe coronary spasm on coronary arteriograms evoked by the two agents were the same in nine of the 11 patients in group 1. In the other two patients in group 1, spontaneous focal coronary spastic stenosis in the baseline coronary arteriogram was relieved by the intracoronary injection of acetylcholine, and a focal coronary occlusive spasm in the same region was induced repeatedly by the subsequent intracoronary injection of ergonovine (paradoxic phenomenon). In contrast, occlusive or near-occlusive coronary spasm was not induced by either agent in any patient in group 2. These results suggest that the two provocative tests for coronary spasm that involve acetylcholine and ergonovine are clinically useful in the diagnosis of vasospastic angina, but testing with intracoronary ergonovine is needed when a spontaneous focal coronary spasm is relieved by the intracoronary injection of acetylcholine. The results also indicate that in many patients with vasospastic angina, nonspecific hypersensitivity to acetylcholine or ergonovine in a definite region of the coronary arteries generally plays an important role in the induction of coronary spasm.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1980

Refractory ergonovine-induced coronary vasospasm: importance of intracoronary nitroglycerin.

Recent experience has suggested that the ergonovine maleate test is a safe procedure for the diagnosis of variant angina pectoris, because ergonovine-induced coronary vasospasm has generally been reversible by sublingual nitroglycerin. This report describes five cases of ergonovine-induced coronary vasospasm that were refractory to sublingual nitroglycerin. Four of these patients had cardiac arrest. In two patients the vasospasm was responsive to intracoronary nitroglycerin administration. Three patients died as a reuslt of the test. The two survivors differed from the nonsurvivors in the total dose or ergonovine given (0.1 and 0.15 mg versus 0.17, 0.3 and 0.3 mg, respectively) and in the method of administration of ergonovine. The survivors were given serial doses of 0.05 mg each whereas the three nonsurvivors received either larger initial doses (0.1 followed by 0.07 mg) or progressive incremental doses (0.05, 0.1 and 0.15 mg serially). Sublingual nitroglycerin, given to all five patients, and intravenous nitroglycerin, given to three of the five, were ineffective in reversing vasospasm. Intracoronary nitroglycerin favorably altered the course of the survivors. Thus, the ergonovine maleate test is not benign and may cause severe coronary vasospasm that is unresponsive to sublingual and intravenous nitroglycerin, but may be reversed by intracoronary nitroglycerin.

Administration, Oral↗

PubMed1987

Relative roles of preload increase and coronary constriction in ergonovine-induced myocardial ischemia in stable angina pectoris.

To assess the relative role of increased ventricular preload and critical coronary lesions in ergonovine-induced myocardial ischemia, 9 normal subjects (group A), 7 patients with stable angina (group B) and 5 with variant angina (group C) were studied. In all patients, the 12-lead electrocardiogram, blood pressure and left ventricular (LV) volume (technetium-99m blood pool) were continuously recorded before and during administration of incremental doses of ergonovine given at 5-minute intervals. In all subjects, an initial LV dilatation developed; in group B and C patients, this was followed by a decrease in stroke volume and ejection fraction with subsequent onset of electrocardiographic changes and angina. The interval between these events was significantly shorter in group C and in 3 group B patients; in these patients, signs of ischemia appeared with smaller ergonovine doses and at minimal preload increase, coronary constriction being the likely mechanism of ischemia. In the remaining 4 group B patients, the onset of stroke volume, ejection fraction, electrocardiographic changes and angina was significantly delayed, occurring after administration of larger ergonovine doses when LV volume was already considerably increased. This finding suggests that the loading effect of ergonovine on LV volume, rather than on coronary constriction, could be the prevailing mechanism of ergonovine-induced ischemia in these patients.

Angina Pectoris↗

PubMed1998

Diagnosis of coronary vasospasm in patients with clinical presentation of unstable angina pectoris using ergonovine echocardiography.

Although coronary vasospasm can contribute to the development of unstable angina, the definite diagnostic method has not been established. The purpose of this study was to determine if ergonovine echocardiography (detection of regional wall motion abnormality during bedside ergonovine challenge) after angiographic confirmation of insignificant fixed disease would be useful and safe in detecting coronary vasospasm in patients with unstable angina. After control of chest pain with medications in patients admitted to the coronary care unit under the tentative diagnosis of unstable angina, diagnostic coronary angiography was performed. All patients with normal or insignificant fixed disease underwent ergonovine echocardiography after discontinuation of medications for 4+/-1 days. Among 208 consecutive patients enrolled for this study, 75% (156 of 208) showed significant fixed disease in the angiography. Ergonovine echocardiography was performed in 52 patients with insignificant disease, and coronary vasospasm was documented in 33 (63%, 33 of 52). No serious procedure-related arrhythmia or myocardial infarction occurred. Esophageal motility disorder and hypertrophic cardiomyopathy were diagnosed in 6 and 3 patients, respectively. Chest pain of undetermined etiology was the final diagnosis at discharge in 10 patients (5%, 10 of 208); among them chest pain redeveloped in 2 patients, and repeated ergonovine echocardiography revealed positive results. Our data suggest that among patients with the clinical presentation of unstable angina, coronary vasospasm is the main cause of myocardial ischemia in a considerable number of patients with a normal or near-normal angiogram, and ergonovine echocardiography after confirmation of absence of significant fixed disease is useful and safe for noninvasive diagnosis of coronary vasospasm in this setting.

Adult↗

PubMed1997

Increasing vasoconstrictor response to ergonovine with oxidative injury in canine coronary artery.

BACKGROUND: The effects of oxygen free radicals on coronary vasoreactivity remain unknown. OBJECTIVE: To examine whether oxygen free radicals increase coronary arterial tone and sensitivity to vasoconstrictor stimulation in closed-chest dogs. METHODS: Oxygen radicals were generated by the reaction of xanthine plus xanthine oxidase (XXO) and effects of these substances on the left coronary artery (the percentage diameter change) and on the constrictor effect of ergonovine were examined in vivo in 19 anesthetized, closed-chest dogs by selective coronary angiography. The effects of XXO solution and ergonovine were assessed in a cumulative fashion using 100, 200, and 300 ml XXO and 50, 100, 150, and 200 micrograms ergonovine, in 5 (group I) and 6 dogs (group II), respectively. The effects of XXO on the constrictor responses elicited by 50 micrograms ergonovine were examined in eight dogs (group III). Changes in the vascular endothelium were examined by postmortem electron microscopic examination. RESULTS: Oxidative injury alone produced slight constriction of the coronary artery, but the change was not significant. However, ergonovine-induced vasoconstriction was enhanced after administration of 100 and 200 ml (cumulative amount) XXO solution (P < 0.05, group II versus group III). The enhancement was no longer observed after administration of 300 ml (cumulative amount) XXO solution. Scanning and transmission electron microscopies revealed the formation of blebs and ulceration in the coronary endothelium after administration of XXO solution. CONCLUSION: These results suggest that oxygen radicals can enhance the ergonovine-induced coronary vasoconstriction in a concentration-dependent manner. There seems to be a critical level of oxygen radicals for the production of the effect.

Animals↗

PubMed1980

Supersensitivity of atherosclerotic rabbit aorta to ergonovine. Mediation by a serotonergic mechanism.

Patients with coronary vasospasm appear to be supersensitive to the coronary constrictor effects of ergonovine. To determine whether atherosclerosis alters arterial reactivity and sensitizes arteries to ergonovine, contractile responses of isolated aortae from control rabbits and from rabbits fed a high-cholesterol diet were compared. Aortic strips were mounted in a myograph for the monitoring of isometric tension, equilibrated in oxygenated Krebs buffer, and exposed to graded concentrations of agonists and antagonists. The concentration-response relation for ergonovine in atherosclerotic arteries exhibited a markedly depressed constrictor threshold concentration (0.5 pM vs. 0.23 muM in controls), a significantly lowered one-half effective dose (ED(50)) value, and an augmented maximal response. Furthermore, atherosclerotic arteries showed similar, although less pronounced changes in the concentration-response relation for serotonin. In contrast, responses to 34 mM KCl were virtually identical, and the concentration-response relation for phenylephrine were similar in the two groups. In control arteries, 0.1 muM phentolamine and 0.1 muM prazosin suppressed responses to 1 muM ergonovine by 71 and 90%, respectively. However, in atherosclerotic arteries alpha-blockers in the same concentration inhibited responses to 0.01 muM ergonovine by less than 10%. On the other hand, 0.1 muM cyproheptadine, a serotonergic antagonist, suppressed these responses by 82%. Thus, the supersensitivity to ergonovine appeared to be mediated predominantly by a serotonergic mechanism. These results indicate that smooth muscle in atherosclerotic arteries may be supersensitive to specific vasoconstricting stimuli, a change that might contribute to arterial dysfunction in vivo.

Animals↗

PubMed1981

Experience with ergonovine provocative testing for coronary arterial spasm.

We reviewed our experience with the ergonovine provocative test for coronary arterial spasm in 40 patients with pain in the chest believed to be angina pectoris and in one patient with a myocardial infarction and normal coronary arteries. Twenty-nine patients had normal coronary arteries, while 12 had mild to moderate lesions. Ergonovine maleate was administered incrementally in total cumulative doses of 0.25 mg to 1.2 mg. The effect of ergonovine on coronary arterial caliber was determined by comparing the arterial diameter from the angiogram obtained after administration of ergonovine with that from the control. Measurements were made at the same preselected points in both films and also at points of greatest response. Excluding the three cases with complete occlusion, the mean reduction in coronary arterial diameter at preselected points was 12 +/- 15 percent. When the points of greatest response were examined, the maximum reduction in coronary arterial diameter was less than 25 percent in 13 patients, 25 to 50 percent in 20 patients, and more than 50 percent in eight patients. The patterns of response included complete occlusion of a vessel in the three patients with variant angina, diffuse narrowing in 16, diffuse and focal narrowing in six, and spasm at the catheter tip in three patients. All patients with maximum reductions of more than 50 percent in coronary arterial diameter and six of those with maximum reductions of 25 to 50 percent had pain in the chest, but only the three with complete occlusion had associated changes in the S-T segment. Thus, the response in patients with variant angina represents one end of a spectrum of responses to administration of ergonovine. In addition, a large number of patients may have ergonovine-induced pain in the chest without electrocardiographic changes and only an intermediate degree of coronary arterial spasm.

Adult↗

PubMed1985

Effect of prostaglandin F2 alpha, phenylephrine and ergonovine on uterine contractions in the ewe.

Two experiments were conducted to determine the effect of prostaglandin F2 alpha (PGF2 alpha), phenylephrine and ergonovine on uterine contractions. In the first experiment, ewes were bilaterally ovariectomized, and a strain gauge force transducer was sutured to the serosa of one uterine horn. Each ewe was treated sc with 2 micrograms of estradiol-17 beta daily to prevent regression of the uterus. Beginning at least 5 d after ovariectomy, four dose levels of PGF2 alpha, phenylephrine and methoxamine were given by im injection and ergonovine was given by im or iv injection. Phenylephrine, methoxamine and ergonovine are alpha-adrenoceptor agonists. Uterine activity was recorded by physiograph for 30 min before and 90 min after treatment. Tracing were analyzed for 20-min periods before treatment and 4 to 24 min and 50 to 70 min after treatment. In Exp. 2, transducers were attached to uteri of intact ewes at d 10 to 12 of an estrous cycle. During subsequent estrus, one or two dose levels of PGF2 alpha, phenylephrine and ergonovine were given by im injection and uterine activity recorded. In Exp. 1, PGF2 alpha and phenylephrine increased (P less than .05 or .01) the number of amplitude of contractions at both 4 to 24 and 50 to 70 min. Ergonovine given im increased the number of contractions. In intact estrous ewes, PGF2 alpha increased the number and amplitude of contractions at 4 to 24 min, phenylephrine increased the number and amplitude at both 4 to 24 and 50 to 70 min, and ergonovine increased the number slightly but significantly at 4 to 24 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Effect of phenylephrine, ergonovine, oxytocin and norepinephrine as an extender ingredient on viability of bovine spermatozoa.

We evaluated effects of three concentrations of phenylephrine, ergonovine, oxytocin and norepinephrine (myometrial stimulants) on viability of spermatozoa when they were included in a seminal extender. Using a split ejaculate technique, ejaculates from each of 10 bulls were extended in egg-yolk citrate to a final concentration of 35 x 10(6) sperm/ml, including 20 mg/ml, 2 mg/ml and .2 mg/ml, of phenylephrine or ergonovine, 20 IU/ml, 2 IU/ml and .2 IU/ml oxytocin or 200 micrograms/ml, 20 micrograms/ml and 2 micrograms/ml norepinephrine prior to freezing. Extended semen without a myometrial stimulant served as the control. Percentage of intact acrosomes was determined prior to freezing for all treatments. Motility and percentage of intact acrosomes were determined immediately after thawing (0 h) and again after 4 h incubation at 37 degrees C. Percentage of intact acrosomes was reduced (P less than .05) prior to freezing by phenylephrine (20 mg/ml) and ergonovine (20 mg/ml) (phenylephrine = 56%; ergonovine = 63%; control = 74%). The same doses of phenylephrine and ergonovine reduced (P less than .05) post-thaw motility and percentage of intact acrosomes at both 0 and 4 h compared with controls. Sperm exposed even to the intermediate concentration (2 mg/ml) of ergonovine had lower (P less than .05) motility 4 h post-thaw. No other compound or concentration of compound or concentration of compound affected percentage of intact acrosome or motility. There were no two or three-way bull x compound and concentration interactions (P greater than .2).(ABSTRACT TRUNCATED AT 250 WORDS)

Acrosome↗

PubMed1981

Use of ergonovine to identify esophageal spasm in patients with chest pain.

We administered intravenous ergonovine maleate to 14 patients with chest pain resembling angina pectoris and to four healthy volunteers. Five of the patients experienced their typical chest pain after ergonovine, and manometric signs of esophageal spasm also developed. The remaining nine patients and the four volunteers did not experience chest pain, but all subjects except one had some symptomatic response to ergonovine, including chest warmth or heaviness, headache, mild choking sensation, facial numbness, flushing, or nausea. Two of the nine patients and one of the four volunteers developed manometric signs of esophageal spasm after ergonovine but experienced no chest pain. Intravenous ergonovine may be useful to identify esophageal spasm in selected patients with chest pain who have normal coronary arteries or in whom coronary artery disease is insufficient to explain symptoms. However, we believe that the potential risks of ergonovine do not justify its routine use as a provocative agent for esophageal spasm.

Adult↗

PubMed1989

Differential inhibition by ergonovine of norepinephrine release in the coronary artery and saphenous vein of the dog.

Experiments were performed to determine the effect of ergonovine on adrenergic neurotransmission in the blood vessel wall. Strips of canine left circumflex coronary arteries and saphenous veins were incubated with [3H]norepinephrine and suspended for superfusion. Ergonovine (10(-6) M) decreased the overflow of [3H] norepinephrine to a modest degree in the coronary artery, whereas a profound inhibition of overflow was observed in the saphenous vein. Methiothepin, but not rauwolscine, reversed the inhibitory effect of ergonovine in both blood vessels. Treatment with atropine or droperidol did not alter the response to ergonovine in the coronary artery. The results demonstrate that ergonovine, by activating prejunctional serotonergic receptors, inhibits adrenergic neurotransmission to a greater extent in the saphenous vein than in the coronary artery. The differential effect of ergonovine on norepinephrine release in these vessels may provide evidence for heterogeneity in the prejunctional modulation of adrenergic neurotransmission.

Animals↗

PubMed1996

Increased basal tone and hyperresponsiveness to acetylcholine and ergonovine in spasm-related coronary arteries in patients with variant angina.

We compared the basal coronary artery tone and the constrictive responses to acetylcholine (Ach) and ergonovine (Erg) among three groups of patients: 31 patients (group 1) with variant angina in whom spasm was provoked by low doses of acetylcholine (intracoronary 20 micrograms) or ergonovine (intravenous 50 micrograms); 35 patients (group 2) in whom spasm was provoked by higher doses of acetylcholine (intracoronary 100 micrograms) or ergonovine (intravenous cumulative dose of 350 micrograms); and 26 control subjects. Patients with variant angina in whom spasm was provoked by low doses of acetylcholine or ergonovine, had a higher incidence of coexisting angiographic evidence of coronary artery disease, multi-vessel spasm and more frequent episodes of angina. The basal coronary artery tone at the spastic and non-spastic sites of the spasm-related artery was significantly elevated in group 1 compared to group 2 (44 +/- 17 vs. 14 +/- 11% and 26 +/- 14 vs. 16 +/- 10%, respectively, P < 0.05), but not in the non-spasm related artery. The magnitude of vasoconstrictive responses to acetylcholine and ergonovine at the non-spastic sites was also greater in group 1 than in group 2 and the control groups (acetylcholine: 40 +/- 20 vs. 26 +/- 11, 27 +/- 12%; ergonovine: 37 +/- 18 vs. 12 +/- 8, 13 +/- 10%, respectively, P < 0.05). However, the basal coronary artery tone was not elevated at the spastic and non-spastic sites in group 2 compared to that in the control subjects. These findings suggest that the basal coronary artery tone is increased in patients with variant angina, with increased frequency of angina suggestive of higher disease activity at the spastic and non-spastic sites of the spasm-related artery, and this may be related to pathogenesis of coronary artery spasm.

Acetylcholine↗

PubMed1998

[Usefulness of intracoronary injection of acetylcholine and ergonovine in patients with variant angina].

The correlation was examined between the angina-producing arteries predicted to be responsible for the sites of ST segment elevation during spontaneous ischemic attacks and the arteries in which spasm was induced by intracoronary injection of either acetylcholine or ergonovine in patients with variant angina. From 1991 January to 1996 June, 42 patients with variant angina, 40 men and 2 women with a mean age of 61.6 years old, underwent the acetylcholine provocation test within 2 weeks of observation of the last ST segment elevation. After discontinuation of antianginal agents for at least 24 hours, a bolus of acetylcholine was injected in incremental doses of 20, 50 micrograms (occasionally 80 micrograms) into the right coronary artery and of 20, 50 and 100 micrograms incrementally into the left coronary artery to provoke coronary spasm. Intracoronary injection of ergonovine was added in nine patients, in whom intracoronary injection of acetylcholine failed to document coronary spasm on the arteries predicted to be responsible for the sites of ST segment elevation during anginal attacks. Ergonovine was injected in total doses of 40 micrograms into the right coronary artery and of 64 micrograms into the left coronary artery. Positive spasm was defined as induction of more than 99% reversible stenosis. The correlation between the arteries predicted to be responsible for the sites of ST segment elevation during attacks and the vessels in which spasm was induced by acetylcholine test was 78.6% for all patients and 80.0% for all sites of ST segment elevation. By adding the ergonovine test after the acetylcholine test, the correlation increased to 95.2% for all patients and 95.6% for all sites of ST segment elevation. The correlation observed agrees with previous studies in which the ergonovine test was performed in patients without induced spasm by intracoronary injection of acetylcholine and that the super-imposed ergonovine test is useful for diagnosing patients with variant angina.

Acetylcholine↗

PubMed1998

Coronary vasoreactivity to ergonovine after angioplasty: difference between the infarct-related coronary artery and the noninfarct-related coronary artery.

BACKGROUND: The vasoreactivity after direct percutaneous transluminal coronary angioplasty (PTCA) in patients with previous myocardial infarction remains unknown. We examined the constrictor response to ergonovine of the infarct-related coronary artery in comparison with that of noninfarct-related coronary artery after angioplasty. METHODS: Ergonovine was administered intravenously to 17 patients with previous myocardial infarction (group I) and to 21 patients with stable angina (group II) 1 year after PTCA. The effects of ergonovine on lumen diameter were analysed quantitatively at the PTCA segment, nonPTCA segment (proximal to the PTCA segment), and nonPTCA artery. RESULTS: The ergonovine-induced decrease in minimal lumen diameter at the PTCA segment was significant in group I (decrease from 2.12 +/- 0.56 to 1.39 +/- 0.74 mm, P < 0.01), but not in group II (decrease from 1.60 +/- 0.35 to 1.43 +/- 0.33 mm, NS). Patients in group I showed a constrictor response at the nonPTCA artery (decrease in diameter from 2.54 +/- 0.90 to 1.94 +/- 0.77 mm, P < 0.01), and a tendency to constrict at the nonPTCA segment (2.56 +/- 0.67 to 2.11 +/- 0.66 mm, P = 0.06), whereas those in group II showed no significant constrictor response to ergonovine at any of the three segments examined. The changes in diameter at the three segments in patients in group I were significantly greater than those in group II (all P < 0.01). Subtotal coronary spasm at the PTCA segment was provoked only in three patients in group I (18%). CONCLUSIONS: The constrictor response to ergonovine of the infarct-related coronary artery was enhanced compared with that of the noninfarct-related coronary artery. This difference in coronary vasoreactivity at the angioplasty segment may be due to previous hypersensitivity of the smooth muscle.

Adult↗

PubMed1978

Ergonovine testing for coronary artery spasm in patients with angiographic mitral valve prolapse.

Coronary artery spasm (CAS) has been postulated to be a pathophysiologic mechanism in the production of ischemic-like chest pain and ECG changes in patients with idiopathic mitral valve prolapse syndrome. To evaluate the possible role of symptomatic CAS evoked by ergonovine maleate, this agent was administered (0.05 to 0.4 mg IV) to 24 patients with chest pain and mitral valve prolapse who had no significant (less than 50%) coronary artery obstruction. Symptoms, ECG and blood pressure changes were monitored in all patients following ergonovine administration. No significant changes were observed in heart rate, systolic blood pressure, or double product. Six patients developed their typical chest pain. In two of these six with chest pain, ST segment shift greater than 1 mm were seen. Post-ergonovine left ventricular end-diastolic pressure (LVEDP) and coronary angiographic changes were also studied in subgroup of 12 of these patients, including five of the six chest pain responders. In the five chest pain responders, pain was associated with a significant rise in LVEDP, whereas no significant change occurred in those patients not experiencing chest pain (p less than 0.01). Chest pain was also associated with significant CAS (greater than 50% lumen reduction) in two patients, each with ST segment shifts greater than 1 mm. In summary, ergonovine stimulation failed to evoke symptoms, ECG or blood pressure changes in three quarters of mitral valve prolapse patients studied. Six patients developed chest pain. Chest pain was assoicated with ECG changes characteristic of CAS in two of these patients, each with angiographic CAS. Thus, symptomatic CAS induced by ergonovine was absent in the majority of these 24 patients with idiopathic mitral valve prolapse syndrome.

Adult↗