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PubMed1997

Disparity between serotonin- and acetylcholine-provoked coronary artery spasm.

BACKGROUND AND HYPOTHESIS: Intrinsic vasoactive substances, such as serotonin and acetylcholine, are known to provoke coronary artery spasm in patients with vasospastic angina. It remains unclear, however, whether these different agents, which activate different receptors, produce spasms at the same sites in these patients. The present study was designed to clarify the disparity of receptor agonist-induced coronary artery spasms in the same patients. METHODS: We conducted sequential provocative tests of coronary artery spasm by acetylcholine, serotonin, and ergonovine in 20 patients with rest angina examined with quantitative coronary angiography. RESULTS: Coronary artery spasms were provoked in all patients at 27 spastic sites. In 13 patients, ergonovine provoked spasms and in 10 of 13 patients who were diagnosed with variant angina, both acetylcholine and serotonin provoked spasms at the same sites where ergonovine also did. In 4 of 13 patients, spasms were provoked by serotonin but not by acetylcholine. In the remaining seven patients, whose spasms were induced by ergonovine, spasms were produced by acetylcholine but not by serotonin. On coronary angiography, the spastic sites for both acetylcholine and serotonin, and those for serotonin alone, were located in the proximal segments of coronary arteries, whereas the spastic sites for acetylcholine alone were located in the distal segments. CONCLUSIONS: This study documented the disparity between serotonin- and acetylcholine-induced spasms. Provocative tests using agents that activate different receptors may produce coronary artery spasms at the same and/or different sites, and this disparity may reflect the clinical heterogeneity of vasospastic ischemic syndrome.

Acetylcholine↗

PubMed1985

Improved coronary supply: prevailing mechanism of action of nitrates in chronic stable angina.

Exercise tolerance before and after sublingual isosorbide dinitrate (ISDN), 10 mg, was assessed in 217 consecutive patients with stable angina, positive exercise test, and angiographically proved coronary artery disease. In 65 patients (30%), ISDN prevented exercise-induced ST segment depression and/or increased exercise time to 1 mm ST segment depression (greater than or equal to 3 minutes), despite the significantly higher (greater than or equal to 25 X 10(2) increment) rate-pressure product attained (increased coronary reserve). On the contrary, in 40 other patients, exercise test remained positive, and neither time to 1 mm ST segment depression nor rate-pressure product increased significantly (fixed coronary reserve). The remaining 106 patients had an intermediate response. To assess the mechanisms underlying the beneficial action of nitrates, we further investigated 13 patients with increased coronary reserve (group 1) and five with fixed coronary reserve (group 2) by the exercise response to ISDN and verapamil, the changes in left ventricular volumes after ISDN and verapamil, the ECG response to intravenous ergonovine, and the changes in coronary stenosis severity following intravenous ergonovine and intracoronary nitrates. ISDN dramatically improved exercise capacity only in group 1 patients. However, it induced a significant reduction of left ventricular volumes in both groups (p less than 0.01). Ergonovine provoked angina and ST segment depression in 62% of group 1 patients and significantly increased the severity of their coronary stenoses (p less than 0.01). In all group 2 patients, ergonovine was negative, and no significant increase in stenosis severity was observed. Intracoronary nitrates reduced stenosis severity in group 1 (p less than 0.01) but not in group 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

Coronary artery spasm after abrupt withdrawal of nitroglycerin in rabbits.

The potential for abrupt withdrawal of nitroglycerin (NTG) to create coronary artery spasm was assessed in New Zealand white rabbits. In the control setting, electrocardiograms were taken from 7 anesthetized rabbits. The administration of intravenous ergonovine did not provoke ST-segment shifts or arrhythmias. Two inches of topical NTG (2%) was applied 3 times daily to a shaved area on the back of each rabbit over a 6-week period. Forty hours after abrupt withdrawal of NTG, intravenous ergonovine and indomethacin were given. Six of 7 rabbits had electrocardiographic changes: ventricular tachycardia in 2, ventricular fibrillation in 1, and significant (1 mm or more) ST-segment shifts in 5 rabbits. Three rabbits died. Sixty-four hours after NTG administration the remaining 4 rabbits were reexamined. One had baseline electrocardiographic evidence of severe myocardial ischemia. Repeat ergonovine and indomethacin testing in the others revealed ventricular tachycardia progressing to asystole in 1, premature ventricular complexes in 1, and ST-segment elevation in another. Two of the remaining 4 rabbits died. Eighty-two hours after NTG administration the remaining 2 rabbits were found dead in their cages. Nitroblue tetrazolium studies revealed extensive myocardial infarction in both animals. Additional studies were performed in 10 normal rabbits. Neither ergonovine nor indomethacin induced ST-segment shifts or arrhythmias in this control population.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Nitroglycerin oral spray: evaluation of its coronary artery dilative action by quantitative angiography.

Twenty patients were studied angiographically before and after administration of glyceryl trinitrate (NTG) spray at a single oral dose of 0.8 mg in either a hydrosoluble (NTG-h) or liposoluble (NTG-I) solution. The assessment was by a randomized double-blind trial involving quantitative coronary angiography and pharmacological stress testing using ergonovine maleate. The peak effect and duration of NTG-induced coronary dilatation were evaluated in 2 groups of 10 patients each, in whom NTG oral spray was given either under resting conditions (group A) or for the release of ergonovine-increased coronary vasomotor tone (group B). The study demonstrates that the 2 different galenic formulations of NTG spray are equally efficacious in dilating the conductance coronary arteries under both conditions. When NTG-h and NTG-I oral spray were given subsequent to ergonovine-testing, the diameters of extramural coronary arteries are not only reset to their dimensions at baseline but furthermore increase above resting values by 15.1% and 15.5%, respectively. Ergonovine-induced coronary vasoconstriction was released significantly for a period of at least 30 minutes. Both the NTG-h and NTG-I oral spray are potent coronary vasodilators in patients with increased coronary vasomotor tone.

Administration, Oral↗

PubMed1995

Fluctuation of spastic location in patients with vasospastic angina: a quantitative angiographic study.

OBJECTIVES: This study sought to determine whether the location of coronary spastic activity may change over time in patients with persistent variant angina. BACKGROUND: Although electrocardiographic studies have provided indirect evidence to indicate that the location of ischemia may change in patients with variant angina, it has not been tested by quantitative angiography whether the location of vasospastic activity may change over time. METHODS: Paired ergonovine provocation tests and coronary angiography were performed at a mean (+/- SD) interval of 43 +/- 13 months apart in patients with persistent symptoms of vasospastic angina in the absence of significant atherosclerosis. A total of 87 spastic and nonspastic segments of 87 major vessels in 29 patients were analyzed by quantitative angiography at baseline, after the administration of ergonovine and after isosorbide dinitrate at the initial and follow-up tests. RESULTS: In 13 patients (group 1), coronary spasm was observed in the same 16 coronary segments at both the initial and follow-up ergonovine provocation tests. In 16 patients (group 2), the following angiographic changes occurred between the initial and follow-up tests in 48 major vessels: Of the 23 segments that developed spasm at the initial test, 10 did not have spasm at the follow-up test; of the 25 vessels that did not demonstrate spasm on the initial test, 12 demonstrated spasm on the follow-up test (a new site of spasm). Thus, in 22 (46%) of 48 vessels, fluctuation of spastic location was observed at follow-up. CONCLUSIONS: Quantitative coronary angiography and repeated ergonovine tests revealed that some patients with persistent vasospastic angina demonstrate fluctuation of vasospastic location, whereas others exhibit a fixed location of vasospasm. Vasospastic angina may not only be a transient disease restricted in location, but may also be a persistent and variable condition involving multiple vessels over many years.

Adult↗

PubMed1991

Effect of H1 receptor stimulation on coronary artery diameter in patients with variant angina: comparison with effect of acetylcholine.

It has been suggested that histamine is involved in the pathogenesis of coronary spasm but its exact role remains unclear. H1 receptor stimulation of the coronary artery was performed with a selective intracoronary infusion of histamine (2 micrograms/min) in 21 patients with variant angina after blockade of the H2 receptor with cimetidine (25 mg/kg) and its effect on the coronary artery diameter was examined. Intracoronary injection of acetylcholine was also performed in 19 of the 21 patients. Ergonovine (0.2 mg) was intravenously administered in one patient. The coronary artery diameter was measured with cinevideodensitometric analysis. A mean plasma histamine concentration in the coronary sinus increased from 4 x 10(-9) to 7 x 10(-8) M 5 min after histamine infusion into the left coronary artery (n = 18). Coronary spasm was induced in 6 patients (29%) with histamine, in 18 (95%) with acetylcholine and in 1 with ergonovine. The effect of histamine on the luminal diameter was analyzed at the site of spasm in the 26 coronary arteries in which spasm was induced by acetylcholine or ergonovine. Of the 20 coronary arteries with a normal arteriogram or a fixed stenosis less than or equal to 50% of luminal diameter, histamine decreased the diameter in 4, increased it in 14 (70%) and caused no change in 2; of the 6 coronary arteries with a fixed stenosis greater than or equal to 75%, histamine decreased the diameter in 5 and increased it in 1. In the coronary arteries in which spasm was not induced by either acetylcholine or ergonovine, histamine increased the diameter, especially in those without advanced atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1991

Epicardial coronary artery tone and reactivity in patients with normal coronary arteriograms and reduced coronary flow reserve (syndrome X)

The vasomotor response of proximal and distal angiographically normal coronary artery segments was studied in 12 patients with syndrome X, 17 age- and gender-matched patients with chronic stable angina and 10 control subjects with atypical chest pain and a normal coronary arteriogram. Ergonovine (300 micrograms by intravenous injection) and isosorbide dinitrate (1 mg by intracoronary injection) were administered to all patients. Computerized coronary artery diameter measurement (angiographically normal segments only) was carried out before and after the administration of ergonovine and nitrate. Baseline intraluminal diameters (mean +/- SEM) of proximal and distal coronary segments were not significantly different in control subjects and patients with syndrome X or coronary artery disease (proximal 2.88 +/- 0.19, 3.01 +/- 0.13 and 2.86 +/- 0.13 mm; distal 1.57 +/- 0.09, 1.70 +/- 0.10 and 1.61 +/- 0.06 mm, respectively). With ergonovine, proximal segments constricted by 10 +/- 2%, 7 +/- 2% and 11 +/- 3% and distal segments by 12 +/- 3%, 14 +/- 3% and 14 +/- 2% in control subjects and patients with syndrome X or coronary artery disease, respectively (p = NS). With isosorbide dinitrate, proximal coronary segments dilated by 11 +/- 2%, 10 +/- 2% and 8 +/- 2% (p = NS) and distal segments by 15 +/- 2%, 11 +/- 3% and 13 +/- 2% (p = NS) in control subjects and patients with syndrome X or coronary artery disease, respectively. Within groups, constriction in response to ergonovine and dilation in response to nitrate were not significantly different in proximal and distal segments.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗

PubMed1984

Refractory coronary artery spasm.

A patient with an episode of refractory myocardial ischemia induced by ergonovine is described. The patient underwent cardiac catheterization 2 weeks after an inferior wall myocardial infarction for evaluation of recurrent rest angina. He developed severe spasm of the proximal right coronary artery in response to ergonovine which was partially relieved with nitrates and calcium channel antagonists. However, myocardial ischemia persisted, culminating in a new inferior wall infarction. The possible mechanism of continuing intense ischemia despite partial relief of the proximal right coronary spasm is discussed. It is suggested that ergonovine testing should perhaps be avoided during the early postinfarction period. Furthermore, if an ergonovine test is anticipated, beta-adrenergic blocking agents should be withheld.

Aged↗

PubMed1996

Relation of basal coronary tone and vasospastic activity in patients with variant angina.

OBJECTIVE: To examine the vasoconstrictor response to ergonovine and the vasodilator response to isosorbide dinitrate in spastic and non-spastic coronary segments from 31 patients undergoing serial angiographic follow up of variant angina. METHODS: Coronary angiograms and ergonovine provocation tests were repeated at an interval of 45 (SD 15) months apart. While all 31 patients showed a positive response to ergonovine initially, vasospastic responsiveness persisted in only 16 patients at follow up (group 1) and not in the other 15 patients in whom symptoms of variant angina had resolved (group 2). Mean luminal diameter of 170 normal or near normal entire coronary segments (American Heart Association classification) were measured (a) at baseline, (b) after the administration of ergonovine, and (c) after the administration of isosorbide dinitrate, during both the initial and follow up angiograms using a computer based quantitative angiography analysis system (CAAS II). RESULTS: In vasospastic patients (initial and follow up angiograms in group 1, and initial angiogram in group 2), basal tone was significantly higher in spastic segments compared to adjacent segments or segments in non-spastic vessels. The diagnostic sensitivity and specificity at 20% increase in basal coronary tone for the prediction of vasospasm were 77% and 73%, respectively. CONCLUSIONS: Coronary artery tone may change in proportion to the activity of variant angina over several years. Contrary to some previous reports, the estimation of basal coronary tone may be useful in the assessment of vasospastic activity in patients with variant angina.

Angina Pectoris, Variant↗

PubMed1990

Effects of atherosclerosis on the coronary microcirculation.

We tested the hypothesis that atherosclerosis potentiates coronary vasoconstriction to serotonin and ergonovine. Coronary microvascular pressures and diameters were measured in the beating left ventricle in normal and atherosclerotic cynomolgus monkeys. Pressures were measured in arteries (190-350 microns diam) that were distal to atherosclerotic lesions. Microvascular pressure and simultaneous measurements of aortic pressure and myocardial blood flow were used to calculate segmental vascular resistance (large artery resistance and microvascular resistance) during serotonin, phenylephrine, and ergonovine dosages. Aortic pressure was maintained constant during all interventions. Administration of phenylephrine (50 micrograms.kg-1.min-1 iv) produced a similar increase in microvascular resistance from base line (P less than 0.05) in atherosclerotic and normal animals, 26 +/- 5 and 14 +/- 9 mmHg.min.g.ml-1, respectively. Serotonin (50 micrograms/min) did not influence coronary resistance in normal animals but produced a significant increase in both large artery (8 +/- 3 mmHg.min.g.ml-1) and microvascular resistance (21 +/- 6 mmHg.min.g.ml-1) in atherosclerotic animals (P less than 0.05). A higher dose of serotonin (200 micrograms/min) produced a modest increase in large artery resistance from base line in normal animals (3 +/- 1 mmHg.min.g.ml-1) and a greater increase in atherosclerotic animals (9 +/- 4 mmHg.min.g.ml-1) (P less than 0.05 vs. normals). Ergonovine (10 micrograms.kg-1.min-1 iv) elevated microvascular resistance in both normal and atherosclerotic animals (P less than 0.05) but increased large artery resistance only in atherosclerotic animals (10 +/- 4 mmHg.min.g.ml-1) (P less than 0.05). In summary, coronary vasoconstrictor responses to serotonin and ergonovine were potentiated by atherosclerosis. Because augmented constrictor responses to serotonin were observed in both the diseased arteries and the microcirculation of atherosclerotic animals, we speculate that the pathophysiological consequences of atherosclerosis extend into the microcirculation.

Adenosine↗

PubMed1982

Spasm of a normal or minimally narrowed coronary artery in the presence of severe fixed stenoses of the remaining vessels: clinical and angiographic observations.

Four patients with medically refractory unstable angina are presented. Each patient had ST-segment abnormalities during some episode of pain. Three patients had at least one episode of documented ST-segment elevation with their spontaneously occurring chest pain. One had recurrent ventricular tachycardia. Two patients had prior myocardial infarction. Angiography demonstrated localized left ventricular akinesis and a severe fixed stenosis in the coronary artery supplying the abnormal segment. There were severe, fixed lesions in two coronary arteries in two patients and in one vessel in two patients. After i.v. ergonovine maleate, coronary artery spasm was documented in a normal or minimally diseased coronary artery in each patient. In two patients, ergonovine-induced spasm not only occluded the vessel, but also markedly decreased retrograde filling of a vessel with severe, fixed narrowing. Each patient's characteristic symptoms appeared with the ergonovine-induced spasm. Thus, ergonovine maleate can provoke spasm of a normal coronary artery, even in the presence of severe fixed stenoses of the remaining vessels. This observation may have an important role in the diagnosis and clinical management of patients with chest pain.

Adult↗

PubMed1985

Significant role of alpha 2-adrenoceptors in coronary artery spasm.

Ergonovine, methoxamine and clonidine were administered intravenously in order to clarify the mechanism of coronary artery spasm in canine experiments. After these administrations, 27.5% of the dogs treated with ergonovine, 59.5% of the dogs treated with methoxamine and 72.7% of the dogs treated with clonidine showed ST segment elevation. The combined application of propranolol with ergonovine or methoxamine could more easily induce ST segment elevation than a single application of ergonovine or methoxamine. Most cases of elevated ST segment returned to the normal after the administration of nitroglycerin and phentolamine. Yohimbine was completely effective for the restoration of normal ST segment. Plasma norepinephrine decreased to 20 +/- 8.0% of the control when ST segment elevation was induced. This is a significantly greater decrease than that seen without ST segment elevation (p less than 0.001). Concomitant with the restoration of normal ST segment, plasma norepinephrine increased after the administration of yohimbine. Methoxamine and clonidine increased (p less than 0.01) and yohimbine decreased (p less than 0.01) coronary vascular resistance. Coronary spasm was visualized on coronary arteriogram after the application of clonidine; also coronary vasodilation was visualized after the administration of yohimbine. These results confirm the hypothesis that coronary artery spasm is mediated by pre- and postsynaptic alpha 2-adrenoceptors.

Animals↗

PubMed1990

The dynamic changes of plasma tissue-type plasminogen activator level and the activity of its inhibitor during coronary vasospasm.

This study aimed to examine the dynamic changes of the fibrinolytic system during coronary vasospasm. Tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor (PAI) and fibrinopeptide A (FPA) levels were measured in the great cardiac venous and arterial blood of 9 patients with clinically and angiographically proven vasospastic angina and 11 controls. Before ergonovine provocation, although there was no difference between the above 2 groups in t-PA levels in the aorta or the great cardiac vein, the PAI level in patients with variant angina was lower than in the controls both in the aorta (4.2 +/- 3.5 IU/ml vs 10.9 +/- 5.2 IU/ml) and in the great cardiac vein (2.3 +/- 2.9 IU/ml vs. 11.9 +/- 4.9 IU/ml). During ergonovine-induced coronary vasospasm in patients with variant angina, the t-PA level in the great cardiac vein significantly increased from 3.4 +/- 0.7 ng/ml to 4.4 +/- 0.5 ng/ml (p less than 0.05), but it did not change in the aorta. The maximal dose of ergonovine (0.4 mg) induced mild diffuse coronary vasoconstriction in the controls, and this diffuse coronary vasoconstriction induced a reduction of PAI levels in the great cardiac vein from 11.9 +/- 4.9 IU/ml to 9.5 +/- 4.8 IU/ml (p less than 0.05). FPA levels in the great cardiac vein did not change during ergonovine-induced coronary vasospasm in either group. Thus, the coronary vasospasm induced the release of t-PA from endothelial cells of coronary vessels and resulted in the reduction in the PAI activity in the great cardiac vein.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Importance of coronary artery spasm in alcohol-related unexplained syncope.

To examine the role of coronary artery spasm in patients with syncope after alcohol ingestion, we performed an intracoronary ergonovine provocation test in 7 male patients (39 to 73 years old, mean 54 years) with alcohol-related syncope which remained unexplained despite noninvasive cardiovascular and neurological examinations. No patients had structural heart disease or significant coronary artery stenosis. Ergonovine was continuously infused into each coronary artery at a rate of 10 micrograms/min for up to 5 min. Coronary artery spasm with ST-segment elevation was induced in 4 of 7 patients. Chest pain before syncope or history of chest pain were not present in 3 of 4 patients with a positive ergonovine test. Multivessel coronary artery spasm was induced in 3 patients. One patient presented with triple vessel coronary artery spasm progressing to near syncope as a result of profound hypotension and ventricular tachycardia during provocation. Coronary artery spasm was promptly relieved by intracoronary isosorbide dinitrate infusion. All patients with a positive ergonovine test were treated with calcium antagonist and did not experience syncope during follow-up. These results suggest that coronary artery spasm is one of the important causes of syncope after alcohol ingestion.

Adult↗

PubMed2002

Myocardial sympathetic denervation, fatty acid metabolism, and left ventricular wall motion in vasospastic angina.

UNLABELLED: Although various noninvasive methods have been used to detect vasospasm, none of them are sensitive enough for patients with sporadic attacks. Because abnormal fatty acid metabolism and cardiac adrenergic neuronal damage are observed in ischemic myocardium, (123)I-15-(p-iodophenyl)-3-R,S-methyl pentadecanoic acid (BMIPP) and (123)I-metaiodobenzylguanidine (MIBG) have recently been proposed as useful tracers for detection of myocardial damage. This study investigated the relationships among the coronary vasospastic regions, abnormal left ventricular regional wall motion, fatty acid metabolism, and sympathetic nerve functions and their changes during treatment in patients with vasospastic angina. METHODS: We evaluated 50 patients with vasospastic angina (25 with clinically documented vasospasm [group A] and 25 with vasospasm induced by ergonovine provocation [group B]) and 25 control subjects who had chest pain but had normal coronary arteries without ergonovine provocation of spasm. Sixteen patients in group A were reevaluated 6 mo after medical treatment. The territorial regions of the vasospasm-induced coronary artery, wall motion determined by left ventriculography, and BMIPP and MIBG uptake were compared. RESULTS: Regions exhibiting a positive reaction to the ergonovine provocation were observed in the right coronary artery in 41 patients, the left anterior descending artery in 33, and the left circumflex artery in 21. Provocation occurred in multiple vessels in 29 patients (58%). Reduction of wall motion was observed in 19 patients (38%). Sensitivity and specificity for the identification of vasospastic angina were 86% (43/50 patients) and 88% (22/25 control subjects), respectively, for BMIPP scintigraphy and 100% (50/50 patients) and 56% (14/25 control subjects), respectively, for MIBG scintigraphy. In the region exhibiting a reduction in left ventricular wall motion, BMIPP or MIBG uptake was decreased. The sensitivity and specificity of determination of vasospasm-induced coronary arteries were 71% (67/95 arteries) and 95% (71/75 arteries), respectively, for BMIPP scintigraphy and 96% (91/95 arteries) and 55% (41/75 arteries), respectively, for MIBG scintigraphy. After 6 mo, during treatment, vasospasm was reinduced by ergonovine provocation in 6 patients (group I) and was not reinduced in 10 patients (group II). Improvements of decreased BMIPP and MIBG uptake were lower in group I (25% +/- 4% and 16% +/- 4%, respectively) than in group II (69% +/- 4% and 50% +/- 3%, respectively; both P < 0.01). The regions in which vasospasm was reinduced exhibited decreased BMIPP and MIBG uptake. CONCLUSION: Abnormal fatty acid metabolism and cardiac sympathetic denervation were observed more frequently than were wall motion abnormalities in the vasospastic region in patients with vasospastic angina. BMIPP and MIBG scintigraphy are highly accurate and noninvasive techniques for determining the presence and location of vasospasm.

3-Iodobenzylguanidine↗

PubMed1987

Evaluation of myocardial perfusion and coronary vascular resistance following withdrawal of chronic nitroglycerin treatment in rabbits.

This investigation was performed to determine whether the abrupt withdrawal of chronically administered nitroglycerin (NTG) alters coronary vascular resistance and myocardial perfusion in an experimental rabbit model. New Zealand white rabbits received 2 inches of topical NTG (2%) applied 3 times daily over a 6 week period. Forty hours after abrupt withdrawal of NTG left ventricular blood flow was assessed by the radioactive microsphere technique. Coronary resistance was significantly increased in NTG-withdrawal rabbits at the baseline (21.5 +/- 3.1) compared to controls (13.5 +/- 1.2) and remained elevated after ergonovine administration at both the early (NTG-withdrawal: 20.9 +/- 3.5 vs controls 12.6 +/- 1.5) and late (NTG-withdrawal: 17.1 +/- 3.1 vs controls: 11.6 +/- 0.9) sampling periods. Neither ergonovine nor indomethacin significantly altered blood flow compared to earlier values. However, the NTG-withdrawal rabbits exhibited significantly lower blood flow to the left ventricle compared to controls after ergonovine administration at both early (NTG-withdrawal: 4.80 +/- 0.72 ml/min/gram vs controls: 6.98 +/- 0.79 ml/min/gram) and late (NTG-withdrawal: 5.30 +/- 0.80 ml/min/gram vs controls: 7/52 +/- 0.66 ml/min/gram) sampling periods and also following indomethacin administration (NTG-withdrawal: 4.24 +/- 0.46 ml/min/gram vs controls: 7.52 +/- 1.26 ml/min/gram). Electrocardiographic evidence of myocardial ischemia was noted in the NTG-withdrawal rabbits following intracardiac injection of microspheres. These studies show that increased sensitivity of NTG-withdrawal rabbits to ergonovine or microsphere injection is associated with increased coronary vascular resistance. However, severe myocardial ischemia was not observed.

Animals↗

PubMed1986

Echocardiographic documentation of myocardial ischemia in presence of angina pectoris without ST-T changes.

A frequent clinical problem is to document the elusive entity of electrocardiographically silent myocardial ischemia. Since echocardiography offers a practical tool to detect reversible mechanical changes due to ischemia, 32 patients with angina on effort, and coronary artery disease, and 15 patients with angina at rest were studied. In all 47 patients electrocardiographic changes during effort or rest pain were inconclusive. Combined 12 lead electrocardiographic and 2-Dimensional echocardiographic monitoring were performed: during ergonovine testing in the 15 patients with angina at rest; during dipyridamole testing in the 32 patients with effort angina and a non diagnostic stress test. Interpretable echocardiograms were obtained in all the patients studied. Positivity of both the Ergonovine-Echocardiographic test and the Dipyridamole-Echocardiographic test was based upon the detection of regional transient asynergy. Of the 15 patients who had chest pain at rest in the absence of diagnostic electrocardiographic changes, Ergonovine-Echocardiographic test was positive in 6 (40%). Of the 32 patients who had chest pain in absence of diagnostic electrocardiographic changes during exercise stress testing, the Dipyridamole-Echocardiographic test was positive in 18 (56%). Echocardiographic monitoring in combination with provocative testing (ergonovine and dipyridamole) may be a practical, non invasive, inexpensive tool which is feasible in all patients with good basal echocardiograms and is able to unmask electrocardiographically silent myocardial ischemia by providing objective mechanical evidence of the ischemic event.

Adult↗

PubMed2002

Chest pain after coronary artery stent implantation.

A sizeable proportion of patients who undergo successful coronary artery stent implantation experiences chest pain immediately after the procedure and/or in the following months in the absence of in-stent restenosis. We investigated this phenomenon in 57 consecutive patients with stable angina who underwent successful stent implantation. Chest pain characteristics were assessed before stent implantation and during 6-month follow-up. All patients underwent coronary angiography within 6 months of the procedure 48 hours after exercise thallium-201 perfusion scintigraphy. Patients who did not exhibit in-stent restenosis underwent an ergonovine test at the end of routine coronary angiography. During follow-up, 15 patients complained of chest pain. Six of these patients exhibited scintigraphic evidence of myocardial ischemia and in-stent restenosis at angiography. In the remaining 9 patients, chest pain occurred in the absence of in-stent restenosis at angiography. In 8 of these patients intracoronary ergonovine administration reproduced their habitual pain, whereas it did not cause any pain in the 42 patients who were completely asymptomatic at follow-up and without in-stent restenosis. Ergonovine caused more intense vasoconstriction and nitroglycerin caused more intense vasodilation of the reference coronary diameter in patients with than in patients without ergonovine-induced pain (-17 +/- 3 vs -9 +/- 3%, p <0.001; 9 +/- 6 vs 5 +/- 4%, p <0.02, respectively). In conclusion, chest pain with features similar to habitual angina occurs in the absence of in-stent restenosis in 1/5 of patients after stent implantation and appears to be associated with more intense coronary vasoreactivity.

Adult↗