Developed Chest Pain Research Articles

The haemodynamic response to ST segment changes during coronary arteriography

Contrast media are known to cause electrocardiographic and haemodynamic changes during coronary arteriography. There is a tendency to proceed with repeated coronary arteriography unless patients develop chest pain, bradycardia or hypotension. We have related the changes in the ST segment to changes in left ventricular end-diastolic pressure, measuring pulmonary arterial diastolic pressure with a transducer tipped catheter. Twenty-five patients were studied, 15 patients with coronary arterial disease, 2 with syndrome X, 3 with coronary arterial spasm (and underlying coronary disease) and 5 normal controls. In control patients, no changes in the ST segment or pulmonary arterial diastolic pressure were recorded. Patients with syndrome X developed ST segment depression in the absence of changes in pulmonary arterial diastolic pressure. Those with coronary arterial spasm and underlying coronary disease developed ST segment depression and a rise in pulmonary arterial diastolic pressure following most injections. In coronary arterial disease, both painful and silent ST segment depression was noted with a rise in pulmonary arterial diastolic pressure. In some instances, a summation effect arose with repeated injections. Major disturbances in the ST segment may occur during coronary arteriography and result in elevation of left ventricular filling pressure.

Premature coronary artery disease and the Prader-Willi syndrome

A 28 year old woman with the Prader-Willi syndrome developed chest pain and loss of anterior R wave amplitude on the electrocardiogram. Cardiac catheterization demonstrated a severe proximal stenosis of the left anterior descending artery with delayed antegrade flow together with antero-apical akinesia consistent with myocardial infarction. Physicians involved in the management of patients with the Prader-Willi syndrome should be aware of this association with premature coronary artery disease.

Anginal attack following a sodium bicarbonate and hydrocortisone injection.

A case of a 73-year-old man with variant angina who developed chest pain and shock following an injection of sodium bicarbonate and hydrocortisone is reported. The electrocardiogram (ECG) during the chest pain attack revealed ST elevation in leads II, III and aVF. It returned to a normal pattern 10 min later. Coronary angiography, performed 2 hours after the anginal attack, showed no significant coronary arterial stenosis. One month later, an injection of ergonovine (16 micrograms) into the right and left coronary arteries induced spasms in segments 4 and 13, with ischemic ECG changes. Possible causes of the anginal attack are a coronary arterial spasm induced by the allergic reaction to hydrocortisone and/or serum alkalosis due to the sodium bicarbonate injection triggered by hyperventilation.

Myocardial Infarction after Dipyridamole-Assisted Thallium-201 Imaging

A 77-year-old woman with suspected coronary artery disease underwent an oral dipyridamole/thallium-201 myocardial imaging study. Approximately 75 minutes after ingestion of dipyridamole 300 mg suspension, the patient developed chest pain, hypotension, nausea, and diaphoresis. An electrocardiogram revealed ST-T wave changes suggestive of inferior ischemia. Appropriate therapeutic measures, including aminophylline and nitroglycerin, were instituted. Delayed thallium images revealed reversible ischemia in the anteroseptal and posterobasal regions with a fixed defect in the inferobasal region. Cardiac enzyme studies were also indicative of acute myocardial injury. The patient subsequently underwent coronary arteriography and four-vessel coronary artery bypass grafting and was discharged without further complication. This report raises concerns about the potential danger of dipyridamole in patients with severe coronary artery stenosis and collateral circulation. Prophylactic aminophylline should be considered in these patients.

Coronary artery spasm induced by intravenous epinephrine overdose

A 27-year-old man was accidentally given 2 mg intravenous epinephrine instead of 2 mg naloxone. He immediately developed chest pain, nausea, and diaphoresis. An ECG taken shortly after the epinephrine administration showed widespread ischemia. Forty-five minutes later the tracing still showed an early repolarization pattern, but ST elevation was less marked and the patient was asymptomatic. Serum potassium was 3.2 mEq/L and serum catecholamines, drawn approximately 20 minutes after the epinephrine administration, were 10 times normal (dopamine, 173 ng/L; epinephrine, 1,628 ng/L; norepinephrine, 1,972 ng/L). There are seven other reports of intravenous epinephrine overdose in the English literature. Two of the previously reported cases had 12-lead ECGs within the first hour. In both there was evidence of transient ischemia similar to that observed in this case. Most of the patients has symptoms consistent with angina, and several developed pulmonary edema. These findings suggest that, in humans, large intravenous doses of epinephrine are likely to produce coronary artery spasm and may decrease coronary artery perfusion.

Usefulness of thallium-201 Scintigraphy in predicting the development of angina pectoris in hypertensive patients with left ventricular hypertrophy

Hypertension and left ventricular (LV) hypertrophy are independent risk factors for the development of coronary artery disease. To determine whether patients at higher risk for coronary artery disease can be identified, 40 asymptomatic hypertensive men with LV hypertrophy were prospectively studied using exercise thallium-201 scintigraphy and exercise radionuclide angiography. Endpoints indicative of coronary artery disease were defined as the subsequent development of typical angina pectoris, which occurred in 8 patients during a median follow-up of 38 months, or myocardial infarction, which did not occur. The exercise electrocardiogram was interpreted by standard ST-segment criteria and by a computerized treadmill exercise score. Abnormal ST-segment responses were present in 16 of the 40 hypertensives (40%), whereas the treadmill score was positive in 8 of those same 40 patients (20%). Scintigraphic perfusion defects assessed both visually and semiquantitatively were observed in 8 of 40 (20%) patients. An abnormal ejection fraction response to exercise was present in 40% (16 of 40) of patients, and 3 of 40 (7.5%) developed new wall motion abnormalities during exercise. Six of 8 patients with either perfusion defects or abnormal treadmill score developed typical angina during follow-up. All 5 patients with concordant positive exercise scintigrams and treadmill score developed chest pain during follow-up and had coronary artery disease confirmed by coronary angiography. However, only 7 of 16 (44%) patients with positive ST changes or abnormal ejection fraction responses during exercise developed chest pain during follow-up. In contrast, of 32 patients with negative scintigrams only 2 developed atypical chest pain syndromes, and significant coronary artery disease was excluded by angiography in 1 patient. Thus, both thallium-201 scintigraphy and treadmill score accurately detect coronary artery disease in asymptomatic hypertensive patients with LV hypertrophy and predict the future development of angina symptoms.

A Comparison of Sublingual Nifedipine Versus Nitroglycerin in the Treatment of Acute Angina Pectoris

The administration of nifedipine by the sublingual rather than the oral route has been suggested to provide a more rapid onset of effect. We compared the safety and efficacy of sl nifedipine to sl nitroglycerin in patients who developed anginal chest pain during diagnostic exercise stress testing. Consecutive patients undergoing diagnostic Bruce treadmill exercise who had not had a recent myocardial infarction or undergone coronary bypass graft surgery and who were not taking nitrates, beta-blockers, digoxin, or calcium antagonists were eligible. Seventy-eight patients meeting the inclusion/exclusion criteria consented to participate. Of these 78, 13 developed chest pain necessitating exercise cessation and were randomized to either nitroglycerin or nifedipine. Nitroglycerin was initially given to seven patients and nifedipine to six patients. Complete pain relief was observed in five of seven (71 percent) nitroglycerin patients at two minutes postdose. At four minutes postdose, the remaining two nitroglycerin patients were essentially pain-free. At two minutes postdose, no patient receiving nifedipine had complete pain resolution, and only one patient (17 percent) had partial (greater than 50 percent) pain relief. At four minutes postdose, four of the nifedipine patients were crossed over to nitroglycerin. At two minutes after the nitroglycerin dose, all four patients had total pain relief. The remaining two nifedipine patients had partial pain relief and were not crossed over to nitroglycerin. Subjective side effects and changes in heart rate and blood pressure were not significantly different between nitroglycerin and nifedipine.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of surgical reduction of left ventricular outflow obstruction on hemodynamics, coronary flow, and myocardial metabolism in hypertrophic cardiomyopathy.

To assess the impact of operative reduction of left ventricular outflow obstruction in hypertrophic cardiomyopathy, measurements of great cardiac vein flow, oxygen and lactate content, left ventricular pressures, and cardiac index were measured at rest and during pacing stress in 20 consecutive patients (13, myotomy-myectomy; six, mitral valve replacement; one, both myotomy-myectomy and mitral valve replacement) who underwent both preoperative and postoperative studies. All had angiographically normal epicardial coronary arteries. Operation resulted in reduction in outflow gradient (64 +/- 38 to 4 +/- 7 mm Hg, p less than 0.001) and in left ventricular systolic pressure (186 +/- 32 to 128 +/- 22 mm Hg, p less than 0.001) and was associated with reduction in great cardiac vein flow (101 +/- 26 to 78 +/- 16 ml/min, p less than 0.001) and oxygen consumption in the anterior left ventricle and septum (11.9 +/- 4.1 to 8.4 +/- 1.9 ml O2/min, p less than 0.001) in the basal state. During rapid atrial pacing, 13 of 20 patients experienced chest pain postoperatively, whereas all 20 developed chest pain during preoperative pacing, with an improvement in pacing anginal threshold (or heart rate 150 if no chest pain was experienced) of 16 +/- 18 beats/min (p less than 0.001). The peak great cardiac vein flow (161 +/- 41 to 131 +/- 45 ml/min, p less than 0.025) and myocardial oxygen consumption (19.4 +/- 6.1 to 14.3 +/- 5.5 ml O2/min, p less than 0.005) during pacing, which correlated directly with the severity of the basal left ventricular gradient (p = 0.011 and p = 0.002, respectively), were also reduced by surgery. Lactate metabolism during pacing changed from net production before surgery to net consumption after operation (-17 +/- 47.6 to 4.4 +/- 29.8 mumol/min, p less than 0.01), with six of 20 patients producing lactate after surgery compared with 13 of 20 before surgery (p = 0.06). The six patients with the highest peak great cardiac vein flow (greater than 175 ml/min) during preoperative pacing had greater symptom and metabolic benefit during pacing after surgery compared with the 14 patients with lower peak coronary flow. Postpacing left ventricular end-diastolic pressure (30 +/- 7 to 23 +/- 7 mm Hg, p less than 0.001) and pulmonary artery wedge pressure (24 +/- 6 to 20 +/- 5, p less than 0.001) were reduced after surgery.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute myocardial infarction in a 22-year-old world class weight lifter using anabolic steroids

A major concern facing the medical profession in dealing with athletes is the widespread use of anabolic steroids despite no proof of their effectiveness on athletic prowess.* Elevated circulating levels of low density lipoprotein (LDL) cholesterol and lowered high density lipoprotein (HDL) cholesterol have recently been reported in powerlifters using anabolic steroids.2 Therefore, anabolic steroid use and resultant unfavorable lipid profiles may increase the risk of cardiovascular disease. We report a case of a world class powerlifter using anabolic steroids who presented with acute myocardial infarction, marked hypercholesterolemia and an abnormal LDL/HDL ratio. The clinical circumstances suggest a causal relationship to anabolic steroid use. A 22-year-old, 330~pound male, world class power weightlifter with no past or family history of cardiac diseases was admitted with severe chest pain that awakened him from sleep. The patient was using intramuscular and oral androgenic steroids daily during the 6 weeks before he developed chest pain. He denied cocaine use. Physical findings on admission were normal. Laboratory studies revealed elevated creatine kinase (6,182 U/ml with 15% MB band). The electrocardiogram disclosed ST-segment elevations and Q waves in leads II, III, aVF, Vs and V6. Cardiac catheterization performed 10 days after infarct demonstrated normal coronary arteries and apical dyskinesia. Total serum cholesterol at admission was 596 mg/dl (LDL 513 and HDL 14 mg/dl). Twenty-four days

５‐ＦＵにより胸痛発作を来した一症例

The authors describe a patient who presented with recurrent chest pain during chemotherapy with 5-fluorouracil (5-FU).A 69-year-old man with metastatic lung carcinoma received 5-FU 1500mg/day by continuous infusion for 5 days. He developed chest pain during the second and third courses of 5-FU infusion, but there were no ischemic changes on the electrocardiogram.Cardiotoxicity as a rare side effect of 5-FU therapy has been reported, but its etiology remains unclear. The ischemic chest pain and EGG changes observed in most cases suggest that coronary artery spasm may be the cause of 5-FU cardiotoxicity. Although cardiotoxicity is a rare complication of 5-FU therapy, the authors think it is advisable to stop the treatment when chest pain occurs.

Implications of positive treadmill exercise tests in asymptomatic adult African blacks.

Maximal exercise tests in 225 apparently healthy adult Africans (148 men, 77 women) aged 26 to 70 years revealed 35 subjects (18 men and 17 women) with ischaemic ST changes. Out of these, 6 men and 4 women developed chest pain that necessitated termination of the tests. Significant ventricular arrhythmias were observed in 27 patients (20 men and 7 women) all of whom had an otherwise negative response to exercise tests. During a follow-up period ranging from 6 months to 4 years, 2 male positive-responders--both of whom developed chest pain during exercise testing--sustained acute myocardial infarction. The coronary arteries of both men were found to be normal at coronary angiography. A third male positive-responder, who also developed chest pain during exercise testing, subsequently experienced repeated attacks of angina with no ECG or serum enzyme changes. Coronary angiography, in this patient, revealed significant proximal vessel disease necessitating coronary angioplasty. One female positive responder, who developed chest pain during exercise-testing, experienced episodes of restrosternal discomfort of considerable duration with no ECG or serum enzyme changes. Her coronary arteries were subsequently shown to be normal. While coronary artery disease would no doubt account for a significant percentage of positive exercise responses in adult African blacks, it seems likely that non-coronary causes play a dominant role.

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.

Incidence of spasm at the site of previous successful transluminal coronary angioplasty: effect of ergometrine maleate in consecutive patients.

The incidence of coronary artery spasm at the site of previous successful angioplasty and its importance in leading to subsequent restenosis or recurrence of symptoms are unknown. Fourteen consecutive patients with single vessel coronary artery disease who had undergone successful percutaneous transluminal angioplasty were studied. All patients were given ergometrine maleate (ergonovine maleate) intravenously during repeat cardiac catheterisation six weeks to three months after angioplasty. Five patients demonstrated excessive luminal reduction (spasm) at the site of previous angioplasty that led to luminal stenoses ranging from 50% to 79%. Two of these patients developed chest pain and ST segment changes during ergometrine maleate provocation and they also showed maximal vasoconstriction. The remaining nine patients did not develop important luminal change at the site of angioplasty after ergometrine maleate. Ergometrine maleate administration resulted in less than or equal to 20% reduction in lumen diameter of adjacent apparently normal sections of the coronary arteries in all but two patients. At the site of previous angioplasty in the five patients with spasm, however, the lumen was constricted by a mean (SD) of 51 (12)%, whereas in the nine patients not demonstrating spasm mean reduction was 12 (7)%. Thus hypersensitivity to ergometrine maleate at the site of previous successful angioplasty was demonstrated in over a third of consecutive patients with single vessel coronary artery disease. The importance of this finding to long term results of coronary angioplasty needs to be investigated further.

The Effect of Acid and Bethanechol Stimulation in Patients with Symptomatic Hypertensive Peristaltic (Nutcracker) Esophagus Evidence That This Disorder May Be a Precursor of Diffuse Esophageal Spasm

The hypertensive peristaltic (nutcracker) esophagus represents a motility disorder characterized clinically by squeezing retrosternal chest pain and manometrically by high amplitude esophageal peristaltic contractions. This study was designed to examine whether the nutcracker esophagus is: (a) a distinct entity, (b) a member of the spectrum of primary esophageal dysmotilities (e.g., diffuse esophageal spasm and achalasia), or (c) is secondary to reflux-induced acid sensitivity. Thirteen patients with a nutcracker esophagus by baseline manometry were subsequently studied after acid perfusion and bethanechol stimulation (0.08 mg/kg). Records were analyzed for symptomatic response and motility changes. Eight of 13 (62%) experienced chest pain during acid perfusion, but none had significant motility changes documented during this period. After bethanechol injection, chest pain occurred in six of 12 (50%) patients; two had burning pain and in the other four (33%) their squeezing chest pain was reproduced. Changes in the motility tracing with evidence of disordered motility suggestive of diffuse esophageal spasm were seen after bethanechol in seven of the 12 tracings analyzed (58%), including all six patients who developed chest pain. We conclude that patients with nutcracker esophagus on baseline manometry may develop motility patterns consistent with diffuse esophageal spasm after provocation with bethanechol. We take this to suggest that the nutcracker esophagus is part of the continuum of primary motility disorders and may actually be a precursor of diffuse esophageal spasm.

Myxoma of the mitral valve diagnosed by echocardiography

effective drugs, and that these should he tried prior to instituting steriod therapy. The importance of recognizing pericarditis in patients with inflammatory bowel disease is demonstrated by the development of cardiac tamponade in the patients described by Breitenstein et a1.6 as well as those reported by Rheingold.4 Pericarditis must therefore be considered in every patient with inflammatory bowel disease who develops chest pain, and conversely, occult inflammatory bowel disease should be excluded when investigating any patient with pericarditis of obscure origin.7

Clinically unrecognized ventricular dysfunction in young diabetic patients

Left ventricular function at rest and during supine bicycle exercise was assessed by gated radionuclide angiography in 20 diabetic patients and 18 normal control subjects without clinical evidence of heart disease. The diabetic patients were aged 21 to 44 years and all except one used insulin. No subject developed chest pain or electrocardiographic changes during exercise. Both groups had a similar rest and exercise heart rate and blood pressure, and both achieved similar work loads. The control group had an ejection fraction at rest of 65.4 +/- 6.2% (mean +/- SD) and only 1 of 18 showed a decrease with exercise; peak exercise ejection fraction averaged 77.1 +/- 7.8%. The diabetic group had a mean ejection fraction at rest of 63.7 +/- 6.5%, similar to that of the control group, but 7 of 20 showed a decrease during exercise; the exercise ejection fraction averaged 67.7 +/- 9.7%, significantly lower than that of the control group (p less than 0.01). The diabetic patients varied widely in ejection fraction response to exercise, ranging from an increase of 25% to a decrease of 21%. This response did not correlate with age, sex, duration of diabetes, smoking, retinopathy, exercise heart rate, blood pressure or rate-pressure product, work load attained or ejection fraction at rest. These data suggest that approximately one-third of patients with diabetes have subclinical left ventricular dysfunction without correlation to risk factors for atherosclerosis or other diabetic complications. Whether this is due to unrecognized coronary artery disease or primary myocardial disease remains unknown.

Cold pressor test during two-dimensional echocardiography: Usefulness in detection of patients with coronary disease

We assessed the feasibility and value of the cold pressor test (CPT) during real-time two-dimensional echocardiography (2DE) in patients with suspected coronary artery disease and normal resting left ventricular wall motion. Twenty patients were studied without knowledge of angiographic findings that demonstrated no significant coronary artery disease in seven (group 1) and significant coronary lesions in 13 (group 2). The increments in physiologic parameters (heart rate, systolic blood pressure, and double product) were not significantly different in both groups. CPT-induced wall motion abnormalities were identified echocardiographically in nine patients in group 2 and in one patient in group 1 (sensitivity 69% and specificity 86%). None of the patients in our study developed chest pain, ST changes, or ectopy during the test. It is concluded that 2DE combined with the CPT is valuable in identifying patients with coronary artery disease who show no left ventricular asynergy at rest.

Effects of low-dose dobutamine on coronary hemodynamics, myocardial metabolism, and anginal threshold in patients with coronary artery disease.

Fourteen patients with coronary artery disease and normal or near-normal left ventricular function were studied at rest and during atrial pacing until the occurrence of angina (12 patients) before and during infusion of dobutamine (3.80 +/- 0.45 micrograms/kg/min). At rest, during the infusion, three patients developed chest pain, mean ST segment depression increased from 0.02 to 0.08 mV (p less than .001), and myocardial lactate extraction fell from +17.5% to -1.4% (p less than .05). These ischemic changes were associated with significant increases in arterial systolic pressure (134 to 149 mm Hg), heart rate (79 to 91 beats/min), coronary sinus flow (89 to 113 ml/min), and myocardial oxygen consumption (10.8 to 13.5 cc/min). In contrast, during atrial pacing, dobutamine did not reduce the pacing threshold or further increase myocardial oxygen consumption or ST segment changes; however, arterial mean and diastolic pressures were significantly lower with pacing during dobutamine infusion compared with control pacing. In the absence of heart failure, dobutamine in low doses can cause myocardial ischemia in patients with coronary artery disease. The absence of increased ischemia from dobutamine during pacing may reflect reversal of pacing-induced ventricular dysfunction.

Esophageal acid perfusion in coronary artery disease: Induction of myocardial ischemia

Although coronary artery disease and gastroesophageal reflux disease are common conditions which, therefore, may coexist, it is unknown whether or not the presence of one affects the other. We performed esophageal acid perfusion tests, with concurrent blood pressure, heart rate, and 12-lead electrocardiographic monitoring, in 37 patients, 25 with angiographically documented coronary disease and 12 with normal coronary arteries. Rate—pressure product, an index of myocardial work load, was calculated. In patients with coronary disease who developed chest pain during acid perfusion, rate-pressure product increased from 10.0 ± 1.0 × 103 (mean ± SEM) basally to 15.2 ± 1.5 × 103 (p < 0.001), and 3 of 9 patients showed concomitant electrocardiogram evidence of myocardial ischemia. In addition, in coronary disease, 64% of patients with infrequent or absent reflux symptoms by history had positive acid perfusion tests, and 56% of patients with coronary disease who developed pain during esophageal acid perfusion could not distinguish that pain from their usual angina. We conclude that in coronary disease, acid perfusion (and, presumably, gastroesophageal reflux) resulting in chest pain causes rate—pressure product elevation and can induce myocardial ischemia. The presence of esophageal acid sensitivity is not accurately predicted by clinical history in coronary disease, and pain of esophageal origin is often confused with angina.

Angina caused by reduced vasodilator reserve of the small coronary arteries

To study the mechanism of chest pain in patients vvith insignificant large vessel coronary artery disease, 22 patients underwent great cardiac vein flow, coronary resistance and lactate determinations at rest and with coronary sinus pacing followed by coronary arteriography. Nine patients experiencing chest pain with pacing demonstrated significantly lesser increase in flow from base-line values (45 ± 30versus86 ± 50% [mean ± standard deviation], p < 0.025), lesser decrease from baseline in resistance (-28 ± 18 versus -44 ± 11%, p < 0.001) and less lactate consumption (25.0 ± 23.6 versus 45.6 ± 19.0 mmol ml/min, p < 0.025) compared with the 13 patients without pacing-induced chest pain. Pacing conducted during the cold pressor test elicited similar abnormalities in those patients experiencing chest pain and those who did not: four of eight patients experiencing chest pain demonstrated a lowered or new anginal threshold compared with that of the control pacing study. Coronary arteriography during the cold pressor test revealed no significant change in epicardial coronary artery dimension. After administration of ergonovine, 0.15 mg intravenously, 2 of 20 patients experienced spontaneous chest pain, which was associated with the greatest decrease in flow ( - 13 and -21%, respectively) and increase in resistance ( + 26 and +39%, respectively) of any patient. Pacing resulted in chest pain in 10 of the remaining 18 patients, including 5 patients who had not experienced chest pain during the control pacing study. Although none of these patients exhibited significant epicardial coronary artery narrowing on arteriography, their flow increased less (38 ± 12 versus 126 ± 68%, p < 0.001), resistance decreased less ( -18 ± 4 versus -50 ± 13%, p < 0.001) and was associated with less lactate consumption (32.7 ± 25.2 versus 70.1 ± 29.4mmolml/min, p < 0.01) than in patients not experiencing chest pain. Eight of the 12 patients developing chest pain demonstrated a decreased or new anginal threshold compared with that elicited by pacing during the control study. These findings suggest that some patients with atypical chest pain have inappropriate coronary arteriolar or small coronary artery constriction with abnormal vasodilator reserve in response to atrial pacing. The abnormality can be unmasked or exacerbated in some patients by vasoconstrictor stimuli, but cannot be identified with standard angiographic assessment of “spasm” because abnormal vasoconstriction occurs in vessels too small to be visualized by angiography.