Transient electrocardiographic changes in patients with unstable angina: Relation to coronary arterial anatomy

The relation between the spontaneous electrocardiographic changes and coronary arterial anatomy in unstable angina pectoris was examined in 97 patients with coronary artery disease and transient electrocardiographic changes during chest pain. Sinus rhythm was maintained during pain in all patients. Heart rate increased significantly in 61 percent (mean ± standard error of the mean 72 ± 2 to 93 ± 2 beats/min, probability [p] < 0.001) and was unchanged or decreased in 39 percent of patients (73 ± 2 to 72 ± 2 beats/min; p = not significant) during pain. S-T segment changes developed in 97 percent of patients, of whom 42 percent had S-T segment elevation and 55 percent S-T depression. The magnitude of the S-T segment shift was greater in patients with triple vessel disease (2.2 ± 0.4 mm) than in those with double (1.5 ± 0.1 mm) or single (1.4 ± 0.1 mm) vessel disease (p < 0.05). In 43 patients with single vessel disease S-T segment elevation developed in 78 percent of those with right coronary artery disease and in only 9 percent of those with left circumflex disease (p < 0.02). Maximal S-T segment changes were more frequent in the inferior leads in patients with right coronary artery disease (56 percent) and in the anterior leads in patients with left anterior descending (65 percent) and circumflex (64 percent) disease (p < 0.05).Thus, patients with coronary artery disease and unstable angina maintain regular sinus rhythm during chest pain, and the heart rate usually increases but may be unchanged or decreased in a significant proportion. S-T segment elevation is common in these patients and the magnitude of the S-T segment shift is related to the extent of the underlying coronary disease. This study suggests that the type and distribution of the repolarization changes are a reflection of the location and severity of the atherosclerotic process.     

Unstable angina pectoris: National cooperative study group to compare surgical and medical therapy: III. Results in patients with S-T segment elevation during pain

A prospective randomized study comparing intensive medical therapy with urgent coronary bypass surgery for the acute management of patients with unstable angina pectoris was carried out by nine cooperating medical centers under the auspices of the National Heart, Lung, and Blood Institute. Between 1972 and 1976, a total of 288 patients were entered into the study; 79 of these (27 percent of the total study group) with 70 percent or more fixed obstruction in one or more coronary arteries had episodes of pain at rest associated with transient S-T segment elevation. Forty-two were randomized to medical and 37 to surgical therapy. The hospital mortality rate was 4.8 percent for the medical and 5.4 percent for the surgical group (difference not significant). The rate Of in-hospital myocardial infarction was 12 percent in the medical and 14 percent in the surgical group (difference not significant).During the 1st and 2nd years of follow-up, 25 percent in the medical and 15 percent in the surgical group complained of New York Heart Association class III or IV angina (difference not significant). During an average follow-up period of 42 months 45 percent of the medically treated patients later underwent surgery to relieve unacceptable angina. In the medical group 65 percent were working full- or part-time at the end of 1 year and 61 percent at the end of 2 years of follow-up; comparable figures for the surgically treated group were 63 and 68 percent.The results indicate that patients with unstable angina pectoris with transient S-T segment elevation during pain at rest with fixed obstruction of 70 percent or more in one or more coronary arteries do not differ significantly from patients with pain at rest associated with transient S-T segment depression or T wave inversion. The condition of such patients can be stabilized, and they can be managed with a maximal medical program including propranolol and long-acting nitrates in pharmacologic doses with good control of pain in most and no increase in rate of early mortality or myocardial infarction. Later, elective surgery can be performed with a lower risk and good clinical results if the patient's angina fails to respond to intensive medical therapy.     

Adjunctive nifedipine therapy in high-risk,medically refractory,unstable angina pectoris

Patients with unstable angina pectoris who remain symptomatic at rest after hospitalization are at increased risk of death or myocardial infarction. This report presents the results of adding the calcium influx blocking agent nifedipine to aggressive therapy with nitrates and beta-blocking drugs in 47 hospitalized patients. The patients were followed up for an average of 12 months. Twenty-two (47%) improved sufficiently to be discharged; despite this symptomatic improvement, 8 had cardiac events within 4 months. Eighteen patients had no symptomatic improvement and 7 of them had cardiac events in 4 months. In 7 others, relief was insufficient to permit discharge, and 1 of these patients had myocardial infarction. In all, 31 patients were treated with medical therapy only. Twenty-one of these patients had a favorable short-term response to nifedipine; 13 died or had an infarction in less than 4 months. Two of 16 patients who underwent coronary artery bypass surgery had cardiac events. The presence of electrocardiographic changes with pain did not identify either a group at higher risk or a group with a better outcome with nifedipine.We conclude that in a high-risk subset of patients with unstable angina pectoris, nifedipine does not reduce morbidity or mortality or the need for bypass surgery, but relieves symptoms in many patients. An early symptomatic response to nifedipine did not predict a reduced incidence of subsequent cardiac events.     

Exercise testing early after myocardial infarction: Predictive value for subsequent unstable angina and death

Recently, modified treadmill exercise testing before hospital discharge has been reported to be safe in patients after uncomplicated myocardial infarction. Accordingly, the frequency of treadmill exercise-induced abnormalities and their prognostic value were evaluated in 130 patients with uncomplicated myocardlal infarction. Seventy-eight patients (60 percent) had one or more treadmill exercise-induced abnormalities; 42 had S-T segment depression, 35 had angina and 17 had an inadequate blood pressure response. During the mean follow-up period of 11 months, 27 patients experienced unstable angina, 12 had a recurrent myocardlal infarction and 10 died of cardiac causes. Compared with patients with no exercise-induced abnormality, patients with S-T segment depression, angina pectoris or an inadequate blood pressure response had a significantly greater (p < 0.001) incidence of all cardiac events during the follow-up period. Furthermore, unstable angina pectoris was significantly more frequent (p <0.005) in patients with S-T segment depression or angina pectoris. Finally, when the patients with ischemic treadmill abnormalities were combined with the patients exhibiting an inadequate blood pressure response, they had a statistically greater (p < 0.005) incidence of cardiac death than that of patients with no treadmill abnormalities. Therefore, these three abnormalities during modified treadmill exercise testing before hospital discharge identify patients with uncomplicated myocardial infarction who are at risk for a future cardiac event.     

Prinzmetal's angina during 5-fluorouracil chemotherapy

Variant angina developed during intravenous 5-fluorouracil therapy in a patient without prior history of angina pectoris. Ambulatory electrocardiography demonstrated S-T segment elevation and ventricular ectopy during pain, whereas no symptoms or S-T segment changes occurred during placebo therapy. Prophylaxis with both nifedipine and diltiazem was successful in preventing recurrence. It is believed that 5-fluorouracil induced coronary vasospasm and that this was prevented by prophylactic calcium antagonist therapy. Drug-induced coronary artery spasm may be the cause of 5-fluorouracil-associated chest pain.     

Chest pain as a predictor of coronary artery disease in patients with obstructive aortic valve disease

To clarify the association between chest pain and significant coronary artery disease in patients who have aortic valve disease, 76 consecutive candidates for aortic valve replacement were evaluated prospectively with use of a historical questionnaire and coronary arteriography. Of the 76 patients, 19 (25 percent) had no chest pain, 21 (28 percent) had chest pain that was not-typical of angina pectoris and 36 (47 percent) had chest pain typical of angina pectoris. In 18 of 19 patients the absence of chest pain correlated with the absence of coronary artery disease. The single patient without chest pain who had coronary artery disease had evidence of an inferior myocardial infarction in the electrocardiogram. Thus, absence of chest pain and the absence of electrocardiographic evidence of infarction predicted the absence of coronary disease in all cases.

The presence of chest pain did not predict the presence of coronary artery disease, but the more typical the pain of angina pectoris the more likely were patients to have significant coronary artery disease. Of the 21 patients with atypical chest pain, 6 (29 percent) had coronary artery disease, but of the 36 patients with typical angina pectoris 23 (64 percent) had significant coronary artery disease. In addition, when patients with chest pain not typical of angina pectoris also had coronary artery disease, the diseased vessels usually supplied smaller areas of the left ventricle than when the pain was typical of angina pectoris. In 21 of 23 patients (91 percent) with typical angina pectoris and significant coronary artery disease, lesions were present in the left coronary artery. There was no systolic pressure gradient across the aortic valve that excluded the presence of coronary artery disease, although all patients with a calculated aortic valve area of less than 0.4 cm² were free of coronary artery disease. Patients with severe left ventricular dysfunction were more likely to have normal coronary arteries.     

Comparison of the data of 24-hour ECG monitoring and the condition of the coronary bed in patients with the variants of the course of unstable stenocardia]

A total of 232 patients with various clinical types of unstable angina pectoris were examined. All the patients underwent coronary angiographic studies, 24-hour ECG monitoring. In 40.5% of the patients, 24-hour monitoring revealed transient ST segment changes which were not accompanied by pain in 47% of the cases. ST segment changes were equally encountered in patients with one-, two-, and three-vessel disease in the presence or absence of pain. Ischemic ST segment changes generally occurred with an anginal episode in patients with crescendo unstable angina, whereas in those with more prolonged and intensified pain and angina at rest in particular, silent myocardial ischemic episodes were significantly more frequently recorded, which were more common in these patients with multivessel disease.     

Rest angina with transient S-T segment elevation correlation of clinical features with coronary anatomy

In 44 consecutive patients with angina at rest associated with transient S-T segment elevation, clinical features were correlated with angiographic coronary anatomy. Patients were divided into three groups depending on the number of major vessels having ?70 per cent luminal narrowing: Group I = no or minimal disease (six patients); group II = single vessel disease (13 patients); and group III = multiple vessel disease (25 patients).The following features did not differ significantly among groups I, II or III: age, sex, risk factors, time from onset of episodes of pain at rest to study or arrhythmias during ischemic episodes. Patients in group III were more likely to have angina on effort (p < 0.001) and an abnormal base line electrocardiogram (p < 0.001) than patients in groups I or II. However, the absence of these features did not separate patients in group I from those in group II.In patients with angina at rest associated with transient S-T segment elevation, clinical features identify patients with multiple vessel disease but do not allow differentiation of patients with no or minimal coronary disease from patients with single vessel disease.     

Detection of acute right ventricular infarction by right precordial electrocardiography

The value of 0.1 mV or greater of S-T segment elevation in at least one right precordial lead (V₄R to V₆R) in defining right ventricular myocardial infarction was assessed prospectively in 43 subjects (33 consecutive patients with enzymatically confirmed infarction of varying type and location, 4 patients with unstable angina and 6 healthy volunteers). Patients with acute myocardial infarction were studied with radionuclide ventriculography and technetium-99m stannous pyrophosphate myocardial scintigraphy 18.2 ± 14.3 (mean ± standard deviation) and 85.1 ± 18.0 hours after the onset of symptoms, respectively. Eleven patients (Group A: 9 patients with transmural inferior infarction, 1 with transmural inferolateral infarction and 1 with transmural anteroseptal infarction) demonstrated right precordial S-T segment elevation and 22 patients (Group B: 6 patients with transmural inferior infarction, 2 with transmural posterior infarction, 3 with transmural inferolateral infarction, 3 with transmural anteroseptal infarction, 3 with transmural extensive anterior infarction, 4 with subendocardial anterior infarction and 1 with unclassified infarction) did not. Right ventricular ejection fraction was significantly lower in Group A (0.47 ± 0.11) than in Group B (0.60 ± 0.12) (p < 0.01). Right ventricular total wall motion score was 63.8 ± 15.6 percent of normal in Group A versus 94.3 ± 8.5 percent in Group B (p < 0.001). Technetium-99m pyrophosphate uptake (2+ or greater) over the right ventricle occurred in nine patients (81.8 percent) in Group A and in one patient (4.5 percent) in Group B (p < 0.001). No patient with unstable angina and no healthy volunteer had S-T segment elevation in a right precordial lead. S-T segment elevation of 0.1 mV or greater in one or more of leads V₄R to V₆R is both highly sensitive (90 percent) and specific (91 percent) in identifying acute right ventricular infarction.     

Left ventricular function during spontaneous angina pectoris: effect of sublingual nitroglycerin

Global and regional left ventricular function was assessed at rest, during spontaneous angina pectoris and after nitroglycerin therapy in 14 patients with ischemic heart disease. Cardiac output, left ventricular pressure and left ventricular volume were measured when patients experienced spontaneous angina pectoris during cardiac catheterization. In every patient control measurements had already been made; further measurements were made after nitroglycerin had relieved pain. Subsequent coronary angiography showed significant two or three vessel disease in all 14 patients. The S-T segment was depressed in every patient during pain (average 0.26 + 0.04 mV; mean + standard error of the mean [SEM]). During spontaneous angina, there was a significant increase in left ventricular end-diastolic pressure (17 ± 2 to 35 ± 2 mm Hg, p < 0.001), left ventricular end-diastolic volume (77 ± 6 to 88 ± 8 ml/m², p < 0.005) and left ventricular end-systolic volume (35 ± 4 to 52 ± 7 ml/m², p < 0.001). Concomitantly stroke index decreased from 42 ± 2 to 36 ± 3 ml/beat per m² (p < 0.01) and ejection fraction from 56 ± 4 to 44 ± 4 percent (p < 0.001).Assessment of regional left ventricular performance during spontaneous angina revealed either development of new areas or extension of already existing areas of abnormal wall motion in all patients. Nitroglycerin restored global and regional left ventricular function to a normal state. In six individual patients there was an excellent correlation between the S-T depression (V₅) and left ventricular end-diastolic pressure during spontaneous angina (correlation coefficient [r] = 0.88 to 0.96) and after nitroglycerin therapy (r = 0.76 to 0.84). For the group, there was a good correlation between change in S-T depression and changes in left ventricular end-diastolic pressure (r = 0.87) and left ventricular end-diastolic volume (r = 0.78). Thus, these data indicate marked systolic and diastolic dysfunction of the left ventricle during spontaneous angina pectoris, characterized by decreases in stroke index and ejection fraction and increases in left ventricular end-systolic and end-diastolic volumes and left ventricular filling pressure.     

Transient S-T segment elevation in unstable angina: prognostic significance

The clinical and prognostic significance of the direction of the S-T segment shift on the 12-lead electrocardiogram was evaluated in medically treated patients with unstable angina pectoris. Long-term mortality and morbidity of 11 patients with transient S-T segment elevation (group I) were compared to that of 21 patients with transient S-T segment depression (group II). The average follow-up duration was 62 months. There was no significant difference between groups I and II with respect to survival or nonfatal myocardial infarction over a five-year period. Mortality was related to the extent of coronary artery disease and left venticular ejection fraction rather than to the direction of the S-T segment shift.     

Unstable angina pectoris: National cooperative study group to compare surgical and medical therapy: II. In-Hospital experience and initial follow-up results in patients with one,two and three vessel disease

A prospective randomized study comparing intensive medical therapy with urgent coronary bypass surgery for the acute management of patients with unstable angina pectoris was carried out by nine cooperating medical centers under the auspices of the National Heart, Lung, and Blood Institute. Between 1972 and 1976, a total of 288 patients were entered into the study. All patients had transient S-T or T wave changes, or both, in the electrocardiogram during pain; 90 percent had pain at rest in the hospital, and 76 percent had multivessel coronary disease. The medically and surgically treated patients were comparable with respect to clinical, electrocardiographic and angiographic characteristics and left ventricular function.During the total study period, the hospital mortality rate was 5 percent in the surgical group and 3 percent in the medical group (difference not significant). The rate of in-hospital myocardial infarction was 17 and 8 percent in the respective groups (P < 0.05). In the last 4 years of the study (1973 to 1976), the hospital mortality rate decreased to 3 percent in the surgical group and to 2 percent in the medical group (difference not significant). During the last 3 years of the study (1974 to 1976), the rate of in-hospital myocardial infarction was 13 percent in the surgical group and 10 percent in the medical group (difference not significant). There were no differences in the subsets of patients with one, two or three vessel disease.In the 1st year after hospital discharge class III or IV angina (New York Heart Association criteria) was more common in medically than in surgically treated patients with one vessel disease (22 percent versus 3 percent, P < 0.05), two vessel disease (40 percent versus 13 percent, P < 0.01) and three vessel disease (40 percent versus 15 percent, P < 0.01). During an average follow-up period of 30 months, 36 percent of the medically treated patients later underwent surgery to relieve unacceptable angina. Late mortality was comparable in the two groups, but the large number of medically treated patients who later underwent surgery prevents definitive conclusions about the relative effect of medical and surgical therapy on long-term mortality. However, the patients who responded to medical therapy did not have a higher late mortality rate than surgical patients.The results indicate that patients with unstable angina pectoris can be managed acutely with intensive medical therapy, including the administration of propranolol and long-acting nitrates in pharmacologic doses, with adequate control of pain in most patients and no increase in early mortality or myocardial infarction rates. Later, elective surgery can be performed with a low risk and good clinical results if the patient's angina fails to respond to intensive medical therapy.     

Clinical relevance of exercise-induced S-T segment elevation

Patients with exercise-induced S-T elevation or S-T depression were evaluated with demographic, treadmill and angiographic data. When 541 patients with S-T depression ware compared with 109 patients with S-T elevation, a greater proportion of the former had chest pain (71 versus 58 percent) and a normal-sized ventricle (86 versus 61 percent) with normal wall motion (54 versus 30 percent). A greater proportion of patients with S-T elevation had had a previous myocardial infarction (61 versus 33 percent). Among patients without prior Infarction (360 with S-T depression and 42 with S-T elevation), these differences disappeared. In this group of 42 patients with S-T elevation, 83 percent had a normal-sized ventricle, 64 percent had normal contractlity and none had a ventricular aneurysm; the severlty of coronary disease and ventricular dysfunction did not differ from the severity in patients with S-T depression. Thus, in patients without prier myocardial infarction, the cause of the development of S-T elevation or S-T depression during exercise does not appear to be related to the the severlty of the coronary lesions, ventricular function or wall abnormalities at rest. In patients with prior myocardial infarction, exercise-induced S-T elevation appears to be a marker of depressed left ventricular function.     

Effects of atrial pacing on QT dispersion in patients with coronary artery disease without angina pectoris and ST segment depression.

The aim of this study was to investigate QT dispersion during atrial pacing in patients with coronary artery disease (CAD) without clinical ischemia, such as angina pectoris and ST segment depression. Thirteen patients with normal coronary arteries and 42 patients with CAD (12 with single-vessel, 16 with two-vessel and 14 with three-vessel disease) having no angina pectoris or ST segment depression during atrial pacing with maximum rate of 120/minute were enrolled in the study. Twelve-lead surface ECGs were recorded at 100 mm/second paper speed before pacing, at maximum pacing rate, and during the recovery period for measurement of QT interval parameters. Corrected QTd (QTcd) increased from 43.4 +/- 8.1 to 49.3 +/- 9.5 ms (p < 0.05) in the control group, from 46.1 +/- 8.1 to 74.3 +/- 7.7 ms (p < 0.0001) in the single-vessel disease group, from 48.5 +/- 10.4 to 93.8 +/- 22.1 ms in the two-vessel disease group (p < 0.0001), and from 49.7 +/- 13.6 to 128.5 +/- 31 ms (p < 0.0001) in the three-vessel disease group at peak atrial pacing period. A positive correlation was found between the severity of CAD and QTcd (r = 0.49, p < 0.0001). It was found that pacing-induced QTc dispersion identifies coronary disease extent, even when there is no ST depression or T wave inversion during pacing.     

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

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

Unstable angina pectoris: A randomized study of patients treated medically and surgically

Fifty patients with the clinical syndrome of unstable angina pectoris were evaluated. Twenty-seven were randomized into medical or surgical treatment groups and subsequently followed up. The results of the study reveal that: (1) there is approximately a 16 percent incidence rate of significant left main coronary artery disease in patients with this entity at our institution; (2) 10 percent of patients do not have angiographically significant coronary artery disease; (3) pain relief is better in the surgically treated patients, but the 1 1/2 year survival rate is not significantly different between the groups; (4) 50 percent of the medically treated patients again had the syndrome of unstable angina pectoris in the initial few months of the follow-up period; (5) the operative and late postoperative mortality rate in patients presenting with unstable angina pectoris and left main coronary artery disease in this small group of patients was 43 percent; and (6) four of six patients with this syndrome whose condition was deemed inoperable and who were not randomized died within the subsequent few months.     

Efficacy of nifedipine therapy for refractory angina pectoris

Nifedipine is a calcium-channel blocking agent that has been effective for patients with angina pectoris when used as single-agent therapy and as part of a combination regimen with conventional antianginal therapy. However, the efficacy of nifedipine in patients with angina refractory to maximum tolerated conventional therapy has not been extensively studied. We present experience using nifedipine in the treatment of three distinct subsets of patients with refractory angina pectoris. One hundred twenty-seven patients with Prinzmetal's variant angina and documented coronary vasospasm were treated with nifedipine after experiencing an inadequate response to conventional therapy. Nifedipine, 40 to 160 mg daily, reduced the mean weekly rate of angina attacks from 16 to 2 (p < 0.001). In 63% of the patients complete control of angina attacks was achieved, and in 87% the frequency of angina was reduced by at least 50%. Nifedipine therapy was well tolerated, and the beneficial response persisted for the 9 months of follow-up. Nifedipine therapy was added to a second group of 11 consecutive patients with refractory episodes of recurrent rest ischemia following acute myocardial infarction. Prior to infarction all the patients had a history of exertional angina only; yet following the infarction, episodes of recurrent ischemia occurred at rest in spite of maximal medical management with beta blockers and/or nitrate preparations. With maximum tolerated conventional therapy the heart rate was lowered to a mean of 65 beats/min and the blood pressure to a mean of $\text{109}\text{70}\text{mm Hg}$. The episodes of rest ischemia were prevented in all but one patient by the addition of nifedipine (mean daily dose 60 mg, range 40 to 120 mg) without causing a change in heart rate or blood pressure. Two patients continued to have myocardial ischemia with minimal exertion, although resting pains were abolished, and they underwent coronary bypass surgery for rellef of exertional pain. Only one patient continued to have episodes of ischemia at rest, and bypass surgery was necessary for pain relief. The other eight patients have been managed medically for a mean of 5.4 months and have remained pain free on combined regimens of nifedipine, beta blockers, and/or nitrate preparations. The third group of patients treated with nifedipine is composed of 239 patients with severe classic exertional angina pectoris without a suspicion of superimposed coronary vasospasm. The anginal episodes in these patients were refractory to maximum tolerated conventional therapy; however, the addition of nifedipine (mean daily dose 60 mg, range 40 to 120 mg) reduced the mean weekly angina attack rate from 20.8 to 6.4 (p < 0.00001). Although only 11% of patients had complete prevention of angina during nifedipine therapy, a total of 70% experienced a reduction in angina frequency of at least 50%. We conclude that the addition of nifedipine therapy may provide further benefit for patients with angina pectoris refractory to maximum tolerated conventional therapy. Randomized, placebo-controlled studies are necessary to confirm the efficacy of nifedipine therapy in patients with refractory angina and to clarify the mechanism of the beneficial response.     

Correlation of computer-quantitated treadmill exercise electrocardiogram with arteriographic location of coronary artery disease

Graded treadmill exercise testing and coronary cinearteriographic studies were carried out on 86 patients with angina pectoris. At rest, all patients demonstrated a normal S-T segment on the modified bipolar lead V₅ recording used. The computer-quantitated S-T segment response to exercise was correlated with the location and extent of obstructive coronary artery disease. The coronary cineartertograms were reviewed by 3 physicians and stenosis of 75 percent or greater was considered significant. All patients showed at least this degree of stenosis in 1 or more major coronary arteries, and 83 of 86 exhibited 90 percent or greater stenosis in at least 1 artery. Thirty-one patients had stenosis in a single artery, 43 had stenosis in 2 arteries and 12 had significant lesions in all 3 major arteries. In 70 of the 86 (82 percent) patients, a positive S-T segment response developed during or immediately after exercise. In 12 of the 16 with a negative response, disease was limited to a single artery. In 11 of the 12 the disease was restricted to the right coronary or left circumflex arteries. Of the 12 patients with an isolated stenosis of the left anterior descending artery, 11 (92 percent) had a positive S-T segment response. Of 55 patients with 2- or 3-vessel disease, 51 (93 percent) demonstrated a positive S-T response. Graded treadmill exercise testing in 80 patients with chest pain, normal coronary art eriograms and normal left ventricular function revealed 4 (5 percent) with a false positive S-T segment response.     

S-T segment elevation and coronary spasm in response to exercise

The prevalence rate of exercise-induced S-T segment elevation of 0.1 mV or greater in symptomatic patients is 3.0 to 6.5 percent in most studies. S-T segment elevation is associated with a more severe degree of myocardial ischemia than depression and frequently implies a high grade coronary stenosis in the vessel that supplies the site of ischemia. Leads V₄ to V₆ and bipolar lead CM₅ have been found to be relatively insensitive in detecting exercise-induced S-T segment elevation.

The pathogenesis of S-T segment elevation is different in three clinical patient subsets reviewed. In patients after infarction, the largest of the three subgroups, exercise-induced S-T segment elevation usually appears in leads with Q waves, is more common after anterior myocardial infarction and implies underlying akinetic or dyskinetic wall motion. Of patients with variant angina, 10 to 30 percent have during exercise S-T segment elevation that is most likely provoked by coronary arterial spasm. The natural history of variant angina is cyclic, and clinical observations and laboratory findings are dependent on particular phases in the disease process and treatment. Finally, 0.2 to 1.7 percent of symptomatic patiënts without infarction or variant angina have exercise-induced S-T segment elevation. Although most of the latter have fixed high grade coronary arterial stenoses at angiography, the exact pathogenetic mechanism of S-T segment shift in this patient group is not yet fully understood.     

Comparison of coronary arteriographic findings during angina pectoris associated with S-T elevation or depression

Coronary arteriographic findings during an attack of angina pectoris associated with S-T segment elevation and angina associated with S-T depression were compared in 54 patients. Thirty-eight attacks with S-T segment elevation included 2 that were spontaneous, 6 induced by methacholine, 4 by epinephrine with or without propranolol, 9 by arm exercise, 5 by hyperventilation with or without Tris-buffer infusion and 12 by ergonovine maleate. Twenty-nine of the 38 attacks were associated with total occlusion, 8 with subtotal occlusion and 1 with diffuse narrowing of a major coronary artery caused by spasm.Twenty-six attacks with S-T segment depression included 3 induced by methacholine, 13 by arm exercise, 3 by hyperventilation with or without Tris-buffer infusion and 7 by ergonovine maleate. Eight of the 26 attacks were associated with subtotal occlusion and 9 with diffuse narrowing of a major coronary artery caused by spasm; 3 attacks were associated with total occlusion of a major coronary artery well supplied with collateral vessels and 2 with total occlusion of a small coronary branch caused by spasm. Four attacks were associated not with spasm but with fixed subtotal occlusion of a major coronary artery (3 attacks) or total occlusion of a major coronary artery receiving collateral vessels (1 attack).Only 2 of the 31 patients with S-T segment elevation had collateral vessels compared with 8 of the 16 patients with S-T segment depression (p < 0.001). It is concluded that angina pectoris associated with S-T segment elevation usually indicates more severe myocardial ischemia than angina associated with S-T segment depression.