Response to exercise early after uncomplicated acute myocardial infarction in patients receiving no medication: long-term follow-up

Cardiovascular function and prognosis have not been adequately defined early after an uncomplicated acute myocardial infarction in patients given no medication. Ninety such patients were studied with treadmill testing submaximally at 3 weeks and maximally at 8 weeks after infarction. The exercise heart rate, rate-pressure product and oxygen uptake were, respectively, 120 ± 17 beats/min, 179 ± 43 and 17.4 ± 1.0 ml/kg per min at 3 weeks and 157 ± 20, 271 ± 55 and 24.3 ± 3.7 at 8 weeks. Exercise variables at submaximal equivalent exercise work did not change from 3 to 8 weeks. At maximal exercise 15.6 percent of patients had S-T changes alone, 8.9 percent had angina alone and 12.2 percent had both. Patients were followed up for a mean of 23.7 months for complications—death, reinfarction, bypass grafting and progression to functional class III and IV. Complications occurred in 27 percent of patients with both angina and S-T changes, 29 percent of those with S-T changes alone, 25 percent of those with angina alone, 8 percent of those with ventricular arrhythmia alone, 12 percent of those with a normal 8 week treadmill test and in 17 percent of the group as a whole. Another 18 patients who were given no medication and whose course was uncomplicated could not perform a maximal 8 week treadmill test because of angina pectoris or S-T segment depression, or both, and 56 percent of these had long-term complications.In conclusion, these reference values serve as safe limits in performing treadmill testing early after acute myocardial infarction. S-T changes or angina, or both, and inability to complete a maximal 8 week treadmill test identify patients at risk for later complications even though these patients may have been considered to be in a low risk category clinically.     

Idiopathic hypertrophic subaortic stenosis: evaluation of anginal symptoms with thallium-201 myocardial imaging.

The evaluation of angina pectoris in patients with idiopathic hypertrophic subaortic stenosis is difficult in those in the age group prone to coronary artery disease. Ten patients with angina pectoris, normal coronary angiograms and idiopathic hypertrophic subaortic stenosis were studied with thallium-201 myocardial imaging performed in conjunction with submaximal treadmill exercise testing. The resting electrocardiogram demonstrated left ventricular hypertrophy with S-T segment abnormalities in seven patients, thereby vitiating the further increase in S-T segment abnormalities that developed in these patients during exercise or in the postexercise period. Of the three patients with a normal resting electrocardiogram, one had significant exercise-induced S-T segment depression. Thallium-201 myocardial imaging revealed no significant perfusion defects in 9 of the 10 patients (90 percent). In one patient with severe left ventricular hypertrophy significant perfusion defects developed after exercise that were not present at rest. Stress thallium-201 myocardial perfusion imaging is a useful noninvasive technique that assists in ruling out the presence of significant coronary artery disease in patients with idiopathic hypertrophic subaortic stenosis.     

Prognostic value of exercise-induced ventricular ectopic activity for mortality after acute myocardial infarction

To evaluate the importance of ventricular ectopic activity on the predischarge treadmill exercise test for predicting mortality in patients after acute myocardial infarction (AMI), 163 patients with uncomplicated AMI were studied using symptom limited low-level treadmill exercise testing and 24-hour ambulatory electrocardiographic monitoring before hospital discharge. All patients were followed for at least 2 years or until recurrent AMI, coronary artery bypass grafting or death. Seventeen patients (10%) died during the follow-up period, 15 patients (9%) had recurrent AMI and 45 patients (28%) underwent bypass surgery. Ventricular ectopic activity was the only single treadmill abnormality that predicted subsequent cardiac death; angina pectoris, electrocardiographic ST-segment depression and a hypotensive blood pressure response did not. The mortality rate in the 20 patients with exercise-induced ventricular ectopic activity was 25%, compared with 8% in those without (p less than 0.004). Furthermore, in this patient population, exercise-induced ventricular ectopic activity was a much better predictor of cardiac death than that detected by ambulatory monitoring. Thus, ventricular ectopic activity on the predischarge treadmill exercise test is an important risk factor for death after AMI.     

Relation of therapeutic response to nifedipine to coronary anatomy and motion of S-T segment during unstable angina pectoris

Of 77 patients hospitalized for unstable angina pectoris and failure of oral, dermal, or intravenous nitrates and/or beta blockade, 81 percent with negligible or single-vessel disease and 55 percent with two- or three-vessel disease showed response (p < 0.05) to nifedipine therapy. Patients with either S-T elevation or no change during pain responded better (31 of 45) than those with any S-T depression (16 of 32; p < 0.05). Patients with negligible or singlevessel disease had a higher prevalence of S-T elevation ( 13 of 16) than patients with two- or three-vessel disease (15 of 31; p = 0.004). S-T motion did not predict response in patients with two- or three-vessel disease, but did predict response in patients with negligible or single-vessel disease. On follow-up study at 9 ± 8 (range one to 33) months, 39 of 42 who had shown response were free from pain. Three died from infarction without unstable angina. Five who showed response had elective bypass surgery. The addition of nifedipine abolished or reduced pain episodes by more than 50 percent in 61 percent of patients with refractory unstable angina pectoris. Patients with negligible or single-vessel disease with S-T elevation benefit most. In patients with two- or three-vessel disease, the type of S-T motion did not predict response. Follow-up of all those with response indicated sustained amelioration by nifedipine therapy. Failure of nifedipine therapy should not be accepted until a dose of 120 mg per day has been achieved, or until intolerable side effects appear.     

Comparison of treadmill exercise testing and psychologic stress testing soon after myocardial infarction.

Are physical or psychologic stressors more useful for evaluating psychologic stress in patients with coronary heart disease? To evaluate this question, patients underwent physical and psychologic testing 7 weeks after myocardial infarction. The psychologic stress test consisted of an open-ended interview, a videotape depicting stressful scenes and a puzzle task. In 20 men whose mean age ± standard deviation was 52 ± 1 years, the interview produced the following peak heart rate and systolic blood pressure responses: 83 ± 18 beats/min and 140 ± 13 mm Hg, which were 8 and 10 percent, respectively, above values at rest (P < 0.05). Symptom-limited treadmill exercise testing in 10 of these patients elicited maximal heart rate and systolic blood pressure values of 152 ± 24 beats/min and 172 ± 32 mm Hg, respectively; ischemic S-T segment depression or angina pectoris occurred in 6 of the 10 patients, whereas none had demonstrated ischemia with psychologic testing. A second consecutive series of 20 patients demonstrated cardiovascular responses to physical and psychologic stress similar to those of the first series. Again, ischemic abnormalities were absent during psychologic stress, whereas exercise-induced ischemic abnormalities were noted in 3 of 20 patients. Ischemic abnormalities are unlikely to appear during psychologic stress testing in patients with a high heart rate and systolic blood pressure threshold for ischemic abnormalities during exercise testing. Standard methods of physical exercise testing are superior to currently available psychologic stress tests for evaluating the cardiovascular response to most commonly encountered psychologic stressors.     

Upsloping S-T segments in exercise stress testing. Six year follow-up study of 438 patients and correlation with 248 angiograms.

A 6 year follow-up study of 438 patients who underwent maximal treadmill stress testing revealed the following annual incidence rate of coronary events (death, myocardial infarction or onset or progression of angina pectoris): 13 percent in 84 subjects whose stress test produced 2 mm downsloping S-T segment depression, 9 percent in 230 subjects with 2 mm horizontal S-T depression and 9 percent in 124 subjects who had an upsloping S-T segment with 2 mm S-T depression measured 0.08 second from the J point. Coronary angiograms were obtained in another group of 248 subjects who underwent maximal treadmill stress testing. They revealed major (greater than 50 percent) obstruction of two or three vessels in 67 percent of 62 subjects with a downsloping S-T pattern on the stress test, in 60 percent of 116 subjects with horizontal S-T depression and in 57 percent of 70 subjects with upsloping S-T depression. Patients with an upsloping pattern of S-T depression during stress testing had the same incidence of coronary events as those with a horizontal pattern of S-T depression. Upsloping S-T depression should not be confused with isolated J point depression. Subjects with an upsloping segment also had the same incidence of major two or three vessel disease as those with horizontal depression. Subjects with a downsloping pattern has a slightly greater incidence of coronary events and major two or three 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.     

The predictive value of a strongly positive stress test in patients with minimal symptoms

The ability of a strongly positive stress test to predict left main coronary artery disease in people with suspected coronary artery disease but with minimal or no angina was investigated in 40 such patients. Nine had a history of myocardial infarction but no angina. Thirty-one had mild angina or a history of mild angina. The stress electrocardiograms were analyzed according to criteria known to be associated with left main coronary artery disease in moderately or severely symptomatic patients; (1) early S-T segment changes (stage I or II of exercise), (2) 2 mm or more S-T segment depression, (3) downsloping S-T segments, (4) associated exercise-induced hypotension, (5) prolonged S-T segment changes after the test (≥8 minutes) and (6) anterior and inferior S-T segment depression. The prevalence of left main coronary artery disease was 35 percent and that of any severe coronary artery disease 75 percent. The criterion of anterior and inferior electrocardiographic changes with exercise was most predictive of left main coronary artery disease (P < 0.01 by χ²). Exercise electrocardiography is useful in the prediction of left main or other severe coronary artery disease even when performed in patients who have minimal angina or in those who are asymptomatic after myocardial infarction.     

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.     

Clinical pharmacology of the new beta-adrenergic blocking drugs. Part 11. Effects of oral labetalol in patients with both angina pectoris and hypertension: a preliminary experience

The safety and efficacy of oral labetalol, an alpha-beta-adrenergic blocking drug, was assessed in six patients with both angina pectoris and essential hypertension. Patients received a placebo for 3 weeks which was followed by a 4 week titration of labetalol (100 to 400 mg. three times a day). The dose was then withdrawn over a 2 day period. With maximum doses of labetalol, exercise tolerance as measured by multistage treadmill testing increased significantly compared to placebo (p < 0.02). At each exercise level (stage), the heart rate, systolic blood pressure, and rate-pressure product were reduced with labetalol treatment. There was no inhibition of exercise-induced increases in heart rate. However, significant inhibition of the systolic pressure increment was seen at Stage II (p < 0.05). While peak heart rate was not significantly different from baseline, the peak systolic blood pressure and rate-pressure product were significanly reduced (p < 0.02). Labetalol treatment significantly reduced the number of weekly spontaneous angina attacks (p < 0.05). The resting supine and standing systolic and diastolic blood pressure were significantly reduced by labetalol (p < 0.01). There was no significant reduction in the standing heart rate, but the supine heart rate was significantly reduced (p < 0.005). There were no rebound hyperadrenergic effects following labetalol withdrawal. When used alone in patients with both angina pectoris and systemic hypertension, oral labetalol is a safe and effective drug for reducing the symptoms of angina pectoris, improving exercise tolerance, and lowering high blood 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.     

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.     

Submaximal predischarge exercise testing after myocardial infarction: prognostic value and limitations

The prognostic value of abnormalities resulting from predischargesubmaximal treadmill exercise testing was evaluated in 222 patientsafter myocardial infarction. The presence of the following variables— ST segment depression and elevation, an abnormal bloodpressure response, limited exercise duration, angina pectoris,ventricular arrhythmias — were predictive of subsequentcardiac events (P<0.001) among the 154 patients with oneor more of these abnormalities. When the presence or absenceof specific variables was assessed, only an abnormal blood pressureresponse, limited exercise duration (P<0.001), and ST segmentelevation and shift (P<0.05), were significantly associatedwith cardiac death. Exercise-induced angina was predictive onlyof the development of subsequent angina (P<0.05), and STdepression was associated only with future coronary surgery(P<0.01). Ventricular arrhythmias had no independent prognosticvalue. Markers of left ventricular dysfunction elicited by submaximalexercise testing are therefore valuable in identifying patientsat high risk of death after infarction. Hallmarks of residualreversible myocardial ischaemia are of limited prognostic importance.The test result may be useful in selecting patients for coronaryangiography.     

Positive treadmill stress tests post myocardial infarction in patients with single-vessel coronary disease

To investigate the possibility that patients with single-vessel coronary artery disease (CAD) and recent myocardial infarction (MI) can have ST segment depression on post infarction treadmill testing due to ischemia, we studied 16 such patients who underwent cardiac catheterization and exercise testing after MI. Of the 11 patients with ST segment depression on treadmill testing, 10 failed to increase their ejection fraction and nine had a focal worsening of wall motion during exercise radionuclide ventriculography. Seven of these 11 patients had hypokinesis or normokinesis in the suspected area of infarction. In contrast, four of the five patients without ST segment depression on treadmill stress testing had an increase in ejection fraction with stress which was significantly greater than that seen in patients with ST depression (7.2% vs 0%, p less than 0.05). Short-term follow-up (1.1 years) revealed continued post infarction angina in 10 of the 11 patients with positive treadmill stress tests. Four of these patients underwent either percutaneous transluminal angioplasty or surgery. We conclude that positive post infarction treadmill tests due to exercise-induced ischemia may occur in patients with single-vessel CAD and may be associated with continued angina that requires surgical intervention.     

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.     

Comparison of silent and symptomatic ischemia during exercise testing in men

OBJECTIVE: To compare angina and ST-segment depression during exercise testing, as markers for coronary artery disease. DESIGN: Retrospective analysis of exercise test responses and cardiac catheterization results. SETTING: A U.S. Veterans Affairs medical center. PATIENTS: Four hundred and sixteen men who were referred for the evaluation of symptoms, postmyocardial infarction testing, or both. Two hundred patients had no clinical or electrocardiographic evidence of previous myocardial infarction, whereas 216 were survivors of a previous myocardial infarction. INTERVENTIONS: All patients did a standard exercise test and had diagnostic coronary angiography with ventriculography within an average of 32 days (range, 0 to 90 days) of their exercise test. RESULTS: Two hundred patients without a previous myocardial infarction were divided into four groups: the no ischemia group had 80 patients; the angina pectoris only group had 23 patients; the silent ischemia group had 40 patients; and the ST-segment depression and angina pectoris group had 57 patients. In patients without a previous myocardial infarction, exercise-induced ST-segment depression was a better marker than exercise-induced angina for the presence of any coronary artery disease (P less than 0.005). Patients with symptomatic exercise-induced ischemia had a higher prevalence of severe coronary artery disease than did those with only silent ischemia (30% compared with 20%; 95% CI, - 7.3% to 27.0%; P = 0.005). For the 216 survivors of a myocardial infarction, divided into the same four groups, ST-segment depression again was a better marker for the presence of severe coronary artery disease compared with angina alone (P = 0.08). The prevalence rates of severe coronary artery disease in the no ischemia plus myocardial infarction group, the angina pectoris only plus myocardial infarction group, the silent ischemia plus myocardial infarction group, and the ST-segment depression and angina pectoris plus myocardial infarction group were 10%, 9%, 23%, and 32%, respectively (P less than 0.01). CONCLUSIONS: Exercise-induced ST-segment depression is a better marker for coronary artery disease than is exercise-induced angina. Symptomatic ischemia during the exercise test is a better marker for severe coronary artery disease than is silent ischemia.     

Repetitive myocardial ischemia of Prinzmetal type without angina pectoris.

In a patient with a normal electrocardiogram, normal treadmill exercise test, normal coronary arteriogram and no symptoms to suggest angina pectoris, continuous monitoring during several days exhibited repetitive (one to two per hour) S-T segment elevations in the precordial electrocardiographic leads and hemodynamic changes typical of Prinzmetal's angina (reduction in arterial pressure and cardiac index and increase in systemic peripheral resistance and pulmonary wedge pressure). This case demonstrates that electrical and dynamic cardiac alterations of Prinzmetal's angina can occur even in the absence of angina pectoris.     

Exercise-induced coronary arterial spasm: Angiographic demonstration,documentation of ischemia by myocardial scintigraphy and results of pharmacologic intervention

Exercise-induced coronary arterial spasm is an infrequently recognized phenomenon whose mechanism and management are not well established. In two patients with reproducible exercise-induced S-T segment elevation and angina pectoris thallium-201 scintigraphy showed areas of reversible anteroapical hypoperfusion, and gated radionuclide ventriculography revealed anteroapical hypokinesia with a decrease in left ventricular ejection fraction at peak exercise. During coronary arteriography, supine exercise provoked occlusive spasm of the left anterior descending coronary artery, which at rest had only minimal plaques'. Consequently, treadmill testing was performed with five different pharmacologically provoked interventions: direct vasodilatation (nitrates), alpha adrenergic blockade (phenoxybenzamine), beta adrenergic blockade (propranolol), calcium flux blockade (verapamil), and prostaglandin inhibition (indomethacin). Exercise-induced coronary arterial spasm, manifested as S-T segment elevation and angina, was prevented by nitrates, but was not eliminated by short-term oral administration of an alpha or beta blocking agent, a calcium antagonist or a prostaglandin inhibitor. Further, beta adrenergic blockade appeared to be detrimental. Thus, this study demonstrates (1) that coronary arterial spasm may be the underlying mechanism of at least some cases of exertional angina associated with transient perfusion deficits and left ventricular dysfunction, and (2) that it may be prevented by oral nitrates.     

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.