The Sensitivity of the Symptom Angina Pectoris as a Marker of Transient Myocardial Ischaemia in Chronic Stable Angina Pectoris

ABSTRACT Therapeutic decisions in patients with angina pectoris are traditionally based on the history reported by the patient, since objective evidence of myocardial ischaemia during daily life is often not available. In this study, ambulatory ST segment monitoring was performed in 60 patients with a history of chronic stable angina pectoris, positive exercise test and/or positive coronary angiography, and a correlation was made between the episodes of chest pain and ST segment change. The patients were grouped according to the results of exercise testing and coronary arteriography, and one group was studied with and without antianginal medication. Overall, 195 episodes of angina were noted, only 94 of which (48%) were accompanied by ST segment depression. Pain and ST segment changes were best correlated in patients with a positive exercise test, positive angiography and who were not receiving antianginal medication. In 101 episodes of chest pain, ST segment change could not be identified; in 18 (18%) there was sinus tachycardia, in 12 (12%) ventricular premature beats, and in 71 (70%) sinus rhythm solely. Thus, anginal pain appears not to be the reliable indicator of transient myocardial ischaemia as was previously thought, a finding which supports the use of objective methods in identifying episodes of transient myocardial ischaemia in daily life.     

Diagnosis of important fixed coronary stenosis in patients with variant angina by exercise tests after treatment with calcium antagonists.

A 12 lead electrocardiogram was recorded during treadmill exercise in 57 patients with variant angina in whom coronary angiography was performed. Thirty six patients performed exercise tests with and without calcium antagonists, and 21 performed them only with calcium antagonists. In 55 patients calcium antagonists had prevented spontaneous attacks of variant angina for more than two days before the test. The other two patients were given a single dose of diltiazem (90 mg) two hours before the test. Exercise testing without calcium antagonists induced ST segment elevation with chest pain in nine patients, ST segment depression in 10 (nine with chest pain), and no important shift of the ST segment in 17. Five patients had severe coronary stenosis (greater than or equal to 75%) and all of them showed positive response. Thirty one patients had no important coronary stenosis and 14 of them showed positive response. The sensitivity of the exercise test in detecting a coronary stenosis greater than or equal to 75% was 100% without calcium antagonists but the specificity was low (55%). When the exercise test was done in patients taking calcium antagonists, only two (specificity 96%) of 48 patients without severe coronary stenosis showed positive response (elevation of ST segment in one and depression in another) whereas all nine patients with severe coronary stenosis had a positive response (depression of ST segment in six and elevation in three (sensitivity 100%). It is concluded that exercise testing with calcium antagonists may be a useful method for detecting severe coronary stenosis in patients with variant angina.     

The haemodynamic response to myocardial ischaemia in ambulant patients with variant angina.

The haemodynamic response to myocardial ischaemia in patients with variant angina during ambulatory activity is unknown. Ambulatory pulmonary artery pressure monitoring with a transducer tipped catheter and simultaneous frequency modulated electrocardiograms was used to assess changes in left ventricular function in five male patients (mean age 51.8 years) during variant angina; four patients had coronary artery stenosis and one had normal coronary arteries. Two hundred and seventy hours of ambulatory recordings were analysed. Twenty episodes (12 painful, 8 silent) of ST segment change greater than 1 mm occurred. Episodes tended to occur more frequently in the early morning hours. Six episodes of painful ST elevation were associated with a rise in pulmonary artery diastolic pressure. In the remaining episodes ST segment elevation was of shorter duration and there was no rise in pulmonary artery diastolic pressure. Pain was usually a late feature. Silent ST segment elevation occurred at rest and pulmonary artery diastolic pressure increased in all but one episode. Silent exertional ST segment depression was associated with a greater increase in pulmonary artery diastolic pressure than that seen during ST segment elevation. ST segment depression preceded or followed ST segment elevation in two episodes. The onset of ST segment elevation nearly always preceded the onset of a rise in pulmonary artery diastolic pressure. Ergometrine maleate provocation produced a rise in pulmonary artery diastolic pressure in three patients. In one there was no response to 1000 micrograms but spontaneous episodes of ST segment elevation were recorded during ambulatory monitoring. Treadmill exercise resulted in both ST segment elevation and depression with a similar haemodynamic response during both types of electrocardiographic change. When there is important coronary artery disease in two or more vessels ST segment changes may occur in different territories during treadmill exercise and during spontaneous episodes. Ambulatory pulmonary artery diastolic pressure monitoring is a useful technique for the investigation of variant angina.     

Intra- and perioperative arrhythmia and ischemic signals in myocardial revascularization patients

In order to evaluate perioperative electrical cardiac disturbances and ST segment changes, 42 patients (38 M, 4 F, aged 57 +/- 6 ys) were studied using 24-hour Holter monitoring before, during and after coronary bypass surgery. In the 4-6 hours before cardioplegic arrest, 38% of patients had ST segment changes. No patient and malignant arrhythmias. The injection of cold cardioplegic solution was followed by bradycardia, ventricular tachycardia, ventricular fibrillation and isoelectric line within 2-4 minutes. After aortic declamping, 30 patients were defibrillated. Impulse formation and conduction disturbances, found in 55% of patients, solved themselves in 1 to 60 minutes. Bundle branch block continued in just 4 cases. A total of 59% of patients had ST segment elevation for 14 +/- 14 minutes and 19% had ST segment depression for 19 +/- 20 minutes. Successive transient ST segment changes were detected in 38% of patients. Sustained ventricular tachycardia occurred during 2 ischemic episodes. Impulse formation and conduction disturbances were not related to the duration of cardiac arrest or ventricular fibrillation, but were more frequent and lasted longer in patients with incomplete revascularization. Transient ST segment depression far from aortic declamping correlated with preclamping ischemia. Transient ST segment elevation correlated with incomplete revascularization. We concluded that ECG signs of intraoperative damage were reversible. Moreover, perioperative transitory ischemia was frequent but could be prevented by coronary active drug administration. On the other hand incomplete revascularization was associated with electrical disturbances and ischemia.     

Submaximal exercise testing early after myocardial infarction. Prognostic importance of exercise induced ST segment elevation.

Seventy four patients (66 men, eight women; mean age 54.3 years) underwent submaximal exercise testing 7-23 days (mean 10.7) after acute myocardial infarction. Follow up was a mean period of 11.3 months. When compared with patients with no exercise induced abnormality, ST segment elevation, ST shift (depression or elevation or both), ST depression, inability to complete five metabolic equivalents, and inadequate blood pressure response to exercise were predictive of subsequent cardiac events (cardiac death, left ventricular failure, recurrent myocardial infarction, angina). When the presence or absence of specific variables was assessed, only ST elevation and ST shift predicted subsequent cardiac events. The presence of exercise induced ST elevation was the only exercise test variable which predicted cardiac death. ST segment elevation was, therefore, the exercise induced abnormality which best predicted the risk of future complications.     

Class I antiarrhythmic drug and coronary vasospasm-induced T wave alternans and ventricular tachyarrhythmia in a patient with Brugada syndrome and vasospastic angina

A 50-year-old man presented with a history of transient chest pain and palpitations. The 12-lead ECG at rest showed normal sinus rhythm. A slight ST segment elevation was observed in leads V1 to V3. During hospitalization, atrial fibrillation developed, and oral pilsicainide was administered. Thirty minutes after the drug was given, the ECG showed marked ST segment elevation in leads V1 to V3, and T wave alternans became visible in leads V2 and V3. Self-terminating ventricular tachycardia was initiated following frequent ventricular premature complexes, which showed a left bundle branch block pattern. The coronary angiogram was normal, but in the provocation test of vasospastic angina, acetylcholine administration into the left coronary artery resulted in complete occlusion of the left anterior descending and circumflex arteries. Marked ST segment elevation developed in leads I, aVL, and V3 to V6 concomitant with visible QT/T alternans in leads V4 and V5, and ventricular tachyarrhythmia was initiated. Brugada syndrome and vasospastic angina coexisted in this patient, and T wave alternans can be used as a predictor of ventricular tachyarrhythmias in such patients.     

Significance of exercise induced ST segment elevation in patients with previous myocardial infarction.

In order to determine the significance of exercise induced ST segment elevation in patients with previous myocardial infarction, we have studied 156 patients, 26 months (mean) after myocardial infarction. Each patient underwent 16 lead precordial electrocardiographic mapping before, during, and after exercise and in addition coronary arteriography was performed. There was no significant difference in the extent of coronary disease or abnormalities of left ventricular function between patients with exercise induced ST segment elevation that was noted to occur in leads with Q waves and those with ST segment elevation plus depression or those with ST segment depression alone. Patients without exercise induced ST segment changes had fewer coronary arteries involved than those who developed ST segment changes. Nineteen patients with exercise induced ST segment elevation alone underwent coronary artery bypass surgery; in 11 this resulted in complete abolition of the exercise induced ST segment elevation and was associated with symptomatic relief and patent grafts without alteration of left ventricular function. Thus, exercise induced ST segment elevation in patients with previous myocardial infarction should be considered as important as ST segment depression in terms of underlying myocardial ischaemia, coronary anatomy, and left ventricular function.     

Submaximal exercise testing early after myocardial infarction. Prognostic importance of exercise induced ST segment elevation

Seventy four patients (66 men, eight women; mean age 54.3 years) underwent submaximal exercise testing 7-23 days (mean 10.7) after acute myocardial infarction. Follow up was a mean period of 11.3 months. When compared with patients with no exercise induced abnormality, ST segment elevation, ST shift (depression or elevation or both), ST depression, inability to complete five metabolic equivalents, and inadequate blood pressure response to exercise were predictive of subsequent cardiac events (cardiac death, left ventricular failure, recurrent myocardial infarction, angina). When the presence or absence of specific variables was assessed, only ST elevation and ST shift predicted subsequent cardiac events. The presence of exercise induced ST elevation was the only exercise test variable which predicted cardiac death. ST segment elevation was, therefore, the exercise induced abnormality which best predicted the risk of future complications.     

Diagnosis of important fixed coronary stenosis in patients with variant angina by exercise tests after treatment with calcium antagonists

A 12 lead electrocardiogram was recorded during treadmill exercise in 57 patients with variant angina in whom coronary angiography was performed. Thirty six patients performed exercise tests with and without calcium antagonists, and 21 performed them only with calcium antagonists. In 55 patients calcium antagonists had prevented spontaneous attacks of variant angina for more than two days before the test. The other two patients were given a single dose of diltiazem (90 mg) two hours before the test. Exercise testing without calcium antagonists induced ST segment elevation with chest pain in nine patients, ST segment depression in 10 (nine with chest pain), and no important shift of the ST segment in 17. Five patients had severe coronary stenosis (greater than or equal to 75%) and all of them showed positive response. Thirty one patients had no important coronary stenosis and 14 of them showed positive response. The sensitivity of the exercise test in detecting a coronary stenosis greater than or equal to 75% was 100% without calcium antagonists but the specificity was low (55%). When the exercise test was done in patients taking calcium antagonists, only two (specificity 96%) of 48 patients without severe coronary stenosis showed positive response (elevation of ST segment in one and depression in another) whereas all nine patients with severe coronary stenosis had a positive response (depression of ST segment in six and elevation in three (sensitivity 100%). It is concluded that exercise testing with calcium antagonists may be a useful method for detecting severe coronary stenosis in patients with variant angina.     

Limited efficacy of magnesium for the treatment of variant angina.

Some patients with variant angina show both ST segment elevation at rest and exercise-induced ST segment elevation. Magnesium deficiency has also been observed in patients with variant angina. This study investigated the correlation between the degree of magnesium deficiency and the efficacy of intravenous administration of magnesium in patients with variant angina. Fifteen patients with angiographically confirmed variant angina were assessed for magnesium deficiency and whether intravenous administration of magnesium (19.2 mEq/l) suppressed exercise-induced ST segment elevation. All 15 patients were studied with a magnesium retention test (0.2 mEq/kg over 4 hr) to analyze magnesium deficiency. In our study, magnesium retention rate in patients with variant angina was not higher than that of controls (57 +/- 24% vs 45 +/- 10%, NS). All 15 patients had anginal attacks during accelerated exercise combined with hyperventilation after placebo infusion, whereas only 8 patients had anginal attacks after magnesium administration. ST segment elevation occurred in 14 patients after placebo infusion, but in only 4 patients after magnesium administration. There were no correlations between disease activity, degree of magnesium deficiency or failure of suppression of ST elevation by the intravenous administration of magnesium. Intravenous administration of magnesium can suppress exercise-induced coronary spasms in some patients with variant angina, but the degree of magnesium deficiency did not correlate with the suppressions of exercise-induced ST elevation after magnesium administration. Intravenous administration of magnesium had limited efficacy in patients with variant angina and exercise-induced ST segment elevation.     

The haemodynamic response to myocardial ischaemia in ambulant patients with variant angina

The haemodynamic response to myocardial ischaemia in patients with variant angina during ambulatory activity is unknown. Ambulatory pulmonary artery pressure monitoring with a transducer tipped catheter and simultaneous frequency modulated electrocardiograms was used to assess changes in left ventricular function in five male patients (mean age 51.8 years) during variant angina; four patients had coronary artery stenosis and one had normal coronary arteries. Two hundred and seventy hours of ambulatory recordings were analysed. Twenty episodes (12 painful, 8 silent) of ST segment change greater than 1 mm occurred. Episodes tended to occur more frequently in the early morning hours. Six episodes of painful ST elevation were associated with a rise in pulmonary artery diastolic pressure. In the remaining episodes ST segment elevation was of shorter duration and there was no rise in pulmonary artery diastolic pressure. Pain was usually a late feature. Silent ST segment elevation occurred at rest and pulmonary artery diastolic pressure increased in all but one episode. Silent exertional ST segment depression was associated with a greater increase in pulmonary artery diastolic pressure than that seen during ST segment elevation. ST segment depression preceded or followed ST segment elevation in two episodes. The onset of ST segment elevation nearly always preceded the onset of a rise in pulmonary artery diastolic pressure. Ergometrine maleate provocation produced a rise in pulmonary artery diastolic pressure in three patients. In one there was no response to 1000 micrograms but spontaneous episodes of ST segment elevation were recorded during ambulatory monitoring. Treadmill exercise resulted in both ST segment elevation and depression with a similar haemodynamic response during both types of electrocardiographic change. When there is important coronary artery disease in two or more vessels ST segment changes may occur in different territories during treadmill exercise and during spontaneous episodes. Ambulatory pulmonary artery diastolic pressure monitoring is a useful technique for the investigation of variant angina.     

Significance of exercise induced ST segment elevation in patients with previous myocardial infarction

In order to determine the significance of exercise induced ST segment elevation in patients with previous myocardial infarction, we have studied 156 patients, 26 months (mean) after myocardial infarction. Each patient underwent 16 lead precordial electrocardiographic mapping before, during, and after exercise and in addition coronary arteriography was performed. There was no significant difference in the extent of coronary disease or abnormalities of left ventricular function between patients with exercise induced ST segment elevation that was noted to occur in leads with Q waves and those with ST segment elevation plus depression or those with ST segment depression alone. Patients without exercise induced ST segment changes had fewer coronary arteries involved than those who developed ST segment changes. Nineteen patients with exercise induced ST segment elevation alone underwent coronary artery bypass surgery; in 11 this resulted in complete abolition of the exercise induced ST segment elevation and was associated with symptomatic relief and patent grafts without alteration of left ventricular function. Thus, exercise induced ST segment elevation in patients with previous myocardial infarction should be considered as important as ST segment depression in terms of underlying myocardial ischaemia, coronary anatomy, and left ventricular function.     

Ventricular arrhythmias during ergonovine-induced episodes of variant angina

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

Brugada syndrome with monomorphic ventricular tachycardia in a one-year-old child.

A one-year-old child with a structurally normal heart presented with monomorphic ventricular tachycardia. Electrocardiogram in sinus rhythm showed right bundle branch block with ST segment elevation suggesting a diagnosis of Brugada syndrome. At a later date, when the ST segment was isoelectric. intravenous procainamide caused ST elevation typical of Brugada syndrome.     

Significance of treadmill stress testing in transmural myocardial infarction: Correlation with coronary angiography

To assess the usefulness of stress testing in predicting multivesselcoronary disease and left ventricular dysfunction, 83 male patientswith a myocardial infarction one to 84 months previously werestudied. In inferior infarction (45 patients), the ST segment depressionhad a sensitivity of 91% and a specificity of 77% to detectmultivessel disease. Patients with multivessel disease had significantlylower exercise capacity and maximal heart rates. ST segmentelevation showed a poor correlation with the number of affectedvessels. In anterior infarction (38 patients), both ST segment depressionand elevation were of little value to detect multivessel disease.However, the predictive value of an exercise test without STsegment changes to exclude multivessel disease was 89%; on theother hand, patients without ST segment changes had significantlyhigher ejection fractions, exercise capacity, maximal heartrates and rate-pressure products than patients with ST segmentchanges. Patients with ST segment elevation had significantly lower ejectionfractions in both groups. The sensitivity of ST segment elevationto detect severe segmental left ventricular dysfunction was84% for anterior infarction and 54% for inferior infarction.Specificity was 84 and 85%, respectively. We conclude that: (1) exercise-induced ST segment depression is useful to predictthe extent of coronary artery disease in inferior infarction,but it is of limited value in anterior infarction, (2) exercise-induced ST segment elevation correlates well withthe presence of severe left ventricular dysfunction in bothanterior and inferior infarction, and (3) an exercise test of considerable intensity without ST segmentchanges makes the existence of multivessel coronary diseaseand/or severe left ventricular dysfunction very improbable.     

Diagnostic Value of Exercise‐Induced ST‐Segment Elevation in Q‐Wave Leads. After Recent Myocardial Infarction

Background: Exercise‐induced ST‐segment elevation in an infarct territory with abnormal Q waves is a known marker for more severe left ventricular wall‐motion abnormalities. However, it is reported, that exercise‐induced ST‐segment elevation in infarct leads may indicate residual viability in the intarctregion. The aim of the study was to test whether exercise‐induced ST‐segment elevation is related to left ventricular (LV) dysfunction or to persistent viability in patients with previous myocardial infarction (MI). Methods: 145 consecutive patients (119 men, 26 women, age 58 ± 11 years) 2–3 weeks after Q‐wave Ml but without ST elevation at rest ECG were enrolled in the study. All patients underwent a target heart rate or symptom‐limited exercise testing (ET) with Bruce protocol. Exercise‐induced ST‐segment elevation < 1 mm above the baseline ST segment level (80 ms after J point) in more than 1 ECG lead with Q wave was considered to be significant. Patients were divided in two groups according to ET results: group I, 25 patients with significant exercise‐induced ST‐segment elevation and group II, 120 patients without exercise‐induced ST‐segment elevation. All patients underwent rest ECHO and low dose dobutamine stress echo (LOSE) within 7 days after ET. LV function was estimated using ejection fraction (EF). Results: More severe LV dysfunction was observed in patients from group 1 (EF 31 ± 8.16% vs EF 45 ± 10.3%). Myocardial viability (defined as an improvement of regional systolic wall thickening in the regions with resting regional wall‐motion abnormalities during LOSE 5 to 15 g/kg/min was recognized in 8 patients (32%) in group I and 31 patients (25.8%) in group II. There was no relation between exercise‐induced ST‐segment elevation and myocardial viability (chi‐square test: 2,809; NS). Conclusions: Exercise‐induced ST‐segment elevation in most cases is associated with left ventricular dysfunction. Patients with exercise‐induced ST‐segment elevation have a lower EF than those without and greater severity of resting wall‐motion abnormalities. Our results suggest that exercise‐induced ST‐segment elevation is not related to residual myocardial viability.     

Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report.

OBJECTIVES. The objectives of this study were to present data on eight patients with recurrent episodes of aborted sudden death unexplainable by currently known diseases whose common clinical and electrocardiographic (ECG) features define them as having a distinct syndrome different from idiopathic ventricular fibrillation. BACKGROUND. Among patients with ventricular arrhythmias who have no structural heart disease, several subgroups have been defined. The present patients constitute an additional subgroup with these findings. METHODS. The study group consisted of eight patients, six male and two female, with recurrent episodes of aborted sudden death. Clinical and laboratory data and results of electrocardiography, electrophysiology, echocardiography, angiography, histologic study and exercise testing were available in most cases. RESULTS. The ECG during sinus rhythm showed right bundle branch block, normal QT interval and persistent ST segment elevation in precordial leads V1 to V2-V3 not explainable by electrolyte disturbances, ischemia or structural heart disease. No histologic abnormalities were found in the four patients in whom ventricular biopsies were performed. The arrhythmia leading to (aborted) sudden death was a rapid polymorphic ventricular tachycardia initiating after a short coupled ventricular extrasystole. A similar arrhythmia was initiated by two to three ventricular extrastimuli in four of the seven patients studied by programmed electrical stimulation. Four patients had a prolonged HV interval during sinus rhythm. One patient receiving amiodarone died suddenly during implantation of a demand ventricular pacemaker. The arrhythmia of two patients was controlled with a beta-adrenergic blocking agent. Four patients received an implantable defibrillator that was subsequently used by one of them, and all four are alive. The remaining patient received a demand ventricular pacemaker and his arrhythmia is controlled with amiodarone and diphenylhydantoin. CONCLUSIONS. Common clinical and ECG features define a distinct syndrome in this group of patients. Its causes remain unknown.     

Prognostic significance of transient myocardial ischaemia after first acute myocardial infarction: five year follow up study.

OBJECTIVE--To assess the five year prognostic significance of transient myocardial ischaemia on ambulatory monitoring after a first acute myocardial infarction, and to compare the diagnostic and long term prognostic value of ambulatory ST segment monitoring, maximal exercise testing, and echocardiography in patients with documented ischaemic heart disease. DESIGN--Prospective study. SETTING--Cardiology department of a teaching hospital. PATIENTS--123 consecutive men aged under 70 who were able to perform predischarge maximal exercise testing. INTERVENTIONS--Echocardiography two days before discharge (left ventricular ejection fraction), maximal bicycle ergometric testing one day before discharge (ST segment depression, angina, blood pressure, heart rate), and ambulatory ST segment monitoring (transient myocardial ischaemia) started at hospital discharge a mean of 11 (SD 5) days after infarction. MAIN OUTCOME MEASURES--Relation of ambulatory ST segment depression, exercise test variables, and left ventricular ejection fraction to subsequent objective (cardiac death or myocardial infarction) or subjective (need for coronary revascularisation) events. RESULTS--23 of the 123 patients had episodes of transient ST segment depression, of which 98% were silent. Over a mean of 5 (range 4 to 6) years of follow up, patients with ambulatory ischaemia were no more likely to have objective end points than patients without ischaemic episodes. If, however, subjective events were included an association between transient ST segment depression and an adverse long term outcome was found (Kaplan-Meier analysis; P = 0.004). The presence of exercise induced angina identified a similar proportion of patients with a poor prognosis (Kaplan-Meier analysis; P < 0.004). Both exertional angina and ambulatory ST segment depression had high specificity but poor sensitivity. The presence of exercise induced ST segment depression was of no value in predicting combined cardiac events. Indeed, patients without exertional ST segment depression were at increased risk of future objective end points (Kaplan-Meier analysis; P < 0.0045). These findings may be explained in part by a higher prevalence of left ventricular dysfunction in patients without ischaemic changes in the exercise electrocardiogram (P < 0.05). CONCLUSION--There seem to be limited reasons to perform ambulatory ST segment monitoring in survivors of a first myocardial infarction who can perform exercise tests before discharge. Patients at high risk of future myocardial infarction or death from cardiac causes are not identified. Ambulatory monitoring and exertional angina distinguish a small subset of patients who will develop severe angina pectoris demanding coronary revascularisation during follow up. Patients without exercise induced ST segment depression comprise a high risk subgroup in terms of subsequent objective end points. The role of ambulatory ST segment monitoring performed in unselected patients immediately after infarction when risk is maximal remains to be clarified.     

Short term reproducibility of exercise testing in patients with ST segment elevation and different responses to the dipyridamole test.

The short term reproducibility of exercise testing in 25 patients who had exercise induced ST segment elevation without baseline regional asynergy or a previous myocardial infarction, who had different responses to the dipyridamole test, was assessed. The patients performed a dipyridamole echocardiography test and a second exercise stress test. All underwent coronary arteriography. Seventeen patients had transient regional asynergy after dipyridamole (group 1) and either ST segment elevation (14 patients) or depression (three patients); a second group of eight had no asynergy and no electrocardiographic changes (group 2). The repeated exercise stress test was positive in 16 of the 17 patients of group 1 (11 with ST elevation and five with ST depression) and in two patients of group 2 (both had ST depression and one had coronary artery disease). The dipyridamole echocardiography test was positive in 17 of the 19 patients with coronary artery disease and was negative in all six patients without coronary artery disease. The repeated exercise stress test was positive in 17 of the 19 patients with coronary artery disease and in one patient without. The dipyridamole echocardiography test and a repeated exercise stress test, but not a single exercise stress test, identified coronary artery disease causing exercise induced ST segment elevation.     

Predicting cardiac mortality after uncomplicated myocardial infarction by exercise radionuclide ventriculography and exercise-induced ST segment elevation.

In 183 consecutive patients with recent, uncomplicated myocardial infarction, the following variables were associated with 4-year cardiac death: haemodynamic decompensation with exercise (P = 0.01), left ventricular ejection fraction at rest (P = 0.004) and at peak exercise (P = 0.003), persistent ST segment elevation at rest in the area of infarction = (P = 0.004), exercise-induced ST segment elevation (P = 0.02), and late aneurysmal evolution (P = 0.01). Exercise left ventricular ejection fraction was the sole variable selected by Cox regression analysis as an independent predictor of cardiac death. In 40 patients with ST segment elevation at rest, left ventricular ejection fraction was 42 +/- 17% at rest and 40 +/- 18% at peak exercise, versus 52 +/- 12% and 52 +/- 14% in the remaining patients (both P less than 0.01). Among these 40, 16 (all with anterior infarction) also had exercise-induced ST segment elevation; their ejection fraction was 32 +/- 13% at rest, 30 +/- 13% during exercise, versus 53 +/- 15% and 53 +/- 15% in 129 patients with no ST segment elevation either at rest, or during exercise (both P less than 0.01). The 4-year risk of death was 20% in the former 40 patients, 36% in the latter 16, while in the complete absence of ST segment elevation, such risk was 3%. All 14 patients with ST segment elevation only during exercise were alive after 4 years: their left ventricular ejection fraction was 47 +/- 12% at rest, 45 +/- 13% with exercise. ST segment elevation was associated with late aneurysmal evolution but not with exercise-induced ischaemia.(ABSTRACT TRUNCATED AT 250 WORDS)