Stress-induced ST-segment elevation in patients without prior Q-wave myocardial infarction

Background

Stress-induced ST-segment elevation is an uncommon finding that usually occurs in patients with prior myocardial infarction (MI). Our purpose was to assess the angiographic and clinical significance of this finding in patients without prior MI.

Methods

Of the 29 002 consecutive ambulatory patients who underwent stress myocardial perfusion imaging over a 5-year period, 205 (0.7%) developed stress-induced ST-segment elevation, of whom 39 (19%) had no Q-wave MI in leads showing ST-segment elevation during either exercise (n = 31) or dipyridamole (n = 8) stress myocardial perfusion imaging. All 39 patients were hospitalized and underwent coronary angiography.

Results

Significant coronary artery disease was found in all 39 patients: 87% had critical (≥90%) stenosis, and 59% had multiple vessel disease. During hospitalization, 37 patients (95%) underwent revascularization.

Conclusions

In patients without prior Q-wave MI, stress-induced ST-segment elevation is associated with critical coronary artery disease. Therefore, these patients should be considered for early coronary investigation.     

Differentiation of myocardial ischemia and left ventricular aneurysm in the genesis of exercise-induced ST-T changes in previous anterior myocardial infarction

We attempted to differentiate between myocardial ischemia and left ventricular asynergy as the underlying mechanisms of exercise-induced ST-segment elevation in patients with previous myocardial infarction (MI). Sixty patients with previous anterior MI, who underwent stress myocardial scintigraphy (SMS) and coronary angiography (CAG), which revealed a single vessel disease of the left anterior descending artery, were entered in this study. SMS and CAG were performed within 3 months of MI onset, and SMS and ECG were quantitatively analyzed. T wave changes to a complete upright position with concomitant ST-segment elevation (T-dominant ST-elevation) was seen in 56% of the patients with post-MI angina pectoris (N = 16) and in 50% of those with significant redistribution in SMS (n = 20). On the other hand, ST-segment elevation without T wave reversion (ST-dominant ST-elevation) was seen in 43% of patients with severe LV asynergy (akinesis and dyskinesis, n = 39) and in 50% of those with severe scintigraphic defect in delayed images (relative thallium uptake less than or equal to 40%, n = 10). When these findings were combined, T-dominant ST-elevation had sensitivity and specificity of 54% and 78%, respectively, for the diagnosis of myocardial ischemia, while the corresponding values for ST-dominant ST-elevation were 44% and 100%, for the diagnosis of severe ventricular asynergy. We conclude that the two underlying mechanisms, ischemia and asynergy, may produce different changes in ST-T shape in patients with previous myocardial infarction.     

Left ventricular wall motion with and without Q-wave disappearance after acute myocardial infarction

Since post-acute myocardial infarction (AMI) Q waves may disappear independent of reinfarction or development of left bundle branch block, the relation between the presence of Q waves and segmental asynergy was assessed in 58 patients with initial Q waves after first AMI. Two-dimensional (2-D) echocardiograms and electrocardiograms were recorded 1 year later. By electrocardiography, 28 had anterior and 25 inferior AMI. At 1 year Q waves had disappeared in 12 of 53 patients (23%): 5 with anterior and 7 with inferior AMI. Segmental asynergy, however, was present in 9 of these 12 patients, although dyskinesia was absent. Presence of Q waves at 1 year (41 patients) was always associated with segmental asynergy. Wall motion score, based on degree of segmental asynergy, was higher in the 41 patients with Q waves compared with patients in whom Q waves disappeared (7.8 +/- 4.4 vs 2.7 +/- 1.9, p less than 0.001). In patients with anterior AMI the number of Q waves at 1 year and the grade of asynergy were correlated. Segmental dyskinesia was rare in patients with inferior AMI (1 of 25) but was common in those with anterior AMI (18 of 28), and was consistently present in patients with more than 2 anterior Q waves.     

Comparison of segmental wall motion abnormalities on echocardiography in patients with anteroseptal versus extensive anterior wall ST-segment elevation myocardial infarction

Objective

Acute anteroseptal ST-segment elevation (STE) myocardial infarction (AS-STEMI), defined as STE limited to leads V1 to V3, has historically been associated with a smaller infarct size than extensive anterior STEMI (EA-STEMI), in which STE extends to leads V4 to V6. We compared the differences in global and regional wall motion by transthoracic echocardiography between patients with AS-STEMI and EA-STEMI.

Methods

Patients who presented with anterior STEMI and underwent primary percutaneous coronary intervention between January 2008 and March 2011 were included. For each subject, a transthoracic echocardiogram that was performed within 24 hours of admission was interpreted by an independent investigator blinded to the patient's electrocardiographic data.

Results

Of the 65 subjects who met our inclusion criteria, 30 had AS-STEMI and 35 had EA-STEMI. No differences were observed between groups in baseline characteristics or the mean number of hypokinetic, akinetic, and dyskinetic segments. Apical inferior segment dysfunction occurred more often in patients with EA-STEMI than in patients with AS-ASTEMI (71.4% vs 43.3%; P = .04). Distribution and extent of wall motion abnormalities were similar between patients with AS-STEMI and those with EA-STEMI.

Conclusion

The term AS-STEMI may be misleading, as it implies that only the anteroseptal segments are involved. We show that regional dysfunction in patients with AS-STEMI extends beyond the anteroseptal region.     

Myocardial ischemia adjacent to infarction enhances the magnitude of exercise-induced ST-segment elevation one month after myocardial infarction

The aims of this study were to compare exercise-induced ST-segment elevation with and without ischemia and to examine the relation between exercise-induced ST-segment elevation and the location of myocardial ischemia. Seventy-nine patients with first anterior myocardial infarction underwent thallium-201 exercise myocardial scintigraphy test one month after myocardial infarction. There were 37 patients showing no reversible defect (non ischemia group), 33 with reversible defect in the territory of the left descending coronary artery (homozonal ischemia group) and 9 with a reversible defect in the territory of the left circumflex or right coronary artery (remote ischemia group). There were no significant differences among the three groups with respect to infarct size, presence of dyskinesis and exercise endurance time. Patients with homozonal ischemia had the highest degree of ST-segment elevation (0.22 +/- 0.09 mV) followed by patients without ischemia (0.13 +/- 0.07 mV) and those with remote ischemia (0.09 +/- 0.08 mV, P <.01). In conclusion, Myocardial ischemia adjacent to infarction amplifies exercise-induced ST-segment elevation.     

Evolution of regional left ventricular wall motion abnormalities in acute Q and non-Q wave myocardial infarction

The evolution of segmental wall motion in Q and non-Q wave acute myocardial infarction was studied in detail in 15 patients without known prior ischemic events. Serial two-dimensional echocardiographic studies were performed beginning early after the onset of chest pain and continuing until 10 to 14 days after admission. An area of apparent infarction was identified on each initial study based on later correlation of ECG and echocardiographic findings. Wall motion of infarct-and noninfarct-related areas was graded in a semiquantitative fashion based on the scoring of a visual analysis. Sequential image data demonstrated significant spontaneous improvement in wall motion of the infarct area in non-Q but not in Q wave events. Patients with non-Q wave infarction and improvement in regional function were at high risk for recurrent infarction within 6 months. Improvement in wall motion inside or outside the area of infarction in Q wave events was related to future risk. We concluded that in patients with initial acute myocardial infarction, failure to develop Q waves correlated with return of function in the apparent area of infarction. Improvement in regional wall motion after the initial study suggested risk for future ischemic events in both ECG types of myocardial infarction. Serial echocardiographic imaging may be a means to identify patients at risk for infarct extension in both non-Q and Q wave events.     

Persistent ST-segment elevation and left ventricular wall abnormalities: A 2-dimensional echocardiographic study

Twenty-three patients with an anterior wall myocardial infarction (MI) and persistent ST-segment elevations (Group I) were examined for wall motion abnormalities using 2-dimensional (2-D) echocardiography. Twenty-two (96%) had dyskinetic wall motion of the infarcted area and 10 (43%) had a left ventricular aneurysm. Among 15 patients who had a chronic anterior wall MI without ST-segment elevation (Group II), 13 (86%) had akinesia of the infarcted segment. To document that dyskinetic wall motion caused the persistent electrocardiographic ST-segment elevations, 15 patients with an acute anterior wall MI (Group III) were followed by serial 2-D echocardiography for 2 to 24 months (mean 8). Of the 10 patients who had dyskinetic wall motion abnormalities on their initial 2-D echocardiogram, persistent ST-segment elevation developed in 9. All 5 patients with akinetic or severely hypokinetic wall motion abnormalities on their first 2-D echocardiogram did not show ST-segment elevation on late follow-up surface electrocardiograms. Infarct size as determined by peak creatine kinase levels for the former subgroup was greater than that for the latter subgroup (2243 ± 429 vs 899 ± 320 IU, respectively, p < 0.01). In conclusion, persistent ST-segment elevation after an acute anterior wall MI is indicative of dyskinetic wall motion rather than aneurysm formation. Dyskinesia precedes the appearance of ST-segment elevation and is probably responsible for these changes on the surface electrocardiogram. Infarct size is larger in persons in whom dyskinetic wall motion abnormalities are likely to develop.     

Clinical characteristics of ST-segment elevation in lead V6 in patients with Q-wave acute inferior wall myocardial infarction

BACKGROUND: Precordial ST-segment depression in acute inferior infarction is well recognized, but few studies have evaluated ST-segment elevation in lateral precordial leads. The present study examined the clinical significance of ST-segment elevation in lead V6 in patients with acute Q-wave inferior myocardial infarction. METHODS: We studied the initial electrocardiography of 125 consecutive patients with acute Q-wave inferior myocardial infarction admitted to hospital within 12 h of the onset of chest pain. They were classified into two groups: group 1 = 34 patients with ST-segment elevation in lead V6; group 2 = 91 patients with no ST-segment elevation in lead V6. RESULTS: Among the seven clinical variables examined, the number of left ventricular asynergic segments (P < 0.001) and pulmonary capillary wedge pressure (P = 0.001) were related to ST-segment elevation in lead V6. The incidences of major arrhythmias (50% compared with 31%, P = 0.04), pericardial effusion (32% compared with 9%, P = 0.003), and pericardial rub (15% compared with 2%, P = 0.02) during the patients' stay in hospital were greater in group 1 than in group 2. Among the patients in group 1, the right coronary artery was the culprit artery in 22 of 24 patients (92%) with ST segment depression in lead I, whereas the circumflex artery was the culprit artery in nine of 10 patients (90%) with isoelectric or ST-segment elevation in lead I. CONCLUSION: The presence of ST-segment elevation in lead V6 in patients with acute Q-wave inferior myocardial infarction was associated with larger infarct size, and greater incidences of major arrhythmias and pericardial involvement during the patient's stay in hospital.     

Clinical significance of ST-segment elevation in lead V1 in patients with acute inferior wall Q-wave myocardial infarction

BACKGROUND: This study was designed to determine the clinical significance of ST-segment elevation in the precordial leads (leads V1 and V2) in acute Q-wave inferior wall myocardial infarction. METHODS AND RESULTS: One hundred fifty-eight consecutive patients with acute Q-wave inferior wall myocardial infarction were classified into 3 groups on the basis of the initial ST-change in V1 (group 1 = 29 patients with ST elevation, group 2 = 97 patients with ST depression, and group 3 = 32 patients with no ST-segment change). The right coronary artery was the infarct-related artery in all the patients in group 1. Although there was no significant difference between groups 1 and 2, the number of left ventricular asynergic segments was larger and the incidence of major in-hospital arrhythmias was higher in groups 1 and 2 compared with group 3. Patients in group 1 had a significantly higher incidence of proximal lesion (86%) and right ventricular infarction (69%) than the other 2 groups did. When ST elevation in leads V1 and V2 was considered, 14 of 15 patients (93%) with ST elevation only in V1 had right ventricular infarction, whereas 6 of 14 patients (43%) with ST elevation in both V1 and V2 had right ventricular infarction (P =.011). CONCLUSIONS: ST-segment elevation in V1 on admission in patients with acute Q-wave inferior wall myocardial infarction indicates a right coronary artery lesion associated with a larger infarct size and a higher incidence of major in-hospital arrhythmias.     

急性ST段抬高心肌梗死患者发生心室游离壁破裂的危险因素分析

目的：分析急性ST段抬高心肌梗死（STEMI）患者发生心室游离壁破裂（FWR）的危险因素。方法回顾性分析武汉亚洲心脏病医院心内科2005年1月至2010年7月间确诊为STEMI患者（1247例）的临床资料,其中发生FWR的患者29例。将患者分为静脉溶栓组、直接经皮冠状动脉介入治疗（PPCI）组和未再灌注治疗组。结果 FWR总体发生率为2.3%,其中静脉溶栓治疗患者128例（10.2%）,发生FWR 6例（4.7%）;接受PPCI患者623例（50.0%）,发生FWR 2例（0.3%）;未再灌注治疗患者496例（39.8%）,发生FWR 21例（4.2%）。FWR组与非FWR组间临床特点比较,高龄（70.2±9.09岁比63.2±11.23岁,P=0.042）、合并高血压病史（62.1%比33.0%,P=0.013）、糖尿病病史（55.2%比23.5%,P=0.022）、合并心力衰竭（Killip分级≥Ⅱ级）（58.6%比21.9%,P=0.012）,既往无陈旧性心肌梗死患者（10.3%比18.4%,P=0.018）等项的差异均有统计学意义;经多因素Logistic逐步回归分析显示年龄（≥70岁）、心功能（Killip≥Ⅱ）、静脉溶栓治疗、高敏C反应蛋白（hsCRP）＞100 mg/L与心肌梗死后发生FWR相关。结论高龄、心力衰竭、静脉溶栓治疗以及hsCRP＞100 mg/L是预测FWR发生的独立危险因素。     

Radionuclide assessment of right ventricular regional wall motion abnormalities in anterior left ventricular infarction

Because of its potential use in the detection of right ventricular myocardial infarction, we performed radionuclide ventriculography in 80 consecutive cases of electrocardiographically anterior acute MI. Regional wall motion of both ventricles was studied on amplitude-phase images. Forty-five patients (56%) showed normal right ventricular function and 35 (44%) regional right ventricular dyskinesia: 19 in the septal, 14 in the apical and 2 in the free wall region. Right ventricular septal, respectively apical asynergy were virtually always associated with asynergy in the homologous parts of the left ventricle. This could be a consequence of the proximity of these regions, or alternatively be due to a common vascular supply. Thus it remains uncertain if asynergy in these regions signifies necrosis of part of the right ventricular wall. Free wall asynergy was considered as evidence of right ventricular wall necrosis. Thus, in our study group the prevalence of right ventricular myocardial infarction in anterior left ventricular myocardial infarction was at least 2.5%.     

Relation of growth-differentiation factor 15 to left ventricular remodeling in ST-segment elevation myocardial infarction

The development of left ventricular remodeling (LVR) after myocardial infarction is associated with a high risk of heart failure and death. LVR is difficult to predict, and limited information is available on the association of cardiac biomarkers and LVR. Growth-differentiation factor-15 (GDF-15) is induced during heart failure development and, in animals models, might influence the different processes involved in cardiac remodeling. The aim of the present investigation was to assess the association between the serum levels of GDF-15 within the first 24 hours of ST-segment elevation myocardial infarction and the development of subsequent LVR at 12 months of follow-up. This prospective study included 97 patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. Echocardiography was performed in all patients within the first 96 hours of admission and at 12 months of follow-up. LVR was defined as a >20% increase in the left ventricular end-diastolic volume at 12 months of follow-up compared to baseline. Blood samples for the determination of GDF-15 and brain natriuretic peptide were obtained within the first 24 hours after symptom onset. According to the pre-established criteria, 21 patients (22%) had LVR. Patients with LVR had greater levels of GDF-15 at study entry (median 3,439 pg/ml, interquartile range 2,391 to 6,168 vs median 1998 pg/ml, interquartile range 1,204 to 3,067, respectively; p <0.001). Multivariate analysis showed that GDF-15 (odds ratio 10.1, 95% confidence interval 2.5 to 40.1, p <0.001) and treatment with angiotensin-converting enzyme inhibitors (odds ratio 3.9, 95% confidence interval 1.2 to 12.3, p <0.01) were independents predictors of LVR. Receiving operating characteristics analysis showed an area under the curve of 0.77 for GDF-15 (95% confidence interval 0.67 to 0.84, p <0.001). In conclusion, the results of the present study have identified GDF-15 as an independent marker of LVR in patients with ST-segment elevation myocardial infarction.     

Clinical characteristics of patients with exercise-induced ST-segment elevation without prior myocardial infarction.

BACKGROUND: Exercise-induced ST-segment elevation is a relatively uncommon problem and occurs more frequently in patients who have had a myocardial infarction. Data is limited on the characteristics of Taiwanese patients without prior myocardial infarction who develop exercise-induced ST-segment elevation. METHODS AND RESULTS: Exercise-induced ST-segment elevation developed in 9 of 6,147 consecutive patients without myocardial infarction who underwent treadmill exercise testing at out institution over a 4-year period. The clinical and angiographic characteristics of these patients were studied. Angiographically normal coronary arteries with coronary vasospasm were found in 5 patients, hemodynamically significant coronary stenosis was found in 3 patients, and coexisting spasm in angiographically normal coronary arteries combined with hemodynamically significant coronary stenosis in the different vessel was found in 1 patient. During a median follow-up of 71 months, 2 patients with coronary vasospasm developed recurrent angina after self-discontinuation of calcium antagonists and 2 patients (1 with coronary vasospasm and 1 with hemodynamically significant coronary stenosis) died of cardiac causes before arrival at the emergency department. CONCLUSION: Coronary vasospasm was a more common underlying pathology of exercise-induced ST-segment elevation in this Taiwanese cohort. Coronary angiography +/- intracoronary ergonovine provocation testing is necessary in these patients to identify the underlying pathology and appropriate treatment.     

Prognostic implications of quantitative evaluation of baseline Q-wave width in ST-segment elevation myocardial infarction

Objectives

To evaluate quantitative relationships between baseline Q-wave width and 90-day outcomes in ST-segment elevation myocardial infarction (STEMI).

Background

Baseline Q-waves are useful in predicting clinical outcomes after MI.

Methods

3589 STEMI patients were assessed from a multi-centre study.

Results

1156 patients of the overall cohort had pathologic Q-waves. The 90-day mortality and the composite of mortality, congestive heart failure (CHF), or cardiogenic shock (p < 0.001 for both outcomes) rose as Q-wave width increased. After adapting a threshold ≥ 40 ms for inferior and ≥ 20 ms for lateral/apical MI in all patients (n = 3065) with any measureable Q-wave we found hazard ratios (HR) for mortality (HR: 2.44, 95% confidence interval (CI) (1.54–3.85), p < 0.001) and the composite (HR: 2.32, 95% CI (1.70–3.16), p < 0.001). This improved reclassification of patients experiencing the composite endpoint versus the conventional definition (net reclassification index (NRI): 0.23, 95% CI (0.09-0.36), p < 0.001) and universal MI definition (NRI: 0.15, 95% CI (0.02–0.29), p = 0.027).

Conclusions

The width of the baseline Q-wave in STEMI adds prognostic value in predicting 90-day clinical outcomes. A threshold of ≥ 40 ms in inferior and ≥ 20 ms for lateral/apical MI enhances prognostic insight beyond current criteria.     

非心肌梗死冠心病患者运动致ST段抬高的临床意义

目的 研究运动致ST段抬高在非心肌梗死患者中发生率及其临床意义。方法 2004年6月至2006年6月共有4601例患者接受了运动平板试验,其中有15例非心肌梗死患者出现ST段抬高,对这15例患者的临床特点与冠状动脉造影结果进行分析。结果 15例（3．2‰）运动致ST段抬高患者中,男性13例,女性2例,年龄40-75岁。单支病变者6例（40％）,2支病变者6例（40％）,3支病变者3例（20％）;12例（80％）累及前降支,1例（6．6％）累及左主干,7例累及右冠状动脉,在累及前降支及左主干13例患者中有8例为重度狭窄病变（狭窄程度为90％-100％）,所有ST段抬高的导联均与病变血管的供血部位一致。结论 运动致ST段抬高在非心肌梗死患者中发生率非常低,多因冠状动脉有严重的固定性狭窄,特别是前降支,可根据出现ST段抬高的导联判断缺血心肌的部位。     

运动诱发ST段抬高者的冠状动脉病变特点及治疗探讨

目的 :观察无心肌梗死 (MI)运动诱发心电图ST段抬高者 6例 ,探讨其冠状动脉 (冠脉 )病变特点及治疗方法。方法 :对无MI而运动诱发心电图ST段抬高的患者进行静息心电图、运动试验及冠脉造影检查 ,运动试验采用Bruce方案。结果 :在 2 86 4例行运动试验检查者中 ,有 6例未患MI而运动诱发心绞痛伴心电图ST段抬高 ,发生率为 0 .2 1%。相应导联ST段抬高 0 .1～ 1.0mV ,停止运动后心绞痛症状消失 ,ST段恢复正常。 6例中 ,1例冠脉病变轻 (狭窄 <35 % ) ,但于冠脉造影后 4周发生急性MI ,梗死部位与ST段抬高导联所对应的部位一致 ;余 5例冠脉均有严重狭窄 (90 %～ 10 0 % ) ,ST段抬高导联与缺血相关血管有良好的对应关系 ,近期内行冠脉腔内球囊成形术效果良好 ,术后症状消失 ,多次复查运动试验 ,结果均阴性。结论 :无MI患者运动诱发心电图ST段抬高多提示心肌透壁缺血 ,冠脉病变重 ,预后差 ,应采取积极的治疗措施。     

Role of myocardial ischemia in the genesis of stress-induced S-T segment elevation in previous anterior myocardial infarction

This study tests the hypothesis that myocardial ischemia is responsible for exercise-induced S-T segment elevation in patients with previous anterior myocardial infarction (MI). Exercise stress testing in conjunction with thallium imaging of the myocardium was performed in 28 patients with previously documented anterior MI. Thallium images were analyzed by computer for the presence of initial uptake defects and evidence of abnormal clearance of the isotope from the myocardium (that is, imaging evidence of ischemia). Total S-T segment elevation (∑ST) in precordial leads V₁ to V₆ at rest was subtracted from ∑ST at peak stress in order to quantitate the extent of S-T elevation induced by stress (ΔST). Two groups of patients were identified; 1 with stress-induced S-T elevation (Group I, ΔST ≥ 4.0 mm) and 1 without this abnormality (Group II, ΔST < 4.0 mm). Evidence of abnormal thallium washout from myocardial scan segments occurred in 12 of 15 Group I patients versus 9 of 13 Group II patients (difference not significant). In addition, abnormal tracer washout from anterolateral or septal scan segments occurred in 5 patients in each group. Likewise, abnormal thallium clearance from inferior or posterior scan segments occurred in 8 of 15 Group I patients versus 7 of 13 Group II patients (difference not significant). The patient with the greatest amount of stress-induced S-T elevation (S-T 11.5 mm) had no evidence of ischemia during the stress test. However, Group I patients did have larger anterolateral plus septal initial thallium uptake defect scores than did those of Group II (10 of 15 with defect score ≥ 350 in Group I versus 1 of 13 in Group II, p <0.002). Similarly, resting left ventricular ejection fraction ≥ 30% was present in only 4 of 15 Group I patients versus 13 of 13 in Group II (p <0.001). Finally, multiple stepwise linear regression analysis demonstrated that ΔST correlated best with the extent of initial anterolateral plus septal thallium uptake defect score (F = 17.3, p < 0.001) and to a lesser extent with resting ejection fraction (F = 5.2, p < 0.05) and change in heart rate from rest to peak stress (F = 8.1, p < 0.01; corrected multiple correlation coefficient = 0.76, p < 0.001). Thus, in patients with previous anterior MI (1) exercise-induced myocardial ischemia occurs as often with as without S-T segment elevation, (2) myocardial ischemia is not required for the production of stress-induced S-T segment elevation, and (3) stress-induced S-T elevation primarily reflects the extent of previous anterior wall damage and to a lesser extent an increase in heart rate between rest and peak stress.     

The role of ischemia and ventricular asynergy in the genesis of exercise-induced ST elevation

Sixty-five patients with ST elevation were retrospectively studied in order to evaluate the clinical significance and underlying mechanisms of ST-segment elevation during exercise. Of these, 50 patients had previous myocardial infarction (Group I) and 15 patients did not (Group II). Exercise thallium-201 imaging was performed on 30 patients, resting gated blood pool imaging was performed on 33 patients, and 23 underwent cardiac catheterization for clinical indications. When the two groups were compared, patients in Group I had more frequent multivessel disease (9/13 vs. 3/10, p less than 0.05), anterior infarctions (33/50 vs. 4/10, p less than 0.02), while Group II patients had more frequent single-vessel disease (7/10 vs. 4/13, p less than 0.05). For Group I patients, the most common reason for termination of exercise was fatigue and/or dyspnea (35/50 vs. 0/15, p less than 0.05), with an irreversible defect noted in both stress and delayed views on thallium imaging (20/24 vs. 1/6, p less than 0.05). In Group II, the most common reason for termination was angina (15/15 vs. 2/50, p less than 0.001), with reversible thallium defects noted more frequently (4/6 vs. 3/24, p less than 0.01). Thus, we conclude that in patients with Q waves, left ventricular dysfunction rather than ischemia is the mechanism for ST elevation. In these patients angina is rare, but fatigue, dyspnea, multivessel disease, and fixed thallium defects are common. In patients with non-Q-wave exertional ST elevation, ischemia is the rule, manifested by frequent chest pain and reversible thallium defects.