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This study compared the 5-electrode-derived EASI electrocardiogram (ECG) with the conventional Mason-Likar ECG in 200 consecutive patients with chest pain transported to 3 hospitals by 2 different emergency medical services. No significant differences were observed between the 2 systems for the detection of relevant electrocardiographic abnormalities. A questionnaire administered to participating emergency medical personnel revealed a high degree of acceptability of the EASI ECG, with some participants commenting that the sternal and mid-axillary locations of the EASI electrodes made them easier to apply, especially to women, than conventional precordial electrodes.

We assessed predicting final infarct size (using predischarge Selvester score) by 3 electrocardiographic variables in 267 patients with first anterior wall acute myocardial infarction (AMI) undergoing (n = 86) or not undergoing (n = 181) thrombolysis. Patients with previous AMI or inverted T waves in leads with ST elevation were excluded. The sum (sigma) of ST elevation, the number of leads with ST elevation, and the initial electrocardiographic pattern were determined on the admission electrocardiogram (absence (QRS-) or presence (QRS+) of distortion of the terminal portion of the QRS inor =2 leads (J pointor =0.5 of the R-wave amplitude in leads I, aVL, V4 to V6, or presence of ST elevation without S waves in leads V1 to V3). There was no association between sigmaST elevation and final infarct size in patients who did or did not receive thrombolytic therapy. Analysis of covariance showed that the number of leads with ST elevation (F = 19.6), thrombolysis (F = 25.2), and QRS+ initial pattern (F = 19.5) were all associated with final infarct size (p0.0001 for all). Among patients who did not receive thrombolytic therapy, the average Selvester score was 19.7+/-9.9 for the QRS- patients and 26.1+/-10.4 for the QRS+ patients (p = 0.02). Among patients who received thrombolytic therapy, the average Selvester score was 11.7+/-9.8 for the QRS- patients and 24.2+/-10.1 for the QRS+ patients (p0.0001). Thrombolysis reduced final Selvester score only in the QRS- group (p0.00001), but not in the QRS+ group (p = 0.45). It is concluded that (1) final Selvester score in anterior wall AMI can be predicted by the number of leads with ST elevation, the initial electrocardiographic pattern, and thrombolysis, and (2) thrombolysis reduces final Selvester score only in patients with QRS- pattern.

This study assessed whether differences in the underlying mechanisms for various patterns of precordial ST-segment depression with inferior acute myocardial infarction (AMI) are associated with poorer prognoses. We studied 1,155 patients with inferior AMI who underwent thrombolysis in the Global Utilization of Streptokinase and TPA for Occluded arteries (GUSTO-I) angiographic substudy: those without precordial ST depression (n = 412; 35.7%), those with maximum ST depression in leads V1 to V3 (n = 547; 47.4%), and those with maximum ST depression in leads V4 to V6 (n = 196; 17.0%) on admission electrocardiogram. We compared the infarct-related artery, presence of left anterior descending or multivessel coronary artery disease, and left ventricular function among groups. Patients with maximum ST depression in leads V4 to V6 more often had 3-vessel disease (26.0%) than those without precordial ST depression (13.5%) or those with ST depression in leads V1 to V3 (15.7%; p = 0.002), and they had a lower ejection fraction (median 54% vs 60% and 55%, respectively; p

The present study compares the on-site interpretation of an admission electrocardiogram (ECG) with core laboratory results in a large, multicenter trial of 516 patients diagnosed with unstable angina pectoris or non-Q-wave myocardial infarction. The local investigators evaluated the admission ECG regarding ST-T changes before the ECGs were sent to the core laboratory for blinded interpretation. The strength of agreement between the observations was described by kappa statistics. There was a poor agreement regarding identification of ST-segment elevation, with 17 patients identified by the local investigator versus 92 by the core laboratory (kappa = 0.05). There was a fair agreement on ST-segment depression with 158 patients diagnosed on-site versus 64 by the core laboratory (kappa = 0.38). Identification of T-wave inversion demonstrated good agreement with 306 patients diagnosed on-site versus 280 by the core laboratory (kappa = 0.63). A moderate agreement regarding identification of a normal ECG was found with 101 patients on-site versus 135 in the core laboratory (kappa = 0.42). Independent variables, including peak creatine kinase-MB and 30-day outcome, were more closely related to core laboratory results than the local investigator's interpretation of the admission ECG. Thus, in the present study, considerable differences were demonstrated between the on-site interpretation of the admission ECG and the blinded evaluation performed in the core laboratory regarding relatively simple electrocardiographic variables. The results suggest that more widespread use of independent evaluation of clinical data should be incorporated in future clinical trials.

Increased T-wave amplitude is one of the earliest electrocardiographic (ECG) changes following coronary artery occlusion. Therefore, higher T waves in the presenting electrocardiogram should represent earlier time to treatment and thus be associated with lower mortality following thrombolytic therapy. However, T-wave amplitude has never been evaluated as a prognostic marker in this setting. We examined clinical outcomes in 3,317 patients with acute myocardial infarction (AMI) who underwent thrombolysis in the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO-I) Study. Patients were classified as either those with high T waves or those with low T waves. Higher T waves were defined as those >98th percentile of the upper limit of normal. T-wave amplitude was also evaluated as a continuous variable according to infarct location (maximum T-wave amplitude) and as the amount of excess T-wave amplitude above normal (excess T-wave amplitude). Patients with higher T waves had lower 30-day mortality than those without (5.2% vs 8.6%, p = 0.001) and were less likely to develop congestive heart failure (15% vs 24%, p

It is clinically important to estimate the size of a myocardial infarction (MI) to predict patient prognosis, to determine the ability of a therapy to limit its size, and to evaluate its effect on left ventricular function. Various electrocardiographic methods have been used for these purposes but their accuracies have not been compared with each other using an identical reference population of anatomically measured infarcts. The capability of 4 electrocardiographic scoring methods (the Selvester score, the Minnesota code, the Novacode, and the Cardiac Infarction Injury Score) to estimate MI size was compared using anatomic MI size in a group of 100 deceased patients. All patients had a standard 12-lead electrocardiogram of sufficient quality to perform manual waveform measurements and without confounding factors such as ventricular hypertrophy, fascicular block, or bundle branch block. The location and size of the left ventricular infarction was measured postmortem using the anatomic method of Ideker et al. All methods' size estimates correlated best with anatomic MI size in the anterior location (r = 0.65 to 0.89). The Selvester score was superior in estimating the sizes of inferior (r = 0.70) and posterolateral (r = 0.74) infarcts. For multiple infarcts all methods performed poorly (r = 0.18 to 0.44).

There is conflicting evidence with regard to the value of electrocardiographic left ventricular hypertrophy (LVH) in myocardial infarction. Of 5,951 patients in the ASSENT-3 trial, 273 (5%) had LVH on baseline electrocardiograms and had significantly higher mortality rates at 30 days (11% vs 6%, p = 0.001) and 1 year (13% vs 8%, p = 0.007). After adjustment for differences in baseline parameters, LVH remained an independent predictor of 30-day (hazard ratio 2.3, 95% confidence interval 1.4 to 3.9) and 1-year (hazard ratio 1.8, 95% confidence interval 1.1 to 2.8) mortality rates. Thus, electrocardiographic LVH is a prognostic tool in identifying short- and long-term mortality rates in patients who have ST-elevation myocardial infarction and receive fibrinolysis.

The consistency of the predictions using the formulas of Aldrich et al1 is dependent on the stability of the ST-segment deviations. In the present study, it was determined that 2 3 of patients were in a period of ST-segment stability, and 1 3 of patients were in a period of ST-segment lability. The clinical decision regarding reperfusion therapy will typically be made on the basis of the appearance of the initial ECG. Continuous ST-segment monitoring during the time required to administer this therapy should determine whether the individual patient is in the stable majority or the labile minority. In a study by Hackett et al7 of 38 patients with acute pain and ST-segment elevation, 8 had documented ST-segment lability before thrombolytic therapy. Because such transient episodes cannot be determined from a single ECG, continuous ST-segment monitoring should be used until the ST segments remain sufficiently stable for the application of the formulas. A further study is required to identify the length of ST monitoring time required to determine the stability of ST-segment deviation in individual patients.

Continuous ST-segment recovery analysis and 5 static methods using ST-segment comparison between a pre- and post-treatment electrocardiogram were compared for their ability to predict infarct-related artery patency in 82 patients with acute myocardial infarction who underwent angiography a median of 124 minutes after onset of thrombolytic treatment. Accuracy at the moment of angiography was 85% (95% confidence interval [CI] 77% to 93%) for the continuous method, and 68% (CI 57% to 78%), 78% (CI 69% to 87%), 83% (CI 74% to 91%), 82% (CI 73% to 90%), and 80% (CI 71% to 89%) for the static methods. At the moment of angiography the most accurate static method and the continuous method agreed in patency assessment in 90% of the patients (CI 84% to 97%). Agreement was reduced to 83% (CI 75% to 91%) of patients when a patency assessment was performed earlier at 90 minutes after treatment onset, and was only 77% (CI 68% to 86%), at 60 minutes. Early disagreement was mainly seen when the continuous ST recording showed ST recovery from a delayed peak ST elevation after the pretreatment static electrocardiogram or when dynamic ST changes suggesting cyclic reperfusion occurred. Continuous ST-segment recovery analysis appears to be as accurate as the most accurate static methods. Continuously updated reference points appear to give important additional information when ST recovery follows a delayed peak ST elevation or when re-elevation occurs, suggesting cyclic flow changes. Such findings appear to affect about half of patients with acute myocardial infarction treated with intravenous thrombolysis, particularly early after administration of therapy.

The use of intravenous thrombolytic therapy to achieve myocardial salvage has become common practice in patients presenting during the early hours of acute myocardial infarction (AMI). 1–3 A prompt, noninvasive estimation of salvage would be useful in determining further therapy for each patient. Clinical indexes of salvage should be accurate, easy to perform, inexpensive, and yield rapid results. Standard electrocardiographic and serum biochemical methods have been shown to indicate myocardial reperfusion. 4–9 Electrocardiographic ST-segment elevation tends to partially resolve immediately after reperfusion, but only 50% of patients have as much as 50% resolution within 90 minutes. 4 Plasma levels of intracellular macromolecules increase early owing to washout through the lymph and blood, but only if irreversible damage has already occurred. 5–9 The present study of patients with AMI was designed to observe serial changes in both the ST segments, and serum levels of creatine kinase-MB and myoglobin after angiographically documented reperfusion; it tests the hypothesis that the ratio of ST-segment decrease to serum macromolecular increase can predict salvage of the jeopardized myocardium.

Cardiac resynchronization therapy (CRT) has emerged as an attractive intervention to improve left ventricular mechanical function by changing the sequence of electrical activation. Unfortunately, many patients receiving CRT do not benefit but are subjected to device complications and costs. Thus, there is a need for better selection criteria. Current criteria for CRT eligibility include a QRS duration ≥ 120 ms. However, QRS morphology is not considered, although it can indicate the cause of delayed conduction. Recent studies have suggested that only patients with left bundle branch block (LBBB) benefit from CRT, and not patients with right bundle branch block or nonspecific intraventricular conduction delay. The authors review the pathophysiologic and clinical evidence supporting why only patients with complete LBBB benefit from CRT. Furthermore, they review how the threshold of 120 ms to define LBBB was derived subjectively at a time when criteria for LBBB and right bundle branch block were mistakenly reversed. Three key studies over the past 65 years have suggested that 1/3 of patients diagnosed with LBBB by conventional electrocardiographic criteria may not have true complete LBBB, but likely have a combination of left ventricular hypertrophy and left anterior fascicular block. On the basis of additional insights from computer simulations, the investigators propose stricter criteria for complete LBBB that include a QRS duration ≥ 140 ms for men and ≥ 130 ms for women, along with mid-QRS notching or slurring in ≥ 2 contiguous leads. Further studies are needed to reinvestigate the electrocardiographic criteria for complete LBBB and the implications of these criteria for selecting patients for CRT.

The prognostic value of myocardial infarct size estimation by QRS scoring in patients with ST-segment elevation myocardial infarction (STEMI) who undergo primary percutaneous coronary intervention (PCI) is unclear. The standard 32-point Selvester QRS score on the discharge electrocardiogram (each point approximately 3% left ventricular mass) was calculated in 4,113 patients with STEMI who underwent primary PCI and survived to hospital discharge in the APEX-AMI trial. QRS scores were divided into tertiles, i.e.,or =3 (10% myocardium), 4 to 7 (10% to 21% myocardium), andor =8 (21% myocardium). Adjusted associations between QRS score and 90-day outcomes (death and composite of death/congestive heart failure (CHF)/shock) were examined. Higher QRS scores were associated with male gender, higher heart rate, worse Killip class, noninferior infarct location, greater ST-segment deviation, and longer times to reperfusion. Higher QRS scores were also associated with impaired culprit artery flow before and after PCI and more frequent multivessel disease. Adverse outcomes occurred more often in patients with higher QRS scores (90-day death: 1.9%, QRS score 0 to 3; 3.4%, 4 to 7; 4.9%,or =8; 90-day death/shock/CHF: 4.5%, 0-3; 7.8%, 4 to 7; 12.1%,or =8). After multivariable adjustment, patients with higher QRS scores remained more likely to develop an adverse outcome versus those with QRS scoresor =3 (score 4 to 7, hazard ratios [HR] for death 2.08, 95% confidence interval [CI] 1.26 to 3.41; HR for death/CHF/shock 2.00, 95% CI 1.26 to 3.17; scoreor =8, HR for death 2.57, 95% CI 1.56 to 4.24, HR for death/CHF/shock 2.93, 95% CI 1.84 to 4.67). In conclusion, infarct size as estimated by QRS scoring at hospital discharge is an independent and prognostically relevant metric in patients with STEMI undergoing primary PCI.

The importance of the timing and completeness of coronary artery reperfusion for limitation of acute myocardial infarction (AMI) size after intravenous thrombolytic therapy was studied in 39 patients. All had electrocardiographic epicardial injury and acute coronary angiography performed

A subset of 3 criteria from the complete Selvester scoring system has been proposed earlier for electrocardiographic screening of healed myocardial infarcts. This subset yielded 95% specificity and high sensitivity for single anterior and inferior infarcts. In the present study, an automated version of these criteria was applied to 1,344 electrocardiograms from normal subjects (473 normal subjects as determined by cardiac catheterization and 871 apparently normal subjects by history and physical examination), to 706 from subjects with single myocardial infarction, and to 131 from subjects with combined anterior and inferior myocardial infarcts. Of the single infarcts, 366 had inferior, 277 anterior and 63 posterolateral locations. Presence and location of infarcts were judged from left ventriculograms and coronary angiograms. Overall specificity was only 86%, whereas overall sensitivity for the infarct population was 77%. Specificity was lower in men than in women; it was also lower in older than in younger subjects. One of the screening criteria (R greater than or equal to 40 ms in V1) may possibly be eliminated to augment specificity; this can be done with only minor loss of sensitivity. Differences in wave form measurements between the manual and computer methods account for a large part of the deterioration of specificity in this study compared with previously published results. Computer application of the screening criteria requires altered criteria limits in comparison with those used in manual application. Probably sex- and age-dependent criteria limits should be used.

The ability of the electrocardiographic ST segment to predict successful reperfusion after thrombolytic therapy remains controversial. To evaluate whether angiographically determined reperfusion could be predicted from changes in ST-segment elevation, the sum of ST-segment elevation in affected leads of the electrocardiogram was compared before and after thrombolytic therapy in 53 patients with acute myocardial infarction (AMI). Reperfusion status of the infarct-related artery was determined angiographically less than 8 hours from onset of symptoms. According to the Thrombolysis in Myocardial Infarction trial (TIMI) criteria, 33 patients had successful reperfusion (TIMI grade 2 to 3 flow) after thrombolytic therapy and 20 patients did not (TIMI grade 0 to 1 flow). Logistic multiple regression analysis showed that the proportional value for the shift in the sum of ST elevation, termed the "% ST change," was more strongly associated with reperfusion than the absolute measured difference in millimeters (chi-square = 11.34 vs 9.22). The entire spectra of sensitivities and specificities were determined to identify a level of the percent ST change with simultaneous high sensitivity and specificity. A 20% decrease in ST elevation provided such a level (88% sensitivity, 80% specificity). The positive and negative predictive values of a 20% decrease in ST elevation were 88 and 80%, respectively. These results suggest that a decrease of only 20% in the sum of ST elevation in the standard electrocardiogram after thrombolytic therapy is a useful noninvasive predictor of reperfusion status in patients with evolving AMI.

The current use of continuous multilead monitoring with high-resolution digital systems 1 during clinically unstable situations has greatly augmented the versatility of the electrocardiogram. A recent study 2 of patients undergoing elective percutaneous transluminal coronary angioplasty (PTCA) reported multilead patterns of peak ST-segment elevation and depression that were reproduced by later reocclusion of the same coronary site. In related work, 3,4 detailed quantitative analyses of dynamic changes in the QRS complex and ST segment during PTCA-induced ischemia were presented in the most active lead of each patient. Occasionally an acute myocardial infarction (AMI) develops spontaneously in the hours after an elective PTCA. Use of continuous electrocardiographic monitoring would facilitate comparisons between the dynamic changes of the “controlled” ischemic period during the PTCA and the spontaneous ischemic period of the AMI by using each patient as his own baseline. Such information may provide a more complete understanding of the evolution of the acute ischemic process. Using continuous 3-lead monitoring in 4 carefully selected patients with elective PTCA who subsequently developed AMI, this study quantitates and compares dynamic characteristics of the ST segment occurring during both ischemic events.

We compared combination fibrinolytic plus glycoprotein IIb/IIIa inhibitor therapy with stand-alone fibrinolysis with respect to speed and stability of reperfusion in patients who had acute ST-segment elevation myocardial infarction; data were obtained from 654 patients in 4 trials (Integrilin to Manage Platelet Aggregation to Combat Thrombosis in Acute Myocardial Infarction, Platelet Aggregation Receptor Antagonist Dose Investigation and Reperfusion Gain in Myocardial Infarction, Integrilin and Tenecteplase in Acute Myocardial Infarction, and the Fifth Global Use of Strategies to Open Occluded Coronary Arteries) that compared thrombolytics plus lamifiban, eptifibatide, or abciximab with standard thrombolysis. We found significantly faster and more stable ST-segment recovery with combination therapy starting at 60 minutes (56.7% vs 48.0% with >/=50% ST-segment resolution, p = 0.03) and sustained over 180 minutes after drug administration; this transient benefit may suggest a time frame when more optimal percutaneous coronary intervention can be performed.

The definition of acute myocardial infarction (AMI) is increasingly dependent on levels of biochemical markers, including troponin. We aimed to determine the levels of biochemical markers associated with definite evolutionary electrocardiographic (ECG) changes in patients with ST-segment elevation myocardial infarction. By examining the database of 855 patients from the troponin substudy of GUSTO-IIa, we selected patients with ST-segment elevation at baseline, evidence of evolution of the QRS, T, and ST-segment waveforms on the predischarge electrocardiogram, and 3 measurements ofor =1 of the following: creatine kinase (CK)-MB, troponin T, or troponin I. We identified 222 patients with evolutionary ECG changes. The median QRS score for this population was 5 points; the fifth percentile was 1. For patients with 3 CK-MB measurements, the fifth percentile as a multiple of the upper limit of normal was 2.1 (upper limit of normal 7.0 ng/ml). For patients with troponin T measurements, the fifth percentile as a multiple of the upper limit of normal was 11.0 (upper limit of normal 0.1 ng/ml). For patients with troponin I measurements, the fifth percentile as a multiple of the upper limit of normal was 3.8 (upper limit of normal 1.5 ng/ml). This study revealed that 95% of the patients with definite ECG evidence of AMI had a more than twofold increase in CK-MB and more than a 3- to 11-fold increase in troponin.

T-wave abnormalities are common electrocardiographic occurrences in patients with non-ST-segment elevation acute coronary syndromes. Although these abnormalities are considered relatively benign, physicians use them to guide therapies. The study objective was to examine the prognostic predictive information of T-wave abnormalities in the setting of unstable coronary artery disease. The T-wave abnormality criterion was based on a new set of normal T-wave amplitude limits differentiated by gender, age, electrocardiographic lead, and QRS axis. Four hundred sixty-eight patients suspected of an acute ischemic incident and considered ineligible for reperfusion therapy were included. Thirteen categories of T-wave abnormalities were tested prospectively. The primary 30-day end point was the combination of refractory angina, myocardial infarction, or death. Quantitative T-wave analysis in an electrocardiographic core laboratory revealed 6 of 13 prespecified categories of T-wave abnormalities that were significantly associated with an adverse outcome. T-wave abnormalities had no prognostic value when ST-segment depression was also present, but this occurred in only 7.9% of patients. T-wave abnormalities as the sole manifestation of ischemia were common (74.4%). Patients with abnormal T waves in > or =1 of 6 selected abnormality categories (70.3%) had a significantly higher risk of death, acute myocardial infarction, and refractory angina (11% vs 3%; p = 0.018). Thus, T-wave abnormalities in patients presenting with non-ST-segment elevation acute coronary syndromes are common and should not automatically be regarded as benign phenomena. Quantitative T- wave analysis provides optimal risk stratification.

Patients presenting in the emergency department with chest pain at rest represent a heterogenous population with varying underlying pathophysiology. Localized ST-segment elevation on the admission electrocardiogram (ECG) is usually an indicator of acute myocardial infarction (AMI), and the treatment of choice for these patients is well documented.1 In patients without such ST-segment elevation, AMI is subsequently diagnosed based on cardiac biochemical markers either at admission or within the first 24 hours. Several studies of patients with acute coronary syndromes have identified electrocardiographic and biochemical variables to be important parameters when assessing the patient’s prognosis 2 and also when estimating effects of various treatments. 3 Based on these findings, it has recently been suggested that patients with low risk indicated by a normal ECG and troponin T or I levels should be assessed for early discharge from the emergency department.4,5 The present study examines both angiographic findings and prognosis in patients with unstable angina pectoris found to be at low risk at admission.

It is unknown whether the risk factors associated with the development of ventricular septal defect (VSD) after acute myocardial infarction (MI) remain the same when thrombolytic therapy is used, nor have specific electrocardiographic patterns of acute MI associated with the development of VSD been identified. Our study population included patients with an anterior MI enrolled in the GUSTO-I study. Baseline clinical data were collected prospectively for all patients. Patients in whom VSD was suspected by the local investigators at each site were evaluated retrospectively. Baseline clinical and electrocardiographic variables were compared between 2 groups: 10,847 patients without VSD (99.6%) and 48 patients with confirmed VSD (0.4%). Multivariate analysis showed the following clinical variables to be independent predictors of VSD: age (odds ratio [OR] 2.19, 95% confidence intervals [CI] 1.62 to 2.98; p

Previous reports indicate that patients who do not develop Q waves after thrombolytic therapy are a different population with a better long-term survival than those who do develop Q waves. However, the use of resources, quality of life, and health status of this population have not been fully evaluated. Using data from the Economics and Quality of Life subset of the Global Utilization of Streptokinase and tPA for Occluded Arteries study, we examined 30-day and 1-year mortality, use of resources, and quality-of-life measures among 1,830 of 3,000 patients with acute myocardial infarction and ST-segment elevation treated with thrombolytic therapy. At hospital discharge, 555 patients (30.2%) had not developed Q waves. These patients had lower mortality than patients with Q waves at 30 days (1.6% vs 4.5%, p

In the prethrombolytic era it was found that infarct size and left ventricular ejection fraction could be predicted using the Selvester QRS score. We evaluated whether infarct size and left ventricular ejection fraction could be predicted by the predischarge QRS score in patients who had received reperfusion therapy and whether considering the configuration of the ST segments and T waves would increase the accuracy of these predictions. We evaluated 51 patients with first anterior wall myocardial infarction who had received reperfusion therapy and predischarge resting technetium-99m-sestamibi scan. The electrocardiograms recorded on the same day of the scan were analyzed for the QRS score and were divided into 3 groups: A, isoelectric ST and negative T waves; B, ST elevation (or =0.1 mV) and negative T waves; and C, ST elevation (or =0.1 mV) and positive T waves. Groups A, B, and C included 12, 23, and 16 patients, respectively. The myocardial perfusion defect extent increased from groups A to C (median 21%, 37%, and 43.5% in groups A, B, and C, respectively; p = 0.023). Similarly, left ventricular ejection fraction decreased (44%, 38%, and 34%, respectively; p = 0.042) from groups A to C. Overall, the correlation between the QRS score and the myocardial perfusion defect extent (rho 0.249; p = 0.08) and ejection fraction (rho -0.229; p = 0.11) was poor. A statistically significant correlation between myocardial perfusion defect size and QRS score was found only in group A (rho 0.599, p = 0.04). Among patients with anterior myocardial infarction who received reperfusion therapy, the predischarge QRS score was predictive of infarct size only in those in whom ST elevation resolved completely. In patients with residual ST elevation there was no correlation between QRS score and infarct size.

The historical time of acute symptom onset is not always an accurate indication of the timing of onset of an acute myocardial infarction (AMI). Consideration of electrocardiographic (ECG) timing parameters could supplement historical timing alone as a clinical guide for decisions regarding the use of reperfusion therapy. Three hundred ninety-five patients from 4 trials of thrombolytic therapy conducted in the northwestern United States and western Canada are included in the present study. A total of 316 patients received either streptokinase or tissue plasminogen activator, and 79 received no reperfusion therapy. Historical time of symptom onset was acquired by emergency or cardiology department personnel and recorded on patient report forms. An ECG method for estimating the timing of the AMI, the Anderson-Wilkins (AW) acuteness score, was calculated from the initial standard 12-lead recording by investigators blinded to the knowledge of symptom duration or any other study variables. Tomographic thallium-201 imaging 7 weeks after hospital admission was used to measure final AMI size. The ECG timing method achieved a relation with final AMI size similar to that previously reported for historical timing. The AW acuteness score proved most useful for anterior AMI location when there was aor = 2 hour delay following symptom onset, but was most useful for the inferior AMI location when there was a2 hour delay. Despite a longer delay, patients with high AW acuteness scores had 50% lower final anterior AMI size than those with low scores; and despite a shorter delay, those with low ECG acuteness scores had 50% greater final inferior AMI size than those with high scores. The AW acuteness score combined with the historical estimation of symptom duration should provide a more accurate basis for predicting the potential for limitation of final AMI size than either method alone. These results could potentially provide the basis for developing a new method for noninvasive guidance of clinical decisions regarding administration of reperfusion therapy in the initial evaluation of patients with AMI.

Patients with unstable coronary syndromes are a heterogeneous group with varying degrees of ischemia and prognosis. The present study compares the prognostic value of a standard electrocardiogram (ECG) obtained at admission to the hospital with the information from 24-hour continuous electrocardiographic monitoring obtained immediately after admission. The admission ECGs and 24 hours of vectorcardiographic (VCG) monitoring from 308 patients admitted with unstable coronary artery disease were analyzed centrally regarding standard electrocardiographic ST-T changes, ST-vector magnitude (ST-VM), and ST change vector magnitude episodes. End points were death, acute myocardial infarction, and refractory angina pectoris within a 30-day follow-up period. ST-VM episodes (≥50 μV for ≥1 minute) during VCG monitoring was the only independent predictor of death or acute myocardial infarction by multivariate analysis. ST-VM episodes during vectorcardiography was associated with a relative risk of 12.7 for having a cardiac event, hypertension was associated with a relative risk of 1.7, and ST depression on the admission ECG was associated with a relative risk of 5.7. Patients with ST depression at admission had an event rate (death or acute myocardial infarction) of 17% at 30-day follow-up. Patients without ST depression could further be risk stratified by 24 hours of VCG monitoring into a subgroup with ST-VM episodes at similar (8%) risk and a subgroup without ST-VM episodes at low (1%) risk (p = 0.00005). Continuous VCG monitoring provides important information for evaluating patients with unstable coronary artery disease. It is recommended that patients not initially estimated at high risk based on the admission ECG are referred for 24 hours of VCG monitoring for further risk stratification.

The method of determining the acuteness score presented in the present study is suggested for use in automated electrocardiographic analysis systems. A potential use of the acuteness score is in combination with historical timing as a guideline for decisions regarding thrombolytic therapy. Patients with an acuteness score above a certain threshold and a brief time from symptom onset may benefit most from thrombolytic therapy. The relation between the levels of acuteness score and the quantity of myocardium salvaged was not determined in the present study because no measure of salvage was available in this population. A future study is suggested in which this relation is determined. An additional use of the acuteness score may be to assess myocardial reperfusion and salvage by examining the time course of progression in score between the ECGs before and sequentially after administration of thrombolytic therapy.