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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 <0.001), female gender (OR 5.07, 95% CI 2.70 to 9.98; p <0.001), and lack of previous angina (OR 2.11, 95% CI 1.12 to 4.29; p = 0.021). Two electrocardiographic variables predicted acute VSD: the magnitude of ST deviation in lead III (OR 1.55, 95% CI 1.12 to 2.21; p = 0.007) and in lead V(2) (p <0.001). However, the relation between the ST amplitude in lead V(2) and the risk for VSD was nonlinear. In patients with anterior MI who underwent thrombolysis, the risk factors for VSD were age, female gender, and lack of previous angina. Previous infarction was not a risk factor. Less ST-segment depression in lead III was a predictor of VSD. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

The authors describe a method to account for patient-to-patient variability in electrocardiographic data. The method yielded criteria for healed inferior myocardial infarction with diagnostic performances better than those of traditional electrocardiographic parameters. [ABSTRACT FROM AUTHOR]

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 <0.01) and at 1 year (4.7% vs 6.8%, p <0.04). Recurrent chest pain and dyspnea were similar at 30 days and 1 year. Patients without Q waves had significantly more angiography and trends toward higher readmission, revascularization, and use of calcium antagonists at 30 days. Angiography, revascularization, readmission, and quality of life were equivalent from 30 days to 1 year, with no sign of late instability. Logistic regression analysis showed an association between in-hospital revascularization and better survival and quality of life at 1 year. Conversely, there was no association between in-hospital use of calcium antagonists and outcome to explain the lower mortality in non-Q-wave patients. The absence of Q waves after thrombolytic therapy is a marker of success, implying better prognosis and equivalent quality of life, use of resources, and health status than for patients with Q-wave acute myocardial infarction and no sign of long-term unstable clinical course. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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 in > or =2 leads (J point > or =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 (p <0.0001 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 (p <0.0001). Thrombolysis reduced final Selvester score only in the QRS- group (p <0.00001), 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. [ABSTRACT FROM AUTHOR]

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 a > or = 2 hour delay following symptom onset, but was most useful for the inferior AMI location when there was a < 2 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. [ABSTRACT FROM AUTHOR]

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 (> or = 50 microV for > or = 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. [ABSTRACT FROM AUTHOR]

The changes in QRS complex morphology associated with acute myocardial infarction (AMI) can resolve spontaneously over time. Whether complete revascularization of the infarct-related myocardial territory after AMI affects this QRS resolution has not been studied adequately. The present study compares the evolution of the changes in the QRS complex associated with AMI during 1-year follow-up in patients treated with or without revascularization after their first thrombolyzed AMI. The study is a substudy of the DANish Trial in Acute Myocardial Infarction (DANAMI) (n = 1,008) that randomized patients with inducible ischemia after their first AMI, treated with intravenous thrombolytic therapy, to conservative treatment or coronary angiography followed by the appropriate revascularization strategy. A total of 817 patients had complete sets of evaluable electrocardiograms. Electrocardiograms were obtained at randomization, and at 3, 6, and 12 months of follow-up and subjected to blinded core-laboratory evaluation according to the Selvester QRS scoring method. This score considers Q-, R-, and S-wave duration and ratios to provide a semiquantitative estimate of AMI size. The median electrocardiographic estimated infarct size in the entire population was 15% of the left ventricle at randomization. At the end of the follow-up period this estimate had decreased to 12% (p < 0.00001). There was no difference in the rate of QRS resolution whether the patients were subgrouped according to randomization or subgrouped according to actual treatment with or without revascularization. The present study confirms the findings from previous studies conducted in the prethrombolytic era, that considerable normalization of the QRS complex also occurs after AMI treated with thrombolytic therapy. This QRS normalization seems unaffected by an aggressive treatment strategy with revascularization via balloon angioplasty or bypass surgery. [ABSTRACT FROM AUTHOR]

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 <0.001). Patients with maximum ST depression in leads V1 to V3 less often had AMIs due to proximal right coronary artery obstruction (23.9%) than patients without precordial ST depression (35.2%) or those with ST depression in leads V4 to V6 (40.0%; p = 0.001) and had larger AMIs as estimated by peak creatine kinase. Different patterns of precordial ST depression are associated with distinctive coronary anatomy. ST depression in leads V4 to V6, but not V1 to V3, confers a greater likelihood of multivessel coronary artery disease. [ABSTRACT FROM AUTHOR]

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 <0.001) or cardiogenic shock (6.1% vs 8.6%, p = 0.023). Higher maximum T-wave amplitude and excess T-wave amplitude were predictive of lower 30-day mortality (chi-square = 67, p <0.001 and chi-square = 33, p <0.001, respectively). These differences remain significant after controlling for other prognostic baseline ECG variables. In addition, T-wave amplitude added prognostic significance after controlling for time to treatment. T-wave amplitude, an often-overlooked component of the electrocardiogram, can add significant prognostic information in initial evaluation of patients with AMI. [ABSTRACT FROM AUTHOR]

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). [ABSTRACT FROM AUTHOR]

Patients with acute myocardial infarction and bundle branch block have a higher mortality rate and more in-hospital complications than patients with normal intraventricular conduction. Patients whose conduction defects revert have an improved prognosis (with outcomes similar to patients who never develop bundle branch block); thus, we analyzed potential predictors of bundle branch block reversion. [ABSTRACT FROM AUTHOR]

Lead distributions of peak ST-segment depression were compared between patients undergoing left circumflex artery percutaneous transluminal coronary angioplasty and exercise tolerance test. Localization of peak ST-segment depression to leads V2 or V3 was 96% specific and 70% sensitive for differentiating ischemia due to occlusion of left circumflex artery occlusion from nonocclusive ischemia. [ABSTRACT FROM AUTHOR]

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.

We investigated the impact of primary angioplasty compared with thrombolysis in 894 patients with ST elevation acute myocardial infarction and electrocardiographic grades II and III ischemia on enrollment. Patients were divided into 2 groups based on the enrollment electrocardiogram-grade III: (1) absence of an S wave below the isoelectric baseline in leads that usually have a terminal S configuration (leads V(1) to V(3)), or (2) ST J-point amplitude > or =50% of the R-wave amplitude in all other leads. To be included in the grade III group, grade III criteria in > or =2 adjacent leads were required. Patients with ST elevation but without grade III criteria were classified as having grade II. In-hospital mortality was 3.2% and 6.8% in the grade II (n = 616) and grade III (n = 278) groups, respectively (p = 0.016). In the grade II group, in-hospital mortality was similar in the thrombolysis and angioplasty subgroups (3.2% and 3.3%, p = 0.941). In patients with grade III, in-hospital mortality was 6.4% and 7.3%, respectively (p = 0.762). The odds ratio for the grade III group for death with thrombolysis was 2.06 (95% confidence intervals [CI] 0.82 to 5.19; p = 0.125); the odds ratio for primary angioplasty was 2.30 (95% CI 0.93 to 5.66; p = 0.07). In the thrombolysis group, reinfarction occurred in 3.3% and 6.5% of the grade II and grade III subgroups (p = 0.137). In the angioplasty group, reinfarction occurred in 1.3% and 4.4%, respectively (p = 0.239). Grade III ischemia on admission was associated with higher in-hospital and 30-day mortality and a higher rate of reinfarction. There was no difference in mortality between primary angioplasty and thrombolysis in the grade II and grade III ischemia patients.

Electrocardiographic recordings used to assess ST-segment deviation are performed using both standard and torso limb lead positions, where bony prominences give more artifact-free signal. Whereas significant QRS artifact can be introduced by such changes in lead location, the impact on ST-segment measurements has never been assessed. Digital electrocardiographic recordings were performed in 29 patients throughout elective angioplasty balloon inflation in the left anterior descending (n = 12), right coronary (n = 14), and circumflex (n = 3) arteries. In all cases, unipolar leads V1, V4, and V6 were affixed to the torso lead positions, allowing reconstruction of simultaneously acquired standard and modified 9-lead electrocardiograms (ECGs). ST levels in the 26 patients who had ST deviation during angioplasty were compared at both baseline and peak ischemia of up to 1,046 microV in the anterior, and 551 microV in the inferior leads. Differences in recorded ST levels for modified versus standard lead locations were all < 100 microV, even at peak ischemia. Although ST-segment elevation in the inferior leads appeared to show slightly more pronounced differences between lead sets than did anterior elevation, all differences were < 100 microV. Thus, measurement of ST-segment levels appears unlikely to be importantly affected by the intermixture of ECGs recorded with standard lead positions and ECGs recorded with monitoring-compatible lead positions on the torso. Recalibration of ST-segment measurements may be necessary for meticulous quantification of ischemia, infarct size, or other measurements that might be affected by variations < 100 microV.

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 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 < 8 hours after symptom onset. Acutely jeopardized myocardium was estimated at baseline, and before and after angiography by quantitative ST-segment analysis. The AMI size was estimated on the final electrocardiogram by the Selvester QRS score. Left ventricular ejection fraction was measured at the time of acute angiography and before discharge in 31 of these patients. In the 21 patients with normal flow (Thrombolysis in Myocardial Infarction [TIMI] trial grade 3) in the infarct-related artery, the amount of jeopardized myocardium decreased from baseline to that before and after angiography (17 to 11 and 11%, respectively; p < 0.00005), and the median final AMI size was reduced (17 to 9%; p = 0.0004). In 6 patients with suboptimal flow (TIMI grade 2), the median amount of jeopardized myocardium decreased slightly from baseline to that before to after angiography (15 to 12%); however, the median final AMI size was not reduced (17%). In 12 patients with no reperfusion (TIMI 0 to 1) flow, the median amount of jeopardized myocardium remained unchanged from baseline to that before angiography (21%), and the final AMI size was not significantly reduced. There was a significant inverse correlation between the change in global left ventricular function and the difference between electrocardiographic estimated jeopardized and final AMI size (rs = -0.53; p = 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)

Proximal limb lead positions are currently used for activity-compatible electrocardiographic monitoring of myocardial ischemia. Two previously described systems for alternate limb lead placement were studied in patients with and without QRS evidence of healed anterior or inferior myocardial infarction. An innovative method was used to simultaneously record 6 standard and 6 modified limb leads, and 3 standard and 3 modified precordial leads on a standard digital electrocardiograph. Both alternate lead placement systems showed rightward frontal plane axis shift and diminished Q-wave durations in lead aVF compared with those of their simultaneous standard controls. Furthermore, potential differences between the standard distal limb lead sites and 5 more proximal sites were explored along each limb. Differences along the left arm were accentuated relative to those along the right arm owing to differences in proximity of the arms to the myocardium. Along the lower limb, and anterior site showed less deviation from standard than did a more lateral site. It is imperative that recordings from alternate sites be labeled accordingly so that their output cannot be confused with that obtained from standard sites.

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.

A subset of 3 screening criteria (Q wave greater than or equal to 30 ms in lead aVF, any Q or R wave less than or equal to 10 ms and less than or equal to 0.1 mV in lead V2, and R wave greater than or equal to 40 ms in V1) has been proposed to identify single nonacute myocardial infarcts. Cumulatively, these 3 criteria achieved 95% specificity, and 84 and 77% sensitivities for inferior and anterior myocardial infarcts, respectively, among patients identified by coronary angiography and left ventriculography. This study establishes the true sensitivities of the set of screening criteria in 71 patients with anatomically proven single myocardial infarcts and 32 patients with multiple myocardial infarcts. In the single inferior infarct group, the aVF criterion was 90% sensitive. The V2 criterion (any Q or R wave less than or equal to 10 ms and less than or equal to 0.1 mV) was 67% sensitive in the single anterior infarct group. No single criterion proved sensitive in identifying a posterolateral infarct. The set of screening criteria performed just as well for multiple infarcts as it did for single infarcts, with a cumulative sensitivity of 72%. The overall sensitivity of the screening set in the 103 patients in all groups was 71%.

Myocardial infarct size is an important risk factor for survival after acute myocardial infarction (AMI). The purpose of this study was to determine the prognostic value of myocardial infarct size, as estimated by the Selvester 54-criteria/32-point QRS scoring system, in the Framingham cohort. During the first 30 years of the Framingham Heart Study, a total of 384 participants developed an AMI requiring hospitalization; from this group, 243 patients met the following inclusion criteria: (1) no electrocardiographic changes due to a previous infarction, (2) survival greater than 3 days after discharge from the AMI hospitalization and (3) no electrocardiographic evidence of conduction disturbances or ventricular hypertrophy at the time of their final in-hospital electrocardiogram. Univariate and multivariate analyses were performed to test the association of the QRS score, and other associated risk factors, with time until coronary heart disease-related death. QRS score was found to be significantly associated with outcome (p = 0.03), as was the systolic blood pressure before infarction (p greater than 0.001). Both univariate and multivariate analysis showed that a history of systolic hypertension was the variable most strongly associated with coronary heart disease-related death. Thus, identification of AMI survivors at high risk for subsequent mortality can be improved by routine blood pressure measurement before AMI, and QRS scoring of the electrocardiogram taken at hospital discharge.

Seventeen new criteria added to the simplified version of the Selvester QRS scoring system to comprise the complete version were evaluated to determine their value in estimating the size of single infarcts. These non-Q-wave criteria might be particularly useful regarding posterolateral infarcts in the distribution of the left circumflex artery. The study population was made up of 21 anterior, 30 inferior and 20 posterolateral single myocardial infarction (MI) patients with no evidences of bundle branch or fascicular blocks, ventricular hypertrophy or previous MI on their final stable electrocardiogram. The complete system's maximum 32 points is capable of indicating MI in 96% of the left ventricle and it estimated a mean electrocardiographic MI size that better approximated the anatomic size compared with the simplified version in all MI locations. The correlation between anatomic and electrocardiographic MI size using the complete system was better and statistically significant for the posterolateral MI group (simplified r = 0.55, p less than 0.01 vs complete r = 0.70, p less than 0.0006). Criteria such as Q and S amplitude less than or equal to 0.3 mV in V1 and less than or equal to 0.4 mV in V2 were particularly helpful. This study documents the improved ability provided by the 17 additional non-Q-wave criteria which have been added in the complete version of this scoring system regarding the sizing of infarcts in the region of the left ventricle supplied by the left circumflex artery.

Successful intravenous thrombolytic therapy early in myocardial infraction has the potential to reduce patient mortality without the additional risk and cost of aggressive invasive therapy. Noninvasive detection of successful reperfusion using resolution of chest pain, ST-segment changes assessed on static electrocardiograms, arrhythmia evolution, early isoenzyme peaking or changes in ventricular perfusion or function has been hampered by poor sensitivity or specificity, or inability to provide timely information. A newly available portable programmable microprocessor-driven real-time 12-lead electrocardiographic monitor has been introduced that may address these limitations. A continuously updated precise digital record of ST-segment activity at the bedside provides valuable information both in monitoring patients during reperfusion therapy to determine the efficacy of such treatment and in the subsequent hours to signal threatened reocclusion. This report describes the salient features of the monitor and presents 4 distinct situations in which the monitor detected timely information regarding coronary patency after reperfusion.

The ability of an independently developed QRS point score to estimate the size of infarcts predominantly within the anterior third of the left ventricular was evaluated by quantitative pathologic-electrocardiographic correlation. The study was limited to 21 patients with a single infarct documented by postmortem examination, for whom an appropriately timed standard 12 lead electrocardiogram was available that did not exhibit signs of left or right ventricular hypertrophy, left or right bundle branch block or anterior or posterior fascicular block. At necropsy the heart was cut into five to seven slices. The location and size of the infarct was quantitated by computer-assisted planimetry of the slices. The electrocardiogram of 19 (90 percent) of the patients exhibited either a Q wave or an R wave of no more than 20 ms in lead V2. The infarct in the two patients without this electrocardiographic finding was small, occupying 2 and 3 percent of the left ventricle, respectively. The percent infarction of the left ventricle correlated with the QRS point score (r=0.80). Thus in patients without complicating factors in the electrocardiogram and with a single infarct, the electrocardiogram provides a marker for infarction in the anterior third of the left ventricle and permits estimation of infarct size.

Eleven percent of 905 consecutive patients with acute myocardial infarction admitted to the coronary care unit at Duke University Medical Center experienced cardiac arrest. Subgroups of patients at high and low risk for cardiac arrest were identified. Cardiac arrest was experienced by 17 percent of patients with signs of heart failure on admission but by only 3 percent of patients without diabetes mellitus, prior myocardial infarction or heart failure by history or on admission. Only 59 percent of patients with cardiac arrest survived hospitalization compared with 88 percent of those without cardiac arrest. Long-term survival for the 765 hospital survivors was significantly greater in the group without than in the group with arrest at each yearly interval from 1 through 5 years; the 2 year survival rate was 50 and 77 percent, respectively, in these two groups. Many of the deaths among the hospital survivors occurred in patients with signs of heart failure during hospitalization. Among 668 hospital survivors who had mild or no heart failure during hospitalization, cardiac arrest continued to be a significant predictor of mortality. The mode of death among hospital survivors did not differ in the groups with and without cardiac arrest; for example, the incidence rate of sudden death in the two groups was 44 and 37 per cent, respectively. In light of recent reports suggesting that the prophylactic use of antiarrhythmic agents can virtually eliminate virtually fibrillation during the hospital phase of acute myocardial infarction, we contend that such use may substantially reduce both long-term and hospital mortality after acute myocardial infarction.

The incidence and prognostic effect of the development of new perioperative ventricular conduction abnormalities were examined in all patients undergoing coronary artery bypass surgery at Duke University Medical Center between 1976 and 1981. Of the 913 patients included, transient (resolved before discharge) ventricular conduction abnormalities developed in 156 (17%) and persistent (until discharge) changes developed in 126 (14%). Complete right bundle branch block (BBB) was the most frequent type of new ventricular conduction abnormality, followed by left anterior hemiblock and incomplete right BBB (found in 60%, 26%, and 9%, respectively, of all patients with transient changes and 29%, 33% and 26% of all patients with persistent changes). Development of new ventricular conduction abnormalities was most strongly related to date of operation (p less than 0.0001, univariate chi 2 = 122), increasing from 2% transient and 7% persistent in 1976 to 36% transient and 22% persistent in 1981. The incidence was also higher in older patients. Preoperative ejection fraction and number of diseased vessels were related to development of perioperative ventricular conduction abnormalities but were not independently related after adjustment for other baseline characteristics. Contrary to findings in other studies, development of new perioperative ventricular conduction abnormalities, including isolated new left BBB, did not worsen the survival rate in patients followed up to 3 years after surgery.

Current coronary care electrocardiographic (ECG) monitoring techniques are aimed at detection of cardiac arrhythmias rather than myocardial ischemia. However, in patients with acute myocardial infarction (AMI) who undergo reperfusion therapy, monitoring ST-segment deviation could provide an early noninvasive indicator of coronary artery reocclusion. In this study, the admission 12-lead ECGs of patients with initial AMI were used to propose optimal lead locations for ST-segment monitoring. The study population was selected from consecutive Duke University Medical Center admissions during 1965 to 1981 who met the following inclusion criteria: chest pain for no more than 8 hours, initial AMI documented by ECG and 3 of 4 enzyme criteria, greater than or equal to 0.1 mV (1 mV = 10 mm) of ST elevation in at least 1 of the standard 12 leads (not aVR) on admission ECG, and no ECG evidence of conduction disturbances, ventricular hypertrophy or tachycardia. ST-segment deviation was quantified; AMI location was assigned based on the lead with maximal deviation. Of the 80 patients who had an inferior AMI, lead III was both the most frequent location for ST elevation (94%) and the most common site with maximal ST deviation. Lead V2 had the highest incidence of ST-segment depression (60%). In the 68 patients who had an anterior AMI, lead V2 had the highest frequency of ST elevation (99%). Leads V2 and V3 were the most common sites of maximal elevation. Thus, for monitoring ST deviation, leads III and V2 may be superior to leads II and V1, which are commonly used in arrhythmia monitoring.(ABSTRACT TRUNCATED AT 250 WORDS)

Studies were performed to determine the chronotropic effect of acetylstrophanthidin during constant infusion through cannulation of the sinus nodal artery. Ten mongrel dogs weighing 13.5 to 18 kg were studied under sodium thiamylal anesthesia. Epicardial atrial and ventricular electrograms were recorded. The sinus nodal artery was cannulated and infused for 20 minutes at a rate of 2 cc/min with a solution containing acetylstrophanthidin, 0.5 microng/cc. Mean results for the group of 10 animals were determined. There was a gradual acceleration of the atrial rate of 45 beats/min after 6 to 8 minutes of infusion. The peak atrial rate of 175 beats/min was achieved by 10 to 12 minutes. This tachycardia persisted for 2 to 4 minutes without atrioventricular block or premature beats. By 12 to 14 minutes, there was a gradual slowing of atrial rate followed by bradycardia, sinus pauses and atrial arrest. Sinus nodal arterial infusion of acetylstrophanthidin produces an initial positive chronotropic effect and, if maintained, a depression of atrial rate and, terminally, atrial arrest. The gradual time course of development and decline of the tachycardia suggests that the "paroxysmal" atrial tachycardia caused by digitalis excess is the result of enhanced pacemaker automatically rather than reentry, and thus is not truly paroxysmal.

Using multiple gated cardiac blood pool imaging and single-plane ventriculography from cardiac catheterization, 2 independent measures of left ventricular (LV) ejection fraction (EF) were determined in each of 21 patients. Patients were seen 2 to 6 weeks after their first acute myocardial infarction and were free of electrocardiographic evidence of conduction abnormalities and left or right ventricular hypertrophy. Differences between the 2 measures of LVEF were examined and then compared with the extent of myocardial necrosis estimated from the standard 12-lead electrocardiogram using the complete 54-criteria/32-point Selvester QRS scoring system. Regression analysis yielded an r value of 0.81 (SEE = 8.05) for the overall relation between the 2 measures of LVEF. Correlation coefficients of -0.70, -0.66 and -0.72 were obtained for the relations of radionuclide LVEF, catheterization LVEF and the mean of these 2 determinations, respectively, compared with QRS score. A QRS score 4 or less achieved 100% specificity and that of 8 or less 100% sensitivity for predicting an LVEF greater than 40%. Thus, the Selvester QRS scoring system may be of value in identifying patients with or without markedly impaired LVEF. This risk stratification may be important in reaching optimal postinfarction therapeutic decisions.

This prospective study compares the estimated size of acute myocardial infarction (AMI) by cumulative serum creatine kinase isoenzyme MB (CK-MB), Selvester QRS score, and 2-dimensional (2-D) echocardiographic dyssynergy of the left ventricle in 63 consecutive patients with their first anterior (n = 31) or inferior AMI (n = 32). The correlations among these parameters were good for patients with anterior AMI (r = 0.74 to 0.78, standard error of the estimate = 29 to 33%) but only fair for those with inferior AMI (r = 0.35 to 0.47, standard error of the estimate = 38 to 73%). Based on previous autopsy studies, estimates of CK-MB and QRS score were then converted to percent of infarcted left ventricle. Linear regression analyses between mean percent AMI size by cumulative CK-MB plus QRS score vs the number of dyssynergic segments by 2-D echocardiography were used to develop a comprehensive formula for estimating AMI size by a combination of all 3 techniques. Thus, a formula is proposed that may optimally estimate AMI size derived from leakage of cytosolic enzymes, changes in the sequence of myocardial depolarization, and irregularities of left ventricular contraction.

The dynamic QRS amplitude changes that appear during 1-vessel percutaneous transluminal coronary angioplasty of the right and left circumflex coronary arteries were studied in 20 patients using continuous 3-lead electrocardiographic recordings representing leads aVF, V2 and V5. The balloon inflations that produced the greatest extent of ST-segment deviation were identified for each lead ("maximally ischemic periods"). QRS amplitude measurements were performed manually at both the PR and shifted J-ST baselines at 10-second intervals during these periods to determine that baseline from which the R and S waves most nearly maintained their control amplitudes. There was no significant baseline relation for either the R or the S waves in leads V2 and V5 during ischemia. However, the R-wave changes in lead aVF were significantly associated with the PR- versus the J-ST-segment baseline (p = 0.007); the S wave, when it occurred, had no tendency for either baseline. The electrocardiographic records were also examined visually for characteristics of left posterior (inferior) "periischemic block" likely to occur uniquely in patients with a dominant right or left circumflex occlusion. There were 2 patients with obstruction of the right circumflex artery who exhibited the characteristics of periischemic block during percutaneous transluminal coronary angioplasty, as evidenced by an increase in R-wave duration, amplitude or both in lead aVF.

Preoperative and serial postoperative electrocardiograms (ECGs) were reviewed in 104 patients undergoing rest and exercise radionuclide angiocardiography before and 1 to 12 months after coronary artery bypass grafting (CABG). Five patient groups were defined by ECG findings before and after CABG: Group I--normal ECG before and no ECG change after CABG; Group II--prior myocardial infarction by ECG before but no QRS change after CABG; Group III--all patients with a minor QRS change (less than 0.04-second Q wave, loss of R-wave amplitude) after CABG; Group IV--all patients with a major QRS change (greater than or equal to 0.04-second Q wave) after CABG; Group V--all patients without new Q waves or loss of R-wave amplitude but with a major QRS change (conduction disturbance) after CABG. Mean resting ejection fraction changed little after CABG in all groups, although the 0.03 increase in Group I was significant (p less than 0.05). Group IV had the largest decrease in resting ejection fraction after CABG (0.04), but this was not statistically significant. Mean exercise ejection fraction increased significantly (p less than 0.0001) in Groups I, II and III but not in Groups IV and V. QRS changes do not consistently reflect impairment of left ventricular (LV) function after CABG.

The decision to administer thrombolytic therapy for limitation of acute myocardial infarction (AMI) size must occur when only the history, physical examination and 12-lead electrocardiogram of a patient are available. A method that could quickly assess the amount of jeopardized myocardium would greatly aid the physician. This study developed formulas from 68 anterior and 80 inferior AMI patients using the extent of initial ST-segment deviation (ST delta) to predict the final AMI size estimated by the Selvester QRS score in a population not receiving reperfusion therapy. Inclusion required: initial anterior or inferior AMI; admission electrocardiogram less than or equal to 8 hours after the onset of symptoms with evidence of epicardial injury; elevated creatine kinase-MB; a predischarge electrocardiogram taken greater than or equal to 72 hours after admission; and no AMI extension before the predischarge electrocardiogram. The extent of epicardial injury was quantified by counting the number of leads with greater than or equal to 0.1 mm ST delta, by the sum (sigma) of ST delta in all leads and by the sigma ST delta in the lead groups associated with each AMI location. These results were compared to the AMI size estimated from the predischarge electrocardiogram. Univariable and multivariable analyses generated these formulas for AMI size: anterior = 3[1.5 (number leads ST increases) - 0.4]; inferior = 3[0.6 (sigma ST increases II, III, aVF) + 2.0]. Thus, formulas based on quantitative measurements of ST delta on the admission electrocardiogram are predictive of final QRS-estimated AMI size, and may be useful in determining the efficacy of acute reperfusion therapy.

The outcome in 126 consecutive patients with nontraumatic out-of-hospital cardiac arrest was analyzed to determine the effectiveness of a standard ambulance system over 22 months. Therapy was limited to basic life support (that is, administration of oxygen by mask, i.v. fluids, closed-chest massage and artificial respiration) by emergency medical technicians in a community in which less than 1% of the population had been trained in cardiopulmonary resuscitation (CPR). Analyses of patient data were performed to determine the relations between survival to hospital admission or discharge and 6 variables; response time, prior CPR, initial rhythm, acute myocardial infarction, initial blood pressure and initial pulse. Of 126 patients, 28 (22%) survived to hospital admission and 11 (9%) to hospital discharge. Two patient subgroups had a higher discharge rate: those with an initial rhythm of ventricular tachycardia or fibrillation (7 of 50, 14%), and those with an initial blood pressure greater than or equal to 90 mm Hg and a pulse rate of greater than 50 beats/min (3 of 6, 50%). For patients in arrest before ambulance arrival, there was no difference in outcome between those who did or those who did not receive prior CPR. Results of this study can be used as a basis for evaluating and comparing interventions directed toward stabilization of patients during the prehospital phase of cardiac arrest.

CK-MB changes were studied using agarose gel electrophoresis in 244 patients admitted to a coronary care unit for suspected acute myocardial infarction (AMI). A range of minimally elevated CK-MB levels, from 1 to 24 IU/liter, was identified as representing uncertain AMI events. Positive AMI events were defined by elevations of 25 IU/liter or more documented in patients with new Q waves or abnormalities in all enzyme and isoenzyme levels. Negative AMI events were defined by elevation of 0 IU/liter, observed in all control subjects. The 1-year cardiac mortality rates in the "positive"-AMI (n = 91) and "uncertain"-AMI (n = 22) groups were identical (22%), and significantly higher than that in the "negative"-AMI group (n = 93) (6%) (p less than 0.05). However, when a larger uncertain-AMI group of 115 patients was compiled by 2 collaborating centers, the 1-year cardiac mortality rate in the 39 patients with chest pain alone was 0%, vs 33% in the 76 patients with accompanying severe medical problems such as cardiac or respiratory failure. Whether minimal CK-MB elevations represent AMI of limited extent is not clear. These elevations occur most often in association with severe medical problems, and in patients without such problems, they may not indicate a poor prognosis.