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The ECG is at a crossroads as to its future integration into modern medical practice. Those most interested in electrocardiography remain the old guard, whose careers evolved with this technology. They remain as enamored by the experiential mythology as by the experimental science of the ECG. Electrophysiologists, who rightly should be carrying on the torch of further ECG development, are too busy with their therapeutic invasive procedures and devices to invest much time in diagnostic decision support. Young physicians in training are too busy learning the plethora of new diagnostic modalities and treatment procedures to even become competent in ECG interpretation. Many of them only have goals to recognize an ST elevation myocardial infarction and atrial fibrillation, and to pass their board examinations. Their understanding of ST elevation myocardial infarction criteria could be easily exposed by asking them to name the contiguous pairs of standard ECG leads. A disappointing number would refer to pairs of leads that are contiguous on the ECG display such as II and III or V1 and V4, rather than the leads separated by 30° going around the surface of the heart as specified in the guidelines.1 Reimbursement provides a further counterincentive: to paraphrase George Bernard Shaw ( The Doctor’s Dilemma , 1926), “the doctor orders the test that pays the most” and that is no longer the ECG, but a panoply of imaging procedures. Examples of the experiential mythology that continue to haunt electrocardiography include the requirement for contiguous or adjacent leads instead of a single lead for fulfilling diagnostic criteria. The contiguous or adjacent lead constraint is a residual from the thick, noisy tracings from the early days of electrocardiography before high-impedance amplifiers, DC coupling, and digital processing produced the high-resolution tracings of today (Figure 1). Applying the criteria to a …

This statement provides a concise list of diagnostic terms for ECG interpretation that can be shared by students, teachers, and readers of electrocardiography. This effort was motivated by the existence of multiple automated diagnostic code sets containing imprecise and overlapping terms. An intended outcome of this statement list is greater uniformity of ECG diagnosis and a resultant improvement in patient care. The lexicon includes primary diagnostic statements, secondary diagnostic statements, modifiers, and statements for the comparison of ECGs. This diagnostic lexicon should be reviewed and updated periodically.

The ECG is the most frequently used tool for evaluating myocardial infarction (MI). The ECG provides an opportunity to describe location and extent of infarction expressed as pathological Q waves or their equivalents. The terminology used for the left ventricular (LV) walls has varied over time,1–7 although the most currently accepted terms by electrocardiographists have been anterior , septal , lateral , and inferior .8–15 However, terminology has been complicated by use of posterior to refer to either the basal lateral or the basal inferior wall (see below). On the basis of correlations with the postmortem anatomic gold standard reported >50 years ago16 and confirmed later,17,18 the presence of abnormal Q waves in leads V1 and V2 was related to septal wall MI; in V3 and V4 to anterior wall MI; in V5 and V6, I, and aVL to lateral wall MI (I, aVL high lateral; V5 and V6, low lateral); and in II, III, and aVF to inferior wall MI. The presence of abnormally increased R waves in V1 and V2 as a mirror image of Q waves in posterior leads was called a posterior wall infarction . Although similar considerations may be applied for ECG location of ST-segment deviation, this report focuses only on ECG localization of the QRS-complex abnormalities indicative of established MI as depicted by cardiac magnetic resonance (CMR) imaging. Although attempts to standardize the terminology applied to the LV walls have been reported,19,20 differences persist among the terms used by anatomists, pathologists, electrocardiographists, cardiac imagers, and clinicians. However, the pathologist’s view of infarcted myocardium lacks insights into the in vivo positioning of the LV walls. CMR imaging with delayed contrast enhancement (CE-CMR) has emerged as a new anatomic …

Background Myocardial salvage is most likely to occur when thrombolytic therapy is administered within 4 to 6 hours of the onset of symptoms of myocardial infarction. The impact of delays within this early time period on final myocardial infarct size are unknown. The purpose of this study was to quantitate the relation between final myocardial infarct size and duration of symptoms before initiation of thrombolytic therapy in patients treated within 6 hours of symptom onset. Methods and Results The findings from patients in four prospective randomized trials of thrombolytic therapy were combined for analysis. The study population consisted of 432 patients presenting within 6 hours of onset of symptoms of first acute myocardial infarction who met ECG criteria that allowed estimation of myocardial area at risk before treatment with thrombolytic therapy and who had thallium-201 myocardial infarct–size measurements performed several weeks after infarction. ECG analysis revealed no difference in myocardium at risk for infarction as a function of duration of symptoms before initiation of thrombolytic therapy. In contrast, univariate and multivariate analysis showed that final infarct size was highly dependent on duration of symptoms before initiation of therapy. Each 30-minute increase in symptom duration before thrombolytic therapy was associated with an increase in infarct size of 1% of the myocardium. Final infarct size in patients treated 4 to 6 hours after symptom onset was indistinguishable from patients who did not receive thrombolytic therapy. Conclusions These findings suggest that for patients treated within 4 to 6 hours of the onset of symptoms, there is a progressive decline in the extent of myocardium salvaged as the duration of symptoms before therapy increases. These results support efforts to minimize the time delay between symptom onset and initiation of reperfusion therapy in all eligible patients.

The detection and assessment of cardiac chamber hypertrophy has long been an important objective of clinical electrocardiography. Its importance has increased in recent years with the recognition that hypertrophy can be reversed with therapy, and that by doing so, adverse clinical outcomes can be

Background : Myocardial scarring from infarction (MI) or nonischemic fibrosis forms an arrhythmogenic substrate. The Selvester QRS-score estimates MI size by quantifying changes in Q-, R- and S-wave durations, amplitudes and morphologies from the 12-lead electrocardiogram (ECG). It provides 32 possible points with each point reflecting scarring of 3% of the left ventricle (LV). Although QRS scoring has been extensively validated for estimating MI scar size in the absence of ECG confounders, it has not been validated in patients with left ventricular hypertrophy (LVH), fascicular/bundle branch blocks or nonischemic scar. We assessed the hypotheses that QRS-scores (modified for each conduction type) correctly identify and quantify both ischemic and nonischemic scar as compared to the reference standard of Cardiac Magnetic Resonance - Late Gadolinium Enhancement (CMR-LGE) and QRS-estimated scar size is associated with inducible sustained monomorphic ventricular tachycardia (MVT) during electrophysiologic (EP) testing. Methods and Results: A prospective 162 patient cohort with LV dysfunction (95 ischemic, 67 nonischemic) received 12-lead ECG and CMR-LGE before defibrillator (ICD) implantation for primary prevention of sudden cardiac death. QRS-scores correctly diagnosed CMR-scar presence with receiver operating characteristics (ROC) area under the curve (AUC)=0.91 and correlation for scar quantification of r=0.74, p Conclusions : Compared to CMR, QRS-scores identify and quantify MI and nonischemic scar despite ECG confounders. Higher QRS-estimated scar size is associated with increased arrhythmogenic potential and warrants further study as a risk-stratifying tool for patients with left ventricular dysfunction.

Background— Primary percutaneous coronary angioplasty is an effective and widely adopted treatment for acute myocardial infarction. A simple method of determining prognosis after primary percutaneous coronary intervention (PCI) would facilitate appropriate care and expedite hospital discharge. Thus, we determined the prognostic importance of various measures of ST-segment–elevation recovery after primary PCI in a large, contemporary cohort of patients with ST-elevation myocardial infarction. Methods and Results— We analyzed ECG data describing the magnitude and extent of ST-segment elevation and deviation before and early after (ie, 30 minutes) primary PCI in the study cohort of 4866 subjects with electrocardiographically high-risk ST-elevation myocardial infarction enrolled in the Assessment of PEXelizumab in Acute Myocardial Infarction (APEX-AMI) trial. Associations among 6 methods for calculating ST-segment recovery, biomarker estimates of infarct size (ie, peak creatine kinase, creatine kinase-MB, and troponin I and T), and prespecified clinical outcomes (ie, rates of 90-day death and 90-day death, heart failure, or shock) were examined. All ST-segment–recovery methods provided strong prognostic information regarding clinical outcomes. A simple ST-segment–recovery method of residual ST-segment elevation measurement in the most affected lead on the post-PCI ECG performed as well as complex methods that required comparison of pre- and post-PCI ECGs or calculation of summed ST-segment deviation in multiple leads (ie, worst-lead residual ST elevation: adjusted hazard ratio for 90-day death rate [reference Conclusions— An ECG performed early after primary PCI is a simple, widely available, inexpensive, and powerful prognostic tool applicable to patients with ST-elevation myocardial infarction.

Background: The potential for salvage of jeopardized myocardium during coronary occlusion decreases as the duration of persistent ischemia is prolonged. Thus, it is important to be able to assess the acuteness of ischemia as a patient presents with signs of acute coronary syndrome. The aim of this study was to compare ECG estimate of ischemic acuteness and time from pain onset for predicting myocardial salvage in patients with first-time myocardial infarction (MI). Methods: Thirteen patients with acutely revascularized first-time MI were studied. All patients had 99mTc tetrofosmin injected and an ECG recorded prior to the PCI. TIMI III flow was obtained in all patients. Single photon emission computed tomography (SPECT) was undertaken within 3 hours of the PCI to assess the myocardium at risk (MaR). Delayed contrast-enhanced magnetic resonance imaging (DE-MRI) was performed 1 week after admission for assessment of infarct size (IS) and infarct transmurality (IT). A salvage index was calculated as (MaR-IS)/MaR. The acuteness of ischemia was estimated both from patient history and from the Anderson-Wilkins (AW) acuteness score of the pre-PCI ECG. Results: The figure shows the relationship between time of symptom onset and salvage index (A) and IT (C) as well as the relationship between AW acuteness score and salvage index (B) and IT (D). The time of symptom onset did not correlate with salvage index or IT. The AW acuteness score, however, showed a significant relationship with both salvage index and IT. Conclusions: The initial ECG changes are superior to time from symptom onset to PCI for predicting myocardial salvage and IT in patients undergoing PCI of first-time MI.

This statement examines the relation of the resting ECG to its technology. Its purpose is to foster understanding of how the modern ECG is derived and displayed and to establish standards that will improve the accuracy and usefulness of the ECG in practice. Derivation of representative waveforms and measurements based on global intervals are described. Special emphasis is placed on digital signal acquisition and computer-based signal processing, which provide automated measurements that lead to computer-generated diagnostic statements. Lead placement, recording methods, and waveform presentation are reviewed. Throughout the statement, recommendations for ECG standards are placed in context of the clinical implications of evolving ECG technology.

Background —Although the stratification of patients with myocardial infarction into ECG subsets based on the presence or absence of new Q waves has important clinical and prognostic utility, systematic evaluation of the impact of thrombolytic therapy on the subsequent development and prognosis of non–Q-wave infarction has been limited to date. Methods and Results —We examined 12-lead ECG, coronary anatomy, left ventricular function, and mortality among 2046 patients with ST-segment elevation infarction from the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries angiographic subset to gain further insight into the pathophysiology and prognosis of Q- versus non–Q-wave infarction in the thrombolytic era. Non–Q-wave infarction developed in 409 patients (20%) after thrombolytic therapy. Compared with Q-wave patients, non–Q-wave patients were more likely to present with lesser ST-segment elevation in a nonanterior location. The infarct-related artery in non–Q-wave patients was more likely to be nonanterior (67% versus 58%, P =.012) and distally located (33% versus 39%, P =.021). Early (90-minute, 77% versus 65%, P =.001) and complete (54% versus 44%, P P P =.0001). In-hospital, 30-day, 1-year, and 2-year (6.3% versus 10.1%, P =.02) mortality rates were lower among non–Q-wave patients. Conclusions —The excellent prognosis among the subgroup of patients who develop non–Q-wave infarction after thrombolysis is related to early, complete, and sustained infarct-related artery patency with resultant limitation of left ventricular infarction and dysfunction.

This report represents our experience with 522 consecutive patients with acute myocardial infarction admitted directly to the Duke Coronary Care Unit. Fifty items of information were used to characterize the patients, their hospital course and follow-up. Serious complications included death, ventricular tachycardia or fibrillation, second- or third-degree heart block, pulmonary edema, cardiogenic shock, persistent sinus tachycardia or hypotension, atrial flutter or fibrillation, and extension of infarction. Forty-nine percent of the patients (252 of 522) experienced a serious complication. All patients who experienced any serious complications had at least one of the above during the first four days of hospitalization. Patients who survived through day 4 were subgrouped on the basis of the occurrence (complicated) or lack of occurrence (uncomplicated) of the above on day 5. Complicated patients had a subsequent hospital mortality of 14% and an incidence of late serious complications of 51%. Patients who were uncomplicated through day 4 had a subsequent hospital mortality of zero and an incidence of late serious complications of zero. These data suggest that it would be feasible and ethically justified to conduct a prospective clinical trial of early discharge (7th day) in patients who meet the above criteria for uncomplicated. The potential economic savings through earlier discharge in uncomplicated patients are of major significance.

This retrospective study correlates electrocardiographic and histopathologic findings in 24 patients with single well-circumscribed infarcts to determine 1) whether ECG terms commonly used to describe the location of myocardial infarcts are significant, and 2) whether the extent of infarct can be determined using QRS characteristics. Transverse sections of the hearts were photographed. Based on histologic sections, the infarct was outlined on the photograph and each section was planimetered via a sonic digitizer into a computer that was programmed to divide the left ventricle into 8 radial sectors and also into basal, mesial, and apical thirds. The percentage of infarct in each of these areas was then calculated. Of the 24 hearts evaluated 12 had posterior infarcts and 12 had anterior infarcts. Posterior infarcts principally involved the basal and mesial levels, whereas the anterior infarcts were more extensive in the apical and mesial thirds, with relative or total sparing of the base. Posterior infarcts were associated with Q waves in leads II, III and aVF in 11 instances. The other posterior infarct was associated with markedly diminished R waves in leads II, III and aVf in the presence of a horizontal axis. All anterior infarcts were associated with Q waves or markedly diminished R waves in the right precordial leads. Eight of the anterior infarcts exhibited circumferential apical involvement and all eight were associated with Q waves or markedly diminished R waves in the left precordial leads. This study documents the electrocardiographic identification of anterior, posterior, and apical infarcts by correlation with pathologic anatomy.

We evaluated a simplified version of a previously developed QRS scoring system for estimating infarct size using observations of Q- and R-wave durations and R/Q and R/S amplitude ratios in the standard 12-lead ECG. Groups of subjects with a minimal likelihood of having myocardial infarcts and minimal likelihood of having common noninfarction sources of QRS modification were studied to establish the specificity of each of the 37 criteria. Only two criteria required modification to achieve 95% specificity. These 37 criteria form the basis of a 29-point QRS scoring system. A 98% specificity was achieved when a score of more than 2 points was required to identify a myocardial infarct. Fifty patients were studied to determine the intra- and interobserver agreement with this scoring system. Each criterion achieved at least 91% intra- and interobserver agreement. These impressive levels of specificity and observer agreement must be matched by high sensitivity of the scoring system and a good correlation between the point score and infarct size in patients with proven infarcts if the point score is to be useful for detecting and sizing infarcts. Sensitivity and correlation between point score and infarct size are evaluated in later studies in this series. The standard ECG is inexpensive and can be obtained repetitively and noninvasively; its QRS complex may be an important means of estimating the size, presence and location of myocardial infarcts.

Frank-lead vectorcardiograms (VCGs) and standard 12-lead electrocardiograms (ECGs) were analyzed to develop simple, linear, quantitative criteria for the diagnosis of right ventricular hypertrophy (RVH). The study subjects included a population with a definite RVH (84 patients with mitral stenosis proved by cardiac catheterization and pulmonary arterial systolic pressure > 40 mm Hg) and a population with minimal likelihood of RVH (173 young, healthy volunteers and 151 normal subjects proved by cardiac catheterization). VCGs were evaluated to identify criteria that provided maximum sensitivity and at least a 95% specificity: the maximum QRS magnitude had to be < 1.8 mV and either (1) the amplitude at -45 degrees (transverse plane) had to be < 0.3 mV or (2) the maximum anterior amplitude plus the maximum rightward amplitude minus the amplitude at -45 degrees must be greater than or equal to 0.5 mV. Application of these criteria achieved 60% (50 of 84) sensitivity in patients with RVH, similar to that for previous VCG criteria but significantly better (p < 0.01) than the best sensitivity with any ECG criteria (27%, 23 of 84). The specificity of the proposed criteria was 96% (310 of 324), significantly better (p < 0.001) than the 78% specificity (252 of 324) of existing VCG criteria. Thus, linear measurements of the QRS complex displayed on the VCG identify 60% of patients with moderate-to-severe RVH and falsely indicate RVH in only 4% of normal subjects.

Two hundred and five patients who received a total of 247 electrode systems-129 transvenous, 68 transmediastinal and 50 transthoracic-are compared after complete uniform two-year follow-up. The transvenous patients had low hospital morbidity (19%) and short hospital stays (75% ≤ 8 days) but a high incidence of electrode failure by 24 months (38%). The transmediastinal and transthoracic patients had more hospital complications (35% and 34%) and longer periods of hospitalization (57% and 70% > 8 days) but fewer instances of failure by 24 months (16% and 11%). Most transvenous electrode failures were secondary to dislodgement. Transmediastinal right epicardial electrodes had the unique problem of threshold elevation and failure between six and 12 months after implantation as well as a high incidence of sudden death in this same period. Although the high incidence of endocardial electrode instability dictates the need for an alternative approach to permanent pacing, the failure of the transmediastinal approach to significantly alter postoperative morbidity (as compared with transthoracic electrodes) and the incidence of threshold elevation remote from right ventricular implantation suggest that limitation of thoracotomy (via the transmediastinal approach) should not take precedence over left ventricular implantation. Development of electrodes which would provide more permanent low resistance fixation to right ventricular endocardium or epicardium may be necessary before the transthoracic approach can be abandoned.

The indication for prophylactic temporary and permanent pacing during acute myocardial infarction (MI) complicated by bundle branch block is high risk of progression via a Type II pattern to second or third degree (high degree) AV block during hospitalization or follow-up. In this study, determinants of high degree AV block during hospitalization and sudden death or recurrent high degree block during the first year of follow-up were examined in 432 patients with MI and bundle branch block. Timing of onset of bundle branch block, the involved fascicles, and the PR interval were examined as determinants of risk of progression to high degree AV block during MI. At highest risk were 186 patients with blocks involving the right bundle and at least one fascicle of the left bundle which were not documented on prior electrocardiograms. Risk was similar with (38%) or without (31%) accompanying first degree AV block. Patients with transient high degree AV block during MI had a 28% incidence of sudden death or recurrent high degree block during the first year of follow-up. Patients not continuously paced had a higher incidence of sudden death or recurrent high degree block than patients continuously paced (65% vs 10%, P less than 0.001). Sudden death during follow-up also occurred in 13% of patients without high degree block during MI. A subgroup with 1) documented prior MI, 2) anterior or indeterminant acute MI, and 3) no symptoms of cardiac failure had a 35% risk of sudden death. The role of permanent pacing in this group is unknown. Thus, patients at high risk of high degree AV block should receive prophylactic temporary pacing. Patients who survive high degree block with MI should receive temporary and then permanent pacing. Patients without high degree AV block during MI who nervertheless have a high risk of sudden death may benefit from permanent pacing.

Vectorcardiograms (VCG) from a consecutive group of 77 patients with significant aortic valve disease were analyzed. All of the patients had complete left and right heart catheterization with normal coronary arteriograms and normal left ventricular contraction. Thirty-five (46%) patients met VCG criteria for anterior myocardial infarction (AMI-35%) and/or inferior myocardial infarction (IMI-14%). This was a significant increase in false positive diagnosis for both criteria compared to a group of 200 normal volunteers under age 30 and 100 patients with normal hearts by cardiac catheterization (P less than 0.01). It was found that if the VCG diagnosis of myocardial infarction was deferred when the maximal transverse plane magnitude was greater than 1.9 mV, the incidence of AMI false positive diagnosis decreased to 3% and the incidence of IMI false positive diagnosis decreased to 1%. The same rule was applied to the aortic valve disease cohort, a group of 124 patients with documented AMI and a group of 158 patients with IMI. This decreased the sensitivity of the AMI criteria from 93 to 83% and of the IMI criteria from 85 to 77%. The increase in average performance was statistically significant fro the AMI criteria (P less than 0.05) but not for the IMI criteria.

Ventriculograms made 9-15 months after surgery in 48 patients with normal preoperative apical contraction were reviewed to determine the influence of apical venting on apical wall motion in patients undergoing coronary bypass surgery. After interpretation of postoperative apical wall motion, the patients were subdivided into two groups. One group consisted of 34 patients who were vented by inserting a catheter through the apex of the left ventricle and the second group included 14 patients in whom no transventricular vent was made. The two groups were similar clinically and hemodynamically before surgery, and the surgical procedures were similar with the exception of vent site. Following surgery, incidences of graft patency and antegrade flow to the apex were also similar. Nineteen (56%) patients in the apically vented group had apical dyskinesia or akinesia observed on the postoperative ventriculogram while none of the patients who were not apically vented had these findings. None of the patients with apical dyskinesia or akinesia had congestive heart failure following surgery. The postoperative ventriculograms of 12 patients with mitral stenosis who underwent valvulotomy by inserting a Tubbs dilator through the apex were also analyzed. Only one patient (8.5%) had apical dyskinesia or akinesia. Since the patients with mitral stenosis probably did not have significant coronary artery disease, it is possible that the combination of the apical vent and ischemic heart disease was responsible for the focal contraction abnormalities observed.

The electrocardiograms of 538 patients with acute myocardial infarction were searched to identify all instances of atrioventricular (A-V) and intraventricular (I-V) conduction disturbances. Data concerning mode of therapy and clinical complications were obtained by review of the record. These variables were then analyzed for significance in relation to the development of type II A-V block acutely and syncope or sudden death during the first year of follow-up. The most accurate predictor for both these events was the status of A-V conduction in combination with the status of I-V conduction. At highest risk (50%) for type II progression were patients with acute adjacent fascicular block plus P-R prolongation, i.e., left anterior hemiblock plus right bundle-branch block (RBBB), or left bundle-branch block (LBBB), or patients with acute nonadjacent fascicular block, i.e., RBBB plus left posterior hemiblock or alternating bundle-branch block. The nonpaced survivors from this same group, plus any other patients with transient type II progression, were also at high risk (45%) for syncope or sudden death in follow-up. No syncope or sudden death has occurred in seven patients with type II progression discharged with a pacemaker. All other patients were at lower risk for these acute and chronic complications. Thus, the electrocardiogram in acute myocardial infarction can identify a high-risk group for acute type II progression in whom prophylactic pacer insertion may be beneficial. Similarly, the electrocardiogram can identify a high-risk group for syncope or sudden death in follow-up and implicates progression to higher degrees of A-V block as an important pathophysiologic mechanism.The possible role of permanent pacemaker therapy in preventing syncope or sudden death in this high-risk group is also suggested.

Twice-daily CPK-MB determinations were performed but not made availabe to the physicians of 179 consecutive patients with precordial pain admitted to a community hospital to evaluate the diagnostic importance of this isoenzyme. Physician decision was based upon history and once-daily ECG and total enzymes (CPK, SGOT, LDH). Following hospital discharge, each patient's clinical record was reviewed to determine the physician diagnostic decision. The patients were subdivided into three groups. The first group consisted of 46 patients with diagnostic QRS changes and elevated total enzymes. All 46 had physician diagnosis of acute myocardial infarction and CPK-MB was present in 44 (96%). The second group included 55 patients with nondiagnostic QRS but elevated total enzymes. Physician diagnosis was acute myocardial infarction in 28 (51%) but 16 (57%) of these had no CPK-MB. The third group contained 50 patients with nondiagnostic QRS and normal enzyme levels. Six (12%) had physician diagnosis of acute myocardial infarction but none had CPK-MB. Thus, absence of CPK-MB failed to confirm physician diagnosis of acute myocardial infarction when based upon history and total enzymes in the absence of QRS changes in 22 of 34 (65%) patients.

To provide an understanding of the clinical characteristics of patients with acute myocardial infarction (MI) and bundle branch block, experience from five centers was accumulated. Patients in whom bundle branch block first appeared after the onset of cardiogenic shock were excluded. In 432 patients, the most common types of block were left (38%) and right with left anterior fascicular block (34%). In 42% of the patients, bundle branch block was new. Progression to high degree (second or third degree) atrioventricular (AV) block via a Type II pattern occurred in 22% of the patients. Hospital and first year follow-up mortality rates were 28% and 28%, respectively. Only 46% of the patients developed pulmonary edema or shock (Killip Class III or IV), and hospital mortality was related to the amount of heart failure (8%, 7%, 27%, 83% for Killip Classes I-IV, respectively). Patients with progression to second degree or third degree AV block via a Type II pattern had increased hospital mortality compared with patients without this complication (47% vs 23%, P less than 0.001). In the absence of pulmonary edema or shock, patients with Type II second degree or third degree AV block still had a higher mortality rate than patients without advanced AV block (31% vs 2%, P less than 0.005), with nearly all the deaths due to abrupt development of AV block. Thus, in many patients MI with bundle branch block is associated with severe heart failure. However, this was not true for a majority of the patients, in whom therapy aimed at preventing morbidity and mortality due to the bradyarrhythmia of advanced AV block might be beneficial.

The epicardial activation sequence of 34 patients with the Wolff-Parkinson-White syndrome was determined. Epicardial pre-excitation occurred at a spectrum of sites over either the free wall of the left or right ventricle or in a paraseptal region, always adjacent to the atrioventricular rings. The site of pre-excitation was related to the spatial position of the 10 msec vector of the vectorcardiogram (VCG) in 15 patients and the 20 msec vector of the electrocardiogram (ECG) in 29 patients with a single accessory pathway. All patients whose 20 msec vector (ECG) was directed to the right had accessory pathways which caused epicardial breakthrough over the free wall of the left ventricle. When the 20 msec vector (ECG) was to the left and inferior, epicardial pre-excitation was over either the right ventricular free wall or in the region of the pulmonary outflow tract. Superior location of the initial forces, especially the 10 msec vector (VCG), strongly suggested the presence of a septal bypass tract. The polarity of the delta wave and maximum QRS forces in precordial lead V1 were discordant in a significant number of patients, pointing to probable shortcomings of a classification based upon the latter.

This study was performed to determine the relationships among angiographic, hemodynamic, clinical, and electrocardiographic data and premature ventricular contractions (PVCs). Arrhythmias were analyzed by 24 hour Holter monitor in 244 patients evaluated for chest pain by coronary angiography and left ventriculography. Using a categorical linear model, the presence of myocardial fibrosis as indicated by both abnormal left ventricular contraction (LVC) and abnormal initial QRS on electrocardiogram was found to be the only independent predictor of both frequent and complex ventricular arrhythmias (P less than .0001). All other descriptors, including the number of diseased vessels (greater than or equal to 75% obstruction), were dependent upon abnormal LVC in their association with PVCs. When the right anterior oblique view of the left ventriculogram was divided into nine segments to allow automated quantiative analysis of LVC, the prevalence of frequent PVCs was directly related to the number of abnormally contracting segments. Of patients with 0 abnormal segments, 11% had greater than or equal to 2 PVC/hr, in contrast to 44%, 73% and 100% of patients with 1-3, 4-6, and 7-9 abnormal wall segments, respectively (P less than 0.01). A similar quantitative relationship was found between premature ventricular contractions and abnormal initial forces indicating previous myocardial infarction on the electrocardiogram.

Vectorcardiograms (VCG) from two patient groups were analyzed to develop and test quantitative criteria for the diagnosis of inferior myocardial infarction. The first group (219 patients) consisted of four subgroups and was used to develop the criteria. Patients were placed in the normal and infarct subgroups by clinical descriptors including history, course in the coronary care unit, and cardiac catheterization findings. The criteria which were found to give the fewest false positive results with acceptable sensitivity were as follows: In the frontal plane, generally clockwise early superior QRS forces must be present, i.e., forces which are initially either a) superior (rightward or leftward) or b) inferior and completely rightward for not more than 10 msec prior to becoming superior, and which subsequently cross the X axis to the left of the 0 point (or less commonly, the entire efferent limb remaining superior to the X axis). One of the following conditions must also be present: 1) Time from the 0 point to leftward X intercept of at least 25 msec and distance from the 0 point to leftward X intercept of at least 0.30 mV; 2) A maximal frontal plane QRS vector less than 15°; 3) A maximal superior deviation of at least 0.1 mV and a ratio of maximal superior deviation to maximal inferior deviation of at least 1:5. The performance of these proposed criteria were then tested prospectively using a second group (255 patients) which was similar to the criteria group. The proposed criteria were found to be statistically superior to both ECG Q wave criteria and to the VCG initial force criteria of Young and Williams. 2 The incidence of false positive diagnosis in the test group was less than 3%.

This report evaluates the morbidity and mortality, during hospitalization and follow-up, of a subgroup of patients with posterior or diaphragmatic myocardial infarction (PDMI) who developed high degree A-V block via a type I mechanism and in the absence of power failure (pulmonary edema or cardiogenic shock). This subgroup was not at any higher risk of hospital morbidity, hospital mortality, or 1-year mortality than three other groups: (a) patients with PDMI but neither high degree A-V block nor initial power failure; (b) patients with other infarct sites who developed high degree A-V block in the absence of power failure; and (c) patients with other infarct sites but neither high degree A-V block nor initial power failure. The significance of subgrouping patients with high degree A-V block by the quantity of clinical heart failure is exemplified by a review of the literature and the present study.

Routine enzymatic and electrocardiographic diagnosis of postoperative acute myocardial infarction (AMI) is frequently inconclusive. The detection and quantitation of isoenzymes of lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), especially the cardiac-specific CPK-MB isoenzyme, have allowed earlier recognition of AMI in nonsurgical patients. Serial monitoring with these methods has been utilized during the postoperative period in 20 noncardiac surgical patients and 100 patients undergoing coronary artery bypass grafting (CABG). In the noncardiac surgery group, both isoenzymes were accurate in diagnosing AMI in the early postoperative period. Of the 100 patients in the CABG group, CPK-MB appearance in 21 correlated with AMI by electrocardiogram. The absence of CPK-MB postoperatively in 49 patients permitted a 73% incidence of new ECG abnormalities to be effectively resolved. Autopsy confirmation of AMI was obtained in two patients with nondiagnostic ECG, but with elevated CPK-MB. The elevated CPK-MB without ECG evidence of AMI in the remaining patients could possibly be explained by varying degrees of myocardial damage produced by intraoperative cardiac manipulation. These data demonstrate the value and sensitivity of CPK-MB isoenzyme determinations in the early recognition of postoperative acute myocardial infarction.

Recurrent supraventricular tachycardia is a frequent complication in patients with the Wolff-Parkinson-White (WPW) syndrome. Our patient was unusual in that the arrhythmia was the predominant rhythm, and it was felt that the sustained tachycardia was responsible for signs and symptoms of congestive heart failure. The arrhythmia could not be controlled adequately with digitalis, quinidine, diphenylhydantoin, or propranolol. Atrial or ventricular pacing also failed to prevent recurrent episodes of tachycardia. Physiological and pharmacological studies suggested that an anomalous pathway was responsible for the WPW abnormality and participated in a re-entrant circuit which sustained the episodes of tachycardia. Isopotential body surface mapping suggested anomalous ventricular excitation at the lateral aspect of the right atrioventricular groove. Epicardial mapping at the time of surgery was used to localize the earliest area of anomalous ventricular activation, and surgical transection of the atrioventricular junction at that point abolished the electrocardiographic features of WPW and the recurrent tachycardia. Five months after surgery neither the ECG features of WPW nor the tachycardia has recurred. The signs and symptoms of congestive heart failure have subsided, and the patient has returned to work.

The specificity of serum CPK-MB for acute myocardial infarction was examined by retrospective analysis of 401 consecutive patients admitted to Coronary Care Unit over a three and one-half year period with suspected infarction in whom the isoenzyme was subsequently detected. Four patients (1 per cent) who died during the hospital admission had no autopsy evidence of acute myocardial infarction. All four had experienced mild iatrogenic cardiac trauma, following which serum CPK-MG persisted for at least 24 hours. In one patient, a permanent pacemaker had been inserted by the transmediastinal approach. Two patients had been subjected to closed chest cardiac massage and intracardiac puncture, and one to external cardiac massage alone. The findings suggest that persistent identification of serum CPK-MB, although specific for myocardial necrosis, cannot be regarded as diagnostic of myocardial infarction. The implications of this are important to treatment of patients after cardiopulmonary resuscitation and operative trauma to the heart.