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The present article introduces the second part of “Recommendations for Standardization and Interpretation of the Electrocardiogram.” The project was initiated by the Council on Clinical Cardiology of the American Heart Association and has been endorsed by the American College of Cardiology

The present article is the fourth in a series of 6 documents focused on providing current guidelines for the standardization and interpretation of the electrocardiogram (ECG). The project was initiated by the Council on Clinical Cardiology of the American Heart Association. The rationale for this

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.

A plea is made for not using in publications the terms J-wave syndromes and early repolarization until such terms are properly defined by appropriate task forces established by recognized authorities. The currently used electrographic terminology, including J-point elevation, meets our needs.

“Life must be lived forward, butunderstood backward.” KierkegaardFor the pat 50 years, I have been an active witness to the scientific developments defining our knowledge of cardiac arrhythmias. This era spans a time period from the formulation of ionic theory of membrane excitation by Hodgkin and Huxley (Nobel prize, 1963) to the understanding of the relation between structure and function of single channels (Nobel prize to Neher and Sakmann, 1991) . From practical point of view, I would like to break down my presentation into 3 parts, the first dealing with successes, the second with failures, and the third, a brief venture into future promises.

(1) Dispersion of QT intervals is the difference between the longest and the shortest QT interval in the ECG. Owing to the relative ease of measurement and the perceived need for new markers of arrhythmogenicity, the method has attracted the interest of clinical investigators but has not reached the level of practical utility. (2) It is postulated that to pass the test of practical utility, the method must meet the following criteria: (a) standardization; (b) establishment of normal values; (c) established sensitivity and/or specificity for diagnosis and/or prognosis; and (d) uniqueness of relevant information. (3) Analysis of the data from the literature suggests that standardization of the method and the range of normal values have not been established, and that the method lacks specificity for separating healthy persons from patients with heart disease. (4) Large values, such as average QT dispersion > 65 msec, have been found predominantly in patients with serious, life-threatening ventricular tachyarrhythmias, and the largest values, i.e., > 110 msec in patients with congenital long QT syndrome. (5) The prognostic value of QT dispersion has been disputed, and the uniqueness of the relevant information has not been tested. (6) It is concluded that the acceptance of QT dispersion as a useful test in practice faces manifold and serious obstacles. It remains to be established whether these obstacles are insurmountable.

(1) Ventricular preexcitation causes both secondary and primary T wave changes. The secondary changes disappear immediately after cessation of preexcitation (ablation of accessory pathways) and unmask the primary T wave changes that regress within days, weeks, or months. (2) The pattern of primary T wave change produced by ventricular preexcitation depends on the location of the accessory pathway connections. The septal and posterior connections are associated with more prominent anteriorly directed T wave deflections and deviation of the T wave vector superiorly. The left lateral connections are associated with rightward deviation of the T wave vector in the frontal plane. (3) The primary T wave abnormalities are believed to be caused by local lengthening of repolarization, but the site of the postulated abnormalities needs to be established. (4) The persistence and slow dissipation of the primary T wave change induced by ventricular pacing, left bundle branch block, and presumably ventricular preexcitation have been attributed to the memory of past events. The nature of these events is not known. Several in vitro models demonstrated phenomena of gradual adjustment of ventricular action potential duration to change in cycle length, or to altered pattern of stimulation, but none of such models has mimicked the long-lasting regression of T wave abnormalities. (5) The terms T wave memory and pseudoprimary repolarization changes lack specificity and are unnecessary additions to the electrocardiographic vocabulary.

In the 2001 edition of the textbook Heart Disease [(1)][1]Brugada syndrome is defined as a “distinct form of idiopathic ventricular fibrillation (VF) in which patients have right bundle branch block (RBBB) and ST elevation in the anterior precordial leads without evidence of structural heart

A plea is made for not using in publications the terms J-wave syndromes and early repolarization until such terms are properly defined by appropriate task forces established by recognized authorities. The currently used electrographic terminology, including J-point elevation, meets our needs.

We describe pathological abnormalities in a 72-year-old male member of a family with a congenital absence of sinus rhythm and a tendency to develop atrial fibrillation at an early age, and in a 54-year-old female member of a family with cardiomyopathy and progressive conduction system disease manifested by first-degree atrioventricular (AV) block, left bundle branch block, and atrial arrhythmias. Both patients died suddenly. The absence of sinus rhythm in case 1 could be explained by marked atrophy, degeneration, and isolation of the sinoatrial (SA) node. The SA node was also diseased in the member of the other family with atrial arrhythmias. Additional common features in both cases included: fatty metamorphosis and degenerative changes of the approaches to the SA node, the atrial preferential fibers, and the approaches to the AV node, a small AV node, degenerative changes of the bundle branches, and floppy AV valves. These findings show that the pathological substrate of familial supraventricular arrhythmias consists of a diffuse involvement of the entire conduction system, bearing resemblance to pathological findings in elderly subjects with acquired sick sinus syndrome.

Objectives . The purpose of this review is to assemble the widely dispersed information about cardiac alternans and to categorize the types and mechanisms of alteraans, their clinical manifestations and possible therapeutic implications. Background . The phenomena of mechanical and electrical alternans have been of continuing interest to both physiologists and clinicians. Recent studies have enhanced this interest because of the reported association of alteraans with experimental myocardial ischemia and cardiac arrhythmias. Methods . The review formulates concepts based on extensive review of published studies and personal observations. Results . Cardiac alternans has been subdivided info the following four categories: 1) mechanical, 2) electrical, 3) in association with myocardial ischemia, and 4) in association with cardiac motion. Mechanical alternans can be explained by hemodynamic or inotropic alterations, or both. Mechanical alternans in the ventricular muscle is accompanied by alternans of action potential shape. In the Purkinje fibers, action potential duration alternates without change in shape and is determined by the duration of the preceding dlastoiic interval. However, in ventricular muscle fiber, alternans can occur in the presence of constant diastolic intervals. T wave alternans reflects changes in action potential duration and is frequently associated with a long QT interval. Electrocardiographic manifestations of conduction alternans occur at many different sites within the conducting system and myocardium. During myocardial ischemia, additional mechanisms of repolariztion alternans have been proposed. Alternans occurring in the presence of a large pericardial efusion is attributed to swinging motion of the heart maintaining two-beat periodicity. Conclusions . Since its origin as “pulsus alternans” described by Traube in 1872, the definition of alternans has evolved into a term encompassing multiple physiologic and pathologic phenomena that, although united by the term cardiac alternans, diverge widely with respect to etiology, mechanism aid clinical significance.

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

I have outlined the approach to therapy of supraventricular tachyarrhythmias practiced by a cardiologist who is not performing special studies in the cardiac electrophysiology laboratory. This review includes the list of common and rare supraventricular arrhythmias, application of diagnostic noninvasive procedures, indications for referral for special electrophysiologic studies, and brief description of drugs and procedures used in the therapy of supraventricular tachyarrhythmias. In addition to general guidelines for treatment of these arrhythmias, I have outlined specific recommendations for patients with acute myocardial infarction, angina pectoris, ventricular dysfunction and congestive heart failure, obstructive cardiomyopathy, hyperthyroidism, AV accessory pathways, chronic obstructive lung disease, diabetes mellitus, hypertension, concomitant ventricular arrhythmias, tachycardia-bradycardia syndrome, and anxiety.

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.

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.

ObjectivesThis study was designed to establish the cause of electrocardiographic (ECG) pattern differences between genders.BackgroundThe male and female patterns of early ventricular repolarization in normal ECGs differ from each other. The male pattern displays a higher J-point amplitude and increased ST angle. The distribution of these patterns between genders has not been studied.MethodsNormal ECGs of 529 males and 544 females, age 5 to 96 years, were subdivided into nine age groups in each gender. We designated the pattern as female if the J point was

Torsade de pointes(Tdp)is a polymorphic ventricular tachycardia(VT)in which the axis of the QRS complex changes direction after a certain number of complexes as if the complex rotated around the baseline. Tdp is usually associated with QT prolongation and dispersion of ventricular repolarlization(DR). Experimental models of tdp are usually associated with induction of early after depolarizations(EADs). Several aspects of the pathogenesis of tdp are incompletely understood. The purpose of this article is to propose the directions in research that may increase our current understanding of the factors responsible for tdp. The most plausible hypotheses requiring further supporting evidence are :1 . The occurrence of tdp requires the presence of DR i.e. tdp does not occur in the absence of DR .2 . EADs appear to play an important role as a trigger to tdp in the animal models but more evidence are needed at the clinical level. 3. EADs may be responsible for arrhythmias other than tdp. 4. The greater incidence of tdp in the females than in tha males may be attributed to differences in the duration of the QT interval and different morphology of the ST‑segment and the T‑wave. The above gender differences may be caused by the effects of gonadal hormones which modulate some of the membrane currents flowing during early ventricular repolarization. (J Nippon Med Sch 2002; 69: 218―223)

Reversible QRS complex changes associated with ST-segment shift during acute myocardial ischemia (AMI) have been reported sporadically in isolated cases or in small patient groups but have not been analyzed systematically in a sizable cohort of patients. During the past 4 years, a purposeful search was made for electrocardiograms with documented reversible QRS changes associated with all acute injury pattern. The measured variables included distribution of leads with ST-segment deviation and reciprocal ST-segment depression, magnitude of the ST-segment shift, amplitude and direction of the initial and terminal QRS deflections, QRS duration, QTc duration, and U wave amplitude. Reversible QRS changes encountered in 29 patients with AMI included new Q waves (n = 3), decreased Q amplitude (n = 2), QS change to qRS or qR (n = 6), disappearance of QS or Q (n = 4), increased R amplitude (n = 9), decreased R amplitude (n = 6), increased S amplitude by more than 75% (n = 18), and increased QRS duration (n = 4). Changes in the initial configuration were present in 24 of the 29 patients. Reversible changes of the terminal QRS portion occurred in all 29 patients, and reversible changes of the initial QRS portion occurred in 23 (79%), whereas QRS duration increased in 4 patients. Reversible QRS changes during AMI are attributed to passive pull by the ST-segment shift and intraventricular conduction disturbance.

Objectives. The purpose of the study was to describe the configuration, and investigate the mechanisms, of QRS changes occurring during percutaneous transluminal coronary angioplasty (PTCA). Background. QRS changes during PTCA have been attributed to both a passive ST segment shift and conduction disturbances (peri-ischemic block). The direct relation between ST segment shift and QRS changes, however, has not been established, and the definition of conduction disturbances remains to be clarified. Methods. Twelve-lead electrocardiograms (ECGs) were recorded before PTCA, at the end of 2 min of PTCA and after return to baseline values in 29 patients (left anterior descending coronary artery [LAD] in 13 patients, right coronary artery [RCA] in 14 and left circumflex coronary artery in 2). Electrocardiographic complexes before and during PTCA were superimposed to determine the amplitudes of initial, terminal and total QRS deflection; the relations of QRS changes to baseline (TP segment) and ST segment shift; and the duration of QRS and corrected QT intervals. Results. 1) The direction of the initial QRS deflection was unchanged, but changes of its amplitude occurred. 2) Terminal QRS deflection changed in all patients with a ST segment shift >17% of the R amplitude, and the correlation between the decrease in the S amplitude and ST segment shift was significant (r = 0.9, p < 0.01) in patients with LAD PTCA. Correlation between changes in total QRS amplitude and ST segment shift in patients with RCA PTCA was weaker (r = 0.54, p = 0.056). 3) Transient conduction disturbance manifested by QRS widening in selected leads occurred in 2 of 29 patients. Conclusions. 1) Changes in terminal QRS deflection during PTCA are proportional to the magnitude of the ST segment shift. 2) Conduction disturbances manifested by increased QRS duration occurred infrequently. We suggest that the term peri-ischemic block be applied only to changes in QRS configuration associated with QRS widening.

Background: Previous studies in small groups of predominantly nongeriatic patients showed that comple ventricular arrhythmias occurring after coronary artery graft (CABG) surgery are of no prognostic significance. The purpose of this study was to compare the prognosis of patients with and without advanced grade ventricular arrhythmias (AGVA) after CABG in a large group of patients. [In this paper, AGVA is used as an abridged definition of frequent premature ventricular complexes (PVCs) and nonsustained ventricular tachycardia (NSVT) which represent advanced grade ventricular arrhythmias.] Methods: Twenty-four hour ambulatory electrocardiographic (ECG) monitoring was performed 3 days after CABG in 185 consecutive patients with and 185 closely matched control patients without AGVA. Of 185 patients with AGVA, 77 had frequent PVCs, 45 had NSVT, and 63 patients had both. The average age of both groups was 65 ± 9.7 years. Patients were followed for 34 ± 10 months, and in 30 patients ambulatory monitoring was repeated at the end of the follow-up. Results: Fifteen AGVA and nine control patients died. In each group seven deaths were noncardiac. Six nonsudden and two sudden cardiac deaths (SCD) occurred in the AGVA group at 2-36 months after CABG and two nonsudden cardiac deaths in the control group at 3 and 35 months after CABG (p = 0.053). Both SCDs occurred 33 months after CABG after new events known to predispose to SCD. In 18 of 30 patients AGVA was no longer present when ambulatory ECG monitoring was repeated 36 ± 11 months after CABG. Conclusions: AGVA after CABG was not a marker of an early sudden cardiac death. In 60% of patients not treated with antiarrhythmic drugs, AGVA was no longer present late after operation.

We compared the effects of a low (0.09 microgram/ml) concentration of propranolol expected to produce only beta-adrenoceptor blockade and a high concentration (0.9 microgram/ml) expected to produce additional direct local anesthetic-like electrophysiological effects on basic and premature action potentials. Both isolated dog cardiac Purkinje and ventricular muscle fibers were examined using conventional microelectrode techniques. The low concentration of propranolol produced no significant electrophysiological change in either fiber type. The high concentration of propranolol shortened the action potential duration and refractoriness while decreasing the maximal upstroke velocity (Vmax) in both Purkinje and ventricular muscle fibers at a constant basic cycle length. In Purkinje fibers, the high concentration also slowed the kinetics of restitution of the action potential duration (tau c from 124.6 +/- 6.5 to 201.4 +/- 16.0 ms, p less than 0.01, n = 7), slowed the recovery kinetics of Vmax, and shifted the early portion of the normalized restitution curve toward longer action potential duration values in both fiber types. The range of premature action potential durations, defined as the difference between action potential durations during the first 100 ms of restitution, was decreased by the high concentration of propranolol in both Purkinje and ventricular muscle fibers by 39.5% and 33.9%, respectively. These findings indicate that (a) low concentrations of propranolol produced no direct electrophysiological effect, and (b) high concentrations of propranolol produced several potential antiarrhythmic effects in addition to the previously reported effects on Vmax and the action potential duration.