Showing papers on "QRS complex published in 1980"

Epicardial and endocardial activation during sustained ventricular tachycardia in man.

Abstract: Ventricular activation during ventricular tachycardia was studied by intraoperative epicardial and endocardial mapping in 21 patients with coronary artery disease and previous myocardial infarction who underwent operation for recurrent ventricular tachycardia. Twenty-nine morphologically distinct tachycardias were mapped; 18 tachycardias had a right bundle branch block morphology and 11 had a left bundle branch block morphology. After cannulation for bypass, the tachycardias were induced and electrograms were recorded at 55-75 epicardial sites. After starting cardiopulmonary bypass, the infarction was incised and electrograms were recorded at 28-55 left ventricular endocardial sites during ventricular tachycardia. All mapping data were analyzed with three simultaneously recorded ECG lead and two reference electrograms. Earliest activation in all tachycardias occured on the endocardial surface of the infarction. In each tachycardia, endocardial electrical activity was recorded before the onset of the QRS complex. Earliest epicardial activation in the 29 tachycardias occurred 10 msec after the onset of QRS complex. Epicardial breakthrough occurred on the right (19 tachycardias) as well as the left ventricle (10 tachycardias). We conclude that ventricular tachycardia associated with ischemic heart disease originates near the endocardial surface of the left ventricle along the border of the infarction and that epicardial mapping alone is insufficient to identify the site of origin of these tachycardias.

Total suppression of ventricular arrhythmias by encainide. Pharmacokinetic and electrocardiographic characteristics.

Abstract: We studied the antiarrhythmic effect of a range of oral doses of encainide in 11 patients with stable high-frequency ventricular arrhythmias. Total suppression of arrhythmia was documented in 10 patients at a wide range of doses and plasma concentrations, and the suppression was subsequently verified in a placebo-controlled crossover study. Drug elimination was rapid (the half-life was 1.9 to 3.8 hours), but the margin between efficacy and side effects was sufficiently wide for therapy every six to 12 hours to be feasible in all 10 patients, with continuing outpatient treatment at six to 12 months. Marked prolongation of PR (mean, 44 per cent) and QRS (mean, 47 per cent) durations coincided with abolition of arrhythmia, but no evidence that these effects were detrimental was observed in radionuclide ventriculograms, exercise testing, or prolonged monitoring. A single patient whose arrhythmia and electrocardiogram were unchanged during therapy eliminated the drug much more slowly than the others a...

QRS wave detection.

Abstract: A QRS complex detector based on optimum predetection with a matched filter is described. In order to improve the accuracy of the QRS complex recognition under conditions of Gaussian noise and variable QRS amplitude, the first derivative of the e.c.g. was used with zero threshold detection. In addition, two nonlinear circuits cut off low amplitude noise and all spikes which appear for a fixed time after QRS detection. Calculation of errors shows that differentiation reduces Gaussian error by √6 and errors caused by variable QRS amplitudes are close to zero. This detector is especially useful with biotelemetry systems since it reduces many interferences due to patient movement and communication channel distortion.

Epicardial Activation in Patients with Left Bundle Branch Block

Abstract: SUMMARY To elucidate the abnormalities in ventricular activation sequence in human left bundle branch block (LBBB), epicardial mapping was performed in five patients, ages 52–58 years, undergoing coronary bypass surgery, and the results were compared with similar data published from patients without conduction defect. Three patients had chronic and two patients intraoperative LBBB. ECGs during LBBB revealed a QRS duration of 130–160 msec and a mean QRS axis of −15° to +45. Epicardial mapping revealed 1) anterior right ventricular (RV) epicardial breakthrough (5–26 msec after QRS onset), normal in site in all patients, but abnormally early in timing relative to QRS onset in three patients with chronic LBBB, and earlier compared with preoperative maps in two patients with intraoperative LBBB; 2) normal location of latest RV epicardial activation in four of five patients, but abnormally late occurrence of this event 100, 108 and 110 msec after QRS onset in three of five patients; 3) absence of discrete left ventricular (LV) epicardial breakthroughs in all patients; 4) slow transseptal epicardial activation (crowded isochrones) from right to left, with anteroseptal crossing preceding inferoseptal crossing; 5) activation of the anterolateral left ventricle before the inferior LV epicardium; 6) more widely spaced isochrones, implying more rapid conduction, over the LV free wall epicardium; and 7) location and timing of latest LV epicardial activation in an abnormal site, and abnormally late relative to QRS onset (113–140 msec, mean 124 msec) in all patients. This event occurred a mean of 20 msec before the end of the QRS in the five patients. In conclusion, with normal axis, human LBBB is associated with initiation of ventricular activation closer to anterior RV recording sites than is normal activation, slow leftward transseptal activation, a generally anteroinferior orientation of LV activation, and probable engagement of the distal LV Purkinje system during the latter part of the QRS.

Treadmill exercise testing in the Wolff-Parkinson-White syndrome

Abstract: Graded treadmill exercise testing was performed in 54 patients with the Wolff-Parkinson-White syndrome and preexcitation (persistent in 36, intermittent in 9 and concealed in 9). Forty-eight patients had previous paroxysmal supraventricular arrhythmia (spontaneous or induced or both). At initiation of treadmill testing, the nine patients with intermittent and the nine with concealed preexcitation had normal conduction. None manifested preexcitation during exercise. Thirty-six patients had preexcitation at initiation of exercise; exercise produced no change in preexcitation in 2, partial normalization of the QRS complex in 16 (due to enhanced atrioventricular [A-V] nodal conduction), and total normalization of the QRS complex in 18 (due to enhanced A-V nodal conduction in 14 and to rate-dependent anomalous pathway block in 4). Exercise-provoked block of the anomalous pathway reflected prolonged anomalous pathway refractoriness, as measured with atrial stimulation. All 18 patients with either total or partial preexcitation at peak exercise manifested more than 1 mm flat or downsloping S-T segment depression. None had evidence of ischemic heart disease. None of the 54 patients manifested either paroxysmal supraventricular tachycardia or atrial fibrillation during or after treadmill exercise. Treadmill exercise testing in patients with preexcitation frequently produces partial or total normalization of the QRS complex due to enhanced A-V nodal conduction and, less commonly, total normalization due to rate-dependent block of the anomalous pathway. False positive S-T segment changes (suggesting ischemia) are always present in patients manifesting preexcitation during treadmill testing. Treadmill exercise testing in patients with preexcitation does not provoke paroxysmal supraventricular tachycardia or atrial fibrillation and is not useful as a provocative test for arrhythmia.

Variability of the body surface distributions of QRS, ST-T and QRST deflection areas with varied activation sequence in dogs

Abstract: Distributions of QRS, ST-T and QRST areas of 192 lead body surface ECG's were measured in dogs for multiple activation orders. Qualitatively, the distributions of QRST area were found to be strikingly similar over all activation orders in contrast to the distributions of QRS or ST-T areas. Quantitative results showed that variability of the QRST areas over all activation orders was consistently less than those of either QRS or ST-T. The factor responsible for the QRS deflection is ventricular activation sequence while those responsible for the ST-T deflection are both activation sequence and ventricular recovery properties. Since the total QRST deflection area was largely independent of activation sequence it is likely the quantity is an index of ventricular recovery properties. The significance of this relation is that QRST deflection area may permit evaluation of intrinsic ventricular recovery properties in the presence of abnormal ventricular activation as occurs with intraventricular conduction disorders and ectopic origin of excitation. Evaluation of intrinsic ventricular recovery properties may also permit recognition of states at risk of ventricular arrhythmias due to increased disparity of these properties.

Hypertrophic Cardiomyopathy: A Disease in Search of Its Own Identity"

Abstract: The search for the identity of hypertrophic cardiomyopathy continues. The paper by Yamaguchi et al.’ in a recent issue of this Journal draws attention to another variation in the spectrum. These workers describe 30 patients in a series of 1,002 consecutive patients investigated with left ventricular angiography and coronary arteriography whose electrocardiograms showed giant inverted T waves with high QRS voltage in the absence of systemic hypertension or occIusive coronary artery disease. In all 30 patients the ventriculogram in the right anterior oblique projection revealed a characteristic spade-like configuration due to concentric apical hypertrophy of the left ventricle and associated with obliteration or elimination of the cavity of the apical portion of the left ventricle at end-systole. Two dimensional echocardiography revealed a similar configuration. No systolic pressure gradient was found even on provocation. The upper half of the septum remained thin instead of bulging into the left ventricle, and systolic anterior motion of the mitral valve was not seen. Many of the cases with apical hypertrophy did not have asymmetric hypertrophy of the septum. The angiographic appearance was contrasted with the “banana” shape observed in hypertrophic obstructive cardiomyopathy in which the authors claim the free wall thickness is increased in all segments. It was not associated with obliteration of the cavity at the apex and the septum was rhomboid in shape in systole in the left anterior oblique projection. All patients showed electrocardiographic abnormalities between the 2nd and 6th decade of life. In four patients, there was a striking progression of electrocardiographic changes over a period of only a few years.

Body surface distribution of electrical potential during atrial depolarization and repolarization.

Abstract: Limited information is available documenting body surface isopotential distributions during atrial excitation and recovery. To expand the current data base, body surface isopotential maps from 40 normal subjects were examined. Data were acquired at a gain of 10,000 and isopotential distributions constructed at 2-msec intervals from the onset of the P wave to the onset of the QRS complex. During the initial half of the P wave, a left midprecordial maximum dominated the distribution. Negative potentials existed over the upper back. Subsequently, the maximum migrated to the left; negative potentials moved into precordial areas. Near the end of the P wave, the maximum shifted to the left back as a minimum evolved over the midprecordium. This minimum increased in intensity and remained stationary throughout the PR segment. These patterns are consistent with previously reported epicardial records from canine preparations documenting initial right and then left atrial activation, and repolarization beginning before the end of excitation and enveloping much of the posterior atrial epicardium with low-level positive potential. All distributions had but a single maximum and/or minimum, consistent with a single dipole equivalent cardiac generator.

Multiple-lead QRS changes with exercise testing. Diagnostic value and hemodynamic implications.

Abstract: To evaluate the diagnostic potential and hemodynamic significance of exercise-induced multiple-lead QRS changes, we studied exercise test responses in 230 patients with chest pain syndromes undergoing Bruce protocol exercise tests. When increases in the R waves of multiple ECG leads (epsilon R) plus ST segment change greater than 1 mm were present, 74 of 75 patients (99%) had coronary disease; this was a higher percentage than that achieved with either measurement alone or when ST change was combined with increase in R in a single lead. Sixty-four of the 75 patients (85%) had multivessel disease, the most severe form of coronary artery disease. Left ventricular end-diastolic pressure (both at rest and after left ventriculography), presence and degree of resting ventricular asynergy, and ejection fraction were all significantly more abnormal in patients whose epsilon R increased, regardless of ST-segment change. Further, in patients who stopped exercise because of cardiac symptoms, exercise duration and the product of heart rate times blood pressure were significantly lower when epsilon R increased. Thus, the mechanism for the increase in epsilon R with exercise in patients with coronary artery disease appears to be related to abnormalities in left ventricular function.

Effects of changes in ventricular size on regional and surface QRS amplitudes in the conscious dog.

Abstract: SUMMARYEight conscious dogs instrumented with wall thickness sonomicrometers and 11 subcutaneous electrodes in a modified McFee vectorcardiographic array were studied during changes in ventricular volume. Simultaneous measurements were made of QRS amplitudes of the endocardial and epicardial ECG, QRS spatial vector magnitudes (SVM), end-diastolic wall thickness (EDT), end-systolic wall thickness (EST) and the amount of systolic thickening (δWT). Ventricular size was decreased by atropine and infulsion of 0.02 μg/kg/min of isoproterenol to increase the mean heart rate from 81 ± 5 beats/min (mean ± SEM) to 174 10 beats/min (p < 0.001), and was reflected by an increased mean EDT (9.06 ± 0.64 mm to 9.94 ± 0.61 mm, p < 0.005). The endocardial QRS amplitude increased in each dog (mean increase 21.55 ± 1.36 mV to 25.13 ± 1.35 mV, p < 0.001), whereas the SVM decreased from 7.69 ± 0.75 mV to 6.18 ± 0.48 mV (p < 0.02). Ventricular size was then increased by rapid saline infusion and was reflected by a decrease of EDT from 9.65 ± 0.66 mm to 9.09 ± 0.66 mm (p < 0.001), while heart rate remained unchanged. Endocardial amplitude decreased in each dog (average decrease 3.59 ± 0.25 mV, p < 0.001), while the SVM increased in each dog (average increase 0.81 ± 0.18 mV, p < 0.005). The mean epicardial amplitudes did not change significantly during either increases or decreases in ventricular volume. In each dog, there was a linear relation between EDT and endocardial amplitudes (r values > 0.88) and an inverse linear relation between EDT and SVM (r values > −0.80). The relations between EST or AWT and regional and QRS surface amplitudes were nonlinear. We conclude that in the conscious dog changes in endocardial QRS amplitudes and SVM respond in an opposite manner to changes in ventricular volume. In this experimental model, alterations in endocardial QRS amplitudes were related directly to changes in diastolic wall thickness; changes in body surface QRS amplitudes were inversely related to wall thickness, a finding that may relate in part to alterations in the distance of the heart from the chest wall.

QRS mapping in the evaluation of acute anterior myocardial infarction.

Abstract: In 42 patients with acute anterior myocardial infarction (AMI), we studied the course of Q-wave development and R-wave reduction during the first 48 hours after the onset of chest pain. We used precordial mapping in relation to clinical features, hemodynamic measurements and enzyme release. Q waves developed within 6-14 hours (mean 9 hours) after onset of symptoms. R-wave amplitudes demonstrated nearly a reflected image: They reduced abruptly 5-11 hours (mean 9 hours) after onset of chest pain, coinciding with ST-segment elevation. In 14 patients (group A, 33%) after initial QRS alterations, there were no further changes. Twenty patients (group B, 48%) had a distinct new increase of Q waves (delta sigma Q = 3.0 +/- 2.0 mV/hours) and further R-wave reduction (-delta sigma R = 1.0 +/- 0.6 mV/hour) simultaneous with new severe chest pain and a delayed second increase of enzyme release corresponding with extension of infarction. There were no significant differences between the groups in age, hemodynamics and infarct size calculated from creatine kinase release. Eight patients (group C, 19%) had contradictory findings. Our findings are consistent with previous results indicating that the critical period for intervention is very small except in patients with extension of necrosis.

Total body surface potential mapping during exercise: QRS-T-wave changes in normal young adults.

Abstract: Total body surface potential distributions were recorded from 20 normal young adults, 20-35 years old, during multistage maximal exercise testing on a bicycle ergometer. Using a system for measuring total body surface potential distributions from measurements at 24 locations, high-quality potential maps were obtained during exercise without requiring wave form averaging or special modes of exercise. Serial maps recorded at 1-msec intervals throughout QRS-T during exercise and during recovery from exercise were compared with corresponding maps recorded with the subjects at rest. During and after exercise, consistent changes appeared in the map patterns during early QRS and the ST segment and in the magnitude of the T-wave potentials. Increases in QRS duration (0-10 msec) also appeared during exercise. The changes in map patterns during early QRS in exercise strongly suggested changes in the initial sequence of activation in the ventricles. The results demonstrate the importance of analyses of total body surface potential distributions in understanding ECG changes during exercise.

Body surface distributions of repolarization forces during acute myocardial infarction. I. Isopotential and isoarea mapping.

Abstract: Although ST-segment abnormalities during acute myocardial infarction are clinically important, the total thoracic distribution of these repolarization potentials has not been reported To provide this information, 24 patients with acute myocardial infarction were studied Isopotential body surface maps were constructed from potentials sensed by 150 anterior and posterior electrodes Patterns from 12 patients with anterior lesions demonstrated the appearance of repolarization potentials 213 +/- 46 msec before the end of the QRS complex During the ST segment, potential distributions were characterized by a single anterior maximum that remained fixed in location but increased in intensity as repolarization progressed Distributions in the remaining subjects with inferior lesions were analogously characterized by (1) the onset of repolarization 346 +/- 124 msec before termination of the QRS complex and (2) a single anterior minimum located on the left anterior superior thorax, with positive potentials distributed around the lower thoracic margins These data suggest that electrocardiographic changes after acute myocardial infarction include (1) marked overlap between activation and recovery patterns and (2) isopotential surface patterns with relatively simple topographic configurations, such as expected of a single-dipole equivalent cardiac generator

Voltage Clamp Studies of the Slow Inward Current

Abstract: As early as 1911, Eiger [l] distinguished two phases in the ECG, the first (QRS complex) being considered as an action current, whereas the second (ST interval and T wave) was interpreted as being the result of biochemical processes. Other authors [2–5] considered that, if QRS was related to excitation, the T wave was related to contraction. Therefore several previous observations suggested that two different mechanisms might be responsible for early and late ECG waves. Moreover the R wave was recognized as being very stable wheras the lability of the T wave was established in many experimental conditions (see [6]).

Initiation and termination of ventricular tachycardia by supraventricular stimuli. Incidence and electrophysiologic determinants as observed during programmed stimulation of the heart.

Abstract: In 7 of 43 patients in whom a sustained ventricular tachycardia could be induced during programmed electrical stimulation by a single ventricular premature stimulus, an identical tachycardia could also be initiated by a single atrial premature stimulus. This phenomenon was observed only in those patients in whom the ventricular tachycardia could be induced by a single ventricular extrastimulus having a prematurity index (ratio between the longest ventricular premature stimulus interval resulting in tachycardia and the duration of the basic cycle length of the paced ventricular rhythm) above 54 percent. No single instance of initiation of ventricular tachycardia by atrial premature stimuli was observed in patients with a ventricular prematurity index below 54 percent or requiring more than one consecutive ventricular extrastimulus to have tachycardia initiated. Other features of patients showing initiation of ventricular tachycardia by atrial premature stimuli were a right bundle branch block configuration of the QRS complex during tachycardia in all seven patients and a relatively slow rate during tachycardia. In one patient ventricular tachycardia was terminated by a conducted atrial premature stimulus.

Torsades de Pointes: Occurrence in myocardial ischaemia as a separate entity. Multiform ventricular tachycardia or not?

Abstract: Torsades de pointes (Tdp) were evaluated with respect to aetiology, morphology and response to treatment in 16 patients admitted to the CCU. Analysis was based on monitor strip charts and conventional 12 lead ECGs. Underlying disease was total AV block in four patients, acute myocardial ischaemia in nine patients, with acute ventricular aneurysms in four patients; one patient had chronic ventricular aneurysm, one idiopathic hypokalaemia, and one was on quinidine therapy. Heart rate was less than 30 beats min−1 in patients with total AV block and above 90 beats min−1 in six out of 12 patients with basic sinus rhythm. QT prolongation was not present in six patients with acute myocardial ischaemia. Tdp were always initiated by PVCs either falling on the downslope of the T wave of the preceding normal beat or shortly after it in the range of a U wave. Coupling intervals in a run of Tdp were variable in most patients, with an increase in eight patients and a decrease in five patients. In patients with total AV block Tdp could be controlled by increasing the heart rate through pacemaker stimulation. Patients in sinus rhythm (heart rate above 60 beats min−1) received antiarrhythmic drugs: propafenon was effective in 80% (eight out often patients). Ten patients were long-term survivors. Outcome of the acute stage of the disease seemed to be determined by underlying myocardial function. Differentiation between Tdp and multiform ventriadar tachycardia (i.e. VT with torsion of QRS complexes occurring in acute myocardial ischaemia) seems unnecessary to us, since morphological features were similar in both groups with the exception of QT prolongation, which was absent in six out of nine patients with acute myocardial ischaemia. Propafenon was active in patients without as well as with QT prolongation.

Characterization of pacemaker arrhythmias due to normally functioning AV demand (DVI) pulse generators.

Abstract: Normally functioning DVI pulse generators with different electronic characteristics may cause complex cardiac arrhythmias that must not be interpreted as pacemaker malfunction. When there is no refractory period after the atrial output, a DVI pulse generator may deliver atrial pacemaker impulses at irregularly shortened intervals and produce an increase in the atrial pacemaker rate compared with the programmed free-running AV sequential rate. Theoretically this variation of the atrial cycle length can occur only within a well-defined range that represents the difference between the ventricular and atrial output escape intervals. In reality, the interplay of the spontaneous sinus rate, duration of AV conduction, time of sensing the ventricular electrogram in relation to the surface QRS complex, and the programmed AV sequential time all influence the atrial pacemaker rate. DVI pulse generators may also create interesting arrhythmias such as pseudopseudofusion beats (delivery of an atrial spike within the QRS complex), double pseudofusion beats, and double pacemaker impulses within the QRS complex according to the electrophysiologic circumstances and specifications of the pulse generator.

Electrocardiogram changes and plasma desipramine levels during treatment of depression.

Abstract: Twenty-six symptomatic subjects who met research diagnostic criteria for major affective disorder and were free of cardiovascular disease were treated for 3 wk with a fixed dosage schedule of desipramine (DMI) to a maximum of 200 mg/day. An electrocardiogram (ECG) and DMI plasma level determinations were obtained before treatment and weekly thereafter. DMI levels during the trial ranged from 13.4 to 882.2 ng/ml. DMI treatment was associated with increase in heart rate (p less than 0.001), prolongation of the PR (p less than 0.001), QRS (p less than 0.001), and QTc intervals (p less than 0.001), and increase in T wave amplitude (p less than 0.001). Significant (p less than 0.001) but relatively weak correlations were noted between DMI plasma levels and heart rate (r = 0.405), QRS interval (r = 0.346), QTc interval (r = 0.534), and T wave amplitude (r = -0.386). PR interval prolongation was independent of DMI levels (r = 0.171). DMI treatment induced no clinically significant ECG alterations or cardiovascular adverse effects. The relevance of DMI plasma level and the possible roles of other contributing factors in the production of these ECG changes are discussed.

Electro- and echocardiographic study of the left ventricle in man after training.

Abstract: Fourteen sedentary middle-aged men underwent a chest X-ray, a 12 lead ECG, a VCG, and an echocardiographic examination prior to and following 5 months of training a moderately severe intensity, on a cycle ergometer. No modification in the X-ray cardiac profile was observed following training. Some electrocardiographic (R wave amplitude in V5 and V6 and Sokolow index: SV1 + RV5 or V6) and vectorcardiographic (maximal QRS vector amplitude, maximal spatial QRS vector, and R wave amplitude) indices of left ventricular hypertrophy were slightly but significantly increased following training. The echocardiographic measurements in diastole (septal and posterior wall thickness, left ventricular internal diameter, and left ventricular mass) were unchanged after training. Results suggest that electrical changes may not provide adequate indications of left ventricular morphological modifications. The lack of echocardiographic evidences of left ventricular hypertrophy suggest that: (1) training does not necessarily induce left ventricular hypertrophy; (2) the large heart sometimes observed in athletes may be the result of a genetic factor or of a prolonged and very intensive training pursued since a very young age, over a number of years; and (3) left ventricular enlargement probably plays a minor role in the increase in aerobic capacity following training.

Influence of left ventricular dimensions on endocardial and epicardial QRS amplitude and ST-segment elevations during acute myocardial ischemia.

Abstract: The influence of acute myocardial ischemia and changes in ventricular dimensions on endocardial and epicardial electrograms were evaluated in 17 anesthetized open-chest dogs before and after left ventricular volume expansion and before and after coronary artery ligation. In eight dogs, regional myocardial blood flow was determined by the labeled microsphere technique. Endocardial QRS (endo-QRS) amplitude in ischemic and nonischemic zones, and epicardial QRS (epi-QRS) in nonischemic zones maintained a negative linear relation with left ventricular end-diastolic dimension before and after coronary artery ligation, although acute ischemia decreased endo-QRS independently. Epi-QRS amplitude in the ischemic zone decreased after coronary artery ligation but changed inconsistently during volume expansion. Ischemia-induced epicardial ST-segment elevation decreased during volume expansion and was associated with improved epicardial blood flow. Changes in epi-QRS in ischemic zones, however, were not related to epicardial blood flow during volume expansion. These findings indicate the potential problems of using changes in QRS amplitude for determining the extent of myocardial ischemic injury.

Initiation and termination of ventricular tachycardia by supraventricular stimuli

Abstract: In 7 of 43 patients in whom a sustained ventricular tachycardia could be induced during programmed electrical stimulation by a single ventricular premature stimulus, an identical tachycardia could also be initiated by a single atrial premature stimulus. This phenomenon was observed only in those patients in whom the ventricular tachycardia could be induced by a single ventricular extrastimulus having a prematurity index (ratio between the longest ventricular premature stimulus interval resulting in tachycardia and the duration of the basic cycle length of the paced ventricular rhythm) above 54%. No single instance of initiation of ventricular tachycardia by atrial premature stimuli was observed in patients with a ventricular prematurity index below 54% or requiring more than one consecutive ventricular extrastimulus to have tachycardia initiated. Other features of patients showing initiation of ventricular tachycardia by atrial premature stimuli were a right bundle branch block configuration of the QRS complex during tachycardia in all seven patients and a relatively slow rate during tachycardia. In one patient ventricular tachycardia was terminated by a conducted atrial premature stimulus.

Optimal use of serum enzyme levels in the diagnosis of acute myocardial infarction. The perspective in 1980.

Abstract: The two clinical studies of the importance of the MB isoenzyme of creatine kinase (CK) presented in this issue of theArchives(see pp 329 and 336) provide important and complementary insights into the current status of the diagnosis of acute myocardial infarction. The ECG remains a most important method for the identification of acute myocardial infarction because of a specificity of new QRS changes accompanied by evolutionary ST segment and T wave changes that approaches 100%. However, the QRS complex is the only aspect of the ECG that should be considered diagnostic, because all variations or changes in repolarization manifested either by elevations or depressions of the ST segment or by inversions of the T wave are, like the history of the classical initial symptoms, indications of acute coronary insufficiency either with or without myocardial necrosis. The QRS complex is a very sensitive indicator of new infarction if it

Transient QRS changes simulating acute myocardial infarction.

Abstract: The purpose of this study was to determine the characteristics and incidence of abrupt occurrence of abnormal initial QRS forces that cannot be explained by acute myocardial infarction or left or right ventricular overload. Computerized data from 3175 patients with suspected acute infarction were reviewed to identify those in whom the ECGs revealed QRS complexes considered to be diagnostic (Q wave or markedly diminished R wave) in the presence of persistently normal profiles of both creatine kinase and lactic dehydrogenase isoenzymes. Lead misplacement had been minimized by obtaining multispace tracings and vectorcardiograms. Eight patients (0.25%) were identified. The abnormal forces were confined to leads V 1-3 in six, V 4-6 in one, and involved all precordial leads in the last. These QRS changes resolved completely within 6 days in all eight patients, which suggests that they did not have an acute infarction. This theory was supported by postmortem examination in one patient. An extremely low incidence (0.25%) has been documented for a syndrome characterized by transient loss of initial anterior forces with persistently normal isoenzyme profiles. Although no etiology could be determined, a transient conduction block of the septal fascicle of the left bundle could have been the cause in seven of the eight patients.

New vectorcardiographic criteria for diagnosing right ventricular hypertrophy in mitral stenosis: comparison with electrocardiographic criteria.

Abstract: 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.

Relation of exercise-induced physiologic S-T segment depression to R wave amplitude in normal subjects.

Abstract: Exercise electrocardiography was performed in 100 asymptomatic male volunteers with a mean age of 42.6 years. The R wave and total RS amplitude and the magnitude of physiologic S-T segment depression at the J junction were quantitated for a modified bipolar CC5 lead and a vertically oriented bipolar lead (VL) using computer-averaged groups of 25 consecutive QRS complexes from each of seven stages of rest and exercise. Computer-generated X-Y plots were used to examine the correlations between the magnitude of S-T depression and the R wave and total RS amplitudes. The magnitude of S-T depression and of the R wave amplitude were unrelated at standing rest but showed increasing correlation with progressive increases in exercise heart rate (correlation coefficient = 0.425, p These data demonstrate a significant relation between the magnitude of R wave and total RS amplitudes and the magnitude of physiologic S-T segment depression in normal subjects during exercise. They suggest the need for evaluation of S-T depression corrected for R wave amplitude in an attempt to improve the diagnostic accuracy of the exercise electrocardiogram. The data also suggest that the criteria for abnormal S-T depression should take into consideration the different R wave voltages reflected by different types of recording leads.

Mechanism of the Repetitive Ventricular Response in Man

Abstract: The electrophysiologic characteristics of the repetitive ventricular response that followed an electrically induced single premature ventricular complex were evaluated to determine its mechanism during atrial pacing or sinus rhythm in 30 patients. Seven patients had preexisting bundle branch block. His bundle or right bundle branch deflections did not precede the repetitive complex in 29 of the 30 patients, which implies that the proximal His-Purkinje system was not involved in the reentry circuit. In 24 of 30 patients the QRS axis of the repetitive complex was divergent 45 ° or more from the stimulated complex. In 22 of 30 patients the repetitive complex had a right bundle branch block configuration. In 14 of 18 patients with two or more repetitive complexes, the QRS pattern changed from beat to beat, which implies that either the reentry pathway or conduction was changing. Thus, the repetitive ventricular response, which can be associated with clinically important ventricular arrhythmias, probably represents intraventricular rather than proximal His-Purkinje system reentry.