Showing papers on "QRS complex published in 1984"

Estimation of QRS Complex Power Spectra for Design of a QRS Filter

Abstract: We present power spectral analysis of ECG waveforms as well as isolated QRS complexes and episodes of noise and artifact. The power spectral analysis shows that the QRS complex could be separated from other interfering signals. A bandpass filter that maximizes the signal (QRS complex)-to-noise (T-waves, 60 Hz, EMG, etc.) ratio would be of use in many ECG monitoring instruments. We calculate the coherence function and, from that, the signal-to-noise ratio. Upon carrying out this analysis on experimentaly obtained ECG data, we observe that a bandpass filter with a center frequency of 17 Hz and a Q of 5 yields the best signal-to-noise ratio.

Fast-Fourier transform analysis of signal-averaged electrocardiograms for identification of patients prone to sustained ventricular tachycardia.

Abstract: Electrocardiograms obtained from patients during arrhythmia-free intervals do not identify those prone to sustained ventricular tachycardia (VT) despite the occult delayed activation that is presumably present. To determine whether frequency-domain analysis facilitates detection of this hallmark of predisposition to VT, fast-Fourier transform analysis (FFTA) procedures were developed and tested with a computer-generated mathematical model. The FFTA approach developed allows inherent limitations of high-gain amplification and a priori filtering used commonly for time-domain analysis to be avoided. After demonstrating that FFTA detected low-amplitude oscillatory waveforms in signal-averaged recordings in the frequency domain, the procedure was applied to signal-averaged X, Y, and Z lead recordings from the following three groups of patients: group I, patients with prior myocardial infarction and episodic sustained VT (n = 16); group II, patients with prior myocardial infarction without overt sustained VT (n = 35); and group III, normal control subjects (n = 10). Results of FFTA demonstrated significant (p less than .0001) differences in the decibel drop at 40 Hz and the area under the curve from the fundamental frequency to the frequency at which the spectral amplitude was decreased by 60 dB for both the terminal 40 msec of the QRS and ST segment in patients in group I compared with those in groups II and III, in whom results were similar. Results were independent of QRS duration (r = .2), left ventricular ejection fraction (r = .19), and complexity of spontaneous ventricular ectopy. Thus, patients known to manifest sustained VT also exhibited relatively greater high-frequency content in arrhythmia-free intervals in the terminal QRS and ST segment than those without VT (88%, 15%, and 0% in groups I through III, respectively). FFTA offers promise for the noninvasive detection of patients at risk for the development of sustained VT.

Identification of patients with ventricular tachycardia after myocardial infarction: signal-averaged electrocardiogram, Holter monitoring, and cardiac catheterization.

Abstract: Electrocardiographic signal averaging techniques have demonstrated a low-amplitude late potential and a long filtered QRS complex in patients with ventricular tachycardia (VT) after myocardial infarction. Complex ventricular ectopy and left ventricular aneurysms have also been associated with VT. The purposes of this study were (1) to determine whether the findings from the signal-averaged electrocardiogram (ECG) were independent of those from Holter monitoring and cardiac catheterization and (2) to determine the combination of findings from the signal-averaged ECG, cardiac catheterization, and Holter monitoring that best characterize patients with VT after myocardial infarction. We studied 174 patients after myocardial infarction, 98 of whom had recurrent sustained VT. By multivariate logistic regression only three parameters were found to be independently significant, listed in order of power: positive signal-averaged ECG (presence of a late potential or a long filtered QRS duration), peak premature ventricular contraction greater than 100/hr, and presence of a left ventricular aneurysm (p less than .001). The signal-averaged ECG provides independent information in identifying patients with VT after myocardial infarction.

Endocardial activation of left bundle branch block.

Abstract: Endocardial catheter mapping was performed in 18 patients with left bundle branch block (LBBB). Four patients had no organic heart disease (group I), six had cardiomyopathy (group II), and eight had coronary artery disease and previous infarction (group III). Twelve patients had one septal site of left ventricular endocardial breakthrough, while six had two left ventricular endocardial breakthrough sites, with one site always being septal. There was no significant difference among the groups with respect to time of left ventricular breakthrough (group I, 44 msec after the onset of the QRS complex; group II, 58 msec; and group III, 51 msec). Total left ventricular endocardial activation time was significantly longer in group III (119 msec) than group I (81 msec; p less than .05) and group II (61 msec; p less than .001). Duration of total right ventricular endocardial activation was 36 msec (seven patients). The final site of right ventricular activation was at 44 msec after the onset of the QRS complex. We conclude that (1) right ventricular activation occurs before initiation of left ventricular activation in patients with LBBB, (2) left ventricular endocardial activation in patients with LBBB most likely occurs as a result of right-to-left transseptal activation, (3) left ventricular endocardial activation sequence in patients with LBBB is heterogeneous, and (4) patients with coronary artery disease and LBBB have significantly longer total left ventricular endocardial activation times than patients with no organic heart disease or those with cardiomyopathies.

Coronary heart diseaseEvaluation of a QRS scoring system for estimating myocardial infarct size: IV. Correlation with quantitative anatomic findings for posterolateral infarcts☆

Abstract: This study correlated the location and size of posterolateral myocardial infarcts (Mls) measured anatomically with that estimated by quantitative criteria derived from the standard 12-lead ECG. Twenty patients were studied who had autopsy-proved, single, posterolateral Mls and no confounding factors of ventricular hypertrophy or bundle branch block in their ECG. Left ventricular anatomic Ml size ranged from 1 to 46%. No patient had a ≥ 0.04-second Q wave in any electrocardiographic lead and only 55% had a 0.03-second Q wave. A 29-point, simplified QRS scoring system consisting of 37 weighted criteria was applied to the ECG. Points were scored by the ECG in 85% of the patients (range 1 to 8 points). Ml was indicated by a wide variety of QRS criteria; 19 of the 37 criteria from 8 different electrocardiographic leads were met. The correlation coefficient between MI size measured anatomically and that estimated by the QRS score was 0.72. Each point represented approximately 4% Ml of the left ventricular wall.

Intraoperative endocardial mapping during sinus rhythm: relationship to site of origin of ventricular tachycardia.

Abstract: Mapping-guided endocardial resection has proved to be an effective therapy for recurrent sustained ventricular tachycardia. However, some patients cannot be mapped during ventricular tachycardia, so that guidance from findings during normal sinus rhythm would be highly desirable. We examined the frequency, timing, and duration of several abnormal types of electrograms recorded endocardially during sinus rhythm and related these findings to activation mapping during sustained ventricular tachycardia. Thirteen patients with extensive myocardial infarction complicated by recurrent sustained ventricular tachycardia were studied intraoperatively during sinus rhythm and induced ventricular tachycardia with a standardized mapping scheme involving the entire endocardial surface. Fractionated electrograms (multicomponent with amplitude less than 1 mV and duration greater than 50 msec) were recorded in all patients. This type of electrogram could be recorded at up to 36% of mapped sites. Split electrograms (two components separated by isoelectric period) were also frequently seen but involved only a mean of 5.8% of mapped sites. Late electrograms (inscribed entirely after the QRS complex) were only recorded in four of 13 patients at a mean of 5% of mapped sites. The location of these electrograms was related to an arbitrary 8 cm2 zone around the earliest site of endocardial activation recorded during ventricular tachycardia. The longest fractionated electrogram was closely related to nine of 22 morphologies of induced ventricular tachycardia, split electrograms were related to seven of 16 morphologies, and late electrograms to two of four morphologies. We have concluded that extremely abnormal electrograms recorded endocardially during sinus rhythm are widespread in patients with extensive myocardial infarction complicated by ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrocardiographic J wave of hypercalcemia.

Abstract: In 1920, Krausl reported electrocardiographic changes in experimental animals with hypercalcemia; we believe that his Figure 1 showed an ST-junctional deflection resembling the J wave of hypothermia. Except for a 1922 article by the same author, we have found no further reports that suggest J waves in hypercalcemia in either experimental animals or humans.2 The electrocardiographic descriptions of hypocalcemia and hypercalcemia have focused on the slope and duration of the ST segment.3 We have repeated the induction of hypercalcemia in the dog and observed that at serum calcium (Ca) levels of 24.6 mg/dl and higher, the QRS widened, largely because of the appearance of a new deflection where the

Differential diagnosis of tachycardia with narrow QRS complex (shorter than 0.12 second)

Abstract: One hundred eighty-seven patients with clinically documented supraventricular tachycardia with a narrow QRS complex were admitted for electrophysiologic study. The diagnoses after this study were circus movement tachycardia using an accessory pathway in 50 patients, atrioventricular nodal tachycardia in 50 patients, atrial flutter in 50 patients, atrial tachycardia in 27 patients and an incessant tachycardia retrogradely using a slowly conducting accessory pathway in 10 patients. On retrospective analysis, 5 criteria on the 12-lead electrocardiogram during tachycardia were analyzed for their value in making the diagnosis of site of origin. These criteria were P-wave location, axis of the P wave, atrial rate, alternation of the QRS complex and atrioventricular relation. Fifty-seven patients with a narrow QRS tachycardia were prospectively studied using the 5 criteria. A correct diagnosis was made in 48 of the 57 patients (84%). Thus, in most patients with a narrow QRS tachycardia, information from the 12-lead electrocardiogram is adequate for diagnosis.

Body surface late potentials: effects of endocardial resection in patients with ventricular tachycardia.

Abstract: We studied 37 patients undergoing endocardial resection for medically refractory ventricular tachycardia (VT). Each was studied before and after surgery by programmed ventricular stimulation and signal-averaged electrocardiography. Low-amplitude late potentials were identified preoperatively in 76% of patients. In the 24 patients without postoperative VT the effect of surgery was to shorten the filtered QRS duration (137 +/- 27 to 121 +/- 26 msec; p = .003), increase the voltage in the last 40 msec of the filtered QRS (16.5 +/- 16.1 to 39.0 +/- 29.4 microV; p = .003), and decrease the incidence of late potentials (71% to 33%; p = .03). The filtered QRS complex was unchanged in 13 patients whose VT persisted after surgery. No preoperative variable predicted which patients would not have inducible VT after surgery. However, loss of a late potential after surgery in nine of 10 patients was associated with absence of inducible VT (p less than .02). Loss of a late potential was not necessary for surgical success. Eight of 18 patients with a persistent late potential did not have inducible VT. The signal-averaged electrocardiogram predicted a successful outcome after endocardial resection if the late potential was no longer present.

Blood pressure, electrocardiogram and echocardiogram measurements in the growing pony foal

Abstract: Summary Twelve newborn pony foals underwent cardiovascular examinations (auscultation, arterial blood pressure measurements, electrocardiograms and M-mode echocardiograms) on their first day of life and then on Days 7, 14, 21, 30, 60 and 90. An age dependent, statistically significant, rapid increase of the arterial blood pressure in the first month was documented together with a slower decrease of the resting heart rate after two and three months of life. Innocent soft systolic murmurs were audible over the left heart base in a large number of the foals. The electrocardiograms showed age dependent increases of the PR-, QRS- and QT- intervals and a trend of the mean electrical axis in the frontal plane to rotate towards the left side. The ventricular dimensions, measured by M-mode echocardiography, increased with the growth of the pony foals. Linear regression equations were calculated for the right and left ventricular internal dimensions in relation to body weight (bwt). The other echocardiographic parameter had low correlations with bwt.

Electrocardiogram of the athlete: An analysis of 289 professional football players

Abstract: The electrocardiogram (EGG) of athletes reflects physiologic cardiovascular adaptations that occur in well-conditioned individuals. To more clearly define electrocardiographic changes seen in predominantly power-trained athletes, the ECGs of 289 apparently healthy professional football players were analyzed in detail. The players, aged 21 to 35 years, one-third of whom were black, had a mean body surface area of 2.24 m2, a mean heart rate at rest of 56 ± 9 beats/min (with 77% (223) having a rate of less than 60 beats/min), and a mean P axis of 30 ± 25 °. A wide QRS-T angle (>60 °) was present in 14% (41 players) of the group. The mean PR interval was 0.18 ± 0.02 second (>0.21 in 9% [26 players]). Although two-thirds of the players had a QRS duration of 0.10 second, only 1 had right bundle branch block and none had left bundle branch block. The sum of S in lead V1 plus R in lead V5 averaged 37 ± 9 mm, with 35% (101 players) demonstrating voltage criteria for left ventricular hypertrophy. The S + R value varied inversely with weight (r = −0.27, p < 0.002). The maximum T height in any lead had a mean of 8.6 ± 3 mm, with 22% (64 players) having a T height ≥11 mm. U waves were universally present. ST-T changes mimicking ischemia were noted in 39 of 289 players (13%), 22 (58%) of whom were black (p < 0.001). The maximal J-point elevation in any lead averaged 1.9 ± 0.9 mm. These findings confirm that the ECGs of power-trained athletes show changes similar to those of endurance-trained athletes. These changes most likely reflect the increased vagal tone and ventricular mass observed in conditioned athletes. Large body size masks the voltage changes expected with increased left ventricular mass. Ischemic-like ST-T-wave deviations were found predominantly in black athletes.

Reevaluation of electrocardiographic criteria for left, right and combined cardiac ventricular hypertrophy.

Abstract: Cardiac chamber weight was determined at necropsy in 323 men to develop correlative studies of electrocardiographic criteria for ventricular hypertrophy. Thirty recommended criteria for left ventricular (LV) hypertrophy, 10 for right ventricular (RV) hypertrophy, and combinations of both criteria for combined hypertrophy were evaluated. Four methods for electrocardiographic diagnosis of LV hypertrophy were derived: (1) a modification of the Romhilt-Estes point system; (2) the presence of any 1 of 3 criteria: (a) S V1 + R V5 or V6 greater than 35 mm, (b) left atrial abnormality, or (c) intrinsicoid deflection in lead V5 or V6 greater than or equal to 0.05 second; (3) a combination of any 2 criteria or of 1 criterion (above) plus at least 1 of the following 3 additional criteria: (a) left-axis deviation greater than -30 degrees, (b) QRS duration greater than 0.09 second, or (c) T-wave inversion in lead V6 of 1 mm or more; and (4) the use of a single criterion--left atrial abnormality. Sensitivity varied from 57 to 66% and specificity from 85 to 93% among these 4 methods. Myocardial infarction increased sensitivity of the foregoing methods, but the specificity was reduced. Method 2 is preferred for the electrocardiographic diagnosis of LV hypertrophy. Two methods were useful for right ventricular (RV) hypertrophy: (1) the use of any 1 of 4 criteria: (a) R/S ratio in lead V5 or V6 less than or equal to 1; (b) S V5 or V6 greater than or equal to 7 mm; (c) right-axis deviation of more than +90 degrees, or (d) P pulmonale; and (2) use of any 2 combinations of the foregoing criteria. Sensitivity ranged from 18 to 43% and specificity from 83 to 95%. Combined hypertrophy was best diagnosed using left atrial abnormality as the sole criteria of LV hypertrophy, plus any 1 of 3 criteria of RV hypertrophy: (a) R/S ratio in lead V5 or V6 less than or equal to 1, (b) S V5 or V6 greater than or equal to 7 mm, or (c) right axis deviation greater than +90 degrees.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmogenic right ventricular dysplasia: a clinical model for the study of chronic ventricular tachycardia.

Abstract: Arrhythmogenic right ventricular dysplasia (ARVD) is a recently individualised clinical entity which sometimes presents with episodes of ventricular tachycardia (VT). These attacks may be resistant to anti-arrhythmic therapy and new therapeutic approaches have been developed for the treatment of this condition. These new methods are mainly surgical, based on the analysis of the electrical activation of the heart in sinus rhythm and during VT. This approach has increased our understanding of the physiopathology of VT, not only in the context of ARVD, but also in the most commonly encountered clinical setting of VT, after myocardial infarction. Electrophysiological study of the epicardial activation of the dysplastic zones has demonstrated the presence of delayed potentials recorded after the end of the QRS complex. This can be explained by the histopathology of these tissues. ARVD is characterised histologically by partial degeneration of the myocardial wall. Most of the muscle fibers are replaced by fatty tissue in the middle of which some healthy fibers survive. These changes are mainly observed in the intramyocardial and subepicardial layers, the subendocardium being almost normal. Strands of isolated muscle fibers within the non-conducting fatty degeneration may lead to very delayed activation with respect to the adjacent healthy tissues. The propagation of activation is delayed as it passes through this plexiform structure and in the zones adjacent to healthy muscle were reentry phenomena may arise. In ARVD, these changes are mainly located over the right ventricle, so explaining the right ventricular origin of most forms of VT observed in this condition. However, we have also observed a case which suggested an isolated arrhythmogenic left ventricular dysplasia. Epicardial mapping localizes the point of origin of VT in zones situated between the slow and normally conducting tissues. Simple ventriculotomy, a full thickness section of the ventricular wall, at the point of epicardial breakthrough of the VT prevents recurrence in the great majority of patients. The same pathophysiological concepts may be applied to VT complicating myocardial infarction but in this situation the myocardial fibers capable of slowly conducting the activation are isolated within the fibrous tissue in the border zone of the infarct. The point of origin of VT is usually within the interventricular septum with a point of epicardial breakthrough which could be located some distance away. Different surgical techniques have been developed to deal with this condition. Encircling endocardial ventriculotomy isolates the arrhythmogenic zone from the rest of healthy tissues by tracin

Systemic venous and pulmonary arterial flow patterns after Fontan's procedure for tricuspid atresia or single ventricle.

Abstract: Despite increasing use of Fontan or modified Fontan repairs, the comparative hemodynamic efficacy of different types of connections are unresolved. Accordingly, we undertook a prospective study designed to determine postoperative flow patterns after Fontan's operation. Seven subjects had tricuspid atresia and eight had single ventricle. Ages ranged from 5 to 38 years (mean 16.4). Ten subjects had nonvalved right atrial-to-pulmonary arterial connection, and four had nonvalved right atrial-to-right ventricular communication. A valved conduit established continuity between the right atrium and right ventricle in one subject. Doppler flow profiles were recorded in the pulmonary artery and in the superior and inferior venae cavae of each. A reference electrocardiogram was used for timing purposes. In 14 patients, forward flow in the pulmonary artery was biphasic. Flow began at the end of the T wave (early ventricular diastole), peaked at or before the P wave (atrial systole), and returned to baseline by the peak of the R wave. Forward flow recommenced at the peak of the R wave (ventricular systole) and returned to baseline at the end of the T wave. Flow in the superior vena cava varied, and could not be recorded in three subjects. Between the end of the P wave and peak of the R wave (atrial systole) flow was reversed in eight, absent in three, and forward in one patient. Forward flow occurred between the peak of the R wave and the end of the T wave and was either continuous or biphasic. Fourteen patients had adequate studies of inferior vena cava flow; reversed flow during atrial systole occurred in 10 subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Heart transplant rejection monitored by signal-averaged electrocardiography in patients receiving cyclosporine.

Abstract: Data from standard and high-frequency signal-averaged electrocardiograms (ECGs) were correlated with the results of 67 endomyocardial biopsies performed in 20 cyclosporine-treated heart transplant recipients. Eight patients (group 1) were in the early postoperative hospitalization period and 12 patients (group 2) were studied after their hospital discharge. The biopsy samples were classified as normal or as indicating early (cellular infiltrate) or definite rejection (myocyte necrosis). The standard ECG parameter studied was the summated QRS voltage in leads I, II, III, V1, and V6. The signal-averaged ECG was evaluated for QRS duration, high-frequency voltage amplitude of the total QRS complex and of its three thirds, peak QRS voltage amplitude, and QRS integrated voltage-time product. The ECG recording obtained at the time of a first normal biopsy sample was considered the normal reference to which additional tracings from the same patient were compared. At the time of subsequent biopsies, the standard ECG parameter showed poor reproducibility (r = .58) and it was inadequate in defining rejection episodes in the early or late postoperative period. The signal-averaged ECG was more reproducible (r = .83) and more accurate in detecting definite rejection during the late posttransplant period than the standard ECG. In group 2 patients, 92% of abnormal signal-averaged ECG recordings were associated with rejection episodes and only 13% of normal tracings were associated with definite rejection. The method was inadequate, however, in monitoring patients during the early postoperative period and in detecting mild forms of rejection in the late postoperative phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Life threatening ventricular tachycardias in late survivors of surgically corrected tetralogy of Fallot.

Abstract: Electrophysiological tests were performed in three patients with surgically corrected tetralogy of Fallot (mean age at evaluation 25 years, mean age at surgical correction 4 years) who had had either a cardiac arrest or transient neurological disturbances (presyncope, syncope) associated with ventricular arrhythmias. All three patients had an excellent haemodynamic result from surgery as judged by echocardiography and cardiac catheterisation. Ambulatory electrocardiographic monitoring and stress exercise testing were normal in two patients and showed complex ventricular ectopy in one. During invasive electrophysiological evaluation all three patients had inducible ventricular tachycardia (monomorphic QRS in two patients, cycle lengths 230 and 240 ms; polymorphic QRS in one patient, mean cycle length 200 ms) with adverse haemodynamic effects in all three patients. These findings suggest that rapid ventricular tachycardia with detrimental haemodynamic consequences, similar to that induced during laboratory study, was the basis for the presenting symptoms in each patient. This possibility was confirmed in one patient who had identical QRS morphology during both spontaneous ventricular tachycardia and that induced during the laboratory study. Thus sudden death or symptoms of syncope postoperatively in patients with surgically corrected tetralogy of Fallot appear to be due to rapid ventricular tachycardia, which may occur despite an apparently excellent surgical result.

Recurrent Ventricular Tachycardia Responsive to Verapamil

Abstract: We describe five young patients with recurrent ventricular tachycardia in the absence of organic heart disease. In all patients tachycardia could be terminated or prevented with verapamil. Tachycardia in four patients was very similar, with a QRS pattern of right bundle branch block and left axis deviation. Electrophysiology studies in two patients showed that VT was inducible in one patient (rapid atrial or ventricular pacing, ventricular extrastimuli) but not in the other. The clinical and electrocardiographic similarities in these patients suggest that their ventricular tachycardias may share a common pathophysiology and may be dependent on slow channel activity.

Experimental amitriptyline intoxication: electrophysiologic manifestations and management.

Abstract: Amitriptyline intoxication can result in severe ventricular arrhythmias that may be refractory to medical management. The mechanisms of these arrhythmias are unclear, and their optimal management is problematic. We studied the cardiac effects of amitriptyline infusion in anesthetized and awake dogs. Amitriptyline significantly increased heart rate, QRS duration, and AH and HV intervals. The concentration-response curves for these effects were, however, quite different, with significant changes beginning at a concentration of 1.5 +/- 0.4 mg/L for heart rate, compared with 2.4 +/- 0.4 mg/L for QRS and HV intervals and 3.7 +/- 0.5 mg/L for the AH interval. Ventricular tachyarrhythmias developed after marked QRS widening had occurred, and appeared in all six awake dogs and five of the six anesthetized dogs studied. Sodium bicarbonate was given to seven animals with ventricular tachyarrhythmias, and it rapidly reversed the arrhythmia in all instances. The benefit from sodium bicarbonate could not be attributed to changes in serum potassium or amitriptyline concentrations. It may have been due to alkalinization or changes in serum sodium concentration. These experiments suggest that: (a) amitriptyline intoxication frequently produces ventricular tachyarrhythmias, if high enough drug concentrations are achieved; (b) these arrhythmias are associated with marked slowing of intraventricular conduction; and (c) sodium bicarbonate is effective therapy for amitriptyline-induced ventricular arrhythmia.

Class 1 antiarrhythmic drugs-Characteristic electrocardiographs differences when assessed by atrial and ventricular pacing

Abstract: Class 1 antiarrhythmic drugs have been subdivided into la, lb and lc according to their effect on the action potential duration. The effects on the surface electrocardiogram of one drug from each subgroup were investigated in nine patients. Electrocardiographs recordings were taken during sinus rhythm and at identical atrial and ventricular paced rates. Disopyramide (la) significantly prolonged the QT interval during sinus rhythm and at the identical paced rates, by increasing both the QRS duration and JT interval. Lignocaine (lb) significantly reduced the Q T interval during sinus rhythm and at the identical paced rates, by reducing the JT interval. Lignocaine had no effect on the QRS duration. Flecainide (lc) significantly prolonged the QRS duration during sinus rhythm, but not the Q Tc. However the Q T interval at the paced rates prolonged significantly, due entirely to an increase of the QRS duration. Flecainide had no effect on the JT interval. These characteristic electrocardiographic differences support the differentiation of class 1 drugs into three separate subgroups.

Determinants of arrhythmogenic ventricular activity detected on the body surface QRS in patients with coronary artery disease

Abstract: The prevalence of arrhythmogenic ventricular activity (AVA) was investigated in 166 patients with coronary artery disease. Thirty patients had documented ventricular tachycardia (VT)/ventricular fibrillation (VF). Bipolar X,Y,Z leads were signalaveraged and filtered with a 40-Hz, bidirectional, high-pass digital filter. The filtered QRS signals were analyzed for the amplitude of the last 40 and 50 ms; duration of low-amplitude potentials ( μ V) in the terminal portion; and duration of the filtered QRS. A positive AVA test result was defined as the presence of 2 or more abnormal indexes. Of the 30 patients with VT/VF, 66% had positive AVA test results (AVA-positive patients). Of the 136 patients without VT/VF, 25% had positive AVA test results. The following univariate variables showed significant correlation with an AVA-positive test: age, previous myocardial infarction, previous VT/VF, left ventricular wall motion abnormalities and left ventricular ejection fraction. Multivariate stepwise discriminant function analysis revealed that the presence of previous myocardial infarction and history of sustained VT/VF were the only independent determinants of AVA. During electrophysiologic studies, sustained VT/VF could be induced in 77% of the AVA-positive patients (24 of 31) and in 30% of the AVA-negative patients (3 of 10). The survival probabilities for 6, 12 and 18 months of follow-up were 92%, 85% and 85% for the AVA-positive and 97%, 92% and 90% for the AVA-negative patients. Our findings support the concept that a positive AVA test result reflects areas of delayed ventricular activation. The areas of delayed ventricular activation are associated with previous myocardial injury and scar tissue and serve as an anatomic basis for reentry. Quantitative analysis of the high-frequency components of the terminal portion of the signalaveraged body surface QRS may be a helpful screening test for detection of patients at high risk of VT/VF.

The QRS morphology in post-myocardial infarction ventricular tachycardia. A study of 100 tracings compared with 70 cases of idiopathic ventricular tachycardia.

Abstract: A hundred tracings of ventricular tachycardia (VT) belonging to 85 patients with myocardial infarction (MI) were compared with 70 cases of incessant, benign, idiopathic VT. The two groups of tracings differed in terms of QRS axis, most often normal in idiopathic VT (75%) and outside normality in MIVT (74%). The sum of QRS amplitude in unipolar limb leads was greater in idiopathic VT (4.3±1.3 mv, mean±S.D.) than in MIVT (2.6±0.8 mv, P>0.001). The QRS width was also different: 135±11 ms in idiopathic VT vs. 171±32 ms in MIVT (P>0.001). The QRS morphology in MIVT was characterized by the presence of a QR pattern in leads other than VR, or a QS pattern in V5–V6. These two aspects were constantly absent in idiopathic VT, and they were present in 89%of MIVT. In only 38 MIVT tracings were the ECG signs of MI observed in the same leads during sinus rhythm and during VT. In 51 MIVT tracings the location of the MI indicated by the VT tracing differed from that displayed in sinus rhythm. Rather than indicating an extension of the infarcted area not apparent in the tracings in sinus rhythm, such a discrepancy suggests that the QRS pattern during VT strongly depends on the point of origin of the VT. Conversely, this explains why the morphology of the QRS is an ureliable means for localizing the VT origin if the location of the MI is not taken into account. We conclude that both factors should be taken into consideration, and this might theoretically permit a better though complex approach to the VT origin in coronary heart disease using surface tracings.

Microtransection of the His bundle with laser radiation through a pervenous catheter: correlation of histologic and electrophysiologic data.

Abstract: This study describes microtransection of the His bundle with a pervenous laser catheter in a live dog. In an adult mongrel dog anesthetized with Nembutol , administered intravenously, electrode catheters (No. 5Fr and 6Fr ) were inserted through a femoral vein and positioned in the high right atrium for atrial pacing and in the His bundle region for recording of His bundle electrograms. The AH and HV intervals were measured during normal sinus rhythm and atrial pacing. Through another femoral vein, a laser fiber was inserted through a lumen catheter (No. 7Fr ) with a preformed curved tip. Under fluoroscopic control, the laser fiber tip was positioned immediately next to the His bundle electrode catheter. During continuous His bundle recordings and fluoroscopic monitoring, short bursts (10 to 60 seconds) of argon laser were delivered (2.5 W) in order to produce His bundle interruption and complete heart block. Escape of a His bundle rhythm (cycle length = 1,100 ms) with QRS morphologic characteristics and duration similar to that of normal sinus rhythm was noted. "Split" His bundle potentials were recorded with an unchanged AH (50 ms) and an H'V interval of 20 ms. After the dog was killed, serial sections of the conduction system of the heart were analyzed. Histologic findings showed excellent correlation with electrophysiologic observations and validated "split" His bundle potentials. The laser radiation produced microtransection of the His bundle with a channel of tissue dissolution 0.2 to 0.3 mm wide in diameter. The latter passed through the His bundle at the junction of penetrating and branching segments, dividing it into superior and inferior portions that retained continuity with proximal and distal His bundle.(ABSTRACT TRUNCATED AT 250 WORDS)