Showing papers on "QRS complex published in 1983"

Relation Between Late Potentials on the Body Surface and Directly Recorded Fragmented Electrograms in patients With Ventricular Tachycardia

Abstract: The relation between low-amplitude, late potentials on the body surface and directly recorded electrograms in 8 patients with and 11 patients without ventricular tachycardia (VT) was studied. Bipolar X,Y,Z leads were signal-averaged and filtered with a digital technique. All patients had catheter endocardial left ventricular maps. The VT group had medically intractable VT and an endocardial excision was performed for control of VT. Before bypass, epicardial maps were obtained in the operating room. All studies were performed during normal sinus rhythm. Four patients without VT, each with a previous myocardial infarction, had fragmented endocardial electrograms recorded at 2.0 ± 1.2 sites. The latest electrogram for each patient ended 87 ± 8 ms after QRS onset, within the high-amplitude portion of the filtered QRS complex. All patients with VT had fragmented electrograms recorded at 6.1 ± 3.1 sites/patient. Eighty-eight percent of the fragmented electrograms were endocardial. The latest fragmented electrogram for each patient ended 161 ± 43 ms after QRS onset, significantly later than the fragmented electrograms from the patients without VT (p = 0.002). Six VT patients had low-amplitude, late potentials at the end of the filtered QRS complex. In these patients, the last 40 ms of the filtered QRS complex contained a higher proportion of fragmented electrograms compared with earlier segments of the QRS complex (68% versus 27%, p It is concluded that the late potential corresponds to delayed, fragmented electrographic activity. Failure to record a late potential may arise from delayed ventricular activation at other sites from bundle branch block or fragmented electrograms of a brief duration.

Evaluation of a QRS scoring system for estimating myocardial infarct size

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.

Quantitative analysis of the high-frequency components of the terminal portion of the body surface QRS in normal subjects and in patients with ventricular tachycardia.

Abstract: Quantitative analysis of the high-frequency components of the terminal portion of the surface QRS was performed in 42 normal subjects (group 1, ages 18-67 years, mean +/- SEM 34.7 +/- 2.2 years) and in 12 patients with symptomatic, sustained ventricular tachycardia (VT) (group 2, ages 48-76 years, mean 59 +/- 2.3 years). Signal averaging and high-pass, bidirectional digital filtering were used for analysis. The total duration of the QRS, the duration of the low-amplitude signals (less than 40 microV) in the terminal portion of the QRS and the amplitude of the signals in the last 40 and 50 msec of the QRS were measured at filter settings of 25 and 40 Hz. Reproducibility of the measurements was tested in 15 normal subjects by comparing results obtained from two consecutive recordings. Significant differences were found between normal subjects and VT patients for all four indexes at both 25- and 40-Hz filters. Specific values for each of the indexes were identified at the 40-Hz filtering, which could separate normal subjects from VT patients (20 microV for the amplitude of last 40 msec; 30 microV for the amplitude of last 50 msec; 120 msec for the total duration; and 39 msec for the low-amplitude signal of the filtered QRS). Using these values for the four indexes, respectively, 90%, 98%, 100% and 90% of the normal subjects and 83%, 83%, 58% and 83% for the VT group were correctly classified. The results show that the high-frequency analysis of the signal-averaged body surface QRS is a reliable, reproducible, noninvasive method for distinguishing patients with VT from normal subjects.

Idiopathic paroxysmal ventricular tachycardia with a QRS pattern of right bundle branch block and left axis deviation: A unique clinical entity with specific properties

Abstract: Eiectrophysiologic evaluation before and after the serial administration of verapamil, lidocaine, propranolol, and procainamide was undertaken in 4 young, asymptomatic patients with recurrent, sustained ventricular tachycardia (VT). No patient had obvious organic heart disease. The electrocardiogram during sinus rhythm showed S-T depression and T-wave inversion over the inferior and lateral precordial leads in 3 patients. QRS morphologic characteristics during episodes of VT showed a pattern of right bundle branch block and left axis deviation. In all 4 patients, VT could be both induced and terminated with electrical stimulation. Verapamil terminated VT and prevented the induction of sustained VT in 3 patients, and markedly slowed the rate of VT in 1 patient. Procainamide effectively prevented the induction of sustained VT in 2 patients, and although ineffective in preventing induction in 2 patients, it slowed the rate of tachycardia in both. Lidocaine and propranolol did not prevent the induction of VT in any patient. These findings suggest that slow-response tissues may be involved in the genesis of VT in these patients, and that VT in these patients may represent a unique clinical entity with distinct electrocardiographic, electrophysiologic, and electropharmacologic properties.

Delineation of the QRS complex using the envelope of the e.c.g.

Abstract: A new algorithm for QRS delineation has been developed. Based on the envelope of the e.c.g. signal a delineation function is defined, which yields a single positive pulse for each complex. From this function the onset and end of the QRS or, alternatively, a fiducial point is determined. To remove low-frequency component such as S-T abnormalities without distortion of the QRS complex, a filter with time-varying characteristics is used. The accuracy of the method has been evaluated in a test set of different QRS complexes obtained from coronary care patients. For QRS onset, the standard deviation of the difference between automated and manual determination was 7 ms in normal beats and 14 ms in ectopic beats. With simulated noise added to each waveform an average dispersion of 7 ms was observed in the recognition of the QRS onset at a signal-to-noise ratio of 15 dB. The corresponding dispersion in the location of a fiducial point was 2 ms. Using simulated e.c.g. data, the stability of the method is demonstrated for transitions between different waveform morphologies.

Ventricular tachycardia induced by atrial stimulation in patients without symptomatic cardiac disease

Abstract: Ten patients with an unusual form of ventricular tachycardia (VT) are described. All were young (mean age 21 years) at the onset of VT, symptoms were of long duration (mean 7 years), none had symptomatic organic heart disease, VT was induced by atrial and ventricular stimulation, VT had a characteristic QRS morphologic picture resembling right bundle branch block with left-axis deviation and 9 had early retrograde His deflections during VT. Supraventricular tachycardia (SVT) was excluded in every patient by electrophysiologic study, although QRS morphologic characteristics and clinical stability of these patients during tachycardia frequently led to the diagnosis of SVT before referral. Four patients received verapamil during electrophysiologic testing. Verapamil slowed and terminated VT in all. Three patients are being treated chronically with oral verapamil, 3 patients with conventional antiarrhythmic agents and 1 with a radiofrequency ventricular pacemaker.

Ambulatory ECG analyzer and recorder

Abstract: An ambulatory cardiac analyzer and recorder includes an allocation and priority scheme which has quotas for classes of QRS events and priority between types of events within a class. The quality of a low priority event is used to replace a similar type of event when the memory is full. The peak detection, QRS identification and classification circuit process and correlate information from both of two input channels. This allows quicker and more accurate determination of QRS waveforms as well as typical QRS waveforms.

Value of QRS alteration in determining the site of origin of narrow QRS supraventricular tachycardia.

Abstract: To determine the value of alternation of QRS morphology in determining the site of origin of sustained narrow QRS supraventricular tachycardia (SVT), we retrospectively studied 163 distinct tachycardias in 161 patients (ages 4 to 91 years) in whom the site of origin of SVT was proven by intracardiac electrophysiologic study. Sustained SVT was defined as lasting longer than 30 sec. Narrow QRS was defined as QRS width less than 0.12 sec. Atrial fibrillation and flutter were excluded. The presence or absence of QRS alternation was judged at least 10 sec after initiation of SVT. Circus movement tachycardia with anterograde AV node conduction and a retrograde accessory AV pathway was seen in 89 patients (58 with Wolff-Parkinson-White syndrome, 31 with concealed accessory pathway); intra-AV nodal reentrant tachycardia (AVNT) was present in 57 cases, and 17 tachycardias were atrial in origin. QRS alternation was present in 36 of 163 cases (22%). In only eight of these 36 did RR interval length alternation accompany alternation in QRS morphology. Thirty-three of 36 (92%) tachycardias with QRS alternation were circus movement tachycardias. Two were atrial in origin and one was AVNT. We conclude that the presence of QRS alternation during sustained narrow QRS SVT is highly indicative of a retrograde accessory AV pathway in the tachycardia circuit.

Isointegral analysis of body surface maps for the assessment of location and size of myocardial infarction.

Abstract: To estimate the location and size of myocardial infarction (MI), an isointegral mapping technique was adopted from among various body surface electrocardiographic mapping techniques. QRS isointegral and departure maps were made in 35 patients with MI. These patients were separated into 3 groups, based on the location of MI: anterior, inferior, and anterior plus inferior. The severity and location of MI were estimated by thallium-201 myocardial perfusion imaging and the degree of scintigraphic defect was represented by a defect score. The extent of MI was expected to be reflected on the QRS isointegral maps as a distribution of negative QRS complex time-integral values. However, the extent and the location of MI were hardly detectable by the original maps. A departure mapping technique was then devised to observe the distribution of departure index on the body surface. Particular attention was given to the area where the departure index was less than −2, and this area was expected to reflect the location and size of specific abnormality of isointegral map due to MI. There were strong correlations between departure area and defect score in the anterior and inferior MI cases (r = 0.88 and r = 0.79, respectively). However, patients with anterior MI plus inferior MI showed no such correlation. Q-wave mapping was compared with QRS isointegral mapping, and QRS isointegral mapping was found to be more accurate in the estimation of the location and size of MI than Q wave mapping. Thus, QRS isointegral mapping, especially departure mapping, is more useful and convenient for detecting the location and size of MI than methods such as isopotential and Q wave mapping.

Bundle branch reentry: a possible mechanism of ventricular tachycardia.

Abstract: Electrophysiologic studies were performed in three patients suffering from attacks of paroxysmal tachycardia with wide QRS complexes. Two patients had atrioventricular dissociation. The arrhythmia could be initiated and terminated by premature ventricular stimulation in all three patients. One patient developed the arrhythmia after rapid atrial stimulation. In each subject, the QRS complexes during tachycardia were identical to recorded supraventricular beats (left bundle branch block pattern in two cases and right bundle branch block pattern in one). A His bundle potential was noted before the QRS complex; the HV interval was equal to or longer than that of the sinus beats. The following observations suggested the presence of a bundle branch reentry mechanism: (1) the relationship between bundle branch block development and tachycardia initiation; (2) the occurrence of tachycardia after electrically induced His-Purkinje reentry; (3) the ability of premature ventricular stimulation during tachycardia to advance the timing of the His deflection and QRS complex, with an unchanged or slightly increased HV interval; and (4) the termination of arrhythmia by premature ventricular depolarization blocked within the bundle branch system. Our results support the idea that bundle branch reentry can play a role in the genesis of ventricular tachycardia.

A mechanism of torsades de pointes in a canine model.

Abstract: A dog model of torsades de pointes (TdP) was developed. Twenty 18-30-kg dogs had cardiopulmonary bypass instituted to maintain stable temperature, perfusion pressure and oxygenation. Quinidine, 30 mg/kg, was then administered and burst ventricular pacing was used to induce arrhythmias. The left anterior descending coronary artery was occluded for 15 minutes and repeat pacing studies were performed. Maps of epicardial activation were made from 27 simultaneously recorded electrograms obtained from 1-mm bipolar electrodes secured to the epicardium with a nylon mesh sock. Arrhythmias in five dogs met criteria for the diagnosis of TdP: All had the characteristic undulating QRS morphology typically associated with TdP, all occurred in the setting of QT prolongation and all ended spontaneously. The epicardial maps demonstrated that each change in QRS morphology was associated with a change in the site of epicardial breakthrough. Those QRS complexes during the transition from one morphology to the next were associated with fusion cycles in which both the old and new sites of epicardial breakthrough were present. In essence, two or more competing activation sequences were vying for control of epicardial depolarization. This conclusion was strengthened by our ability to simulate TdP in the surface ECG and in epicardial maps by simultaneously pacing from two widely separated ventricular sites at slightly different, varying rates.

Evaluation of a QRS scoring system in acute myocardial infarction: Relation to infarct size, early stage left ventricular ejection fraction, and exercise performance

Abstract: Recent studies suggest that the QRS scoring system (QRSs) using observations of Q- and R-wave duration and R Q and R S amplitude ratios in the standard electrocardiogram (ECG) is useful in estimating left ventricular function after acute myocardial infarction (AMI). The correlation of QRSs with infarct size determined by serum creatine kinase MB changes and early stage left ventricular ejection fraction (LVEF) determined by multiple gated equilibrium cardiac blood pool scintigraphy was studied in 32 patients with AMI using ECGs taken 3 and 7 days after onset. The relation of QRSs to exercise performance was also examined in 45 other patients who underwent heart rate limited low level exercise test (LLET) soon after AMI (12.3 ± 5.6 days, mean ± standard deviation). The QRSs of 7 days after onset significantly correlated with both infarct size and LVEF; infarct size (CK·g·Eq) = 5.24 QRSs + 8.50 (r = 0.72, p Patients with exercise tolerance of 12 minutes (9.0 ± 3.3 versus 4.5 ± 2.4 and 3.6 ± 2.2, p 5 minutes, whereas all patients who could not exercise for > 5 minutes (10 of 45 patients) had QRSs > 5. The relation between QRSs and the reasons for termination of LLET showed that patients with fatigue or dyspnea, or both, had significantly higher QRSs (8.7 ± 4.6) than those in target heart rate (5.4 ± 2.2, p These data suggest that QRSs will be clinically useful not only as a variable correlating with infarct size and LVEF but also as an aid in early identification of exercise performance soon after AMI.

Comparison of total body surface map depolarization patterns of left bundle branch block and normal axis with left bundle branch block and left-axis deviation.

Abstract: Total body surface maps from 15 subjects with left bundle branch block and normal axis (LBBB-NA) and 10 subjects with left bundle branch block and left axis (LBBB-LA) were analyzed and compared with maps from normal subjects. In 19 of the 25 subjects with LBBB, the timing of early upper sternal positivity was similar to that of normal subjects, indicative of timely but oppositely directed septal activation. The right ventricular breakthrough was normally located in all, but was earlier after the onset of QRS than expected in some. The initial portion of the positivity produced by left ventricular activation was located in the upper anterior chest in both LBBB-NA and LBBB-LA, but its onset was generally delayed compared with that in normal subjects, presumably because of the time taken by the right-to-left septal activation. Also, the total duration of this positivity was longer than in normal subjects and extended considerably beyond 90 msec, indicating prolonged activation of the anterior free wall of the left ventricle. In LBBB-NA, this upper anterior positivity remained anterior throughout depolarization, but in LBBB-LA it moved toward the left shoulder and the left upper back, presumably due to the posterior orientation of the terminal portion of depolarization. This terminal orientation in patients with LBBB-LA was thought to be due to the additional delay in the activation of the anterobasal portion of the left ventricle caused by selective involvement of the left anterior fascicle.

Quantitative assessment of myocardial ischemia and necrosis by continuous vectorcardiography and measurement of creatine kinase release in patients.

Abstract: The accuracy of the use of the maximal QRS vector difference to estimate myocardial infarct size irrespective of infarct location was compared with that of measurement of cumulative creatine kinase (CK) release. Sixty patients with acute myocardial infarction and a history of symptoms of less than 4 hr duration were followed for 24 to 72 hr with orthogonal vectorcardiography and CK release analysis. Spatial QRS vector differences were calculated between the first QRS complex recorded and subsequent QRS complexes at timed intervals. The QRS vector difference increased rapidly and reached a plateau at an average 12.1 hr after onset of symptoms, as compared with 34.0 hr for the cumulated CK release. In 42% of the patients a stepwise progression of infarct evolution was observed. Irrespective of infarct location the maximal spatial ST vector magnitude was related to the ultimate QRS vector difference (r = .80) and to the cumulative amount of CK released (r = .64). Furthermore, maximal QRS vector difference correlated well with the maximal cumulative CK release (r = .64) Ten patients had possible infarct expansion, as indicated by recurrent QRS changes without concomitant CK release. Fifteen patients had infarct extension that was indicated by secondary CK release and that in seven patients was associated with further QRS changes. Infarct extension caused an approximate 25% increase in infarct size. Spatial ST vector magnitude, QRS vector difference, and cumulative CK release are complementary measures in the quantification of evolving myocardial injury after acute coronary occlusion and in the determination of sequels to therapeutic interventions.

A quantitative relationship of electrocardiographic criteria of left ventricular hypertrophy with echocardiographic left ventricular mass: a multivariate approach.

Abstract: The purpose of this study was to evaluate the sensitivity of various electrocardiographic (EKG) criteria of left ventricular hypertrophy (LVH) in relation to echocardiographic left ventricular mass (LVME) and to assess the relative strength of various EKG variables used in the diagnosis of LVH by multivariate analysis. An attempt was also made to determine if a new combination of precordial and T-wave voltage could improve the sensitivity of EKG. In 89 patients, M-mode echocardiograms and standard EKGs were studied. Correlation of Romhilt-Estes point-score system with LVME was r = 0.621, sensitivity and specificity was 57 and 81%, respectively. Other voltage criteria had lower sensitivity. Various combinations of precordial and T-wave voltage were not superior. The quantitative relationship of individual EKG variable, QRS duration, S V1-3, R V4-6, strain T wave, left atrial abnormality, intrinsicoid deflection and axis, with LVM was, r = 0.661, 0.595, 0.429, 0.42, 0.347, and 0.225, respectively. By multivariate analysis, QRS duration, S V1-3, T-wave and R V4-6 voltage had F-value (relative strength) of 27.95, 27.15, 22.02, and 4.03, respectively, other variables were statistically insignificant. In conclusion, the most important EKG variables predictive of LVH are QRS duration, S V1-3, strain T-wave and lateral voltage in decreasing value. Rescoring these variables in accordance to their correlation to LVM may improve EKG sensitivity for the diagnosis of LVH.

Electrocardiographic, echocardiographic and ventriculographic characterization of hypertrophic non-obstructive cardiomyopathy

Abstract: HNCM tends to have more diffuse or generalized hypertrophy than HOCM, although these two types are not fundamentally different in aetiology (genetic). Extreme ASH is primarily related to a hereditary factor while HNCM, including apical hypertrophy, seems to be based on an abnormal disposition to produce myocardial hypertrophy in response to endogenous or exogenous stimulation such as catecholamines, chronic anoxia, hypertension or even aging. Hypertension by itself, however, can not be a cause of apical hypertrophy. The configuration of left ventricular hypertrophy in HCM can be divided roughly into several patterns: ASH, apical, postero-inferior, generalized or diffuse types, etc. ASH is not an essential morphology for HNCM. Apical hypertrophy is the only specific hypertrophic pattern which shows characteristic ECG abnormalities (giant negative T waves and high QRS voltage in left precordial leads). Inverted T waves combined with high QRS voltage tends to be a reflection of a localized hypertrophic portion in the left ventricular free wall. Abnormal Q waves associated with left axis deviation usually suggest marked septal hypertrophy. They seem to be related to conduction disturbances in myopathic septum.

Left bundle branch block and mechanical events of the cardiac cycle

Abstract: Left bundle branch block (LBBB) is associated with a prolongation of the interval from the QRS onset to the onset of left ventricular (LV) ejection. The locus and prevalence of specific sites of delay were examined in 56 patients with complete LBBB using echocardiography, phonocardiography and external pulse recordings. The results were compared with those in 52 control subjects without LBBB. The onset of the QRS complex was used as the initial reference point of measurement of time intervals. The following abnormalities were found in patients with LBBB: (1) delayed mitral valve closure (Q-MC greater than 0.08 second) was the major site of delay in 23% of patients; (2) prolongation of the LV isovolumetric contraction time (greater than 0.06 second) was the major site of delay in 41%; (3) both Q-MC and LV isovolumetric contraction time were prolonged in 18%; and (4) in 26% of patients the onset of ventricular contraction determined by the onset of the increase of the apex impulse was delayed (Q-VC greater than 0.07 second). The most common cause of delayed ejection was a prolonged LV isovolumetric contraction time, which occurred in 59% of patients. A control group of 20 patients with abnormal LV function but without LBBB had a low incidence of the 3 types of delay in LV ejection (0 to 15%). Thus, the major abnormalities in the cardiac cycle in LBBB are due to the conduction defect and not to LV dysfunction. The results of this study suggest the presence of variable abnormalities of conduction in complete LBBB.

Electrocardiographs criteria for the diagnosis of anterior myocardial infarction: Importance of the duration of precordial R waves

Abstract: A systematic evaluation of a large number of electrocardiographic (ECG) variables that might be useful for diagnosing anterior myocardial infarction (MI) is reported. Previous anterior MI was shown to be present or absent by cardiac catheterization in 199 patients. The best discriminator between cases and noncases of anterior MI in most patients is the presence of a Q wave of any magnitude or an initial R wave < 20 ms in lead V2. In patients with ECG evidence of associated left ventricular or type C right ventricular enlargement, the more stringent criterion of a Q wave of any magnitude in lead V2 yielded the optimal combination of sensitivity and specificity for diagnosing anterior MI. The diagnostic performance of the proposed criteria for anterior MI is superior to that of more traditional criteria that use measurements of the absolute and relative amplitudes of precordial R waves.