Showing papers on "QRS complex published in 1994"
TL;DR: Results of this investigation suggest that regression of ECG features of left ventricular hypertrophy confers an improvement in risk for cardiovascular disease, whereas serial worsening imposes increased risk.
Abstract: BACKGROUNDDuring the past half-century, the ECG has been used extensively for the diagnosis of left ventricular hypertrophy. Persons with ECG evidence of left ventricular hypertrophy are at increased risk for the development of cardiovascular disease.METHODS AND RESULTSSubjects from the Framingham Heart Study with ECG evidence of left ventricular hypertrophy were eligible for this investigation if they were free of cardiovascular disease and did not have complete bundle-branch block or Wolff-Parkinson-White syndrome. Logistic regression analyses of pooled biennial examinations were used to determine risk for cardiovascular disease as a function of baseline voltage (sum of R wave in aVL plus S wave in V3) and repolarization and as a function of serial changes in these ECG features of hypertrophy. The eligible sample consisted of 274 men (mean age, 60 years) and 250 women (mean age, 64 years) who contributed 2660 person-examinations. During follow-up, there were 269 new cardiovascular events. Compared with ...
616 citations
TL;DR: A 54‐year‐old man received a four chamber pacing system for severe congestive heart failure and his clinical status improved markedly with a weight loss of 17 kg and disappearance of peripheral edema.
Abstract: A 54-year-old man received a four chamber pacing system for severe congestive heart failure (NYHA functional Class IV). His ECG showed a left bundle branch block (200-msec QRS duration) with 200-msec PR interval, normal QRS axis, and 90-msec interatrial interval. An acute hemodynamic study with insertion of four temporary leads was performed prior to the implant, which demonstrated a significant increase in cardiac output and decrease of pulmonary capillary wedge pressure. A permanent pacemaker was implanted based on the encouraging results of the acute study. The right chamber leads were introduced by cephalic and subclavian approaches. The left atrium was paced with a coronary sinus lead, Medtronic SP 2188-58 model. An epicardial Medtronic 5071 lead was placed on the LV free wall. The four leads were connected to a standard bipolar DDD pacemaker, Chorus 6234. The two atrial leads were connected via a Y-connector to the atrial channel of the pacemaker with a bipolar pacing configuration. The two ventricular leads were connected in a similar fashion to the ventricular channel of the device. The right chamber leads were connected to the distal poles. The left chamber leads were connected to the proximal poles of the pacemaker. Six weeks later, the patient's clinical status improved markedly with a weight loss of 17 kg and disappearance of peripheral edema. His functional class was reduced to NYHA II. Four chamber pacing is technically feasible. In patients with evidence of interventricular dyssynchrony, this original pacing mode probably provides a mechanical activation sequence closer to the natural one.(ABSTRACT TRUNCATED AT 250 WORDS)
522 citations
TL;DR: Prolonged QRS duration and increased dispersion of repolarization make independent contributions to the risk of arrhythmic cardiac death in patients with coronary artery disease.
Abstract: In a recent prospective study of myocardial ischemia, arrhythmic cardiac death occurred in 17 of 936 patients (2%) during a 2-year follow-up after acute myocardial infarction or unstable angina. Dispersion of ventricular repolarization was evaluated on the 12-lead electrocardiogram at enrollment in 17 patients who subsequently died of cardiac arrhythmia and in 51 matched survivors. The aim of this study was to evaluate the relation between various measurements of dispersion of repolarization and subsequent arrhythmic cardiac death, and to determine if dispersion of repolarization makes an independent contribution to the risk of arrhythmic cardiac death. Ventricular depolarization quantitated in terms of mean QRS (QRS-m) duration, and ventricular repolarization quantitated in terms of mean (m), maximal-minimal dispersion (d), standard deviation (s), and coefficient of variation (cv) of QT and JT intervals, were determined. Univariate analyses revealed that 2 standard electrocardiographic parameters, QRS-m and QT-m, and 3 dispersion variables, JT-d, JT-s, and JTc-d, were associated with arrhythmic cardiac death (p < 0.01). Multivariate analyses revealed that the combination of the dispersion parameter (JT-d, JT-s, or JTc-d) and QRS-m made an independent contribution to the risk of arrhythmic cardiac death. The findings highlight the importance of both delayed depolarization and heterogenous repolarization as risk factors for arrhythmic cardiac death. Thus, increased dispersion of repolarization is associated with an elevated likelihood of arrhythmic cardiac death. Prolonged QRS duration and increased dispersion of repolarization make independent contributions to the risk of arrhythmic cardiac death in patients with coronary artery disease.
342 citations
TL;DR: The hypothesis that QTd after AMI depends on reperfusion status as well as infarct site and size is supported, as successful thrombolytic therapy is associated with lessQTd and JTd in post-AMI patients.
Abstract: BACKGROUNDQT dispersion (QTd, equals maximal minus minimal QT interval) on a standard ECG has been shown to reflect regional variations in ventricular repolarization and is significantly greater in patients with than in those without arrhythmic events.METHODS AND RESULTSTo assess the effect of thrombolytic therapy on QTd, we studied 244 patients (196 men; mean age, 57 +/- 10 years) with acute myocardial infarction (AMI) who were treated with streptokinase (n = 115) or anistreplase (n = 129) at an average of 2.6 hours after symptom onset. Angiograms at 2.4 +/- 1 hours after thrombolytic therapy showed reperfusion (TIMI grade > or = 2) in 75% of patients. QT was measured in 10 +/- 2 leads at 9 +/- 5 days after AMI by using a computerized analysis program interfaced with a digitizer. QTd, QRSd, JT (QT minus QRS), and JT dispersion (JTd, equals maximal minus minimal JT interval) were calculated with a computer. There were significant differences in QTd (96 +/- 31, 88 +/- 25, 60 +/- 22, and 52 +/- 19 milliseco...
269 citations
Patent•
19 Mar 1994TL;DR: In this article, a fiducial point of each successive QRS complex is detected prompting the storage of sampled and digitized waveform data within a timing window bridging the point in time of fiducual point detection.
Abstract: An implantable cardioverter/defibrillator system provided with method and apparatus for discrimination between monomorphic arrhythmias, e.g. ventricular tachycardia from polymorphic arrhythmias, e.g. ventricular fibrillation. A fiducial point of each successive QRS complex is detected prompting the storage of sampled and digitized waveform data within a timing window bridging the point in time of fiducial point detection. Stored sets of such sampled wave shape data are compared data point to data point resulting in a sampled morphology index value for each compared set. The magnitude of the sampled morphology index value or a series such index values are analyzed to determine the presence of a single or a progression of beat-to-beat waveform changes indicative of a polymorphic single transition or progression of QRS complexes from monomorphic to polymorphic waveforms indicative of an arrhythmia that should be treated with aggressive cardioversion/defibrillation therapies. The system is preferably provided with a closely spaced and widely spaced pairs of electrodes for sensing each QRS complex of the patient's electrocardiogram. The closely spaced electrode pair is coupled to sense detect circuitry for identifying a predetermined fiducial point in the electrical signal associated with a ventricular depolarization and to counting and comparison circuitry for developing rate and onset data. The widely spaced pair of electrodes is coupled to sense and digitizing circuitry for developing the sampled waveform amplitude data from which the morphology index values are derived.
218 citations
TL;DR: Using the algorithm derived, a right-sided accessory pathway can be reliably distinguished from one that is left-sided, right free wall from right septal, right anterolateral from posterolateral and anteroseptal from other right sePTal pathways.
213 citations
TL;DR: Serial electrocardiograms revealed diagnostic features of embolism in an additional 3 patients and two-dimensional Doppler echocardiography at admission revealed tricuspid valve regurgitation and an increased right ventricular end-diastolic diameter in all cases.
Abstract: In 49 consecutive patients (27 men and 22 women, age range 44 to 86 years) presenting with acute symptoms and with subsequently proven pulmonary embolism, and without previous lung disease, the 12-lead electrocardiograms obtained at hospital admission were reviewed in a blinded fashion to identify electrocardiographic features suggestive of right ventricular overload. Pulmonary embolism was considered probable in 37 patients (76%), from the presence of > or = 3 of the following abnormalities: (1) incomplete or complete right bundle branch block (n = 33); which was associated with ST-segment elevation (n = 17) and positive T wave (n = 3) in lead V1; (2) S waves in leads I and aVL of > 1.5 mm (n = 36); (3) a shift in the transition zone in the precordial leads to V5 (n = 25); (4) Q waves in leads III and aVF, but not in lead II (n = 24); (5) right-axis deviation, with a frontal QRS axis of > 90 degrees (n = 16), or an indeterminate axis (n = 15); (6) a low-voltage QRS complex of 7 days. In the 12 patients with normal electrocardiograms at admission, serial electrocardiograms revealed diagnostic features of embolism in an additional 3 patients. Two-dimensional Doppler echocardiography at admission revealed tricuspid valve regurgitation and an increased right ventricular end-diastolic diameter in all cases.(ABSTRACT TRUNCATED AT 250 WORDS)
168 citations
TL;DR: There was a clear link between age and QRS duration, which increased linearly from about 1 year of age to adolescence, and Upper limits of normal heart rate tended to be higher in women than in men in the two adult populations.
155 citations
TL;DR: Though QT dispersion and distribution are abnormal in left ventricular hypertrophy these findings do not support the hypothesis that Qt dispersion reflects arrhythmic risk in eitherhypertrophy or heart failure.
Abstract: OBJECTIVE--To study QT dispersion in left ventricular hypertrophy and chronic heart failure and to determine the relation to ventricular arrhythmias. SETTING--Investigational laboratory of a tertiary referral centre. STUDY DESIGN--Patients with left ventricular hypertrophy and normal systolic function (n = 14) and patients with chronic heart failure (n = 18) were matched with controls (n = 17). The QT dispersion was examined in relation to abnormalities in resting mechanical and autonomic function and to the findings of 24 hour Holter monitoring. MAIN OUTCOME MEASURES--QT dispersion is the difference between the maximum and the minimum QT values from the 12 lead electrocardiogram. Mean(SD) QT dispersion from the 10 lead electrocardiogram was also examined once the 12 lead minimum and maximum values had been removed. The QT distribution is the curve describing the distance from the mean for all QT intervals (ms). RESULTS--All measures of QT dispersion were increased significantly in left ventricular hypertrophy and tended to increase in those with heart failure. The QT distribution was abnormal in both heart failure and left ventricular hypertrophy. There was no relation between the degree of change in QT dispersion and the incidence of ventricular arrhythmia on 24 hour Holter monitoring. Also there was no relation between QT dispersion and autonomic or mechanical abnormalities. The QT dispersion was related to QRS duration. CONCLUSION--Though QT dispersion and distribution are abnormal in left ventricular hypertrophy these findings do not support the hypothesis that QT dispersion reflects arrhythmic risk in either hypertrophy or heart failure.
142 citations
TL;DR: Radiofrequency ablation therapy is effective and safe in patients with idiopathic left ventricular tachycardia and should be considered as the primary therapeutic modality in these patients.
Abstract: BACKGROUNDThe feasibility and efficacy of radiofrequency ablation therapy in idiopathic left ventricular tachycardia has not been assessed in a large group of patients.METHODS AND RESULTSTwenty consecutive patients with idiopathic left ventricular tachycardia and without structural heart disease underwent electrophysiological study, pharmacological interventions with administration of verapamil and adenosine, and radiofrequency ablation therapy. There were 17 men and 3 women with a mean age of 28 +/- 8 years. The QRS configuration during tachycardia was of right bundle branch block and superior axis in 13 patients, indeterminate axis in 6 patients, and right axis in 1 patient. The tachycardia was electrically inducible and responsive to verapamil but not to adenosine. Thirteen patients demonstrated entrainment. Activation and pace-mapping studies disclosed that the tachycardia originated from the inferior apical septum in 15 patients, the midseptum in 4 patients, and the anterior lateral wall of the left ...
139 citations
TL;DR: In most patients with dilated cardiomyopathy and an electrocardiographic pattern of left bundles branch block or intraventricular block, the onset of mechanical systole is strikingly and symmetrically delayed in both ventricles, compatible with bilateral bundle branch block.
Abstract: OBJECTIVE--To investigate the nature of ventricular activation and its relation with mechanical events in patients with dilated cardiomyopathy. STUDY DESIGN--Retrospective and prospective study with 12 lead electrocardiograms, signal averaged electrocardiograms, and M mode and Doppler echocardiograms. SETTING--Tertiary cardiac referral centre. PATIENTS--77 patients (mean (SD) age 59(13)) with dilated cardiomyopathy, four after aortic valve replacement and three after coronary bypass surgery, and six patients with a normal sized left ventricle and complete right bundle branch block were studied. 15 normal subjects (age 45(20)) were used as controls. RESULTS--In patients with dilated cardiomyopathy, QRS duration was longer (127(25) ms v 90(10), P < 0.05) than normal and was normally distributed (r = 0.991, P < 0.01) on a normal probability plot. 20 had classic left bundle branch block, 29 intraventricular conduction delay, four right bundle branch block, and one bifascicular block. The PR interval was prolonged (185(30) ms v 150(15), P < 0.05). Electromechanical delay, Q to the onset of thickening of the interventricular septum as seen on the transverse M mode echocardiogram, was 75(15) ms in controls, but reduced to 43(15) ms in the patients (P < 0.01). Q to the onset of mitral regurgitation was also short (50(15)) ms, and correlated inversely with PR interval (r = -0.67, n = 73, P < 0.01). Early potentials (< 40 microV) were recorded on the signal averaged electrocardiogram in 33 representative patients and in all controls. Their overall duration was 30(12) ms in the patients, much longer than normal (12(7), P < 0.01)). Early potential time correlated positively with PR interval (r = 0.75, P < 0.01) and QRS duration (r = 0.60, P < 0.01) on a 12 lead electrocardiogram, and negatively with apparent electromechanical delay (r = -0.71, P < 0.01, n = 33), but not with true electromechanical delay (73(15)ms) or true PR interval (163(30)ms), calculated by correcting apparent values for early potential. The onset of left ventricular free wall motion was delayed with respect to the septum beyond 95% of the upper normal limit in all the patients with classic left bundle branch block and intraventricular conduction defect. Motion in the right ventricular free wall was delayed in 13 of 20 patients with left bundle branch block and 24 of 29 with intraventricular conduction defect by 65(20) ms, similar to that (75(10) ms) in patients with right bundle branch block. CONCLUSION--In most patients with dilated cardiomyopathy and an electrocardiographic pattern of left bundle branch block or intraventricular block, the onset of mechanical systole is strikingly and symmetrically delayed in both ventricles, compatible with bilateral bundle branch block. Complete atrioventricular block does not occur. The ventricle is activated through the upper septum and this activation is detectable only by signal averaged electrocardiography. The anatomical substrates for this abnormal activation could be the high connections described by Mahaim and Winston.
TL;DR: Fetal magnetocardiography is used as a method of measuring the time intervals of the fetal heart during the antenatal period to establish the reliability of this method.
TL;DR: Delayed conduction is an important feature of severe cardiac hypertrophy in guinea pigs and man and is associated with accentuated conduction delay and altered repolarisation during ischaemia.
Abstract: Objective: The aim was to investigate why cardiac hypertrophy causes increased vulnerability to arrhythmias during myocardial ischaemia. Methods: The electrophysiological basis for this increased vulnerability was studied in isolated perfused guinea pig hearts obtained 50 and 150 d after aortic constriction, and in sham operated controls. Cellular electrophysiology, conduction, and refractory periods were examined during control perfusion and during low flow (coronary flow reduced to 10% of control) and zero flow ischaemia. ECGs in patients with left ventricular hypertrophy and in controls matched for age and heart rate were also studied. Results: Aortic constriction increased heart weight:body weight ratio by 33% at 50 d and by 69% at 150 d. Action potentials were unchanged in hypertrophied hearts. Significant conduction delay occurred in 150 d hypertrophied hearts [conduction time index 23(SEM 4) ms v 18(3) ms, p<0.001; QRS width 40(1) ms v 35(1) ms, p<0.01], but not in 50 d hypertrophied hearts. Conduction delay was also present in humans with left ventricular hypertrophy [QRS width 96(13) ms v 87(8) ms, p<0.01]. Although the QTc interval was increased in humans, at 422(23) ms v 411(17) ms in controls, p<0.05, this could be explained by the increased QRS duration. During ischaemia, ventricular arrhythmias tended to occur earlier in hypertrophied hearts. Hypertrophy was also associated with a greater increase in conduction delay. Ischaemia reduced action potential duration and refractory periods; the reduction in action potential duration was attenuated by hypertrophy (p<0.01), although the reverse was apparent during low flow ischaemia at 50 d. Conclusions: Delayed conduction is an important feature of severe cardiac hypertrophy in guinea pigs and man. Hypertrophy is associated with accentuated conduction delay and altered repolarisation during ischaemia.
Cardiovascular Research 1994; 28 :47-54
TL;DR: Recurrent ventricular fibrillation was observed in a 67‐year‐old woman following catheter ablation of the AV junction using radiofrequency energy, followed by QTc prolongation of the QRS escape rhythm 1 day after the procedure.
Abstract: Recurrent ventricular fibrillation was observed in a 67-year-old woman following catheter ablation of the AV junction using radiofrequency energy. This serious complication has been reported following direct current energy ablation of the AV junction, but not after using radiofrequency energy. This life-threatening arrhythmia seemed pause and bradycardia dependent. It was followed by QTc prolongation of the QRS escape rhythm 1 day after the procedure. Ventricular arrhythmias were suppressed by rapid ventricular pacing.
TL;DR: The rate-corrected JT interval (JTc) is a more accurate measurement of ventricular repolarization than the QTc, and therefore may be a more sensitive means of assessing abnormalities.
Abstract: A prolonged rate-corrected QT interval (QTc) may be associated with an increased risk of developing ventricular arrhythmias and sudden death, particularly in patients with the hereditary long QT syndrome (LQTS), myocardial ischemia, or antiarrhythmic medication toxicity. It is known that there are some patients with LQTS who sometimes have a borderline or normal QTc (< or = 0.45 second). Although the QTc has been the standard measurement of ventricular repolarization, it includes both depolarization and repolarization and may not always be a sensitive indicator of the type of repolarization abnormalities seen in LQTS. Intraventricular conduction abnormalities complicate evaluation of the QTc interval. The rate-corrected JT interval (JTc) is a more accurate measurement of ventricular repolarization, and therefore may be a more sensitive means of assessing abnormalities. The QTc on a resting electrocardiogram was determined in 40 patients with LQTS and in 31 patients with right bundle branch block after tetralogy of Fallot repair. These were compared with 1,000 age-matched control subjects. The right bundle branch block group had normal JT and JTc measurements, despite having prolonged QT and QTc intervals compared with controls. The JTc identified 85% of patients affected with LQTS compared with only 58% identified using only the QTc as a marker for the syndrome. The JTc is a more specific measurement of ventricular repolarization than the QTc by eliminating QRS duration variability. It appears to be a more sensitive predictor of repolarization abnormalities, and may be helpful in identifying patients with LQTS who have borderline or normal QTc measurements on resting electrocardiograms.
TL;DR: A significant number of patients with dilated or hypertrophic cardiomyopathy may have a long QTc interval on the surface ECG, and ventricular hypertrophy/dilation may be additional rare causes of acquired prolongation of the QT interval.
TL;DR: A 43-year-old white woman with a well-documented history of a carrier state for Fabry’s disease who presented with palpitations and a short PR interval, and underwent detailed electrophysiologic testing is reported.
Abstract: Fabry’s disease is an X-linked lysosomal storage disease caused by a deficiency of a-galactosidase-A that results in an accumulation of intracellular glycolipid in the heart and other organs. l Several electrocardiographic changes have been described in affected patients, including varying degrees of atrioventricular block, ST and T-wave changes, and a short PR interval.24 These changes are thought to be due to glycosphingolipid deposition involving the myocardial fibers and conduction system.24 However, the etiology of a short PR interval in Fabry’s disease is not completely understood. We report a patient with heterozygous Fabry’s disease who presented with palpitations and a short PR interval, and underwent detailed electrophysiologic testing. A 43-year-old white woman with a well-documented history of a carrier state for Fabry’s disease (based on decreased levels of a-galactosidase)presented with palpitations and dyspnea. On examination, her pulse was irregular, with a rate of 150 beats1 min. An initial electrocardiogram demonstrated atrialBbrillation, with an average ventricular response of approximately 150 beatslmin and shortest RR interval of 350 ms. A total of 0.75 mg of digoxin was administered in sequential doses, followed by conversion to normal sinus rhythm. Further digoxin dosing was held. An electrocardiogram recorded during sinus rhythm (Figure 1) showed a short PR interval of 110 ms, with a normal QRS duration and no evidence of preexcitation. The echocardiogram was normal. To assess the etiology of the short PR interval, an electrophysiologic
TL;DR: It is concluded that in patients with an AMI the use of thrombolytic therapy/angioplasty is associated with a significantly decreased prevalence of abnormal SAECG and an abnormalSAECG is predictive of an increased incidence of arrhythmic events in all patients regardless of prior thrombectomy.
Abstract: Thrombolytic therapy and angioplasty during the early phase of an acute myocardial infarction (AMI) have been shown to improve prognosis. Time-domain analysis of the signal-averaged electrocardiogram (SAECG) provides strong, independent prediction of arrhythmic events (arrhythmic death/resuscitated cardiac arrest) after AMI. To determine whether the prognostic significance of an abnormal SAECG (QRS duration ≥120 ms) measured after AMI is influenced by thrombolytic therapy/angioplasty given in the AMI period, the predictive value of SAECG was compared in patients with and without prior thrombolysis/angioplasty in a substudy of the Cardiac Arrhythmia Suppression Trial. Information was available in 787 patients. The average follow-up was 10 ± 3 months and arrhythmic events occurred in 33 patients (4.2%). The prevalence of abnormal SAECG in patients with and without thrombolytic therapy/angioplasty was 9.4% (34 of 363 patients) and 14.9% (63 of 424 patients), respectively (p
TL;DR: It is concluded that although significant differences were detected between normal subjects and the 3 groups of athletes by routine ECG, the signal-averagedECG, and echocardiography, only an increased QT dispersion from the 12-lead ECG was helpful in distinguishing athletes with VT from other athletes.
Abstract: Sudden cardiac death in well-trained athletes is most often superimposed on the presence of structural heart disease. However, some athletes die suddenly in the absence of overt heart disease. To improve identification of athletes at high risk for ventricular tachycardia (VT), ventricular repolarization, the signal-averaged electrocardiogram (ECG), and the echocardiogram from 13 male athletes with symptomatic VT and without evidence of manifest cardiac disease were compared with data obtained in 3 matched control groups (15 apparently healthy professional road cyclists, 10 professional basketball players, and 15 normal control subjects without any sports activity). All patients had apparently normal QRS duration on the routine ECG, and none were taking antiarrhythmic drugs. Echocardiography and signal-averaged electrocardiography were useful in distinguishing the group of athletes with tachyarrhythmias from the group of normal nonsporting controls, but not from both groups of normal athletes. The QT interval (V4) and the QT interval corrected with the cubic root were shorter for the nonsporting controls. Three parameters for QT dispersion showed significant differences (p < 0.003) between athletes with disease and all other groups. It is concluded that although significant differences were detected between normal subjects and the 3 groups of athletes by routine ECG, the signal-averaged ECG, and echocardiography, only an increased QT dispersion from the 12-lead ECG was helpful in distinguishing athletes with VT from other athletes.
TL;DR: The characteristic findings of electrocardiogram (ECG) in 11 patients with acute myocarditis were clarified and Corticosteroid treatment was effective for patients who had edematous myocardial thickening and AV conduction disturbances.
Abstract: The purpose of the present study was to clarify the characteristic findings of electrocardiogram (ECG) in 11 patients with acute myocarditis ST elevation without reciprocal ST depression was one of the conspicuous findings in the acute stage Total QRS amplitudes at the acute stage were significantly decreased as compared to those before illness and during the convalescent stage Abnormal Q waves were present in 7 patients and disappeared in a short period The number of leads showing Q waves was inversely correlated to left ventricular (LV) ejection fraction (r = -087, p < 001) Conduction disturbances were present in 7 patients Second degree and advanced AV block was transient while bundle branch block remained over months Corticosteroid treatment was effective for patients who had edematous myocardial thickening and AV conduction disturbances As the serial ECG findings in acute myocarditis are so characteristic, and this help to differentiate it from acute myocardial infarction (AMI)
TL;DR: This study shows that body surface mapping enables precise localization of the origin of postinfarction ventricular tachycardia in 62% and regional approximation in 30% of tachycardsias.
TL;DR: It is suggested that use of the time-voltage integral of the QRS complex, a method that can be readily implemented on commercially available computerized ECG systems, can improve the accuracy of ECG methods for the identification of left ventricular hypertrophy.
TL;DR: The results indicate that artificial neural networks may be of interest in the attempt to improve computer-based electrocardiographic interpretation programs.
Abstract: Artificial neural networks are computer-based expert systems that learn by example, in contrast to the currently used rule-based electrocardiographic interpretation programs. For the purpose of this study, 1,107 electrocardiograms (ECGs) from patients who had undergone cardiac catheterization were used to train and test neural networks for the diagnosis of myocardial infarction. Different combinations of QRS and ST-T measurements were used as input to the neural networks. In a learning process, the networks automatically adjusted their characteristics to correctly diagnose anterior or inferior wall myocardial infarction from the ECG. Two thirds of the ECGs were used in this process. Thereafter, the performance of the networks was studied in a separate test set, using the remaining third of the ECGs. The results from the networks were also compared with that of conventional electrocardiographic criteria. The sensitivity for the diagnosis of anterior myocardial infarction was 81% for the best network and 68% for the conventional criteria (p < 0.01), both having a specificity of 97.5%. The corresponding sensitivities of the network and the criteria for the diagnosis of inferior myocardial infarction were 78% and 65.5% (p < 0.01), respectively, compared at a specificity of 95%. The results indicate that artificial neural networks may be of interest in the attempt to improve computer-based electrocardiographic interpretation programs.
TL;DR: A QRS onset and offset detection algorithm has been developed for use in body surface QRS integral mapping of ventricular tachycardia and revealed an identical or adjacent localization of the site of origin.
Abstract: A QRS onset and offset detection algorithm has been developed for use in body surface QRS integral mapping of ventricular tachycardia. To determine QRS intervals, the algorithm uses two computed signals: the sum of the absolute values of the first derivatives of all leads and the sum of the absolute values of all leads. The second order derivative of the latter parameter is used to detect the time instants of QRS onset and offset. Using the algorithm, QRS integral maps are subsequently computed, which are correlated with a database of QRS integral maps in order to localize the site of origin of ventricular tachycardia. Comparison of the performance of the algorithm with visual evaluation by a human expert in this procedure revealed, in 95% of the cases, an identical or adjacent localization of the site of origin. >
TL;DR: Traditional clinical markers such as resolution of chest pain and ST‐segment elevation failed to distinguish successful and failed reperfusion in patients treated with thrombolytic agents for AMI.
Abstract: The hypothesis that an increase in the amplitude (root-mean-square voltage) of the high frequency (150-250 Hz) components of the QRS complex occurs with successful reperfusion following thrombolytic therapy in acute myocardial infarction (AMI) and fails to occur when thrombolysis fails was tested. Clinical markers for successful or failed reperfusion following thrombolytic therapy for AMI are notoriously insensitive. The amplitude of the high-frequency components of the QRS complex decreases during ischemia and returns to normal with resolution of ischemia, but neither the variability in measurement of these potentials nor their patterns of change during the course of AMI have been described. In 32 control subjects, the average coefficient of variation for the amplitude of the highfrequency QRS complex was 10% or 0.3 uV. Based on these data, for the acute infarction population a significant change in this measurement was therefore defined as a change in amplitude > 20% or 0.6 uV on two consecutive recordings. In 30 patients with AMI treated with a thrombolytic agent, either cardiac catheterization, serial serum myoglobin, or complete resolution of ST-segment elevation were used to define successful or failed reperfusion. High-frequency QRS electrocardiograms were obtained at the start of treatment with a thrombolytic agent and for 3 h thereafter using a signal-averaging technique and digital filtering. Standard 12-lead electrocardiograms were obtained at the same time. In patients who reperfused successfully, the high-frequency QRS amplitude increased significantly (1.2 ± 0.9 uV above its nadir at 83 ± 36 min after initiation of thrombolytic therapy) in 23 of 25 patients. In contrast, the highfrequency QRS amplitude did not change or declined in all five patients who failed to reperfuse (-0.4 ± 0.4 uV, p < 0.05 compared with successful reperfusion). Traditional clinical markers such as resolution of chest pain and ST-segment elevation failed to distinguish successful and failed reperfusion. High-frequency QRS electrocardiography is a rapid, reliable bedside technique for discriminating between successful and failed reperfusion in patients treated with thrombolytic agents for AMI.
TL;DR: Clinically significant cardiovascular toxicity occurs rarely in patients with toxic carbamazepine concentrations, and ECG findings do not correlate with serum carbamazepsine concentration.
TL;DR: The present study confirms that acute oral antiarrhythmic drug loading is simple and effective and that patients with heart failure or significant cardiac dysfunction are not treated with these agents.
Abstract: sient hypotension, and 2 had a significant QRS widening with induction of a transient complete left bundle branch block in I. Electrocardiographic QRS intervals measured immediately after conversion to sinus rhythm were unchanged compared with baseline for placebo, but for flecainide and propafenone a mean lengthening of 25% and 21% occurred, respectively. The efficacy of propafenone and flecainide in converting recent-onset AF to sinus rhythm has been studied, but no direct comparison between these 2 drugs administered as acute, oral loading doses in a placebocontrolled study has been previously reported. The present study confirms that acute oral antiarrhythmic drug loading is simple and effective. Because spontaneous conversion of AF to sinus rhythm may occur in 39% to 48% of patients within 8 hours,3 we believe a placebo group is essential to assess drug efficacy. The use of class 1C antiarrhythmic drugs like propafenone or flecainide carries the risk of inducing atria1 flutter with a fast ventricular response,5,6 and we observed this. However, spontaneous atria1 flutter with 22: 1 AV conduction ratio and a heart rate of 1150 beats/min occurs relatively often, even with placebo, especially during the time preceding conversion to sinus rhythm. The negative inotropic effect of class 1C drugs mandates that patients with heart failure or significant cardiac dysfunction are not treated with these agents. The negative chronotropic response (long pause at the time of conversion from AF to sinus rhythm) was observed with both drugs but was not associated with an adverse outcome.
TL;DR: STT changes of a small magnitude are seen in about half of the cases of stroke patients without primary heart disease and that they do not resemble the typical pattern of acute myocardial ischaemia.
Abstract: Consecutive electrocardiograms were recorded in 28 stroke patients without signs of primary heart disease. Individuals with subarachnoidal haemorrhage, or electrolyte disturbances were excluded. A computerized tomography of the brain was performed in each case and showed a cerebral haemorrhage (n = 4), cortical infarction (n = 6), subcortical infarction (n = 14) and normal finding (n = 4). One patient developed atrial fibrillation but no other case of serious disturbances in rate of rhythm occurred. None developed AV block, bundle branch blocks or significant changes in QRS complexes. The most common abnormalities in ECG were transient STT changes in lateral leads, which were seen in 13 cases. The typical findings were flat or slightly negative T waves, horizontal or down-sloping ST segments and sometimes a small ST depression. In no case did ECG show typical signs of acute myocardial infarction. A transient prolonged QT interval was seen in three patients and transient U waves in four. ECG did not correlate to the location of the vascular lesion seen on CT or the clinical outcome. It is concluded that STT changes of a small magnitude are seen in about half of the cases of stroke patients without primary heart disease and that they do not resemble the typical pattern of acute myocardial ischaemia.
TL;DR: A method of quantitative comparison of body surface potential maps can be used in normal hearts to localize ventricular pacing sites within a 4-mm range and may have utility in determining potential ablation sites for therapy of ventricular tachycardia or preexcitation syndromes.
Abstract: BACKGROUNDSeveral studies have related 12-lead ECG waveform during ventricular tachycardia to ECG waveform during ventricular pacing to identify ablation sites for therapy of ventricular tachycardia. QRS isopotential maps and QRS isointegral maps derived from body surface isopotential maps have also been correlated with left ventricular pacing sites with the same objective. The comparison process used is subjective and only semiquantitative. Improved accuracy of catheter placement may improve success rates of ablation therapy.METHODS AND RESULTSThis animal study was performed to determine the spatial resolution with which left ventricular pacing sites could be distinguished by body surface isopotential mapping. Potentials were recorded from 64 evenly spaced thoracic leads. Hexapolar or octapolar pacing catheters with 2-mm interelectrode spacing were placed percutaneously in the left ventricle in each of six dogs, and bipolar endocardial pacing was performed using each pair of adjacent electrodes. QRS isop...
TL;DR: A new stepwise approach with three criteria for the electrocardiographic differential diagnosis between ventricular tachycardia in coronary artery disease and preexcited regular tachycardsia is designed.
Abstract: The 12-lead surface electrocardiogram is a simple and useful tool for the differential diagnosis of regular wide QRS complex tachycardia. However, criteria do not as yet exist to discriminate between ventricular tachycardia and supraventricular tachycardia with anterograde conduction over an accessory pathway (preexcited tachycardia). Therefore, we designed a new stepwise approach with three criteria for the electrocardiographic differential diagnosis between ventricular tachycardia and preexcited tachycardia and prospectively studied 267 regular tachycardias with electrophysiologically proven mechanism and a wide QRS complex (> or = 0.12 s): 149 consecutive ventricular tachycardias and 118 consecutive preexcited regular tachycardias. Underlying heart disease was old myocardial infarction in 133 of 149 (89%) ventricular tachycardias. The patients presenting with preexcited tachycardia had no additional structural heart disease. Atrial fibrillation with preexcited QRS complex was not included. The criteria favoring ventricular tachycardia were: (1) presence of predominantly negative QRS complexes in the precordial leads V4 to V6, (2) presence of a QR complex in one or more of the precordial leads V2 to V6, and (3) AV relation different from 1:1 (more QRS complexes than P waves). The final sensitivity and specificity of these three consecutive steps to diagnose ventricular tachycardia were 0.75 and 1.00, respectively. This new stepwise approach is sensitive and highly specific for the differential diagnosis between ventricular tachycardia in coronary artery disease and preexcited regular tachycardia.