Parietal Block Research Articles

A New Case of Epsilon Wave on Loop Recorder.

Epsilon wave in ARVD is the marker of slow conduction (parietal block) observed on the right precordial leads as opposed to the left precordials. It is the result of a slowdown of conduction in the epicardial layers of RV and LV apex due the presence of a trouble in development producing apoptosis and fat (Kim Nature 2013) instead of cardiomyocytes.

The electrocardiographic manifestations of arrhythmogenic right ventricular dysplasia.

The ECG is abnormal in most patients with arrhythmogenic right ventricular dysplasia (ARVD). Right ventricular parietal block, reduced QRS amplitude, epsilon wave, T wave inversion in V1-3 and ventricular tachycardia in the morphology of left bundle branch block are the characteristic changes that reflect the underlying genetic predetermined pathology and pathoelectrophysiology. Recognizing the characteristic ECG changes in ARVD will be of help in making a correct diagnosis of this rare disease.

Electrocardiographic Pattern in Arrhythmogenic Right Ventricular Cardiomyopathy

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a cardiac disease characterized by progressive myocardial atrophy and fibrofatty replacement. Standard electrocardiograms (ECGs) and signal-averaged ECGs (SAECGs) were relatively low cost and repeatable diagnostic tools. In this study, ECGs and SAECGs of patients with ARVC were analyzed with the aim to assess the diagnostic capability of these noninvasive techniques. A total of 205 patients with ARVC were analyzed. ECGs were abnormal in 74% of patients and SAECGs were positive in 60%, with normal ECGs mostly related to mild forms of the disease. The most common electrocardiographic abnormalities were localized right QRS prolongation, poor r wave progression in the right precordial leads, incomplete right branch bundle block, prolonged S-wave upstroke in V(1) to V(3), parietal block, ST-segment elevation in V(1) to V(3), inversion of T waves beyond V(2), and epsilon wave. Low QRS voltages in the precordial leads were frequently present in all patients with ARVC compared with a group of 120 healthy subjects (p = 0.00001). T-wave inversion beyond V(3) characterized subjects with severe right ventricular dilatation, whereas in subjects with left ventricular involvement, T-wave inversion in lateral leads was more commonly detected. Overall, the extent of electrocardiographic abnormalities was related to disease extent. In conclusion, abnormalities in ECGs and SAECGs were frequent in patients with ARVC and correlated with disease extent, even if a stereotypical electrocardiographic pattern did not exist. ECGs and SAECGs remain an important tool for the diagnosis and assessment of ARVC extent. Nonetheless, a normal ECG does not exclude the presence of the disease.

Prolonged RV endocardial activation duration: A novel marker of arrhythmogenic right ventricular dysplasia/cardiomyopathy

Parietal block, defined as intra right ventricular (RV) conduction slowing, is a major diagnostic criterion for arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). We evaluated the utility of total RV endocardial activation duration (EAD) measured by 3-dimensional electroanatomic mapping during sinus rhythm in the diagnosis of ARVD/C. Twenty-five consecutive patients with frequent left bundle branch block morphology premature ventricular complexes who underwent electroanatomic mapping as a part of the evaluation for ARVD/C were included in the study. All patients were evaluated using standard protocol that included electrocardiogram (ECG), signal-averaged ECG, Holter monitoring, echocardiography, and magnetic resonance imaging. Invasive testing was performed as indicated. Total RV EAD was measured as the time interval between the onset of RV activation to the latest activated region in the RV. The mean age of the study subjects was 38 +/- 11 years, and 32% were men. Fourteen subjects were diagnosed with ARVD/C using task force criteria, and the remainder had idiopathic ventricular tachycardia. Although the surface QRS durations were similar, the total RV EAD was significantly prolonged in ARVD/C compared with idiopathic VT (83.9 +/- 10 ms vs. 50.8 +/- 7 ms, P <.001). None of the idiopathic VT subjects had RV EAD of >65 ms. RV EAD also showed significant negative correlation with RV ejection fraction. Total RV EAD obtained by 3-dimensional electroanatomic mapping is a sensitive marker of intra-RV conduction delay in ARVD/C, and a total RV EAD of >65 ms accurately differentiates ARVD/C from idiopathic VT.

Abstract 4116: Electrocardiographic Markers of Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy: A reappraisal

Background: The Task Force criteria for diagnosis of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) rely on depolarization and repolarization abnormalities detected on a surface ECG. Terminal activation delay (TAD) has recently been presented as specific and sensitive marker of ARVD/C. The purpose of this study was to evaluate the sensitivity and specificity of TAD in patients with ARVD/C. Methods : In a cohort of 74 patients with definite ARVD/C (51% male); age 36 ± 12 years) and 48 phenotypically normal non cardiac patients (35% male); age 35 ± 14 years) we studied the ECG criteria used to diagnose ARVD/C with specific a focus on TAD. The parameters analyzed were: T wave inversion (TWI) in ≥ V2, TWI ≥ V3, epsilon wave, QRS ≥ 110ms in V1 to V3, parietal block defined as QRSd V1–V6 or V2–V6 or V3–V6 &gt;25 ms in the presence of QRS ≥ 100ms in at least 2 right precordial leads, TAD in V1-V3 and QRSd in V1+V2+V3/V4+V5+V6 ≥ 1.2. Sigma scan software was used for the ECG analysis. Results : In the ARVD/C group, the prevalence of TWI ≥ V2 was 82%, TWI ≥ V3 was 66%, epsilon wave: 1%, QRSd ≥ 110ms V1-V3: 39%, parietal block: 16%, TAD: 46 %, QRSd ratio ≥ 1.2: 19%. In the non cardiac group the prevalence of TWI ≥ V2 was 6 %, TWI ≥ V3: 6%, epsilon wave: 0%, QRSd ≥ 110ms V1–V3: 4%, parietal block: 2%, TAD: 12%, and QRSd ratio ≥ 1.2: 4% (Figure). Conclusion : The results of this study reveal that terminal activation delay has only moderate sensitivity and specificity for the diagnosis of ARVD/C. Our results also reveal that T wave inversion in the right precordial leads is a very sensitive marker of ARVD/C.

Progressive Cardiac Conduction Defect is the Prevailing Phenotype in Carriers of a Brugada Syndrome SCN5A Mutation

Loss-of-function mutations in the SCN5A gene encoding the cardiac sodium channel are responsible for Brugada syndrome (BS) and also for progressive cardiac conduction disease (inherited Lenègre disease). In an attempt to clarify the frontier between these two entities, we have characterized cardiac conduction defect and its evolution with aging in a cohort of 78 patients carrying a SCN5A mutation linked to Brugada syndrome. Families were included in the study if a SCN5A mutation was identified in a BS proband and if at least two family members were mutation carriers. Sixteen families met the study criteria, representing 78 carriers. Resting ECG showed a spontaneous BS ECG pattern in 28 of 78 (36%) gene carriers. Intraventricular conduction anomalies were identified in 59 of 78 gene carriers including complete (17) or incomplete (24) right bundle branch block, right bundle branch block plus hemiblock (6), left bundle branch block (1), hemiblock (1), and parietal block (10). PR and QRS duration were longer in the gene carrier cohort in comparison with their relatives carrying no mutation. Finally, in the gene carrier cohort conduction defect progressively aggravated with aging leading in five occasions to pacemaker implantations. The present study shows that the most common phenotype of gene carriers of a BS-type SCN5A mutation is progressive cardiac conduction defects similar to the Lenègre disease phenotype. In consequence, we propose that carriers of a SCN5A mutation need a clinical and ECG follow-up because of the risk associated with severe conduction defects.

Electrocardiographic features of inherited diseases that predispose to the development of cardiac arrhythmias, long QT syndrome, arrhythmogenic right ventricular cardiomyopathy/dysplasia, and brugada syndrome

Analysis of the 12-lead electrocardiogram (ECG) provides important diagnostic and prognostic information in the long QT syndrome. The clinical diagnosis of long QT syndrome is determined by the presence of a QTc≥0.44 sec. A normal QTc does not exclude a family member from being a genetic carrier. The ECG patterns of depolarization, the ST segment and shape of the T-wave can provide important clues as to the affected gene, particularly in conjunction with clinical information as to the precipitating causes of syncope or cardiac events. In arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D), the typical ECG pattern consists of T-wave inversion beyond lead V 1. Evidence of right ventricular parietal block is manifest by a QRS duration in V 1≥110 msec and a longer QRS duration in the right then left precordial leads. Evidence of slow fractionated conduction is present as epsilon waves. The signal averaged ECG may show exceedingly long and low late potentials. Information regarding the risk of sudden death may also be obtaioned from the ECG. The ECG changes alone or in combination can provide strong evidence for the diagnosis of ARVC/D and helps to differentiate ARVC/D from right ventricular outflow tract (RVOT) tachycardia. The typical pattern of the ECG in the Brugada syndrome is ST segment elevation in the right precordial leads. This abnormality can be dormant and elicited by administration of drugs that cause Na channel blockade, such as ajmaline or type 1a or 1C antiarrhythmic drugs. Individuals who do not have the Brugada ECG findings at baseline but have this pattern induced by antiarrhythmic drugs are also at risk for sudden death. Further risk stratification may be obtained in the asymptomatic patients if ventricular fibrillation is induced at electrophysiological study.

Arrhythmogenic right ventricular dysplasia

Arrhythmogenic right ventricular dysplasia is a relatively newly described clinical entity that is more and more frequently recognized. It may explain an increasing number of unexpected, sudden deaths in young adults that are or are not preceded by cardiac symptoms. A genetic transmission of the disease has been suggested by the study of familial cases. A location on chromosome 14 appears to be responsible for this disease. In some patients, a superimposed inflammatory process mixed with the pattern of arrhythmogenic right ventricular dysplasia may explain the progressive deterioration of left ventricular function. The systematic study of electrocardiograms demonstrates prolongation of the QRS complex and repolarization abnormalities in the right precordial leads due to a parietal block. Multiple therapeutic approaches are now available. The first line of therapy remains antiarrhythmic drugs, which are effective in most cases. Ablative techniques, implantable defibrillators, and heart transplantation have been used in the most severe examples of the disease.

Cerebral amyloid angiopathy in chinese

Cerebral amyloid angiopathy (CAA) affects only the cerebral vasculature and 1s common 1n Caucasians. The frequency of finding CAA in autopsy material 1n Caucasians rises from 8* 1n the 7th decade to 60% 1n the 10th decade. The incidence of CAA 1n Chinese has not been previously documented. A retrospective study on autopsy material from Jan 86 to April 89 was performed to study the incidence of CAA 1n Chinese. Cases were selected 1f the patient was older than 40 and a parietal block was available. Paraffin sections were stained by H&E, congo red and examined under light microscopy and polarized light. Cases which showed vessles with positive congophllla and an apple green birefringence were diagnosed as CAA. EM was performed 1n some cases. The hippocampi and parietal cortex were studied for the presence of senile plaques. The overall incidence of CAA is 9.8% and 1s age-related. CAA 1s associated with histological features of Alzheimer's disease 1n <i>5%</i>. To conclude, the incidence of CAA in Chinese 1s much lower than the Caucasians, the reasons for the difference 1s uncertain. Table 1. Age40+50+60+70+80+90 +TotalNo. studied7226570337204CAA01477120Incidence %04.56.110.021.214.39.8

Left ventricular parietal block: Diagnostic and clinical study

Fifty-five patients with widened QRS complexes due to the presence of slurred S waves or of terminal slurrings on R waves, in more than three leads, with no infarction or bundle branch and fascicular blocks, were studied with the usual clinical examinations as well as vectorcardiographic recording. A parietal block of the left ventricle was diagnosed when, in the presence of a normal development of ventricular depolarization in the initial and middle phases, the terminal QRS loop was delayed, sometimes irregular and displaced leftward and posteriorly. When this delay was directed to the right, the ventricular localization was puzzling. The comparison of the electrocardiographic (ECG) and vectorcardiographic (VCG) data on the terminal part of ventricular depolarization showed some discrepancies and revealed the greater importance of VCG investigation for the study and the localization of parietal blocks. The pathogenesis of such minor conduction disturbances is not yet clear, since the experimental data on the anatomical-functional structures are different: the Purkinje network, Purkinje fiber-muscle junction or common myocardium. In some cases we think it is possible to localize the structure concerned; in any case we can always localize it at the level of the free ventricular wall.

Nature of the conduction disturbance in selective coronary arteriography and left heart catheterization

The electrocardiographic changes associated with coronary arteriography were compared with those occurring during left ventricular catheterization in 16 patients. In 1 patient, a 36 year old man, transient left anterior divisional block was documented when the catheter tip was in the outflow tract of the left ventricle. The ÂQRS shifted from +90 to −50°, the initial 0.02 second QRS forces shifted interiorly and to the right, and the QRS interval increased from 0.07 to 0.09 second, fulfilling previously described criteria for the diagnosis of left anterior divisional block. This was attributed to transient injury of the anterior division of the left bundle branch. During recovery, several progressively decreasing degrees of left anterior divisional block were recorded. In the same patient and in the other 15, selective opacification of the coronary arteries shifted the main QRS forces, without change in the direction of the initial QRS forces. The axis shifts occurring during coronary arteriography are attributed to parietal block. Selective opacification of the coronary arteries does not affect the intraventricular conducting fascicles and Purkinje fibers.

The pathologic basis of the electrocardiographic pattern of parietal block

Extensive pathologic examination of hearts of patients with parietal block and varying clinical pictures indicates that parietal block and left axis deviation can result from a variety of anatomic lesions and that no specific area of the heart or conduction system is consistently involved.

Vectorcardiographic Analysis of Left Axis Deviation, in the Differentiation of Diaphragmatic Infarction and Parietal Block

Vectorcardiographic analysis of abnormal left axis deviation (mean electrical axis between 270°-330° in the frontal plane of the scalar electrocardiogram) has shown that this condition results from an abnormal pathway of depolarization. The two most common entities responsible for this condition are parietal block and diaphragmatic infarction. An rS complex in aVF may be found in a significant proportion of diaphragmatic infarctions and when associated with abnormal left axis deviation, may superficially resemble parietal block on the scalar electrocardiogram. The major feature differentiating these two abnormalities has been shown to be the direction of inscription of the QRS sE-loop in the frontal plane. Parietal block is characterized by counterclockwise inscription, whereas diaphragmatic infarction always produces clockwise inscription of some portion of the QRS sE-loop. We believe that the initial r wave in aVF in the presence of diaphragmatic infarction results from inferiorly directed septal forces in most instances. An rS complex in aVF in cases of parietal block, on the other hand, is probably dependent upon early depolarization of the inferior wall. Septal fibrosis and infarction complicating parietal block requires vectorcardiographic display for correct interpretation.

The electrocardiogram in diphtheritic myocarditis

Hospital records of 229 children with diphtheria revealed evidence of myocarditis affecting 47 (20 per cent), both by physical signs and abnormal electrocardiograms. The 437 electrocardiograms taken on the 47 patients were analyzed by the conventional and the electrovectorcardiographic method of Grant, and the QRS-T spatial angles were evaluated. A high predictability of survival from diphtheria is afforded by the electrocardiogram. Cases were grouped according to their most severe ECG abnormalities. If only the P-R interval was prolonged (Group A), or the T vector was shifted (Group B), causing the QRS-T angle to widen, the prognosis for complete recovery was excellent. Prolongation of the P-R interval tended to persist, whereas primary T-wave changes subsided. An intraventricular block (Group C) involved the superior branch of the left main bundle branch to the left ventricle in 8 children; and of these, 4 died, but only one as a result of myocarditis. One child with only incomplete right bundle branch block recovered. Of 14 children with a major conduction block (Group D), 11 died. Six of these children had complete bundle branch block: there were 3 fatalities. Complete A-V block was the most ominous ECG sign, in that it was consistently followed by death in 8 children. However, in one of these children the block regressed and death resulted from polyneuritis and respiratory failure. Out of the total 229 cases, 15 deaths occurred in that group of 47 patients in whom there was evidence of myocardial involvement; 10 deaths were due to this involvement and peripheral vasodilatation. One child died early from obstructive, laryngeal diphtheria, and 4 succumbed to the late effects of progressive polyneuritis complicated by pulmonary hypoventilation and infection. Autopsy was carried out on 8 children, for whom correlations of ECG, clinical, and pathologic data were presented. Early death in 3 children (Cases 40, 44, and 47) was associated with complete A-V block and histologic evidence of extensive myocardial disease, and in one child (Case 35), with right bundle branch block and a hemorrhagic myocardium. The child who died early from laryngeal obstruction (Case 31) had parietal block by ECG and interstitial edema of the myocardium. Death due to peripheral neural and respiratory causes late in the course of illness of 3 children (Cases 33, 38, and 46) was associated with regression of ECG changes and much less severe histologic evidence of myocarditis.

Vectorcardiographic and electrocardiographic findings in myotonia atrophica: A study employing the frank lead system

1. 1. Seventeen patients with classic myotonia atrophica, as manifested by clinical findings and electromyographic studies, were investigated by chest x-ray film, electrocardiogram, and spatial vectorcardiogram employing the Frank lead system. Twenty-seven normal individuals were studied with the Frank system and are reported on to validate our method and to add to the normal findings in the literature. 2. 2. In 12 (71 per cent) of the 17 patients there was a total of 12 different abnormal electrocardiographic findings. These consisted primarily of conduction defects (P-R interval greater than 0.20 sec., 29.5 per cent; QRS interval greater than 0.09 sec., 41 per cent; Q-T interval in excess for rate, 35 per cent). Five patients (29.5 per cent) were found to have left axis deviation. S-T segment elevation was present in 4 patients (23.5 per cent). Three patients (17.5 per cent) were thought to have a form of left ventricular parietal block. The other major abnormalities included T-wave changes (17.5 per cent), and changes consistent with myocardial infarction (12 per cent). Seven patients (41 per cent) had a sinus rhythm of 60 per minute. 3. 3. Spatial vectorcardiography revealed 3 patients with normal loops (17.6 per cent), 4 patients with S 1S 2S 3 loops (23.5 per cent), 4 with left ventricular parietal block (23.5 per cent), and 6 with displacement of instantaneous vectors in anterior, diaphragmatic, or posterior areas identical to that seen in myocardial infarction (35.4 per cent). The cause of left axis deviation in the electrocardiogram of 5 of our patients was either “infarction” or left ventricular parietal block by vectorcardiographic findings. The findings of “infarction” and left ventricular parietal block in 10 patients (60 per cent) would imply involvement of myocardial tissue. Prolongation of the QRS interval in the electrocardiogram (greater than 0.09 sec.) and vectorcardiogram in this study was due to either “infarction” or left ventricular parietal block. The vectorcardiogram proved to be superior to the standard 14-lead electrocardiogram in the detection of abnormalities of the ventricular activation process. The electrocardiogram was the better measurement of P-R and Q-T intervals, rate, rhythm, and S-T segment and T-wave changes. 4. 4. The findings of conduction defects in the electrocardiogram, and of significant changes in the ventricular activation process in 60 per cent of patients in the vectorcardiogram, would seem to be consistent with the reported autopsy findings of myocardial involvement. 5. 5. The findings of “infarction” in the absence of clinical history would imply that cardiac involvement in myotonia atrophica brings about another “infarction pattern” without true coronary artery disease with myocardial infarction.

Results of ventriculomyotomy in muscular subaortic stenosis

The results of surgery in 4 cases of muscular subaortic stenosis are described. An incision through the center or the anterior extremity of the abnormal muscle mass in the ventricular septum with blunt separation of the cut edges, was performed under direct vision using cardiac bypass. The obstruction to left ventricular outflow was abolished in all 4 cases, and marked symptomatic and hemodynamic improvement was noted in 3. Following surgery, the contour of the aortic pressure pulse was altered in that the tidal wave became greater than the previously dominant percussion wave. The altered physical findings reflected both the relief of the obstruction to left ventricular outflow and the improvement in the filling characteristics of the left ventricle. The fourth patient has had a prolonged postoperative illness, and final clinical improvement cannot be assessed. The postoperative electrocardiograms revealed left bundle branch block when the center of the ventricular septum was incised. When the anterior extremity of the septum was incised, the postoperative electrocardiograms revealed either left ventricular parietal block or anterolateral peri-infarction block. The results of this operative procedure appear promising and worthwhile pursuing in significantly disabled patients with muscular subaortic stenosis.

Left ventricular parietal block produced by transventricular aortic commissurotomy

Preoperative and postoperative electrocardiograms of 29 patients who underwent transventricular aortic commissurotomy were reviewed. Fifteen of 26 tracings which showed normal ventricular depolarization forces preoperatively showed left axis deviation with significant changes in direction of the terminal depolarization forces postoperatively. In 3 patients in whom the electrocardiogram was monitored during operation, these changes were observed as soon as the aortic dilator was advanced toward the aortic valve. The tracings taken in a comparable number of patients who were subjected to right ventriculotomy or left atriotomy failed to show similar changes. The acute occurrence of this conduction defect in the apparent absence of myocardial infarction is attributed to the mechanical trauma to the fibers of the superior division of the left bundle caused by the dilator as it is passed through the outflow tract of the left ventricle.

Left Axis Deviation

Our understanding of the meaning of the electrocardiogram is greatly furthered by careful comparison of cardiac hypertrophy and cardiac damage observed post mortem with electrocardiograms taken during the last weeks of life. An electrocardiographic-pathologic correlation of 672 cases is reported in which the roles of left ventricular hypertrophy, myocardial infarction, and other factorsin the production of left axis deviation are examined. A heretofore unrecognized QRS-complex syndrome of infarction is described in which the QRS forces are diagnostically abnormal but no "Q waves" are seen in the conventional leads. The roles of hypertrophy, variations in body build, chronic pulmonary disease, and various types of "parietal block" in the production of left axis deviation are studied.