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The prevalence of adults with congenital heart disease has dramatically increased during the last decades due to significant advances in the surgical correction of these conditions. As a result, patient's survival has been prolonged and arrhythmias have become one of the principal causes of morbidity and mortality for these patients. The surface 12-lead ECG may play a critical role in the identification of the underlying heart disease of the patient, the recognition of the arrhythmia mechanism and may also help in the planification of the ablation procedure in this setting. Finally, important prognostic information can be also obtained from the ECG in these patients. The present review will offer an overview of the principal utilities of the surface ECG in the diagnosis and management of patients with CHD and arrhythmias., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Objectives: Complete heart block has not been reported in association with left ventricular hypertrabeculation (LVHT)/noncompaction, nail-patella syndrome (NPS), and mitochondrial myopathy (MMP)., Case Report: A 47-year-old man with congenital NPS from a 17-bp deletion in exon 5 of the LMX1B gene, MMP from the A3243G mitochondrial DNA transition, and LVHT was acutely admitted after a syncope followed by dizziness. Cardiological examinations revealed bradycardia. Blood pressure was 70/30 mm Hg. Blood work revealed a creatine kinase of 389 U/L (normal, <175 U/L), renal insufficiency, anemia, and reduced calcium, phosphorus, and magnesium. Electrocardiogram showed complete heart block with an escape rhythm of 30/min. A temporary pacemaker was inserted. During the procedure, the patient became asystole but was successfully resuscitated. One day later, he received a permanent pacemaker. Echocardiography showed normal systolic function and LVHT. The patient recovered without sequelae., Conclusion: In single cases, LVHT may be associated with complete heart block. Most likely, complete heart block was due to MMP. Patients with NPS and MMP require multidisciplinary surveillance, including regular electrocardiograms, for indicating anticipatory intervention in time.

An electrocardiogram (ECG) showing sinus tachycardia with sinus rate exceeding the ventricular rate suggesting atrio-ventricular (AV) block in a patient with old anterior wall infarction is presented. The presence of varying PR intervals, irregular RR intervals and P-QRS relationship not consistent with 2nd degree type 1 AV block was seen. The possible site(s) and degree of AV block in the case is discussed.

We report a 37-year-old man with type I second-degree atrioventricular (AV) block (atypical Wenckebach's periodicity) referred to our department for pacemaker implantation because of an episode of syncope. After exhaustive evaluation, including electrophysiological test, in which Wenckebach's cycles with block within the AV node was demonstrated, syncope was considered to be neurally mediated. Head-up tilt testing with sublingual isosorbide dinitrate was positive. The decrease in atrial rate at the beginning of the vasovagal reaction was not immediately accompanied by a depressed AV node conduction. Only at the moment of syncope did incomplete AV block appear. This observation illustrates (1) a neurally mediated origin of syncope in a patient with chronic AV block, and (2) the different time-course responses of the sinus and AV nodes to autonomic tone.

An 87-year-old man was referred to our institution to undergo radiofrequency catheter ablation for typical atrial flutter. A decapolar electrode catheter with an interelectrode spacing of 1mm positioned at the cavotricuspid isthmus (CTI) exhibited 2 discrete potentials. The first electrogram was recorded at a site close to the tricuspid annulus and the second at a site close to the inferior vena cava at the CTI. Entrainment study showed that the first component was crucial to maintain the artrial flutten; however, the second one was found to function as a bystander portion of the reentrant circuit. Radiofrequency energy application at the site where the first potential was inscribed could terminate the atrial flutter creating a complete bidirectional conduction block at the CTI.

A 63-year-old diabetic man was admitted with general fatigue. Electrocardiogram (ECG) on admission showed complete atrioventricular (AV) blockade associated with prominent bifid T waves. The second component of the bifid T waves was distinguished from U waves by the beat-to-beat varying bifidity and the nadir between the two components located at > or = 1 mm above the isoelectric line. Range of absolute QT interval was 535 to 650 ms. Hypokalemia (3.6 mEq/L) was noted at admission. Partial restoration of the potassium level (3.9 mEq/L) prior to temporary ventricular demand pacing obscured the bifid T waves and attenuated the QT prolongation and dispersion to some extent (absolute QT interval ranging 520 to 620 ms). It was concluded that marked bradycardia caused by complete AV blockade (ie, a junctional escaped rhythm at a rate of 42 beats/min), hypokalemia, and underlying diabetes mellitus contributed in concert to the QT prolongation and dispersion leading to the prominent bifid T waves.

A 53-year-old patient had a complex ventricular arrhythmia, which most likely was an intermittent pure (nonmodulated) parasystole, due to protection limited to the first part of the cycle coexisting with exit block. However, other interpretations of the observations were possible. Foremost among these was modulated parasystole with partial protection or with an attenuated or nondetectable early delaying phase, with exit block. Interestingly, the parasystole appeared to have fulfilled the dynamic rules regarding the number of sinus beats interposed between manifest parasystolic beats, as has been reported for pure or weakly modulated parasystole. This case corroborates unusual manifestations of an arrhythmia, which because of its newly found complexities and various possible interpretations seems to be discussed with decreasing frequency in most textbooks on general cardiology.

A 65-year-old woman who had shown no delta waves or atrioventricular block when seen in February 1989, suddenly developed advanced atrioventricular block in April 1990. The first electrophysiologic study revealed that atrioventricular block was caused by His ventricular block, and only weak retrograde conduction was documented. A DDD-type permanent pacemaker was implanted. One month after implantation, delta waves developed. The second electrophysiologic study, performed in February 1993, disclosed that a Kent bundle with bidirectional conduction capacity was located at the posterior septum and that the normal conduction system remained blocked at the His ventricular site. The etiology of the newly developed delta waves seems to be the disappearance of impedance mismatch at the ventricular insertion site of the Kent bundle.

Coronary vasospasm may result in recurrent angina pectoris and cause acute myocardial infarction. The extent to which the "sudden death syndrome" occurs is unknown. The case described herein is unique in that the clinical features, including hypotension, AV block, and ventricular arrhythmias, were similar to those seen in myocardial infarction with a poor prognosis, yet infarction was not documented. In subsequent, long-term follow-up evaluation, chest pain has been recurrent, but despite close observation, no further major cardiac complications have been documented. Long-term use of verapamil has contributed to better control of clinical symptomatology.

His bundle electrogram was recorded in a young adult male with corrected transposition of the great vessels and single ventricle. Prolonged PA and AH intervals, wide diphasic His spike, and normal HV intervals were found. These findings are suggestive of the diffuse nature of conduction delay in this congenital lesion involving intra-atrial, AV nodal, and intra-His regions.

A patient with intermittent ventricular parasystole is reported in whom the presence of second degree entrance block with supernormal conduction was suggested for the first time. In this patient, ventricular extrasystoles with variable coupling frequently occurred. The QRS configuration of the extrasystoles was different from that of the parasystolic beats. When extrasystoles did not occur, the parasystolic beat was never seen because the conducted sinus impulse always reset the parasystolic rhythm. When an extrasystole occurred 0.52 sec or more after the preceding sinus beat, this extrasystolic impulse also reset the parasystolic rhythm. On the other hand, when an extrasystole occurred between 0.47 and 0.51 sec after the sinus beat, the parasystolic focus was protected from this extrasystolic impulse. When, however, an extrasystole occurred in a short terminal portion of the T wave of the preceding sinus beat, this extrasystolic impulse reset the parasystolic rhythm again, suggesting entrance block failure during the supernormal phase.

A 65-year-old man with Wolff-Parkinson-White syndrome type A had a rapid ventricular response over an accessory pathway during atrial fibrillation. Four months later, electrophysiological study revealed the following properties: 1) The antegrade accessory pathway conduction showed phase 3 and phase 4 block. 2) The retrograde concealed accessory pathway conduction eliminated phase 4 block in the antegrade accessory pathway conduction. 3) Premature ventricular excitation arose from the accessory pathway or from the ventricular muscle close to its distal end. 4) Atrial fibrillation during isoproterenol infusion did not show rapid ventricular response. Spontaneous impairment of accessory pathway conduction due to phase 3 and phase 4 block was suspected.

Rate dependent first degree block, which was followed by a complete block, between a pacemaker electrode and the ventricular myocardium, was observed in a patient with inferior myocardial infarction. These conduction disturbances which occurred during pacing at the postero-basal wall of the right ventricle and not during pacing at the apex, suggested that the posterior part of the right ventricle was damaged. This hypothesis was supported by hemodynamic findings which indicated a right ventricular infarction.

The ECGs of 1,095 patients with coronary angiographic evidence of significant coronary artery disease (greater than or equal to 50% obstructive lesion in at least one major coronary artery) were reviewed. Five patients had left posterior hemiblock (LPHB), an incidence of 0.5%. Three of five patients also had a right bundle branch block (RBBB). Of the five patients with LPHB, all had significant right coronary artery (RCA) disease (four complete occlusions, one 90% obstructive lesion). All five patients having LPHB also had evidence of critical disease (greater than or equal to 75% obstruction) of at least one of the major branches of the left coronary artery; four of the five had complete occlusion of the left anterior descending coronary artery (LAD). The left circumflex coronary artery (CFx) was critically diseased in three patients. The ECGs of four patients showed evidence of only one myocardial infarction while one patient had evidence of an anterior and an inferior infarction. It is concluded that the presence of LPHB in patients with coronary artery disease is an ominous electrocardiographic finding, and is associated with extensive coronary artery disease.

Clinical, radiologic and histo-pathological observations have suggested that conduction disturbances (CD) are frequent in patients with calcified mitral annulus (CMA). To determine the incidence of CD, 65 consecutive patients with CMA were studied. Sixty-five normal individuals, matched for age and sex served as a control group. CMA has been identified by M-mode echocardiography, cross-sectional echo and image amplifier fluoroscopy. CD were present in 23 patients with CMA as compared to seven patients in the control group (p less than 0.01). Three patients developed complete atrioventricular block (4.6%) during hospitalization requiring artificial pacemakers. We conclude that, 1) early detection of CMA in the elderly is useful in predicting a higher incidence of CD. 2) Complete heart block is more frequent in patients with CMA. 3) Frequent ECG follow-up in these patients has proven to be useful in avoiding serious clinical complications.

A patient with primary cardiomyopathy and long standing atrial fibrillation presented with atrial tachycardia and AV block. Atrial pacing sequentially converted the atrial tachycardia to atrial flutter (biatrial) and to the dissimilar atrial rhythms of right atrial fibrillation with left atrial flutter, right atrial flutter with left atrial electrical standstill and right atrial fibrillation with left atrial standstill. The clincial milieu and intracardiac recordings are presented.

The electrocardiograms (ECGs) of 55 patients with mitral valve prolapse were analyzed. Twelve of these demonstrated conduction abnormalities. Five patients had first degree heart block. Three had the classic ECG changes of the Wolff-Parkinson-White syndrome. Two patients had left anterior hemiblock, one of whom also had incomplete right bundle branch block. One patient had episodes of advanced atrioventricular block and periods of sinus arrest, which resulted in recurrent syncopal attacks. One patient had incomplete left bundle branch block. The presence of conduction disturbances points to the diffuse nature of the myocardial abnormality in mitral valve prolapse.

A 55 year old healthy man with chronic bifascicular block (right bundle branch block and left anterior hemiblock) had a near syncopal episode. A treadmill test showed exercise induced Mobitz type II AV block manifested clinically by paradoxical slowing of the heart rate and decreased blood pressure. True His Purkinje block and pseudo AV block due to His extrasystoles were documented by an electrophysiological study.

A case of ventricular parasystole firing at the extremely rapid rate of 214 beats per minute in a 73 year old woman is described. Manifest cycle lengths of parasystolic complexes varied widely due to variable degrees of exit block, which could be best interpreted by the concept of multilevel block or alternating Wenckebach periodicity in the ventriculo-ectopic junction. Discontinuation of digoxin reduced the degree of exit block and unmasked parasystolic tachycardia.

The long term prognosis was studied in 50 patients treated for the sick sinus syndrome with pacemaker insertion. The mean age of the patients was 71 years. There were 31 females and 19 males in the series. Nine patients (18%) died during the average follow-up period of 19 months. Dizzy and syncopal episodes were abolished in most patients with pacemaker therapy. However only two of the nine patients in congestive heart failure improved with the pacemaker. Thus the long term prognosis of patients with the sick sinus syndrome is poor despite pacemaker therapy. This is particularly true for the patient in chronic congestive heart failure who does not respond to the pacemaker treatment.

A criterion to determine the indication for pacemaker implantation in the sick sinus syndrome by overdrive suppression is proposed. Overdrive suppression was performed in 10 patients with the sick sinus syndrome (SSS) and another 10 patients with normal sinus rhythm (NSR) who served as controls. In the SSS group, 9 patients had complained of such severe symptoms as Adams-Stokes attack and/or congestive failure and were referred to our laboratory for pacemaker implantation. One other patient, an apparently robust young man (20 years old) referred for detailed cardiac examination, had no remarkable symptoms except for arrhythmias, but was found dead two months later. Atrial pacing for overdrive suppression was carried out at first at various rates ranging from 60 to 180 beats/min for 15 sec, and then at a rate of 100 beats/min for various durations ranging from 5 to 180 sec. After cessation of the atrial pacing, asystolic pauses were measured and the maximum (maximum pause) among the pauses obtained was used as a parameter indicating depression of cardiac automaticity. The maximum pause in the SSS group ranged from 5.6 to 9.0 sec (mean +/- SD = 7.0 +/- 1.2), WHILE THOSE IN THE NSR group ranged from 0.7 to 1.5 sec (mean +/- SD = 1.2 +/- 0.14). Therefore, the maximum pause was considered not only to reflect the severity of the symptoms necessitating pacemaker implantation in the 9 patients of the SSS group but to have warned us of sudder death in another patient. We concluded that overdrive suppression is useful as a supplementary challenge to determine indications for pacemaker implantation for the sick sinus syndrome, and that prolongation of the maximum pause beyond 5.0 sec is the critical level for pacemaker implantation.

Hypogonadotropic hypogonadism with anosmia was found in a 38 year old female. Cardiac abnormalities were manifested by a second degree heart block as well as a conduction delay below the AV node. Striking T wave inversions developed in the absence of any symptoms. These changes probably reflect a central nervous system defect.

To assess the prognostic significance and the clinical implications of the electrocardiographic findings of the first acute myocardial infarction, the in-hospital mortality and complications and three-year follow-up of 180 patients were analyzed. The patients were divided according to the infarction type (transmural, non-transmural), the site, (anterior, inferior including posterior) and the absence or presence of ST depression in leads facing the site of infarction. The peak enzyme concentrations were significantly higher in those with transmural infarcts than in those with non-transmural infarcts, in anterior infarcts compared to inferior infarcts, and in those sites with ST depression than those without. The early complications of cardiogenic shock, congestive cardiac failure, and complete heart block were significantly higher in transmural infarcts compared to non-transmural, while late complications and mortality were the same in all groups and subgroups. This study demonstrated that ECG changes in the first acute myocardial infarction are of prognostic significance for the early clinical course, but cannot predict the late course or subsequent coronary events.

The ECGs of 72 patients with an unequivocal vectorcardiographic diagnosis of either left anterior hemiblock (LAH) or inferior myocardial infarction (IMI) or both were reviewed. Our intention was to identify definite electrocardiographic criteria for the diagnosis of the left anterior hemiblock and of inferior myocardial infarction when both were present vectorcardiographically. All patients with left anterior hemiblock, accompanied or not by IMI, had a left axis deviation, a negative terminal deflection (S wave) in leads II, III and a VF; the majority of them also had a terminal r wave in lead a VR (50 of 52, 96%). The diagnosis of LAH was therefore always possible in the concomitant presence of both entities. A negative initial deflection (Q wave) significant in size or not significant was present in a minority of patients with both LAH and IMI (9 of 24, 37.5% in lead II; 7 of 24, 25% in lead III; and 12 of 24, 50% in lead aVF). In the patients with insignificant Q waves, as well as in the rest of the patients with rS configuration, the electrocardiographic diagnosis of IMI was not possible due to the concomitant presence of LAH.

A rare instance showing non-conducted atrial parasystole coexisting with ventricular parasystole is presented and a related subject is briefly discussed. The importance of recognizing parasystole is again emphasized because the ordinary extrasystoles, particularly ventricular in origin, are frequently digitalis-induced, while parasystole, which superficially resembles the ordinary extrasystoles, does not seem to be related to digitalis.

A case is presented in which left anterior hemiblock (LAH) appeared transiently after the pause terminating atrial pacing, after atrial premature beats and during the slowing of sinus rhythm induced by carotid sinus massage. The transient LAH is attributed to phase-4 block, and is reported in order to add weight to the hypothesis that phase-4 block is a significant factor in the genesis of discrete conduction blocks in the human heart.

The effect of adrenergic enhancement (stimulation of a stellate ganglion or administration of norepinephrine) on arrhythmias induced by ventricular overdrive ("overdirve excitation") was studied in dogs with complete atrioventricular block. The following results were obtained. (1) Adrenergic enhancement may lead to abnormal ventricular rhythms. (2) A brief drive during adrenergic enhancement induced or enhanced fast ventricular rhythms. (3) The induced rhythms were characterized by an abrupt onset, a fast rate of discharge, and a moderate degree of slowing before an abrupt cessation. (4) The induced rhythms were accelerated by further drive. (5) Increasing the duration of overdrive during adrenergic enhancement resulted in overdrive suppression and not in overdrive excitation. (6) Prolonged drive could induce a few beats (instead of suppression) but at a rate below control ("inhibited excitation"). (7) The arrhythmogenic effects of overdrive and adrenergic enhancement were potentiated by the simultaneous administration of calcium. It is concluded that interventions which increase the inward calcium current (overdrive, adrenergic enhancement and higher [Ca]o) favor the onset and the maintenance of overdrive excitation.

The electrocardiographic diagnosis of myocardial infarction in patients with ventricular pacemakers is often difficult. This report describes the electrocardiograms of two patients with permanent ventricular pacemakers in whom the diagnosis of acute anterior myocardial infarction could be made with confidence by observing the evolution of primary ST and T wave abnormalities in the absence of specific QRS changes.

The electrocardiographic findings in two children with sustained atrial tachycardia and exit block are reported. The exit block was dependent on the atrial pacemaker rate, being present only at rapid rates of discharge. In one case propranolol enhanced the exit block, and on an appropriate dose the heart rate was maintained within a well tolerated range.

Extra AV nodal Wenckebach periodicity was diagnosed in seven patients. The most frequent form of this conduction abnormality was an exit block. The underlying block was localized in the sinoatrial junction and in the atria in two patients; the AV junction and the ventricle were the site of the Wenckebach periodicity in one case each. In extra AV nodal exit block, the actual conduction delay is not seen on the ECG and the diagnosis is based on the progressive shortening of the P-P or R-R intervals followed by a pause which is less than twice the shortest P-P (R-R) interval depending on the level of the block. A Wenckebach periodicity in the bundle branches or within the reentry pathway each occurred in one patient. In these forms of Wenckebach periodicity, the diagnosis is established more readily because the conduction delay can be demonstrated on the surface ECG. The clinical significance of extra AV nodal Wenckebach periodicity is discussed.

Coexistent sino-atrial and atrioventricular block with Wenckebach phenomenon is an extremely unusual cardiac arrhythmia. Observations on the natural history of sinus node dysfunction are rare. For over six years our elderly patient has been followed without symptoms but with increasing severity of atrio-ventricular block.

Pacemaker capture during the supernormal period was seen in a case of modulated parasystole where ectopic cycles occurred without any interposed nonparasystolic beat. This contrasts with previous clinical reports, since, in the latter, the parasystolic cycle length could not be measured directly. As in experimental studies, supernormal modulation resulted in a triphasic phase response curve. Although less likely, similar electrocardiographic changes could be produced by a conceptually different phenomenon, namely full parasystolic resetting due to loss of protection occurring exclusively early in the cycle, combined with modulation in the other (late) parts of the cycle.

Four of 32 patients with left anterior hemiblock and an acute anterior wall myocardial infarction died. Left anterior hemiblock was present on admission in 24 patients, and subsequently appeared in 8. Of the 28 survivors, 21 are still alive an average of 2.8 years after the acute myocardial infarction.

Twelve patients with inferior wall myocardial infarction complicated with complete atrioventricular block during the acute stage were studied. The His-bundle electrogram was studied in the convalescent stage at an average of 6 months after the acute attack. The age of the patients was 62 +/- 16 years. The width of the QRS complex was within the normal range and the PR interval was less than 200 msec. AH time was 74 +/- 18 msec (mean +/- SD). No split H activity was observed. HV time however, was significantly prolonged in the 12 patients; 54 +/- 12 msec vs. 42 +/- 9 msec in the control group (p less than 0.02). Five patients had HV time equal to or more than 60 msec. Intra-His block was suggested to exist in a high frequency in the patients who had previous complete AV block during the acute stage of myocardial infarction of the inferior wall.

Two cases of transient hemiblock occurring during the course of acute myocardial infarction are reported. The transient manifestation permits the accurate evaluation of the diagnostic features of the hemiblocks as modified by acute infarction. One case reflects the development of left bundle branch block due to bilateral post-divisional block which inter alia permits the study of left bundle branch block in the presence of acute myocardial infarction.