Premature Ventricular Excitation Research Articles

Simultaneous development of complete AV block and WPW phenomenon after COVID-19 in a child with severe systemic pathology

Simultaneous development of atrioventricular (AV) blockade and Wolf–Parkinson–White syndrome (WPW) are described extremely rarely and mainly in adults. A few observations have shown the appearance of A-B blockade against the background of the already existing permanent form of premature ventricular excitation (WPW). We have described a case of simultaneous primary development of the WPW phenomenon and complete A-B blockade in a child with severe systemic disease after undergoing COVID-19.

ПРОГНОСТИЧЕСКИЕ ФАКТОРЫ СИНДРОМА ВОЛЬФА-ПАРКИНСОНА-УАЙТА В ДЕТСКОМ ВОЗРАСТЕ

Objective: to determine the prognostic factors determining the severity of Wolff-Parkinson-White syndrome (WPW) in children. Methods: a retrospective analysis of the course of the disease was performed in 108 children with WPW syndrome aged 13.6 (12-16) years. Depending on the number of attacks of paroxysmal tachycardia (PT), all children were divided into 2 groups: group A consisted of 47 children (43.5%) with a history of no more than three attacks of PT and they were rare; group B included 61 children (56.5%) with frequent (more than once a month) attacks of PT, more than four in the history. We studied: the family history, the clinical picture of the disease, the nature of paroxysmal tachycardia, the effectiveness of treatment, and the results of instrumental studies. Using the method of mathematical modeling, the informative value of each feature was determined, and the diagnostic value was determined. Results: age and gender differences in the development of WPW syndrome in children were established. The presence of a family history of ECG signs of ventricular preexcitation is a reliable sign (p=0.02), contributing to more frequent PT attacks. More frequent development of PT attacks was noted in patients with mitral valve prolapse (p=0.03) and additional chords in the left ventricular cavity (p=0.001). In the group with frequent PT attacks, signs of sinus node dysfunction were detected more often (<0.001). According to the echocardiographic study, children with frequent PT attacks were more likely to have disorders in the form of thickening of the interventricular septum in the diastole (p=0.010) and signs of diastolic dysfunction of the right ventricle (p = 0.010). Conclusion: The factors of prognostic value include: male gender, the presence of the expressed symptoms of the attack of PT and PT frequency more than once per month, low vagal efficiency on relieving the attack, a history of frequent attacks, a family history of ECG characteristics of premature ventricular excitation, the presence of signs of sinus node dysfunction during 24 hours without the attack and the signs of arrhythmogenic myocardial dysfunction by echocardiography.

Mechanically Induced Ectopy via Stretch-Activated Cation-Nonselective Channels Is Caused by Local Tissue Deformation and Results in Ventricular Fibrillation if Triggered on the Repolarization Wave Edge (Commotio Cordis).

External chest impacts (commotio cordis) can cause mechanically induced premature ventricular excitation (PVEM) and, rarely, ventricular fibrillation (VF). Because block of stretch-sensitive ATP-inactivated potassium channels curtailed VF occurrence in a porcine model of commotio cordis, VF has been suggested to arise from abnormal repolarization caused by stretch activation of potassium channels. Alternatively, VF could result from abnormal excitation by PVEM, overlapping with normal repolarization-related electric heterogeneity. Here, we investigate mechanisms and determinants of PVEM induction and its potential role in commotio cordis-induced VF. Subcontusional mechanical stimuli were applied to isolated rabbit hearts during optical voltage mapping, combined with pharmacological block of ATP-inactivated potassium or stretch-activated cation-nonselective channels. We demonstrate that local mechanical stimulation reliably triggers PVEM at the contact site, with inducibility predicted by local tissue indentation. PVEM induction is diminished by pharmacological block of stretch-activated cation-nonselective channels. In hearts where electrocardiogram T waves involve a well-defined repolarization edge traversing the epicardium, PVEM can reliably provoke VF if, and only if, the mechanical stimulation site overlaps the repolarization wave edge. In contrast, application of short-lived intraventricular pressure surges neither triggers PVEM nor changes repolarization. ATP-inactivated potassium channel block has no effect on PVEM inducibility per se, but shifts it to later time points by delaying repolarization and prolonging refractoriness. Local mechanical tissue deformation determines PVEM induction via stretch-activation of cation-nonselective channels, with VF induction requiring PVEM overlap with the trailing edge of a normal repolarization wave. This defines a narrow, subject-specific vulnerable window for commotio cordis-induced VF that exists both in time and in space.

A Dynamical Threshold for Cardiac Delayed Afterdepolarization-Mediated Triggered Activity

Ventricular myocytes are excitable cells whose voltage threshold for action potential (AP) excitation is ∼−60 mV at which INa is activated to give rise to a fast upstroke. Therefore, for a short stimulus pulse to elicit an AP, a stronger stimulus is needed if the resting potential lies further away from the INa threshold, such as in hypokalemia. However, for an AP elicited by a long duration stimulus or a diastolic spontaneous calcium release, we observed that the stimulus needed was lower in hypokalemia than in normokalemia in both computer simulations and experiments of rabbit ventricular myocytes. This observation provides insight into why hypokalemia promotes calcium-mediated triggered activity, despite the resting potential lying further away from the INa threshold. To understand the underlying mechanisms, we performed bifurcation analyses and demonstrated that there is a dynamical threshold, resulting from a saddle-node bifurcation mainly determined by IK1 and INCX. This threshold is close to the voltage at which IK1 is maximum, and lower than the INa threshold. After exceeding this dynamical threshold, the membrane voltage will automatically depolarize above the INa threshold due to the large negative slope of the IK1-V curve. This dynamical threshold becomes much lower in hypokalemia, especially with respect to calcium, as predicted by our theory. Because of the saddle-node bifurcation, the system can automatically depolarize even in the absence of INa to voltages higher than the ICa,L threshold, allowing for triggered APs in single myocytes with complete INa block. However, because INa is important for AP propagation in tissue, blocking INa can still suppress premature ventricular excitations in cardiac tissue caused by calcium-mediated triggered activity. This suppression is more effective in normokalemia than in hypokalemia due to the difference in dynamical thresholds.

ROLE OF FIBROUS MYOCARDIAL DISORGANIZATION IN FORMATION OF RHYTHM DISTURBANCE IN PREMATURE VENTRICULAR EXCITATION SYNDROMES

Aim. The aim of the study was to assess the markers of synthesis and degradation of collagen, the parameters of structural-functional status of myocardium in patients with Wolff-Parkinson-White (WPW) syndrome and phenomenon, as well as idiopathic atrial fibrillation (AF) and to evaluate their predictor value in the development of tachyarrythmias. Materials and methods. Seventy three patients were examined. The main group included 43 patients with premature ventricular excitation syndromes (16 with WPW phenomenon and 27 with WPW syndrome, mean age 25 ± 9,15 years, 29 (67 %) men and 14 (33 %) women). The comparison group joined 30 patients with “idiopathic” AF (mean age 28,8 ± 4,25 years, 67 % of men and 33 % of women) and practically healthy persons of the same age. To assess disturbance of fibrous matrix of the myocardium, quantitative value of tissue inhibitor of metalloproteinase-1 (TIMP-1), matrix metalloproteinase-9 (MMP-9) and carboxyterminal propeptide (PIP) - blood serum type I procollagen was studied. Structural-functional status of myocardium was investigated with echocardiographic method. Results. The study indicated participation of matrix metalloproteinases and their inhibitors in formation of structural-functional changes in the myocardium among WPW syndrome and phenomenon patients, with maximum dysbalance of type I collagen exchange registered in patients suffering from WPW syndrome combined with AF. When carrying out statistical processing, reliable difference between the indices of extracellular matrix status depending on WPW syndrome and phenomenon, as well as on the presence or absence of AF paroxysms against he background of ventricular preexcitation syndrome were found out. Conclusions. Presence of dysbalance of the fibrosis seromarkers, which correlate with geometry of the left atrium and have a predictor value for the development of atrial fibrillation with WPW, was stated.

ROLE OF COLLAGEN SYNTHESIS AND DEGRADATION SEROMARKERS, STRUCTURAL-FUNCTIONAL HEART PARAMETERS IN PROGNOSIS OF ATRIAL FIBRILLATION AMONG PATIENTS WITH PREMATURE VENTRICULAR EXCITATION SYNDROMES

Aim. The aim of the study was to optimize the diagnosis and prognosis of developing arrhythmias in this cohort and to reveal the possible role of fibrous matrix disturbance in development of arrhythmia. Materials and methods. The main group included 43 patients with premature ventricular excitation syndromes (WPW phenomenon, WPW syndrome), the comparison group - 15 practically healthy persons of the similar age. The mean age of patients belonging to the main group was 25,3 ± 9,15 years. All the groups were comparable by gender distribution ( p = 0,45, Fisher criterion) and age ( p = 0,27, U-criterion). Results. The greatest matrix metalloproteinase-9 (MMP-9) indices were assessed in patients with WPW syndrome - 96,1 ± 33,2 ng/ml, with WPW phenomenon - 54,3 ± 21,8 ng/ml; p = 0,0003). Practically healthy persons had minimum MMP-9 values - 27,4 ± 10,9 ng/ml ( p = 0,00014; p = 0,000002). Maximum values of tissue inhibitor of matrix metalloproteinases (TI MP-1) are presented in WPW phenomenon group and practically healthy persons (418,5 ± 69,8 ng/ml and 461,7 ± 72,2 ng/ml; p = 0,27). In patients with WPW syndrome, TIMP-1 was reliably lower - 341,1 ± 90,1 ng/ml ( p = 0,002; p = 0,00012). Procollagen type 1 carboxyterminal propeptide (PICP) level in patients with WPW syndrome was 179,9 ± 76,2 ng/ml, with WPW phenomenon - 97,8 ± 31,7 ng/ml ( p = 0,00014). All patients, included into the study, significantly differed from practically healthy persons by PICP level - 69,4 ± 23,9 ng/ml ( p < 0,05, U -criterion). Statistical processing of material showed reliable differences between extracellular matrix status indices depending on WPW syndrome and phenomenon, as well as presence or absence of AF paroxysms against the background of ventricular preexcitation. Conclusions. Changes in fibrous matrix, namely, increase in MMP-9, PICP concentrations and decrease in TIMP-1was registered. WPW syndrome is characterized by significant dysbalance of collagen synthesis and degradation seromarkers than WPW phenomenon. The studied seromarkers of fibrosis, probably, participate in formation of rhythm disturbance of the heart with actual syndromes available.

Modification by KCNE1 variants of the hERG potassium channel response to premature stimulation and to pharmacological inhibition

human Ether-à-go-go-Related Gene (hERG) encodes the pore-forming subunit of cardiac rapid delayed rectifier K+ current (IKr) channels, which play important roles in ventricular repolarization, in protecting the myocardium from unwanted premature stimuli, and in drug-induced Long QT Syndrome (LQTS). KCNE1, a small transmembrane protein, can coassemble with hERG. However, it is not known how KCNE1 variants influence the channel's response to premature stimuli or if they influence the sensitivity of hERG to pharmacological inhibition. Accordingly, whole-cell patch-clamp measurements of hERG current (IhERG) were made at 37°C from hERG channels coexpressed with either wild-type (WT) KCNE1 or with one of three KCNE1 variants (A8V, D76N, and D85N). Under both conventional voltage clamp and ventricular action potential (AP) clamp, the amplitude of IhERG was smaller for A8V, D76N, and D85N KCNE1 + hERG than for WT KCNE1 + hERG. Using paired AP commands, with the second AP waveform applied at varying time intervals following the first to mimic premature ventricular excitation, the response of IhERG carried by each KCNE1 variant was reduced compared to that with WT KCNE1 + hERG. The IhERG blocking potency of the antiarrhythmic drug quinidine was similar between WT KCNE1 and the three KCNE1 variants. However, the IhERG inhibitory potency of the antibiotic clarithromycin and of the prokinetic drug cisapride was altered by KCNE1 variants. These results demonstrate that naturally occurring KCNE1 variants can reduce the response of hERG channels to premature excitation and also alter the sensitivity of hERG channels to inhibition by some drugs linked to acquired LQTS.

Electroconvulsive therapy-induced Wolff–Parkinson–White syndrome: a case report

ObjectiveWolff–Parkinson–White (WPW) syndrome is characterized by premature ventricular excitation due to the presence of an abnormal accessory pathway. Electrocardiography (ECG) of patients with WPW syndrome portrays a short PR interval and a wide QRS interval with a delta wave. MethodsHerein, we report the case of a patient with schizophrenia who developed a wide QRS interval with a delta wave immediately following electroconvulsive therapy (ECT). ResultsInitially, the delta wave disappeared within 2 days after ECT. However, the duration of the delta wave increased exponentially to 4 months when ECT was repeated. ConclusionAlthough the patient's cardiocirculatory dynamics remained normal, we continued to monitor her ECG until the delta wave disappeared because WPW syndrome can lead to serious arrhythmia.

Association of Smoking, Sleep Apnea, and Plasma Alkalosis With Nocturnal Ventricular Arrhythmias in Men With Systolic Heart Failure

Excess sudden death due to ventricular tachyarrhythmias remains a major mode of mortality in patients with systolic heart failure. The aim of this study was to determine the association of nocturnal ventricular arrhythmias in patients with low ejection fraction heart failure. We incorporated a large number of known pathophysiologic triggers to identify potential targets for therapy to reduce the persistently high incidence of sudden death in this population despite contemporary treatment. Eighty-six ambulatory male patients with stable low (≤ 45%) ejection fraction heart failure underwent full-night attendant polysomnography and simultaneous Holter recordings. Patients were divided into groups according to the presence or absence of couplets (paired premature ventricular excitations) and ventricular tachycardia (VT) (at least three consecutive premature ventricular excitations) during sleep. In multiple regression analysis, four variables (current smoking status, increased number of arousals, plasma alkalinity, and old age) were associated with VT and two variables (apnea-hypopnea index and low right ventricular ejection fraction) were associated with couplets during sleep. We speculate that cessation of smoking, effective treatment of sleep apnea, and plasma alkalosis could collectively decrease the incidence of nocturnal ventricular tachyarrhythmias and the consequent risk of sudden death, which remains high despite the use of β blockades.

Navigational error in the heart leads to premature ventricular excitation

In the normal heart, an insulating barrier separates the atria and ventricles. The only way in which electrical impulses can cross this barrier is via the atrioventricular (AV) node, which delays impulse conduction to ensure the forward flow of the blood. However, in some individuals, additional muscular bundles (accessory pathways) allow rapid conduction of electrical impulses from the atria to the ventricles, resulting in premature ventricular excitation and contraction. In this issue of the JCI, two independent research groups demonstrate that erroneous development of the embryonic AV canal, which performs a similar function to that of the adult AV node, is a novel mechanism by which accessory pathways can form.

A simple automated stimulator of mechanically induced arrhythmias in the isolated rat heart

Transient stretching of the ventricle can trigger arrhythmias and evoke ventricular fibrillation, especially when the stimulation occurs in the vulnerable period. To explore the sensitivity of small hearts we used a commercial pressure servo to study the kinetic relationship of left ventricular pressure to excitability and arrhythmias in the rat heart. Stimulation protocols were readily composed on the computer and programmed to vary the stimulus amplitude and timing relative to pacing. The pressure-induced premature ventricular excitations were similar to those observed in larger hearts, but the convenience of using small hearts allows the use of inexpensive transgenic animals to explore the molecular basis of transduction.

Electrophysiologic Interaction between Class I Antiarrhythmic Drugs and Volatile Anesthetics in Depressant Effects on Ventricular Activation in a Canine Myocardial Infarction Model

Previous studies showed that volatile anesthetics depressed ventricular delayed activation in a canine myocardial infarction model. It is well known that class I antiarrhythmic drugs depress the ventricular activation in the infarcted myocardium. In the present study, we examined the electrophysiologic interaction between volatile anesthetics (sevoflurane, isoflurane) and class I antiarrhythmic drugs (lidocaine, procainamide) in effects on the ventricular delayed activation in a canine myocardial infarction model. The conduction time of the premature stimulation-induced ventricular excitation was measured in both normal and infarcted zones of the ventricle. An interval from the premature stimulus artifact to the epicardial activation was measured on bipolar electrograms as an index of conduction time, i.e., activation time. In the infarcted zone, the volatile anesthetics and class I antiarrhythmic drugs prolonged the activation time in the infarcted zone, and the combination of the volatile anesthetics and the class I antiarrhythmic drugs markedly prolonged the activation time or blocked the delayed activation. In the normal zone, a similar synergistic interaction was observed, but the effect of these drugs was less compared with that in the infarcted zone. From these results, possible mechanisms to explain the synergistic interaction were discussed.

Electrophysiological effects of myocardial stretch and mechanical determinants of stretch-activated arrhythmias.

Although the existence of myocardial mechanoelectrical feedback is well established, the mechanism of arrhythmia induction by ventricular dilatation or stretch remains insufficiently defined. In particular, controversy exists when comparing the arrhythmogenic potential of chronic versus acute myocardial stretch. Also, assessment of cellular electrophysiological effects of myocardial stretch has been incomplete. To evaluate the electrophysiological and arrhythmogenic effects of slow versus rapid ventricular wall stretch, we developed an isolated Langendorff-perfused rabbit heart model in which left ventricular (LV) volume can be changed by a computer-controlled servopump. Cellular electrophysiological effects and premature ventricular excitations (PVEs) and their origin produced by the volume increases were assessed by a multiple-site monophasic action potential (MAP) recording system and by volume-conducted ECGs obtained by immersing the entire preparation in a saline-filled tank. Volume was increased either gradually with slow volume ramps (0.1 ml/sec) or suddenly by volume pulses of varying pulse waveforms (three different amplitudes and five different rise velocities) applied randomly 250-350 times to each of eight hearts. Gradual LV volume loading caused gradual decreases in MAP resting and action potential amplitude, whereas rapid, transient volume pulses caused transient depolarizations. Despite similar membrane potential effects of stretch, gradual volume increases rarely (11%) produced PVEs, even with large volume loads, whereas rapid volume pulses of moderate amplitudes regularly triggered PVEs (45-100% of interventions). Logistic regression analysis showed that the probability of PVE occurrence increased independently with both the amplitude and the velocity of the volume increase, with the greatest sensitivity to stretch velocity exhibited at low and intermediate pulse amplitudes. Faster volume pulse rise velocities triggered PVEs at a lower instantaneous pulse amplitude than lower rise velocities, further corroborating the dependence of stretch-activated arrhythmias on the velocity of stretch. In contrast, an increase in the basic ventricular volume had no effect on the probability of PVE occurrence during the volume pulses. The MAP recordings demonstrated spatial variability in the extent of local depolarizations and site of PVE origin; transient depolarizations occurred, and PVEs originated most often in the posterolateral region of the left ventricle. Membrane depolarization is caused by both gradual and rapid ventricular stretch, but PVEs are more easily elicited by rapid stretch. Regions of greater myocardial compliance that experience greater relative stretch may act as "foci" for stretch-activated arrhythmias during dynamic ventricular loading. These whole-heart data corroborate the existence of stretch-activated membrane channels in ventricular myocardium and may help explain ventricular ectopy under conditions of differential ventricular loading, as in ventricular dyskinesia, or regional muscle traction, as in mitral valve prolapse syndrome.

Magnetocardiographic localisation and modelling

In our magnetocardiographic (MCG) localisation studies, two modelling approaches have been applied: (a) modelling the sources with dipole and quadrupole moments in a general multipole expansion and using a homogeneous, semi-infinite volume conductor, and (b) using a single current dipole source in a homogeneous, realistically shaped torso. Both approaches have been successfully applied in localising the premature ventricular excitation site in patients suffering from the Wolff-Parkinson-White syndrome. In addition, we have participated in developing a model of propagation of electrical activation in the ventricles. Anisotropic conductivity properties and spiral arrangement of myocardial fibres are included in the model.

Effects of halothane with and without histamine and/or epinephrine on automaticity, intracardiac conduction times, and development of dysrhythmias in the isolated guinea pig heart.

Histamine is released during allergic reactions, and is known to produce cardiac dysrhythmias. The authors compared the cardiac effects of histamine and epinephrine during exposure to halothane in the isolated perfused guinea pig heart. Responses studied were spontaneous sinus rate, intra-atrial conduction time, atrial-septal conduction time (ASCT), intraventricular conduction time (IVCT), and left ventricular pressure (LVP). The incidence and type of dysrhythmias with histamine and halothane and with epinephrine and halothane were analyzed from electrograms. The authors found that halothane alone (0.7 to 2.1 vol%) causes dose-dependent depressions of sinus rate and LVP, prolongs ASCT and IVCT, and produces atrioventricular (AV) block with junctional bradycardia. Histamine alone (.01-10 microM) increases sinus rate and LVP but, like halothane, prolongs ASCT. Halothane antagonizes the inotropic and chronotropic effects of histamine, but enhances ASCT compared with histamine alone. Histamine with halothane greatly increases the incidence of junctional tachycardia with AV dissociation from 0% with histamine alone up to 48%. Epinephrine alone (0.1-5 microM), like histamine, increases sinus rate and LVP, but does not cause a relative increase in ASCT. Halothane antagonizes the inotropic and chronotropic effects of epinephrine, but increases the incidence of ventricular tachycardia from 6% to 28%, and the incidence of premature ventricular excitations from 0% to 40%, compared with epinephrine alone. The authors' in vitro findings show that histamine and halothane, like epinephrine and halothane, can cause dysrhythmias, but that the genesis and type of dysrhythmias induced by these agents are dissimilar. Consequently, the release of histamine with an anaphylactoid reaction during halothane anesthesia, and the treatment of the reaction with epinephrine, could result in dangerous ventricular tachydysrhythmias.

Intermittent wolff-parkinson-white syndrome due to phase 3 and phase 4 block: Disappearance of rapid ventricular response during atrial fibrillation

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.

Epicardial Mapping in Wolff-Parkinson-White Syndrome

The syndrome of Wolff-Parkinson-White (WPW) is classically defined by an electrocardiogram with a short PR interval, a prolonged QRS complex that begins with an abnormal initial force known as the delta wave, and is seen in patients who are predisposed to tachyarrhythmias. 1 Figure 1 shows the ECG of WPW compared with a normal ECG. The PR interval is short because the QRS (the delta wave) begins abnormally early in relationship to the end of the P wave. Thus, the PR interval is shortened to the same extent that the QRS is prolonged. The diagram on the right depicts atrial activation in phase 1. Phase 2 demonstrates premature ventricular excitation (preexcitation) over an accessory atrioventricular connection that conducts without the delay exhibited by the atrioventricular node. The anomalous, premature depolarization is indicated by the darker grain pattern in the heart and in the ECG. During phase 3, the ventricle is

Alternate Patterns of Premature Ventricular Excitation during Spontaneous Atrial Bigeminy

This report documents two instances of spontaneous alternate patterns of premature ventricular during atrial bigeminy (alternating premature ventricular excitation). Previous reports of alternating premature ventricular excitation have required control of electrophysiologic parameters by atrial pacing methods. Illustration of this arrhythmia and a discussion of its mechanism constitute the substance of this report.

Alternate patterns of premature ventricular excitation during induced atrial bigeminy.

Alternate patterns of premature ventricular excitation have been observed during induced atrial bigeminy in 18 subjects, including five normal volunteers. Each study was performed in the cardiac catheterization suite where a transvenous catheter electrode was positioned in the right atrium. Coupled or paired stimuli were delivered to the atrium by an isolated battery-powered source at an adjusted interval which resulted in alternate patterns of ventricular excitation from alternate premature beats ("alternating premature ventricular excitation"). In most instances "alternating premature ventricular excitation" occurred when parameters of preceding cycle length, premature coupling interval, and atrioventricular conduction time were constant. In man also some observations were made of His bundle excitation during premature atrial stimulation, and in the intact dog heart some observations were made of alternating premature ventricular excitation during His bundle stimulation. A tenable explanation for alternating premature ventricular excitation is advanced which rests on three postulates: (1) A long cycle length is followed by a long refractory period. (2) The refractory period of each branch of the specialized conduction system is dependent on its preceding cycle length or recovery period; and (3) the diastolic recovery period of a blocked segment of the specialized conduction system is shorter than the recovery period when blockade does not occur.

Electrocardiographic criteria in the differential diagnosis of pre-excitation (Wolff-Parkinson-White syndrome) and arteriosclerotic heart disease.

THE electrocardiographic picture of prolonged QRS-complex duration with short PR interval was the subject of isolated reports1 , 2 until Wolff, Parkinson and White3 described the clinical syndrome of "bundle-branch block with short PR interval in healthy young people prone to paroxysmal tachycardia."Subsequent studies have demonstrated that premature ventricular excitation, not delayed conduction, prolongs QRS-complex duration. Block of neither the right nor the left bundle branch interferes with premature excitation, suggesting that the main bundles are not pathways for the premature impulse.Many synonyms for the Wolff–Parkinson–White syndrome have appeared. These include accessory-bundle syndrome,4 bundle-of-Kent syndrome,5 anomalous atrioventricular excitation,6 pre-excitation7 and . . .