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Abstract: Since its initial description by Jervell and Lange‐Nielsen in 1957, the congenital long QT syndrome (LQTS) has been the most investigated cardiac ion channelopathy. Although congenital LQTS continues to remain the domain of cardiologists, cardiac electrophysiologists, and specialized centers, the by far more frequent acquired drug‐induced LQTS is the domain of all physicians and other members of the health care team who are required to make therapeutic decisions. This report will review the electrophysiological mechanisms of LQTS and torsade de pointes, electrocardiographic characteristics of acquired LQTS, its clinical presentation, management, and future directions in the field. [ABSTRACT FROM AUTHOR]

Aims: The present study attempts to develop an objective, statistically based set of criteria for activation time determination from unipolar electrograms (U-EGMs) using a standard of activation related to biophysical theory. Methods: A high-resolution assembly of U-EGMs obtained from the epicardial surface of the canine postinfarction heart were analyzed in order to achieve the best prediction of local versus distant activation. An activation time standard (ATS) consisted of three properties: (1) propagation of activation, evidenced by a linear temporal shift of waveforms from closely spaced U-EGMs with little or no decay in amplitude; (2) cycle length-dependent changes of those propagating waveforms; and (3) evidence of electrotonic deflections, seen as nonpropagating potentials having decaying amplitude with distance. Results: A number of U-EGM features were calculated and subjected to analysis by comparing their occurrence with the ATS. A discriminant function analysis incorporating multiple features (Voltage, −dV/dt and Ratio) of major U-EGM deflections improved prediction of activation time of complex fractionated EMGs from ischemic canine epicardium to 90%. Conclusion: A unique discriminant function based on sound biophysical principles markedly improved prediction of activation time of complex U-EGMs from ischemic canine epicardium. A computerized version of the algorithm could be developed to provide more accurate activation maps for both basic and clinical use. (PACE 2011; 34:1105-1115) [ABSTRACT FROM AUTHOR]

A 74-year-old man with past history of near syncope presented with frequent periods of second-degree atrioventricular block (2° AVB). An electrophysiological study revealed prolonged atrial-His and His-ventricular (HV) intervals and frequent His bundle (H) extrasystoles. The latter manifested in the surface electrocardiogram as premature atrial, junctional, or ventricular beats, as well as 2° AVB that mimicked Wenckebach or Mobitz II block. Procainamide markedly suppressed H extrasystole. However, because of the presence of prolonged HV interval and history of presyncope, a permanent pacemaker was inserted. The case illustrates the varied manifestation of H extrasystole and presents guidelines for management. (PACE 2010; 1-4) [ABSTRACT FROM AUTHOR]

Aims: To compare patients with atrial flutter (AFl) and 1:1 atrioventricular conduction (AVC) with patients with AFl and higher AVC. Methods: The characteristics of 19 patients with AFl and 1:1 AVC (group A) were compared with those of 116 consecutive patients with AFl and 2:1 AVC or higher degree AV block (group B). Results: Age, gender, and left ventricular function were similar in the two groups. In group A versus group B, more patients had no structural heart disease (42% vs 17%, P < 0.05) and syncope/presyncope (90% vs 12%, P < 0.05). The AFl cycle length (CL) in group A was longer than in group B (265 ± 24 ms vs 241 ± 26 ms, P < 0.01). The transition from AFl with 1:1 to 2:1 AVC or vice versa was associated with small but definite changes in AFl CL, which showed larger variations in response to sympathetic stimulation. In group A patients who were studied off drugs, the atrial-His interval was not different from group B, but maximal atrial pacing rate with 1:1 AVC was faster. In group A, five patients were misdiagnosed as ventricular tachyarrhythmias, and three with a defibrillator received inappropriate shocks. Four patients had ablation of AVC and six had ablation of AFl circuit. Conclusions: The main difference between groups A and B may be an inherent capacity of the AV node for faster conduction, especially in response to increased sympathetic tone. The latter affects not only AVC but also the AFl CL. One should be aware of the different presentations of AFl with 1:1 AVC to avoid misdiagnosis/mismanagement and to consider the diagnosis in patients with narrow or wide QRS tachycardia and rates above 220/min. [ABSTRACT FROM AUTHOR]

Introduction: Atrial standstill is a rare heterogeneous arrhythmia characterized by electrical and mechanical standstill and electrical inexcitability. A long-lasting progressive form is seen with cardiac and neuromuscular diseases, and a familial or idiopathic form may have a genetic basis. A transient form was described secondary to drug intoxication, electrolyte imbalance, cardiac inflammation, and ischemia. Methods: We investigated three patients with long-standing atrial tachyarrhythmia (AT) (atrial flutter in two, and focal atrial tachycardia in one). All patients underwent a complete electrophysiological study with mapping of right and left atrial activity and radiofrequency ablation (RF Abl) of AT. Results: Following RF Abl of AT, all three patients manifested transient atrial electrical silence in the absence of known reversible causes. Atrial electrical silence was observed when, following AT termination, an escape atrioventricular (AV) junctional rhythm (in two patients) and an escape VVI pacemaker rhythm (in one patient) showed transient ventriculo-atrial (VA) conduction block (up to 30 seconds). A dominant sinus rhythm was observed to return 30 minutes, 90 minutes, and 12 hours, respectively, in the three patients. Two patients received a dual chamber pacemaker and a decision was made not to upgrade the patient with VVI pacemaker. Discussion and Conclusions: The present report expands the spectrum of the syndrome of atrial standstill and raises interesting questions regarding possible electrophysiologic mechanism(s) of prolonged post overdrive atrial standstill. The report suggests that chronic overdrive of sinus and subsidiary atrial pacemakers may result in calcium overloading of cardiac cells, which is known to cause suppression of pacemaker activity as well as increased intracellular resistance. These mechanisms can possibly result in either prolonged suppression of sinus and atrial pacemaker activity and/or pacemaker exit block. [ABSTRACT FROM AUTHOR]

Available evidence supports the hypothesis that cardiac resynchronization therapy (CRT) results in favorable structural as well as electrical remodeling. Electrical remodeling seems to be related, to a large extent, to structural remodeling, usually referred to as reverse remodeling of left ventricular (LV) dysfunction. This can lead to amelioration of the arrhythmogenic substrate associated with depressed LV systolic function and heart failure. However, a direct electrophysiological effect due to favorable remodeling of repolarization with reduction of the dispersion of repolarization cannot be ruled out. On the other hand, in a small subgroup of patients, CRT could increase the dispersion of repolarization and induce malignant ventricular tachyarrhythmias. Clinical trials have consistently shown improved outcome with CRT-defibrillators (CRT-D) and more trials have demonstrated the benefits of the defibrillator in the population with depressed LV function. However, some physicians argue that implanting the less expensive and less complicated CRT-pacemaker (CRT-P) may be appropriate in certain groups of patients. Before this position is accepted, it is imperative that criteria for the selection of this group of patients with presumably low risk for sudden arrhythmic death as well as the proarrhythmic effect of CRT be clearly defined. [ABSTRACT FROM AUTHOR]

The cardiovascular drug carvedilol is characterized by multiple pharmacological actions, which translate into a wide-spectrum therapeutic potential. Its major molecular targets are membrane adrenoceptors, ion channels, and reactive oxygen species. Carvedilol's favorable hemodynamic effects are due to the fact that the drug competitively blocks β1-, β2-, and α1- adrenoceptors. Several additional properties have been documented and may be clinically important, including antioxidant, antiproliferative/antiatherogenic, anti-ischemic, and antihypertrophic effects. The antiarrhythmic action of carvedilol may be related to a combination of its β-blocking effects with its modulating effects on a variety of ion channels and currents. Several studies suggest that the drug may be useful in reducing cardiac death in high-risk patients with prior myocardial infarction and/or heart failure, as well as for primary and secondary prevention of atrial fibrillation. This article will review experimental data available on the electrophysiologic properties of carvedilol, with a focus on their clinical relevance. [ABSTRACT FROM AUTHOR]

Previous tridimensional activation mapping showed that the development of functional conduction block at the onset of torsades de pointes was regionally heterogeneous; conduction block was frequently observed in the L V and the interventricular septum (IVS) but not in the RV, in the canine anthopleurin-A (AP-A) model of long QT syndrome (LQTS). This may be related to the distribution of mvocytes with M celllike electrophysiological characteristics. To better understand the regional difference of arrhythmogenicity in LQTS, the authors investigated cycle length related modulation of ventricular repolarization among three different layers: the endocardium (End), mid-myocardium (Mid), and epicardium (Epi) of the LV and RV and at two different areas: the Epi and septum (Sep) in the IVS. The LQT3 model was produced by AP-A in dogs. Using constant pacing and single premature stimulation (S1S2), the ventricular repolarization pattern was analyzed from 256 unipolar electrograms. Activation-recovery intervals (ARIs) were used to estimate local repolarization. In seven experiments, AP-A increased regional AW dispersion to 88.1 ± 36.0 ins in the LV, to 72.9 ± 35.7ms in the IVS. and to 23.0 ± 8.7 ms in the RV at the pacing cycle length (CL) of 7,000 ms. Development of the large ARI dispersion was due to greater ARI prolongation at the Mid site in the LV and at Sep site in the IVS. As the S1S2 interval was shortened, regional ARI dispersion decreased gradually, and finally, ARI dispersion showed a reversal gradient of repobarization between the Mid and Epi sites in the LV and between the Sep and Epi sites in the IVS. Two factors contributed to create the reversal gradient of repolarization: (1) a difference in restitution kinetics at the Mid site in the LV and at the Sep site in the IVS, characterized by a larger Δ ARI and slower time constant (τ), and (2) a difference in diastolic intervals at each site resulting in different input to restitution at the same CL. However, the RV showed small alteration in the transmural dispersion of repolarization in the S1S2 protocol. S2 created heterogeneous functional conduction block in the LV and IVS but not in the RV. In the LQT3 model, the arrhvthmogenicity of torsades do pointes is primarily due to dispersion of repolarizatian in the LV and IVS because of prominent distribution of M cells. The RV seems to participate passively in reentrant excitation during torsades de pointes. [ABSTRACT FROM AUTHOR]

The effects of a single intravenous infusion of 750 mg of procainamide was studied in 12 patients with symptomatic chronic recurrent venlricular tachycardia in whom arrhythmias could reproducibly be initiated and terminated by programmed electrical stimulation of the heart. Sustained ventricular tachycardia was induced in 6 patients and non-sustained tachycardia was induced in the remaining 6 patients during control studies. Following procainamide (plasma level 10.3 ± 3.7 mcg/ml], ventricular tachycardia could be induced in 10/12 patients, sustained in 4 patients and non-sustained in the remaining 6 patients. In 8/12 patients (66%). induction of ventricular tachycardia was facilitated as demonstrated by: (1) tachycardia zone was widened in 4 patients and was unchanged in another 3 patients; (2) non-sustained ventricular tachycardia was changed to sustained ventricular tachycardia in one patient. The ventricular tachycardia had a faster rate and a different QRS morphology; [3] in 4 patients tachycardia was inducible with a lesser number of extrastimuli and/ or by spontaneously occurring ventricular premature depolarization and; (4) increase of the number of induced ventricular responses of non-sustained ventricular tachycardia. In 4/12 patients )(33%), procainamide abolished or modified the induction of ventricular tachycardia as demonstrated by: (1) inability to induce ventricular tachycardia in 2 patients; (2) narrowing of the tachycardia zone and conversion from sustained into non-sustained ventricular tachycardia (one patient) and; (3) decrease in the number of induced ventricular responses in one patient. The response to procainamide could not be predicted from rates of spontaneous ventricular tachycardia, induced ventricular tachycardia during control studies, degree of slowing of ventricular tachycardia or from prolongation of the coupling interval after procainamide. These results suggest that instead of abolishing the arrhythmia, procainamide in frequently employed doses in patients with chronic recurrent ventricular tachycardia can facilitate its initiation sometimes at even faster rates. Patients not responsive to the usual doses of procainamide should undergo acute drug testing trials to determine the optimal dose/drug levels. [ABSTRACT FROM AUTHOR]

A case is described in which ventricular pacing from the middle cardiac vein produced an electrocardiographic pattern which mimicked the morphology of the normally conducted beats. The possible etiologies of this unusual phenomenon and its implications concerning the functional anatomy of the normal conduction system in the human heart are discussed. [ABSTRACT FROM AUTHOR]

Malfunction of both temporary and permanent demand transvenous pacemakers was caused by contact between the two endocardial electrodes. Contact between these electrodes created spurious potentials which resulted in irregular inhibition of both demand units. The potentials were demonstrated by recording from the temporary wire. There was no interference with either pacemaker in the fixed rate mode and malfunction ceased when the temporary wire was removed. [ABSTRACT FROM AUTHOR]

The LQTS is a prime example of bow molecular biology, ion channel, cellular, and organ physiology, coupled with clinical observations, promise to be the future paradigm for advancement of medical knowledge. Both the congenital and acquired LQTS are due to abnormalities (intrinsic and/or acquired) of the ionic currents underlying cardiac repolarization. In this review, the continually unraveling molecular biology of congenital LQTS is discussed. The various pharmacological agents associated with the acquired LQTS are listed. Although it is difficult to predict which patients are at risk for TdP, careful assessment of the risk-benefit ratio is important before prescribing drugs known to be able to cause QT prolongation. The in vivo electrophysiological mechanism of TdP in the LQTS is described using, as a paradigm, the anthopleurin-A canine model, a surrogate for LQT3. In the LQTS, prolonged repolarization is associated with increased spatial dispersion of repolarization. Prolongation of repolarization also acts as a primary step for the generation of EADs. The focal EAD induced triggered beat(s) can infringe on the underlying substrate of inhomogeneous repolarization to initiate polymorphic reentrant VT, sometimes having the characteristic twisting QHS configuration known as TdP. The review concludes by discussion of the clinical manifestations and current management of both the congenital and acquired LQTS. The initial therapy of choice for the large majority of patients with the congenital LQTS is a beta-blocking drug. This therapy seems to be effective in LQT1 and LQT2 patients, but may not be as effective in LQT3 patients. Other therapeutic options include pacemakers, cervicothoracic sympathectomy, and the implantable cardioverter defibrillator. Recent molecular genetic studies have suggested several genotype specific therapies; however, long-term efficacy data are not available. [ABSTRACT FROM AUTHOR]

The value of signal-averaged P-wave electrocardiogram and echocardiography for predicting recurrent atrial tachyarrhythmias was prospectively investigated in 60 patients presenting with paroxysmal atrial fibrillation or flutter. All patients were followed up for 1 year after restoration of sinus rhythm. A stepwise discriminant function analysis sac used to identify variables predicting recurrent atrial tachyarrhythmias. Analyzed variables included signal-averaged P-wave duration in 3 bipolar orthogonal leads (X,Y,Z) and their vector magnitude as well as left and right atrial dimensions and volumes. During follow-up, 25 patients had recurrent curial tachyarrhythmias, while 35 did not. Using discriminant function analysis, the left atrial antero-superior dimension was found to be the only variable predicting the recurrence of atrial tachyarrhythmias (P< 0.0038) and was able to correctly classify 65% of the study patients. It was concluded that, in patients with paroxysmal atrial fibrillation or flutter, the traditionally used determination of left atrial dimension was the variable most closely associated with a high risk for recurrent tacharrhythmias. The signal-averaged P-wave duration did plot improve tachyarrhythmia prediction. [ABSTRACT FROM AUTHOR]

T or U wave alternans in association with long QTU and torsade de pointes (TdP) is uncommon and its mechanism(s) is unknown. We studied three patients with TU alternans, long QTU, and TdP: patient 1 was a newborn with congenital long QTU; patient 2 had marked hypokalemia and hypomagnesemia; and patient 3 was receiving procainamide. In the three patients, TU alternans was tachycardia dependent and preceded the onset of TdP. In the patient on procainamide, TU alternans and TdP occurred at long cardiac cycles. In this patient, endocardial monophasic action potential (MAP) recordings showed that TU alternans was associated with alternation of the duration of the plateau. A deflection consistent with early afterdepolarization (EAD) arose at a constant time interval from phase 0 but alternated from high and low levels of phase 3. The first ectopic heat of TdP arose on the descending limb of the EAD. TU alternans was investigated by MAP recordings in six normal dogs, following the administration of anthopleurin-A (AP-A), a drug shown to delay sodium inactivation and to induce bradycardia dependent long QTU, EADs, and TdP. In two dogs TU alternans was associated with 2:1 recordings of EAD and nearly constant plateau duration. In three dogs, TU alternans was associated with EAD that occurred in consecutive beats at constant time intervals from phase 0, but alternated from high and low phase 3 because of alternation of the duration of the plateau. In one dog, alternation of EAD and plateau duration occurred. In 36 separate episodes of TdP that were analyzed in the six dogs, 32 were bradycardia dependent but four developed on abrupt shortening of the cardiac cycle associated with alternation of action potential duration. Our results suggest: (1) TU alternans may be due to 2:1 propagation of an EAD or to alternation of the recovery kinetics of u repolarization current; (2) The constant occurrence of EAD in relation to phase 0 in spite of alternation of plateau duration suggests an ionic mechanism synchronized to depolarization; (3) Tachycardia dependent TdP in clinical and experimental examples of long QTU seems to be characteristically associated with TU alternans. Dispersion of repolarization may underlie the increased ventricular electrical instability in these cases. [ABSTRACT FROM AUTHOR]

The signal averaged electrocardiogram (SA-ECG), programmed electrical stimulation (PES), and left ventricular ejection fraction (EF) studies were utilized for risk stratification and management of patients with complex ventricular arrhythmias and nonsustained ventricular tachycardia (VT). The study population included 90 patients (63 with coronary artery disease and 27 with dilated cardiomyopathy). Sustained monomorphic VT was induced in 22 cases (24%), ventricular fibrillation (VF) in 10 (11%), and no sustained VT/VF in 58 (64%). An abnormal SA-ECG was recorded in 23 patients (26%) and was more common in patients with than in those without induced sustained VT (68% vs 12%, P < 0.0001). None of 33 patients with normal SA-ECG and EF ≥ 40% had induced VT. Patients were followed-up for 2.5 ± 0.8 years off antiarrhythmic therapy, unless they had induced sustained VT. The 3-year sudden death rate was 19% in the group with induced sustained VT, 0 in that with induced VF, and 9% in that without induced VT/VF (P = NS). The 3-year total cardiac mortality was higher in patients with than in those without EF < 40% (27% vs 7%, P < 0.05). It is concluded that patients with organic heart disease and spontaneous nonsustained VT may not need PES or antiarrhythmic therapy if SA-ECG is normal and EF is ≥ 40%, since their risk of induced VT and sudden death is low. On the other hand, patients with abnormal SA-ECG and/or EF < 40% may require PES, since their risk for induced VT is high. Antiarrhythmic therapy may also be considered in these patients. [ABSTRACT FROM AUTHOR]

The presence of late potentials on the body surface recording was correlated with ventricular activation maps of reentrant circuits in the postinfarction canine model of reentrant excitation. Late potentials were found to correlate with delayed myocardial activation. However, during a reentrant rhythm complete diastolic activity on the body surface could not be detected if the mass of electrically active cells was too small and/or if very slow conduction in part of the reentrant circuit generated low amplitude extracellular potentials. Myocardial zones responsible for late potentials during a basic rhythm (e.g., sinus rhythm) may not necessarily be part of the critical zone of slow conduction during reentrant activation. Dynamic changes in late potentials are not amenable to temporal signal averaging techniques but could be detected by a high resolution beat-to-beat recording. A thorough understanding of the electrophysiological limitations of late potentials in the signal-averaged ECG could result in better utilization of the technique in clinical practice as well as in the development of new approaches for the detection of the arrhythmogenic substrate. [ABSTRACT FROM AUTHOR]

The article focuses on percutaneous cardiac mapping and ablation registry. After the first published reports of therapeutic electrode catheter ablation appeared in 1982, the Percutaneous Cardiac Mapping and Ablation Registry was formed to collect and disseminate information relative to these nonpharmacological techniques for control of refractory cardiac tachyarrhythmias. Thus, the Registry allows physicians to assess the risks and benefits of these procedures. Because this field is evolving, it was considered important to devise a central registry for tracking the course of not only catheter electrode ablation techniques but also those catheter techniques using alternative forms of energy.

Asynchronous pacing during the presence of electromagnetic interference or other sources of "noise" is a protective mechanism available to prevent pacemaker output inhibition. We describe a patient with a DDD pacemaker who had asynchronous dual chamber or noise reversion pacing as a consequence of repetitive signals (QRS complexes) falling into the noise sampling period (NSP) of the pacemaker ventricular refractory period. During supraventricular tachycardi at a rate of 215 bpm, noise reversion mode pacing occurred when QRS complexes were well detected immediately after the termination of a normal pacemaker ventricular refractory period and treated as a premature ventricular depolarization, resulting in automatic refractory period extension. Recycling of this extended refractory period occurred when consecutive QRS complexes were detected during the NSP and forced asynchronous dual chamber pacing at the programmed lower rate. The mechanism is presented and was supported by subthreshold esophageal pacing simulating the tachycadia and initiating the noise reversion response. [ABSTRACT FROM AUTHOR]

Focuses on the importance of reentrant excitation as a mechanism for cardiac arrhythmia. Difficulty of obtaining information on the electrophysiological requirements for reentry; Role of reflection in clinical arrhythmia; Demonstration of the multiple muscular connections between the atrium and ventricle in the human heart.

Presents summaries of pertinent data on attempted ablation of the atrioventricular juntion and ventricular tachycardia foci. Catheter ablation of the atrioventricular junction; Analysis of catheter ablation of ventricular tachycardia foci.

The mechanisms of resetting, entrainment. acceleration, or termination of reentrant ventricular tachycardia by programmed electrical stimulation were studied in the canine post-infarction model. In this model, reentrant circuits were localized in the epicardial layer overlying the infarction and were accessible to detailed mapping by multiplexer techniques. The reentrant circuit has a characteristic figure-eight configuration in the form of two circulating wavefronts around arcs of functional conduction block that coalesce into a slow common reentrant wavefront. Termination of reentrant tachy-cardia occurred when a stimulated wavefront arrived earlier to a strategically located area in the proximal portion of the zone of slow conduction, before refractoriness expired distally, resulting in conduction block. The three factors that determined if the stimulated wavefront could reach this zone in time for conduction block were: (1) the cycle length of stimulation; (2) the number of stimulated beats, and (3) the site of stimulation. The most optimal situation for stimulated termination of reentry was a critically coupled single stimulus applied to the ischemic zone close to the proximal side of the zone of slow conduction that captured locally and conducted prematurely to the strategic zone for conduction block. When a single stimulated wavefront failed to terminate reentry, one or more subsequent wavefronts succeeded. However, the stimulated train had to be terminated following the beat that interrupted reentry. Otherwise, a subsequent stimulated beat could reinitiate the same reentrant circuit or induce a different circuit. The new circuit could have a shorter revolution time, resulting in tachycardia acceleration , and occasionally degeneration into ventricular fibrillation. Overdrive termination of reentry required both a critical cycle length of stimulation and a critical number of beats in a stimulated train. Otherwise, the stimulated train could establish a new.. [ABSTRACT FROM AUTHOR]

Catheter ablation of ventricular tachycardia is a procedure of last resort in critically III patients. The Percutaneous Cardiac Mapping and Ablation Registry was able to collect data on 88 patients undergoing ablation of ventricular tachycardia foci. The mean following interval for the group was 10 ± 8 months. Results were divided into three categories: Group I patients remained asymptomatic and were on no antiarrhythmic medications (33%); Group 11 remained asymptomatic and took antiarrhythmic agents (38%); Group III patients were considered unsuccessful and consisted of 29 percent of the total. More than one-third of patients received two shocks; the remainder received from one to five shocks. Overall mortality included four procedure-related deaths and total follow- up mortality was 25 percent. Catheter ablation for ventricular tachycardia should be undertaken only in highly specialized centers with an expert and experienced electrophysiologist with immediate surgical back-up available. [ABSTRACT FROM AUTHOR]

Provides information about the Percutaneous Cardiac Mapping and Ablation Registry in the U.S. in 1982. Executive management of the registry; Purpose of the registry; Responsibilities of the registry.

There are three current prognostic indicators of ventricular electrical instability: (1) categorization and stratification of spontaneous ventricular arrhythmias from standard EGG recordings; (2) programmed electrical stimulation; (3) direct recording of delayed depolarization potentials, usually referred to as late potentials. Of the three, the latter offers a new and promising approach. Late potentials represent delayed activation potentials of diseased myocardial zones and may prove to be a strong independent marker of the propensity to develop reentrant ventricular arrhythmias and sudden cardiac electrical death. The problem in identifying late potentials on the body surface is that the signal is smaller than the electrical noise produced by various sources. Two different techniques have been utilized to improve the signal-to-noise ratio: first, signal averaging, which is applicable to regular repetitive electrocardiographic signals but cannot detect moment-to-moment dynamic changes in the signal; second, low-noise or high-resolution electrocardiography that utilizes spatial averaging techniques as well as other noise-reducing measures to record the late potentials on a heat-to-beat basis. This technique has the potential of directly identifying malignant "reentrant" versus benign "focal" ventricular rhythms. The present report discusses the electrophysiologic basis of late potentials and the clinical results of both signal-averaged and low-noise recordings for evaluation of ventricular electrical instability, particularly in patients with ischemic heart disease. [ABSTRACT FROM AUTHOR]

A 44-year-old man developed recurrent pulmonary embolization after implantation of a permanent transvenous DVI pacemaker connected to polyurethane leads. Thrombus was found in the left innominate and subclavian veins around the pacemaker leads, but not in the right atrium or in the venous system of the pelvis and the lower extremities. The recurrence of pulmonary embalization followed discontinuation of treatment with Coumadin. This case demonstrates that lifelong anticoagulation is indicated in patients who have had pulmonary, embolization and/or venous thrombosis around the pacemaker leads. [ABSTRACT FROM AUTHOR]

Presents a case report of an elderly female patient who was referred for cardiac resynchronization therapy (CRT) due to refractory heart failure. Medical history; Effect of CRT on ventricular function; Discussion on transmural dispersion and intraventricular conduction disorder; Impact of CRT on the frequency of ventricular tachyarrhythmias.

We describe a patient with Wolff-Parkinson-White syndrome in whom a steerable catheter became entrapped in the mitral valve apparatus, during radiofrequency ablation. Treatment consisted of surgical removal of the catheter. The occurrence of this previously unreported complication stresses the need for on-going monitoring of risk and benefits of electrophysiological interventions. [ABSTRACT FROM AUTHOR]

Presents a response by Nabil El-Sherif and Gioia Turitto to a letter to the editor about their article "The Long QT Syndrome and torsade de pointes," in a 1999 issue.