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Biomedical subjects

Melvin M Scheinman

Publications and source records attributed to Melvin M Scheinman.

At least 19 recordsLinked to original sources
PubMed2005

Method to predict isthmus location in ventricular tachycardia caused by reentry with a double-loop pattern.

BACKGROUND: During electrophysiologic study, induction and mapping of clinical reentrant ventricular tachycardia can be difficult. Hence, analysis of sinus-rhythm electrograms for reentry localization is of potential clinical relevance. Herein is described a method of sinus-rhythm electrogram shape analysis, that does not require arbitrary threshold values, for localization of double-loop reentrant circuits that drive clinical tachycardias. METHODS AND RESULTS: Reentrant ventricular tachycardia was induced by premature stimulation in 23 postinfarction canine hearts 4-5 days after left anterior descending (LAD) ligation. Sinus-rhythm activation maps were constructed from bipolar electrograms acquired at 196-312 sites in the epicardial border zone. The timing of all electrogram peak deflections during one cycle of sinus rhythm was determined, and the mean (MPD) and deviation (DPD) were taken, respectively, as estimates of the time of activation wavefront crossing, and the duration of local electrical activity. These variables were then mapped on a computerized grid. The line of most uniform and sharp MPD gradient predicted the propagation direction through the double-loop reentrant circuit isthmus that would occur upon tachycardia induction. The sharpest transitions in DPD bounding this line predicted the positions of arcs of block that would border the reentrant circuit isthmus during tachycardia. The actual and estimated isthmuses overlapped by a mean of 84.1 +/- 3.8%. In six experiments lacking inducible reentrant tachycardia, no line of sharp MPD gradient was present in the MPD maps. CONCLUSIONS: Analysis of multiple sinus-rhythm deflections can localize the reentrant ventricular tachycardia isthmus without introduction of arbitrary threshold points and peak choices that may lead to error.

Algorithms↗
PubMed2005

Site specificity of transverse crista terminalis conduction in patients with atrial flutter.

INTRODUCTION: The causes of transcristal conduction (TC) in patients with atrial flutter (AFL) are unknown. METHODS AND RESULTS: In two groups of patients referred for AFL ablation, 36 had cavotricuspid isthmus (CTI) dependent flutter (Group I) and 24 had lower (n = 21) or upper loop reentry (n = 5) (Group II). After ablation, isthmus block was evaluated by pacing from the coronary sinus (CS) and low lateral right atrium and by alternative techniques, including mapping with electrodes spanning the CTI or electroanatomic mapping. After bidirectional CTI block was verified, 21/36 (58%) in Group I showed TC with CS pacing, including low TC in 16 (including 11 showing "pseudo" CTI conduction), higher TC in 6 and multiple breaks in 3. However, 8 with low TC during CS pacing showed unidirectional block by pacing outside of the CS os. Twelve (50%) in Group II had TC during CS pacing after bidirectional CTI block, with low TC in 5 (2 mimicking residual CTI conduction) and higher breaks in 9. There was no significant difference in the incidence of TC during CS pacing after CTI block between groups. In seven autopsied hearts, the muscle orientation between the proximal CS musculature and Eustachian ridge were examined. Muscular connections between the CS and Eustachian ridge coursing toward the orifice of inferior vena cava were found in one of the hearts. CONCLUSIONS: It is concluded that in patients with bidirectional CTI block, pacing from the CS may be associated with TC mimicking a conduction leak through the isthmus. Pacing just outside the CS os helps distinguish pseudo from true isthmus block.

Aged↗
PubMed2005

History of Wolff-Parkinson-White syndrome.

While Drs. Wolff, Parkinson, and White fully described the syndrome that bears their names in 1930, prior case reports had already described the essentials. Over the ensuing century this syndrome has captivated the interest of anatomists, clinical cardiologists, and cardiac surgeons. Stanley Kent described lateral muscular connections over the atrioventricular (AV) groove, which he felt were the normal AV connections. The normal AV connections were, however, clearly described by His and Tawara. True right-sided AV connections were initially described by Wood et al., while Ohnell first described left free wall pathways. David Scherf is thought to be the first to describe our current understanding of the pathogenesis of the Wolff-Parkinson-White (WPW) syndrome in terms of a reentrant circuit involving both the AV node--His axis as well as the accessory pathway. This hypothesis was not universally accepted and many theories were applied to explain the clinical findings. The basics of our understandings were established by the brilliant work of Pick, Langendorf, and Katz who by using careful deductive analysis of ECGs were able to define the basic pathophysiological processes. Subsequently, Wellens and Durrer applied invasive electrical stimulation to the heart in order to confirm the pathophysiological processes. Sealy and his colleagues at Duke University Medical Center were the first to successfully surgically divide an accessory pathway and ushered in the modern area for curative therapy for these patients. Morady and Scheinman were the first to successfully ablate an accessory pathway (posteroseptal) using high-energy direct-current shocks. Subsequently, Jackman, Kuck, Morady, and a number of groups proved the remarkable safety and efficiency of catheter ablation for pathways in all locations using radiofrequency energy. More recently, Gallob et al. first described the gene responsible for a familial form of WPW. The current ability to cure patients with WPW is due to the splendid contributions of individuals from diverse disciplines from throughout the world.

Cardiology↗
PubMed2004

Use of ibutilide in cardioversion of patients with atrial fibrillation or atrial flutter treated with class IC agents.

OBJECTIVES: We sought to assess the efficacy and safety of ibutilide cardioversion for those with atrial fibrillation (AF) or atrial flutter (AFL) receiving long-term treatmentwith class IC agents. BACKGROUND: Attenuation of ibutilide-induced QT prolongation has been observed in a small number of patients pretreated with class IC agents. The clinical significance of the interaction between ibutilide and class IC agents is unknown. METHODS: Seventy-one patients with AF (n = 48) or AFL (n = 23), receiving propafenone 300 to 900 mg/day (n = 46) or flecainide 100 to 300 mg/day (n = 25), presented for ibutilide (2.0 mg) cardioversion. RESULTS: The mean durations of arrhythmia episode and arrhythmia history were 25 +/- 48 days and 4.4 +/- 6.4 years, respectively. Sixty-five patients (91.5%) had normal left ventricular systolic function. Twenty-three of 48 patients (47.9%; 95% confidence interval, 33.3% to 62.8%) with AF and 17 of 23 patients (73.9%; 95% confidence interval, 51.6% to 89.8%) with AFL converted with mean conversion times of 25 +/- 14 min and 20 +/- 12 min, respectively. There was a small increase in corrected QT interval after ibutilide (from442 +/- 61 ms to 462 +/- 59 ms, p = 0.006). One patient developed non-sustained polymorphous ventricular tachycardia and responded to intravenous magnesium. Another developed sustained torsade de pointes and was treated effectively with direct-current shock and intravenous dopamine. CONCLUSIONS: Our observations suggest that the use of ibutilide in patients receiving class IC agents is as successful in restoring sinus rhythm and has a similar incidence of adverse effects as the use of ibutilide alone.

Aged↗
PubMed2004

Effectiveness of sotalol treatment in symptomatic Brugada syndrome.

We describe a 53-year-old man with recurrent syncopal events and a malignant family history who was treated for 13 years with sotalol drug therapy with no further occurrence of Brugada syndrome symptoms. Genetic testing revealed that he carried a Brugada syndrome sodium channel SCN5A mutation (4189delT). This finding suggests that sotalol may be of therapeutic benefit in such patients.

Adult↗
PubMed2004

Famotidine and long QT syndrome.

Numerous drugs have been implicated in causing a prolonged QT interval and Torsades de pointes. However, the association of famotidine and acquired long QT syndrome has rarely been reported. We report 2 cases of famotidine-associated acquired long QT syndrome.

Aged↗
PubMed2004

Left septal atrial flutter: electrophysiology, anatomy, and results of ablation.

BACKGROUND: We describe the clinical and electrophysiological characteristics of a novel macroreentrant form of left atrial flutter circuit. METHODS AND RESULTS: A total of 11 patients were included in the study. The mean tachycardia cycle length was 278+/-41 ms. Nine of the 11 patients were treated with antiarrhythmic drugs at the time of the study for concomitant atrial fibrillation. With the use of entrainment pacing and either the CARTO Biosense mapping system (9 patients) or conventional mapping (2 patients), the flutter circuit was found to rotate around the left septum primum with a critical isthmus located between the pulmonary veins posteriorly and/or mitral annulus anteriorly and the septum primum. In 5 patients, radiofrequency ablation was performed from the septum primum to the right inferior pulmonary vein (group 1), and in 6 patients, a lesion was made from the septum primum to the mitral annulus (group 2). After a follow-up of 13+/-6 months, 2 patients in group 1 and all patients in group 2 remained in sinus rhythm without recurrence. CONCLUSIONS: Slowing of electric conduction in the left atrial septum due to antiarrhythmic drugs and/or atrial myopathy seems to promote left septal atrial flutter. Radiofrequency ablation of this arrhythmia is usually effective and safe. A line of block between the septum primum and the mitral annulus proved to be effective for cure of tachycardia.

Aged↗
PubMed2004

Lower loop reentry as a mechanism of clockwise right atrial flutter.

BACKGROUND: Right atrial reentrant tachycardia resulting from lower loop reentry (LLR) around the inferior vena cava (IVC) has been described recently. However, all reported cases of LLR in the literature have negative flutter waves on the inferior surface ECG leads similar to that of counterclockwise typical atrial flutter around the tricuspid annulus (TA). Right atrial flutter with positive flutter waves in the inferior ECG leads has been assumed to rotate as a single reentrant activation wave front around the TA, and the role of LLR in those patients is not known. METHODS AND RESULTS: Twelve consecutive patients with flutter wave morphology on surface ECG consistent with clockwise atrial flutter were studied. The endocardial activation pattern recorded from conventional multipolar electrode catheters was characteristic of clockwise atrial flutter around the TA. Entrainment pacing in all 12 patients and 3D activation sequence mapping in 7 patients, however, revealed clockwise LLR involving the lower right atrium around the IVC in 7 patients, figure-of-8 double-loop reentry around both the IVC and TA in 4, and single reentrant loop around the TA in 1. Linear radiofrequency ablation in the isthmus between the TA and IVC (TI isthmus) terminated the tachycardia in all patients. CONCLUSIONS: Surface ECG flutter wave morphology and limited recording intracardiac sites proved insufficient to delineate the precise mechanism of the TI isthmus-dependent clockwise right atrial flutters. Most right atrial flutters with positive flutter wave on surface ECG may be supported by a reentrant circuit around the IVC or a figure-of-8 double-loop reentry involving both the IVC and TA.

Aged↗
PubMed2004

Usefulness of a ventricular extrastimulus from the summit of the ventricular septum in diagnosis of septal accessory pathway in patients with supraventricular tachycardia.

To compare usefulness of a ventricular extrastimulus (VES) from the right ventricular (RV) apex versus the RV septum in patients with a septal accessory pathway (AP), VES was applied from the RV apex and the summit of the RV septum in patients with septal APs. A VES from the RV apex and from the summit was diagnostic of the presence of an AP in 13 of 28 patients (83%) and in 10 of 12 patients, respectively (46% p <0.05), and VES proved an AP as a part of the tachycardia circuit in 5 of 28 patients (18%) and 6 of 12 patients, respectively (50%, p <0.05). A VES during His bundle refractoriness from the RV summit increases the diagnostic yield for both the presence of an AP and its participation in the tachycardia circuit with respect to RV apical VES.

Adolescent↗
PubMed2004

Characterization of a KCNQ1/KVLQT1 polymorphism in Asian families with LQT2: implications for genetic testing.

Congenital long QT syndrome (LQTS) is a genetic disease that predisposes affected individuals to arrhythmias, syncope, and sudden death. Mutations in several ion channel genes have been discovered in different families with LQTS: KCNQ1 (KVLQT1, LQT1), KCNH2 (HERG, LQT2), SCN5A (LQT3), KCNE1 (minK, LQT5), and KCNE2 (MiRP1, LQT6). Previously, the P448R-KVLQT1 missense mutation has been reported as an LQT1-causing mutation. In this report, we demonstrate the presence of the P448R polymorphism in two, unrelated Chinese LQTS families. Although absent from 500 reference alleles derived from 150 white and 100 African-American subjects, P448R was present in 14% of healthy Chinese volunteers. Given the inconsistencies between the genotype (LQT1) and clinical phenotype (LQT2) in our two LQTS families, together with the finding that the P448R appears to be a common, ethnic-specific polymorphism, mutational analysis was extended to the other LQTS-causing genes resulting in the identification of distinct HERG missense mutations in each of these two families. Heterologous expression of P448R-KVLQT1 yielded normal, wild-type (WT) currents. In contrast, the two unique HERG mutations resulted in dominant-negative suppression of the WT HERG channel. Our study has profound implications for those engaged in genetic research. Importantly, one child of the original proband was initially diagnosed with LQT1 based upon the presence of P448R-KVLQT1 and was treated with beta-blockers. However, he did not possess the subsequently determined LQT2-causing mutation. On the other hand, his untreated P448R-negative brother harbored the true, disease-causing HERG mutation. These findings underscore the importance of distinguishing channel polymorphisms from mutations pathogenic for LQTS and emphasize the importance of using appropriate ethnically matched controls in the genotypic analysis of LQTS.

Alleles↗
PubMed2004

Catecholamine dependent accessory pathway automaticity.

Automaticity from extra nodal accessory pathways appears to be rare. We report the case of a man with the WPW syndrome who presented for repeat electrophysiological study and catheter ablation. After successful ablation of a para-Hisian accessory pathway, an isoproterenol challenge produced an accelerated wide complex rhythm that was dissociated from sinus rhythm and matched the previous pattern of maximal preexcitation. This automatic rhythm was transient and dependent on catecholamine administration. One month after successful ablation, an exercise treadmill test (ETT) did not demonstrate any pre-excitation or ectopy.

Adult↗
PubMed2003

ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary. a report of the American college of cardiology/American heart association task force on practice guidelines and the European society of cardiology committee for practice guidelines (writing committee to develop guidelines for the management of patients with supraventricular arrhythmias) developed in collaboration with NASPE-Heart Rhythm Society.

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Anti-Arrhythmia Agents↗