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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

Idiopathic ventricular tachycardia: Diagnosis and management.

Idiopathic ventricular tachycardia (VT) is an uncommon form of VT that is seen in patients without structural heart disease. It is commonly seen in young patients and usually has a benign course. Recent studies have delineated the mechanisms and anatomical locations of this form of VT. Recognition of various forms of idiopathic VT based on characteristic QRS morphology from the 12-lead electrocardiogram (ECG) has important prognostic and therapeutic implications. The understanding of the mechanisms of idiopathic VT has led to the use of specific antiarrhythmic drugs targeting particular arrhythmias. Recent technological advances in the field of mapping and catheter ablation have led to a suitable alternative to drug therapy with a very high cure rate. This review describes the clinical features, ECG recognition, and management of idiopathic monomorphic VT.

Adult↗

The 12-lead electrocardiogram in supraventricular tachycardia.

The 12-lead electrocardiogram (ECG) is an invaluable tool for the diagnosis of supraventricular tachycardia (SVT). Most forms of SVT can be distinguished with a high degree of certainty based on specific ECG characteristics by using a systematic, stepwise approach. This article provides a general framework with which to approach an ECG during SVT by describing the salient characteristics, ECG findings, and underlying electroanatomical relationships of each specific type of SVT encountered in adults. It concludes by providing a systematic algorithm for diagnosing SVT based on the findings of the 12-lead ECG.

Electrocardiography↗

Exercise-induced ventricular arrhythmias in patients with no structural cardiac disease.

We review the clinical and genetic disorders associated with exercise-induced ventricular arrhythmias in patients with normal hearts. Foremost are those with catecholaminergic polymorphic ventricular tachycardia due to abnormalities in either the ryanodine receptor 2 genes (RyR2) or the calsequestrin genes (CASQ). These patients manifest ventricular premature beats and polymorphic ventricular tachycardia in response to exercise or on exposure to catecholamines. A great deal of basic information has been accumulated suggesting that these arrhythmias are caused by abnormalities in Ca2+ metabolism. The ensuing cytosolic Ca2+ overload results in delayed after-depolarizations and extrasystolic Ca2+ waves, leading to polymorphic ventricular tachycardia. Most of these patients will respond to beta-blocker therapy but a significant minority (30%) will require a defibrillator. Advances in genetic testing allow better understanding of this syndrome.

Calcium↗

Ratio of late to early T-wave peak amplitude in 24-h electrocardiographic recordings as indicator of symptom history in patients with long-QT Syndrome types 1 and 2.

UNLABELLED: We reviewed 24-h electrocardiographic recordings from 214 genotyped subjects--97 with long-QT syndrome type 1 (LQT1), 62 with LQT2, and 55 unaffected--to record maximal diurnal amplitude ratios between late and early T-wave peaks. Maximal amplitude ratios between late and early T-wave peaks were higher in symptomatic than in asymptomatic patients both in LQT1 (3.2 +/- 1.0 vs. 2.3 +/- 0.8; p < 0.001) and in LQT2 patients (2.6 +/- 1.0 vs. 1.7 +/- 0.5; p < 0.001). The maximal amplitude ratio between late and early T-wave peaks was independently associated with symptom history in both LQT1 and LQT2 patients. OBJECTIVES: We tested the hypothesis that in long-QT syndrome types 1 (LQT1) and 2 (LQT2), the diurnal maximal ratio between late and early T-wave peak amplitudes correlates with a history of symptoms better than QT interval durations. BACKGROUND: Genotype and phenotype studies have delineated clinical profiles of the most prevalent LQT1 and LQT2 subtypes of inherited LQT, but prediction of arrhythmia risk remains uncertain, the baseline QTc interval being the best predictor. In experimental long-QT syndrome models, the ratio between late and early T-wave peak amplitude predicts onset of torsade de pointes. METHODS: We reviewed 24-h electrocardiographic recordings from 214 genotyped subjects--97 with LQT1, 62 with LQT2, and 55 unaffected-to record maximal amplitude ratios between late and early T-wave peaks by use of a computer-assisted program. RESULTS: Maximal amplitude ratios between late and early T-wave peaks were higher in symptomatic than in asymptomatic patients both in LQT1 (3.2 +/- 1.0 vs. 2.3 +/- 0.8; p < 0.001) and LQT2 patients (2.6 +/- 1.0 vs. 1.7 +/- 0.5; p < 0.001). Although the QTc interval also was longer in symptomatic patients, only the maximal amplitude ratio between late and early T-wave peaks was independently associated with symptoms in both LQT1 and LQT2 patients. CONCLUSIONS: Maximal diurnal ratio between late and early T-wave peak amplitude improves noninvasive risk assessment both in LQT1 and LQT2 syndromes. We propose this new indicator in clinical evaluation of arrhythmia risk in LQT1 and LQT2.

Adult↗

Atrial tachycardia arising from the coronary sinus musculature: electrophysiological characteristics and long-term outcomes of radiofrequency ablation.

OBJECTIVES: We sought to describe the electrophysiological features and long-term outcome after radiofrequency catheter ablation (RFCA) of atrial tachycardia (AT) arising from the coronary sinus (CS) musculature. BACKGROUND: Atrial tachycardia requiring RFCA deep within the CS has been described in isolated case reports. However, the mechanism and exact site of origin of this tachycardia have not been well elucidated. METHODS: The study included 8 patients (5 men) of a consecutive series of 283 patients undergoing RFCA for focal AT. RESULTS: In sinus rhythm, a discrete potential (P) was noted after the CS atrial electrogram and during tachycardia, the CS (P) preceded the surface P-wave by 30 to 50 ms. The CS (P) always preceded the earliest electrogram in the left atrium (LA). Three-dimensional electroanatomical mapping was available in four patients, and in one case it showed earliest activation in the CS with rapid spread to the proximal CS and then to the LA. Ablation of the AT initially attempted from the earliest site in the LA in three patients was unsuccessful. In all patients the tachycardia was safely and successfully ablated at a site 3.6 cm within the CS. There has been no recurrence over a follow-up of 37 +/- 13 months. CONCLUSIONS: Focal AT emanating deep within the CS musculature can be recognized by a discrete potential associated with the CS atrial signal both during sinus rhythm and tachycardia. Long-term success without complications can be accomplished by ablating within the CS in close proximity to the CS (P).

Adolescent↗

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↗

Protected circumferential conduction in the posterior atrioventricular vestibule of the left atrium: electrophysiologic and anatomic correlates.

BACKGROUND: The anatomic substrate for protected isthmus conduction in the right atrium has been well defined. Little is known of similar substrates in the left atrium (LA). METHODS: Patients (pts) with reentrant tachycardia (AVRT) supported by a single left-sided accessory pathway were studied retrospectively (n = 64) and prospectively (n = 31). Intracardiac electrograms were recorded from the His bundle position and coronary sinus (CS). The LA was mapped with a steerable catheter using the transseptal approach. LA anatomy was examined grossly and histologically in six cadaver hearts after removal of endocardium. RESULTS: A distal-to-proximal CS activation sequence during AVRT was seen in all patients with a left lateral accessory pathway before ablation. After one to three radiofrequency (RF) energy deliveries that did not interrupt accessory pathway conduction, the CS activation sequence was reversed in three patients in the retrospective group and bidirectional conduction block in the posterior atrioventricular vestibule of the LA (PAVV) was demonstrated in nine patients in the prospective group. Four of the six cadaver hearts showed a distinct circumferential inferoposterior myocardial bundle that coursed parallel to the CS in the PAVV. CONCLUSIONS: We described evidence of bidirectional intraatrial block in the PAVV after application of RF energy during accessory pathway ablation. Such conduction block may mimic the presence of a second accessory pathway. Our data suggest that circumferential conduction in the PAVV may be poorly coupled to the rest of the LA and may be involved in the macro-reentrant circuit around the mitral annulus. The circumferential inferoposterior myocardial bundle may serve as the underlying anatomic substrate.

Adult↗

Reentry within the cavotricuspid isthmus: an isthmus dependent circuit.

BACKGROUND: We describe a new cavotricuspid isthmus (CTI) circuit. METHODS: This study includes 8 patients referred for atrial flutter (AFL) ablation whose tachycardia circuit was confined to the septal CTI and the os of the coronary sinus (CS(OS)) region. Entrainment mapping was performed within the CTI, CS(OS), and other right atrial annular sites (tricuspid annulus (TA)). Electroanatomic mapping was available in 2 patients. RESULTS: Sustained AFL occurred in all patients with mean tachycardia cycle length (TCL) of 318 +/- 54 (276 - 420) ms. During tachycardia, fractionated or double potentials were recorded at either the septal CTI and/or the region of CS(OS) in all, and concealed entrainment with post-pacing interval (PPI)--TCL < or = 25 ms occurred in this area; but manifest entrainment with PPI > TCL was demonstrated from the anteroinferior CTI and other annular sites in 7/8 patients. In one, tachycardia continued with conduction block at the anteroinferior CTI during ablation. Up to three different right atrial activation patterns (identical TCL) were observed. The tachycardia showed a counterclockwise (CCW) pattern in 6, a clockwise pattern in 2, and simultaneous activation of both low lateral right atrium and septum in 5. Electroanatomic mapping was available in 2, showing an early area arising from the septal CTI in 1, and a CCW activation sequence along the TA in another. Radiofrequency application to the septal CTI terminated tachycardia in 4, and tachycardia no longer inducible in all. CONCLUSIONS: We describe a tachycardia circuit confined to the septal CTI/CS(OS) region, and hypothesize that this circuit involves slow conduction within the CTI and around the CS(OS), which acts as a central obstacle.

Aged↗

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↗

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↗

The history of AV nodal reentry.

Though patients with AV nodal reentry are now routinely cured by catheter ablation, the basic mechanism of this disorder is still under debate. The putative mechanism of AV node reentry was first discovered by the elegant work of Gordon Moe. He demonstrated the existence of dual pathways and echo beats in rabbits. Building on these seminal observations, the mechanism of AVNRT has burgeoned to include the possibility of left atrial input into the node. The first curative nonpharmacologic procedures involved surgical dissection around the AV node and the procedure was rapidly supplanted by catheter ablation procedures. The initial ablative procedure targeted the fast pathway, but later observations showed that ablation of the slow pathway was more effective and safer. Cure of AV nodal reentry which is the most common cause of paroxysmal supraventricular tachycardia became possible through the cooperative efforts of anatomists, physiologists, surgeons, and clinical electrophysiologists.

Cardiology↗