Slow conduction in the infarcted human heart. 'Zigzag' course of activation.

Bakker, Jacques M.T. de; Capelle, F. J. L. Van; Janse, Michiel J.; Tasseron, Sara; Vermeulen, Jessica; Jonge, N. De; Lahpor, Jaap R.

doi:10.1161/01.cir.88.3.915

Cited by 720 publications

(541 citation statements)

References 38 publications

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“…İlginç bir bulgu olarak koroner arter hastalığı ve dilate kardiyomyopati tanılı ve ventriküler aritmisi olan hastalarda endokardiyal haritalamada skar alanlarının çevresinde fragmante intrakardiyak elektrokardiogramlar alınmış-tır (19)(20). Transplantasyon yaıplacak korner arter hastalarının papiller kaslarının intersitisyel fibrozis ile ayrılan alanlarında yavaşlamış ileti ve iletinin zikzak şeklinde bir yol takip ettiği bunun da intramiyokardiyal iletiyi yavaşlattığı sonuç olarak ''reentry'' tetiklenmesi yapabileceği düşünülmüştür (21)(22) fQRS varlığı antiartimik ilaç kullanmayan ve fonksiyonel kapasitesi 3 altında olan sistolik kalp yetmezliği olan hastalarda ICD şoklamala-rını predikte etmekte olup bu grup hastalarda ventriküler artimiye yatkınlık açısından yapıla-cak randomize kontrollü bir çalışma bu grup hastalara klinik yaklaşım açısından önemli biligiler sunabilir.…”

Section: Ekokardioyografi Ve Rutin Tetkiklerunclassified

The Association Between Fragmeted QRS and ICD Shocks in patients with Left Ventricular Systolic Heart Failure

Özcan¹,

Turak²,

Tok³

et al. 2013

Turk J Bioch

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Amaç: Sol ventrikül sistolik disfonksiyonu olan hastalarda fragmente QRS'in (fQRS) mortalite ve ventriküler aritmi ile ilişkisine dair farklı bilgiler mevcuttur. Biz çalışmamızda fQRS'in fonksiyonel kapasitesi 3 altında olan ve herhangi antiaritmik ilaç kullanmayan implante edilebilir şok cihazı (ICD) taşıyan hasta grubundaki yaşanmış şok olayları ile ilişkisini saptamak istedik.

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Section: Ekokardioyografi Ve Rutin Tetkiklerunclassified

The Association Between Fragmeted QRS and ICD Shocks in patients with Left Ventricular Systolic Heart Failure

Özcan¹,

Turak²,

Tok³

et al. 2013

Turk J Bioch

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“…A major structural change in ventricles post infarction is the dissociation of the formerly compact myocardial architecture into single bundles separated by connective tissue, forming a loose conductive network, with sparse coupling among the branches. 92 The clinical observation that patients with an obvious structural substrate (eg, scar) have episodic post myocardial infarction arrhythmias suggests a role for intermittent triggers in the setting of chronic maladaptation. 93 Clinically, several triggering events have been suggested 94,95 : (1) transient ischemia; (2) fluctuations in the activity of the autonomic nervous system; (3) changes in general body homeostasis (eg, electrolytes, circulating hormones); (4) drugs that prolong the QT interval; and (5) regional sympathetic denervation induced by infarction.…”

Section: Ventricular Tachycardia and Fibrillationmentioning

confidence: 99%

“…106, 107 The main determinants of the slow propagation appear to consist of (1) the tortuous or "zig-zag" pathways traveled by the impulse that are many times longer than the distance between entry and exit points, and (2) the conduction delay at branching points of the fiber bundles. 92,106,108,109 Not only do alterations in conduction occur, but these are accompanied by alterations in the density and function of membrane ion channels in tissue surviving myocardial infarction. 18 The sequence of events responsible for these changes may derive from the altered (and excessive) mechanical load that often eventuates in the periinfarction zone and that leads to cellular hypertrophy.…”

Section: The Relationship Of Electrophysiologic Mechanisms To the Arrmentioning

confidence: 99%

“…116,117 There is also a reduction in Ca 2+ inward current that arises from both reduced channel density and acceleration of calcium channel inactivation 103,118 and reducedadrenergic responsiveness. 90,92 A reduction in transient outward current, Ito, and a loss of the phase 1 notch of the action potential are prominent features of myocytes isolated from 5 day old infarcts. 103,118 In animals that are 30 days or more post-infarction, progressive reduction in IK and ICa,L density is seen in the hypertrophied cells adjacent to the infarct.…”

Section: The Relationship Of Electrophysiologic Mechanisms To the Arrmentioning

confidence: 99%

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The Search for Novel Antiarrhythmic Strategies

Gambit¹

1998

Jpn Circ J

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he first 2 meetings of the Sicilian Gambit focused on a pathophysiologic approach to evaluate antiarrhythmic drugs in light of the electrophysiologic mechanisms for cardiac arrhythmias; 1,2 on the extent to which this approach was effective in identifying the most appropriate therapy for clinical arrhythmias; and on areas where further information was needed to provide rational directions for therapy. 3 The stimulus for the third Sicilian Gambit meeting (the subject of this report) was continued concern over the future of antiarrhythmic drug therapy, based on (1) the increased mortality reported with d-sotalol in the SWORD trial; 4 (2) the failure of amiodarone to reduce all-cause mortality in CAMIAT 5 , EMIAT 6 and CHF-STAT 7 ; and (3) the extent to which international differences in perceived needs and guidelines for drug development might reduce enthusiasm for drug discovery. Participating in the meeting were basic and clinical scientists, investigators involved in drug trials and representatives of regulatory and funding agencies.In the following pages we emphasize that (1) traditional modalities of antiarrhythmic drug development have reached a near-impasse; (2) new perspectives should, nonetheless, lead to novel antiarrhythmic approaches; (3) information derived from molecular technology should facilitate the identification of specific targets for pharmacologic intervention; (4) at least one condition, congenital long QT syndrome, may soon represent "proof of concept" of the linkage between molecular biology and novel treatment strategies; (5) common arrhythmias like atrial fibrillation and ventricular tachycardia and fibrillation may be amenable to a similar approach; and (6) new thinking on development of novel compounds must be complemented by innovative decisions in clinical trials. We stress, as well, that a major market for antiarrhythmic drug therapy still exists: the frequency of lethal ventricular tachyarrhythmias as well as of atrial fibrillation is such that therapies having widespread applicability at modest cost must be sought. RationaleEarly approaches to antiarrhythmic drug development involved the serendipitous identification of antiarrhythmic actions of natural compounds such as cinchona 8 or compounds synthesized for other applications such as procaine. 9 This was followed by synthesis of derivative molecules (respectively, quinidine 10 and procainamide 11 ) and their testing in animal models and in human subjects. Identification of a perceived benefit in human subjects (eg, suppression of ventricular premature depolarizations) could lead to a search for related molecules the effects of which might be more sustained, less toxic and/or more potent, or with properties that might be modified advantageously. These molecules also were tested in animal models for their antiarrhythmic efficacy and toxicity and, if they passed muster, were tested in patients. Shortcomings of this approach are that molecules thus identified tend to incorporate not only the potential benefits of the so-called paren...

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“…1 This results from complex zigzag assembly of surviving myocyte channels in the scar and the expanse of its distribution. [2][3][4] Entrainment mapping is the foremost method for finding the channels that support VT. However, several limitations can significantly constrain its application in the laboratory.…”

mentioning

confidence: 99%

Development of Time- and Voltage-Domain Mapping (V-T-Mapping) to Localize Ventricular Tachycardia Channels During Sinus Rhythm

Nayyar

Kuklik

Ganesan

et al. 2016

Circ: Arrhythmia and Electrophysiology

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Background-In ventricular scar, impulse spread is slow because it traverses split and zigzag channels of surviving muscle.We aimed to evaluate scar electrograms to determine their local delay (activation time) and inequality in voltage splitting (entropy), and their relationship to channels. We reasoned that unlike innocuous channels, which are often short with multiple side branches, ventricular tachycardia (VT) supporting channels have very slow impulse spread and possess low entropy because of their longer protected length and relative lack of side-branching. Methods and Results-Patients with ischemic cardiomyopathy and multiple VT were studied. In initial mapping stage (16 patients and 58 VTs), left ventricular endocardial mapping was performed in sinus rhythm. Detailed pace mapping was used to identify VT channels and confirmed, when feasible, by entrainment. Scar electrograms were analyzed in time and voltage domains to determine mean activation time, dispersion in activation time, and entropy. Predictive performances of these properties to detect VT channels were tested. In the application stage (7 patients and 20 VTs), these properties were prospectively tested to guide catheter ablation. A mean number of 763±203 sampling points were taken. From 1770 pace maps, 47 channels corresponded to VTs. A combination of scar electrograms with the latest mean activation time and minimum entropy, in a high activation dispersion region, accurately recognized regions containing VT channels (κ=0.89, sensitivity=86%, specificity=100%, positive predictive value=93%, and negative predictive value=100%). Finally, focused ablation within 5-mm rim of the prospective channel regions eliminated 18 of 20 inducible VTs. Conclusions-Activation time and entropy mapping in the scar accurately identify VT channels during sinus rhythm. The method integrates principles of reentry formation to recognize VT channels without pace mapping or mapping during VT. (Circ Arrhythm Electrophysiol. 2016;9:e004050.

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Slow conduction in the infarcted human heart. 'Zigzag' course of activation.

Abstract: Slow conduction perpendicular to the fiber direction in infarcted myocardial tissue is caused by a "zigzag" course of activation at high speed. Activation proceeds along pathways lengthened by branching and merging bundles of surviving myocytes ensheathed by collagenous septa.

Cited by 720 publications

References 38 publications

The Association Between Fragmeted QRS and ICD Shocks in patients with Left Ventricular Systolic Heart Failure

The Association Between Fragmeted QRS and ICD Shocks in patients with Left Ventricular Systolic Heart Failure

The Search for Novel Antiarrhythmic Strategies

Development of Time- and Voltage-Domain Mapping (V-T-Mapping) to Localize Ventricular Tachycardia Channels During Sinus Rhythm

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