Electrotonic modulation of the T wave and cardiac memory

Rosenbaum, Mauricio B.; Blanco, Horacio H.; Elizari, Marcelo V.; Lázzari, Julio O.; Davidenko, Jorge M.

doi:10.1016/0002-9149(82)90169-2

Cited by 384 publications

(229 citation statements)

References 19 publications

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“…17 During ventricular pacing, the T wave changes, but T wave concordance reappears after several days when normal activation is restored (''cardiac memory''). 55 Our model provides a possible explanation for this phenomenon by assuming that electrical remodeling of cardiomyocytes is triggered by changes in mechanical work.…”

Section: T Wave Concordance and Cardiac Memorymentioning

confidence: 95%

“…When normal activation is restored, the normal T wave reappears after several days. This phenomenon is known as ''cardiac memory'' and was first described by Rosenbaum et al 55 Herweg et al 20 observed changes in the atrial T wave (Ta wave) after changing the activation sequence in canine atria, indicating that cardiac memory is possible in the atria. In contrast, no evidence for ''atrial memory'' has been found in the goat.…”

Section: Introductionmentioning

confidence: 95%

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Mechanoelectric Feedback as a Trigger Mechanism for Cardiac Electrical Remodeling: A Model Study

et al. 2008

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Abstract-Regional variation in ionic membrane currents causes differences in action potential duration (APD) and is proarrhythmic. After several weeks of ventricular pacing, AP morphology and duration are changed due to electrical remodeling of the transient outward potassium current (I to ) and the L-type calcium current (I Ca,L ). It is not clear what mechanism drives electrical remodeling. By modeling the cardiac muscle as a string of segments that are electrically and mechanically coupled, we investigate the hypothesis that electrical remodeling is triggered by changes in mechanical load. Contractile force generated by the sarcomeres depends on the calcium transient and on the sarcomere length. Stroke work is determined for each segment by simulating the cardiac cycle. Electrical remodeling is simulated by adapting I Ca,L kinetics such that a homogeneous distribution of stroke work is obtained. With electrical remodeling, a more homogeneous shortening of the fiber is obtained, while heterogeneity in APD increases and the repolarization wave reverses. Our results are in agreement with experimentally observed homogeneity in mechanics and heterogeneity in electrophysiology. In conclusion, electrical remodeling is a possible mechanism to reduce heterogeneity in cardiomechanics induced by ventricular pacing.

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Section: T Wave Concordance and Cardiac Memorymentioning

confidence: 95%

Section: Introductionmentioning

confidence: 95%

Mechanoelectric Feedback as a Trigger Mechanism for Cardiac Electrical Remodeling: A Model Study

et al. 2008

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“…5 Subsequent studies by Rosenbaum and colleagues, and more recently by Wecke and colleagues, have delineated many of the basic features of the phenomenon of cardiac memory. [6][7][8] The onset of cardiac memory is rapid; as little as 15 minutes of pacing results in T wave changes. In humans, continuous pacing for approximately one week results in a steady state change in the T waves.…”

Section: Cardiac Memorymentioning

confidence: 99%

“…Intriguingly, accumulation occurs even in the absence of overt T wave changes. Both Rosenbaum and colleagues and del Balzo and colleagues 6,9 demonstrated that multiple trains of pacing stimuli resulted in progressively more cardiac memory, even when enough time was left between trains for apparently complete resolution of the alterations in T wave morphology. This observation suggests that the changes observed in the T wave in cardiac memory do not provide an accurate reflection of the underlying pacing-induced electrical changes that have transpired in the ventricular myocardium.…”

Section: Cardiac Memorymentioning

confidence: 99%

Mechanisms linking short- and long-term electrical remodeling in the heart .....is it a stretch?

Marrus

Nerbonne²

2008

Channels

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Ion channels play a central role in the normal electro-mechanical functioning of the heart and are implicated in a variety of disease processes. In response to electrical or mechanical perturbations, cardiac myocytes exhibit remarkable changes in the expression and/or the function of sarcolemmal ion channels, a process that is broadly described as electrical remodeling. This remodeling has beneficial, as well as adverse, effects on myocardial function, including increased risk of fatal arrhythmias. One specific example of cardiac electrical remodeling is cardiac memory, a phenomenon induced in the heart following abnormal myocardial activation patterns produced by artificial pacemakers. Recent studies have shed new light on the molecular mechanisms underlying cardiac memory and suggest intriguing parallels between cardiac memory and heart failure. In both situations, abnormal mechanical stretch of the myocardium results in direct alterations in ion channel properties, as well as in the activation of angiotensin-dependent signaling cascades. With time, altered gene transcription and protein synthesis lead to persistent changes in ion channel levels and activities, changes that can significantly impact normal cardiac function and increase arrhythmia susceptibility.

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“…There are at least 2 types of remodeling that may occur alone, or together. One, electrical remodeling, may be either physiological and unassociated with evidence of cardiac disease (so-called cardiac memory 14,15 ) or may be pathological, as in the shortened atrial effective refractory periods seen after resolution of even brief periods of atrial tachycardia or fibrillation. 16 The second type of remodeling, structural, also may be physiological or pathological.…”

Section: Emerging Concepts Suggesting New Strategies For Prevention Amentioning

confidence: 99%

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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Electrotonic modulation of the T wave and cardiac memory

Cited by 384 publications

References 19 publications

Mechanoelectric Feedback as a Trigger Mechanism for Cardiac Electrical Remodeling: A Model Study

Mechanoelectric Feedback as a Trigger Mechanism for Cardiac Electrical Remodeling: A Model Study

Mechanisms linking short- and long-term electrical remodeling in the heart .....is it a stretch?

The Search for Novel Antiarrhythmic Strategies

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