Heart Remember or cardiac memory

 Background Can heart remember?

What is heart remembers?  Heart remembers:  Characterized by Rosenbaum et al. in 1982  T wave changes induced by ventricular pacing or arrhythmia that persist long after normal ventricular activation has resumed

 Heart remembers:  Physiological process  Continuance and reversible process  Persist for a variable period (minutes to months)

Other terminology about heart remember  Heart remember is neither secondary T wave changes, nor primary T wave changes

 Secondary T wave changes: a change in repolarization induced by an altered pathway of activation: bundle branch block; Wolff-Parkinson-White Syndrome et al

 Primary T wave changes origin from: (a) structural (reflecting hypertrophy, myocyte destruction or fibrosis) (b) Hyperkalemia or hypokalemia induced; pharmacologic (antiarrhythmic drug induced), or pathologic (electrolytic abnormalities) (c) T wave evolution after myocardial infarction

 Heart remember : electrotonic modulation T wave  “electrical remodeling”

Why we should study heart memory?

First reason: This phenomenon is induced not only by pacing, but by the occurrence of spontaneous ventricular premature depolarizations or tachycardias

The second reason: It impacts on the determinants of ventricular repolarization and refractoriness and, therefore, potentially on the expression (or prevention) of arrhythmias

The third reason: It can be confused with the ST-T wave changes of ischemia

The fourth reason: It can induces changes in ion channel physiology that are also seen with cardiac failure or that follow an ischemic insult

Forms of heart memory  Short term memory: labile form which lasts seconds to minutes and depends on covalent modification of preexisting proteins

 Long term memory: consolidated form which lasts days to weeks or longer and requires transcriptional activation and new protein synthesis

Mechanisms of heart memory

Model for memory in the heart A stimulus (pacing), via activation of endogenous cardiac angiotensin-II system, initiates transduction cascade that results in occurrence of memory.

 short memory: Angiotensin coverting enzyme (ACE) or angiotensin II receptor blockers can prevent induction of short term memory  When the transient outward potassium current is blocked by 4-AP, the memory does not occur

 Protein synthesis inhibitors like cyclohexamide can delay the onset and magnitude of cardiac memory (long memory) in dog

Clinical importance of cardiac memory  Action potential duration and refractory periods tend to be prolonged in cardiac memory

 Could memory be an antiarrhythmic intervention?

 The therapy of arrhythmias with individual drugs is beset with seemingly inexplicable variability because of the complex interdigitating events that govern cardiac rhythm and the plasticity of the heart.

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