1. Heart Remember or cardiac memory

2.  Background Can heart remember?

3. 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

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

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

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

9.  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

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

11. Why we should study heart memory?

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

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

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

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

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

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

18. Mechanisms of heart memory

19. 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.

20.  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

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

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

24.  Could memory be an antiarrhythmic intervention?

26.  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.

27. Thank you