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 mon

ths)

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 heartA stimulus (pacing), via activation of endogenous cardiac angiotensin-IIsystem, 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.

Thank you