Ventricular repol. - why epi before endo?

[nvshelat]

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Why is it that the epicardium repolarizes before the endocardium in the ventricles (resulting in an upswinging T wave - Lead 2)? Guyton says that it may be due to high BP in the ventricles causing a reduction in coronary blood flow to the endocardium... I dunno if I buy that... Lilly Pathophys of Heart Disease says its due to the Purkinjes having the prolonged APs (I'm guessing due to the L type Ca channels??). Does anyone know the answer?

Thanks!

 

[SeventhSon]

Why is it that the epicardium repolarizes before the endocardium in the ventricles (resulting in an upswinging T wave - Lead 2)? Guyton says that it may be due to high BP in the ventricles causing a reduction in coronary blood flow to the endocardium... I dunno if I buy that... Lilly Pathophys of Heart Disease says its due to the Purkinjes having the prolonged APs (I'm guessing due to the L type Ca channels??). Does anyone know the answer?

Thanks!

well whatever the primary etiology, it has to converge on the differential action potential duration, with epicardium APs being shorter than endocardial APs.

Since there never is true ischemia, I doubt the relatively low endocardial perfusion during systole has anything to do with it. You said it yourself... what is the AP determined by? L-type Ca channels are responsible for depolarization, not repolarization. K+ channels are responsible for repolarization and, and these are regulated by Gi-betagamma and Go. I think a subtype may be controlled by a PKA signal too.

Some possible explanations include differential expression of proteins or receptors involved in this response between endo and epicardium, but I have no idea. If your book says "it may be due", then perhaps it just isn't known.

 

[nvshelat]

well whatever the primary etiology, it has to converge on the differential action potential duration, with epicardium APs being shorter than endocardial APs.

Since there never is true ischemia, I doubt the relatively low endocardial perfusion during systole has anything to do with it. You said it yourself... what is the AP determined by? L-type Ca channels are responsible for depolarization, not repolarization. K+ channels are responsible for repolarization and, and these are regulated by Gi-betagamma and Go. I think a subtype may be controlled by a PKA signal too.

Some possible explanations include differential expression of proteins or receptors involved in this response between endo and epicardium, but I have no idea. If your book says "it may be due", then perhaps it just isn't known.

Thanks!!

 

[MtnGntx]

The cardiac sodium channel is primary carrier of depolarization signal as it propogates through the myocardium, including the specialized conduction pathways (SA, AV, and purkinjes). The calcium channels are secondarily stimulated and drive contractive forces... they are NOT the primary depolarizing mechanism. There are beta subunit protiens (and a mess of other things ) that exist in a gradient across the LV wall that modulate the expression levels and biophysics of the voltage sensing mechanisms within the sodium channels. These differences account to much of the repolarization kinetics that lead to the aforementioned epicardial repolarization ahead of the M-zone or endocardial channel resetting. Physiologically, these differences occur to reduce the possibility of re-entrant depolarizations that lead to pathological arrhythmias. The entire contraction process is a delicate balance of temporal-spatial depolarization and contraction optimized for pump function. No offense to Guyton, but I have never heard of this ballet being contingent on coronary vascularization processes which seem to be downstream to pump function essentials. Nor have I heard this sequence directly atributed to the AP duration of purkinje fibers... although this seems a more plausible hypothesis assumg that purkinjes manifested predominately in the endocardium... But I dont believe that to be the case...

I would suggest that the "reason" is as stated above. Mutations in the sodium channels that effect the repolarization sequence (by prolonging or reducing depolarization abnormally and differentially across the myocardial wall) are well known to produce re-entrant arrhythmias. There has been a lot of good work on dog hearts reproducing Long-QT syndrome and Brugadas by disrupting temporal conditions. Much more could be said about all of this!😉