PVCs and Heart Transplants

I've been researching PVCs and heart transplantation recently in the hopes of learning more clues to the causes of PVCs.  The reason is because there's a lot of discussion about the autonomic nervous system (ANS) and its role in causing PVCs.  When someone receives a heart transplant all of these nerves are cut so I thought it would be interesting to see what the occurrence of PVCs in heart transplants.   If the ANS played any role in increasing PVCs, I'd expect to see a decreased incidence of PVCs in tranplants.

My father was another reason why I decided to research this.  He had a heart transplant back in 1988 and he's done amazingly well so far.

What I learned from the literature is that PVCs occur in about 75% of post transplant patients.  This isn't surprising because the heart was without 02 for a number of hours. I also learned that since the ANS is cut to the heart and therefore this heart rate control mechanism is gone the heart will revert to its own internal pacing rate which is about 100 BPM.  The only way a transplanted heart will increase its rate is by adrenaline.  A transplant patient will increase their HR when exercising but that's only due to adrenaline.  Adrenaline alone can bring the rate up to near max levels.  This is interesting insight into some of the assumptions I think some of us make about how the heart works.

I also learned that PVCs lessen over time for heart transplants.

My father doesn't recall any PVCs post transplant.  He has isolated - infrequent PVCs now.  His ANS actually re-enervated his heart!  This happens to about 40% of transplants.  We know this because his resting rate is mid 70s now which means the internal rate of the heart is being overridden by the parasympathetic nerve (a.k.a. vagus nerve)

Some really basic conclusions:

benign PVCs can occur with NO influence from the ANS.  They are completely internally driven by the heart.
PVCs change over time even for a heart damaged while outside the body on ice for a number of hours

I now second guess the ANS as a primary trigger for PVCs.  I think it might be a secondary cause, meaning when it sends signals to change the HR this might cause already excitable ventricular pacers to fire.

PVC are so complex and there are so many possible underlying causes.  It's no wonder they are so difficult to treat.

[itdood]

p.s., I wanted to add that when you peel back all the layers of the PVC onion, at its core are excitable ventricular pacers.  Treating the root cause is critical.  All we are left with is trying to treat secondary factors, to dull those with meds, and it never really gets to the root of the problem.

The only way I know of to deal with excitable ventricular pacers is to kill them, ablation.  Ablation for benign PVCs is a very complex and delicate issue, save that for another disucssion.

A blanket medication would dull all the pacers and possibly dull all the heart's backup pacers.  I think this is why doctors have found that treating with class III antiarrhythmics can actually be detrimental to benign PVC sufferers.

[Mom2four85]

wow great info, so am I reading this correctly - the ANS/vagus nerve may not play as an important role as it seems to? meaning it's the secondary cause and the heart is primary?

[ireneo]

Absolutely interesting bits of information. Thank you for doing the research on this and explaining it so well. Again, I see why cardio docs are so reluctant to treat PVC's as a rule. Ablation is tricky and difficult with poor success rates and meds just cover up the problem. I just live with mine (hiccup, hiccup)

[itdood]

Hi Lisa, I think that's the best way to think about it.  ANS can play a role but I think of it as more of a secondary thing.  I feel this is the reason Docs look at people like they have 2 heads when they swear there's something vagus related going on.  I was one of them.  I know for sure there wasn't something random going on.  I had positional PVCs, certain time of day...   I certainly think there's some correlation to vagus activation and PVCs but what it all boils down to is that ventricular pacers are firing when they aren't supposed to.

Hi Irene, thanks for the comments :-)