Why does everyone always assume PVCs and not PACs as benign palpitations?

[Losingmymind47]

This is here, other boards and including doctors? Are PAC's not just as common?

I ask because everyone thought PVCs were causing my palpitations however it is actually PACs once caught...

Why are these never brought up as a possible cause?

[Losingmymind47]

Also I have read that when the PAC does not conduct due to being blocked compared to the normal beat this results in an even longer pause then when the PAC conducts itself - the pause is the worst part.

I think you will find this study very interesting:

http://onlinelibrary.wiley.com/doi/10.1002/jcph.679/full

You can see that when people get PVCs they seem to get more of them, but more people tend to get PACs, at least that is the conclusion I draw.

In terms of what is benign and what isn't - I can find studies that say PVCs are predictors of mortality, trigger VTach, Vfib etc as well - but you really have to know what you are reading. Most of the time the people with the most PACs or PVCs are old, male, have high blood pressure, diabetes and existing heart conditions which are all factors that increase mortality. In almost all studies though low burdens of either are not really associated with much of anything.

[Losingmymind47]

I would also add in addition to nothing but a long pause, they might fire when only part of the heart is reset and ready resulting in some very strange beats, or they may fire on time so you may feel almost no difference. The problem I think with PACs is they result in all kinds of strange sensations.

[2210485]

Happy to explain my rationale:

So, in terms of PAC's not necessarily being more common, my argument is not that they are LESS common, rather that theres some fundamental flaws in studies regarding burden.

Let's take a look at what we know:

According to 24 hour holter results (the best standard imo)

1. As you stated there have been some findings that the occurence of a single pac may be more common. In fact, its almost universally prevelant in every human being alive (75% - 99% depending the study cited)

2. The prevelance of PVC > 100 is roughly 4% - 5% among randomly selected individuals free of detectable heart disease; based on Data available.

3. The prevelance of PAC > 70 is roughly 25% among randomly selected patients over age 50.

Based on this one could conclude that PAC burden = 25%, PVC burden = 5%... BUT theres a problem!

Armed with the knowledge that PVC and PAC burden increases with Age and Carsiovascular Disease; We can conclude:

1. Using a MultiVerse approach we find that different studies target different populations.

2. To qualify for the PVC study participants were first screened with a full cardiac workup. Participants with any indication of cardiac disease were excluded.

The Afib study, due to its unique end point (correlation to disease and mortality) included patients that were both healthy and those who had detectable cardiac disease. Including conduction diseases, sss, afib, atrial enlargement, regurgitation, familials etc.

Therefore by design the most comorehensive studies looking at actual Atrial Burden, and hence from the perspective of burden on all the heartbeats of the world can not compare to more comprehensive looks at PVC prevelance.

3. Age! There is a lack of data that can be used to compare prevelance of PVC in one age group vs PAC in another with similar selection criteria.

4. Variability in Endpoints with regards to how patients with a 'high burden' are determined. The closest we get is a comparison of 70 PAC vs 100 PVC in 24 hours. Even without the age or disease consideration undoubtably the percentage of 100 PAC will be lower than 70 PAC. While it is unlikely that this difference would be as dramatic as 80%, we have no way to prove this without the unpublished raw data.

5. Of note here as well is that these studies have also found a mdoerate correlation between PVC burden and PAC burden. However no in depth analysis of this data was performed to determine to precise ratio of change or to try to make predictions that did not support the end point of prospective studies.

Point being despite all of this we can not simply say 'PAC/PVC burden = 25% vs 5%'

Rather what we CAN say is this:

1. More people experience a single PAC then PVC. While this is true I am not sure this is the best measure of what constitutes "common". In my opinion the best measure would be what kind of burden PACs have on the population at large vs PVC. This could,be correlated to Holter Results of symptomatic individuals to better support my second point; that PVC tend to present as symptomatic.

2. Individuals Older than 50, regardless of heart health have more PAC's then the general population with otherwise perfectly normal hearts tend to have PVC's. This is a summation that could have been drawn with or without a study and doesn't necessarily resolve the question of whether or not PAC are more "common" per se.

Sources:

https://www.google.com/url?sa=t&source=web&rct=j&url=http://circ.ahajournals.org/content/circulationaha/126/19/2302.full.pdf&ved=2ahUKEwi_sNiMhIPZAhUL-GMKHeg6DsQQFjACegQIEhAB&usg=AOvVaw1qBLXSeKBc1TATaCpFz7gf

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4390755/#!po=34.0909

https://www.mdedge.com/ccjm/article/95979/cardiology/evaluation-and-management-premature-ventricular-complexes

https://www.ncbi.nlm.nih.gov/m/pubmed/20404258/

https://www.ncbi.nlm.nih.gov/pubmed/10995861

http://circ.ahajournals.org/content/63/6/1351

[2210485]

Also included in some of those sources is data regarding PAC and Mortality.. I have more studies to support this as well.

There is well documented evidence that draws relatively precise correlation between various degrees of PAC burden and Superventricular events vs mortality. So we have the foundation to develop better criteria in terms of what types of PAC are benign.

I can't speak for whether or not this goes into practice, but its something to consider with regards to your original post.

Of course the same types of study shed light on PVC burden and mortality.

[2210485]

Sorry, to clarify further.

Existence of the criteria if used could potentially help seperate patients based off history and symptomology. Which may lead to a physician "shrugging off" any consideration for a superventricular source. Opting instead to get "tunnel vision" on more ambiguous the ventricular aspect

[2210485]

Lastly, in terms of my summation that PAC are less likely to be felt.

I haven't read into it. Admittedly this was said based off purely anecdotal evidence observed on my part.

There seems to be a trend, at least in my own little bubble for:

1. Patients presenting for holter being more likely to have a burden of a statistically significantly higher value then average. However PAC burden, while elevated, is not often an impressive number.

2. Journao entries more frequently correlating with periods of elevated ventricular ectopy, or ventricular events. This as opposed to periods of elevated Atrial events in the absence of an equal or greater relative change in ventricular ectopics.

Objectively there are studies that support the theory that most patients presenting for palpitations are diagnosed with PVC.

However there is no such study with data sufficient to conclude that the symptoms,were in fact caused by the PVC and not a corresponding PAC burden.

[Losingmymind47]

But it conducts as a normal heartbeat at the wrong time - which feels even more alarming and irregular speaking  to anyone who gets both.

I just read a study of 18-45 year used showed 58% of otherwise healthy people (the aim of the study was not cardiac related so basically people without obvious heart issues) get PACs on a 24 hour compared to 40% getting PVCs. Only 27% get both so not sure where you are getting your facts from. In the older age group its 86% PACs 73% PVCs and 66% both

[Losingmymind47]

There is also an associated pause and force beat the same as a PVC. The difference being unlike a PVC you actually feel the "wrong" beat as well as it conducts fully - sometimes when the valves are closed etc

[Losingmymind47]

The only thing I agree with you on is that they are sometimes more troubling (although usually benign as well) but they do seem to cause more issues than PVCs from what I have read. The benefit being though that the issues are less likely to suddenly kill you.

[2210485]

I would be suprised to see any significant cannon A's solely from a PAC, assuming the following is true.

1. No R-on-T phenomenon
2. No Accessory Conduction Pathways.
3. No AV Block

Even at the tightest coupling interval allowed under these circumstances, the mechanical response to the P wave would occur at the very tail end of systole.

The SL Valve would likely close during this period and the ventricle will have entered active relaxation. This would result in a premature opening of the AV valve, and consequent obliteration or shortening of the IVRT on echo. Potential exists for a small cannon A Wave, which would probably be short lived, delayed SL valve closure would also be possible.

Some hemodynamic effects would be measured as a result of these events, however I can't see such changes being as noteworthy as those occurring during a PVC. Thus I wouod anticipate the contraction itsself to generate symptoms in a smaller percentage of the patient population.

[2210485]

1. PAC are not necessarily as common.

2. PVC are more likely to be felt as a forceful contraction. This is because they occur at an inappropriate time relative to the cardiac cycle wheras a pac conducts as a normal heartbeat.

3. PAC are actually probably less beningn. They are more likely to precipitate SVT and could be a sign of broader conduction disease. They are also ominous for AFIB remmission. Someone with a higher PAC burden then PVC burden would be suprising.