CPAP vs APAP and heart disease

[Snoredog]

these stupid research doctors, they still don't get it.

They waste millions and millions of grant dollars on these meaningless repeat studies to discredit the efficacy of the autopap all in order to protect their cash-cow business and keep you coming back for more frequent office visits.

Yet the people that remain on therapy "long-term" nearly always end up on some kind of therapy provided by an autopap machine. All the patients they insist be on cpap end up bailing on therapy.

They need to make these X-pap machines OTC then they could waste that money on finding a cure.

[YourLeftVentrical]

[quote="Snoredog"]these stupid research doctors, they still don't get it.

They waste millions and millions of grant dollars on these meaningless repeat studies to discredit the efficacy of the autopap all in order to protect their cash-cow business and keep you coming back for more frequent office visits.

Yet the people that remain on therapy "long-term" nearly always end up on some kind of therapy provided by an autopap machine. All the patients they insist be on cpap end up bailing on therapy.

They need to make these X-pap machines OTC then they could waste that money on finding a cure.

[Snoredog]

[quote="YourLeftVentrical"][quote="Snoredog"]these stupid research doctors, they still don't get it.

They waste millions and millions of grant dollars on these meaningless repeat studies to discredit the efficacy of the autopap all in order to protect their cash-cow business and keep you coming back for more frequent office visits.

Yet the people that remain on therapy "long-term" nearly always end up on some kind of therapy provided by an autopap machine. All the patients they insist be on cpap end up bailing on therapy.

They need to make these X-pap machines OTC then they could waste that money on finding a cure.

[YourLeftVentrical]

Sorry, i guess I veered away form my point. My point was that apap's aren't smart enough to evaluate all the reponsces to indicate where the optimal pressure is. It seems like a doc might be able to find a good range for at least some people, though.
Please note I say "optimal" not just "AHI less"

[Bookbear]

IMHO (and I really mean that... I'm no doctor and not a trained scientist. I made my living for 35 years as a reference librarian.)

IMHO, as a general rule of thumb, the more data points the better. A great deal depends on how the patients were selected for the study, and what criteria were used. 31 strikes me as a small number. People differ in so very many ways, and their responses to pap therapy varies greatly, as a casual reading of this forum bears out. I would be much more concerned about these findings if it involved several hundred over a similar span of time. And of course, no one first study is the final word. These findings would need to be validated by at least one (preferably more) subsequent studies. As it stands, it certainly suggests an interesting topic for further research. Personally, I am willing to go either way, cpap or apap, to achieve good long term treatment that reduces my risk of cardiovascular problems, so I have no apap ax to grind!

BTW, this forum would not make a good pool for such a study. We all self-select to be here... and that makes us a rather particular subset of the apnea patients out there. We are motivated and intelligent enough to want to take a hand in our health, and willing to expend a fair amount of effort in monitoring our treatment and investigating possible options. It would seem that that makes us atypical!

_________________

[StillAnotherGuest]

Well, I guess a (the?) important concept in the APAP approach to OSA is that these machines not only increase pressure in response to events, but also decrease pressure in response to the absence of events (lest everybody always end up on 20 cmH2O by the end of the night). In other words, they're periodically "trolling" until they generate an event to try to insure lowest effective pressure.

Looks like these guys were using the European version of the A10 algorithm with an Autoset T, where the pressure reduction time constant due to apnea is 20 minutes, to flow limitation is 10 minutes, and to snoring is 10 minutes. That's a "I think", because as has been discussed before, details of the APAP algorithms of these machines is often not completely clear:

Bench Evaluation of FL by APAP
Musings on A10

In this Montano study, APAP range was 4-15 cmH2O, and residual AHI of fixed CPAP vs APAP as measured by PSG was 2 vs 6 after 3 months (residual AHI 6, "trolling" constant of 10 minutes, get it?). Course, one could argue the wide pressure range thing. But if the minimum APAP pressure is set to take care of all obstructive events, and the upper limit is set to avoid unnecessarily high pressures (like, "Hey, my APAP is at 8.2 cmH2O minimum and 8.5 cmH2O maximum"), well, then fine, I would think that that's getting pretty darn close to fixed CPAP.

Perhaps a better way to look at this would be that if you're having x-number of pressure increases per night (not "reported AHI"), then I would argue that you're having at least that many events.

Or even better, as far as this study goes, if there's no improvement in blood pressure or glucose control, then you gotta ask whether or not your therapy is optimal.

And again, it looks like AHI>5 is the magic number.
SAG

[DreamStalker]

Sorry, i guess I veered away form my point. My point was that apap's aren't smart enough to evaluate all the reponsces to indicate where the optimal pressure is. It seems like a doc might be able to find a good range for at least some people, though.
Please note I say "optimal" not just "AHI less"

No offense ... but you also veered away from topic. The study was not intended to evaluate APAPs for the effectivness of finding an "optimal" pressure but rather to compare the effects between APAP and CPAP on the cardiovascular system. In fact, study abstract states that all 31 patients were initially titrated using standard CPAP. So one question that arises is how they established the pressure range for the APAP group (as SAG mentioned)? If the APAP group was set to 4-15 then they were set up for failure ... significantly skewing the study results (even if they had been based on sound assumptions about sample population ... which I don't think is realistically possible with 31 samples/patients).

Nevertheless, your original point regarding Bilevels and CO2 also illustrates the complexity of OSA treatment (CPAP, APAP, or BIPAP) on the cardiovasular system which supports the view that the investigators may have over-simplified their approach to the study.

[cwsanfor]

What is with -SWS, still getting over Memorial Day?

[Snoredog]

What is with -SWS, still getting over Memorial Day?

every time someone asks: Where's SWS? after he's been gone a while

I usually say: ah he left cause he was wrong all the time!

then he has to come back here and defend himself

[Snoredog]

[quote="StillAnotherGuest"]Well, I guess a (the?) important concept in the APAP approach to OSA is that these machines not only increase pressure in response to events, but also decrease pressure in response to the absence of events (lest everybody always end up on 20 cmH2O by the end of the night). In other words, they're periodically "trolling" until they generate an event to try to insure lowest effective pressure.

Looks like these guys were using the European version of the A10 algorithm with an Autoset T, where the pressure reduction time constant due to apnea is 20 minutes, to flow limitation is 10 minutes, and to snoring is 10 minutes. That's a "I think", because as has been discussed before, details of the APAP algorithms of these machines is often not completely clear:

Bench Evaluation of FL by APAP
Musings on A10

In this Montano study, APAP range was 4-15 cmH2O, and residual AHI of fixed CPAP vs APAP as measured by PSG was 2 vs 6 after 3 months (residual AHI 6, "trolling" constant of 10 minutes, get it?). Course, one could argue the wide pressure range thing. But if the minimum APAP pressure is set to take care of all obstructive events, and the upper limit is set to avoid unnecessarily high pressures (like, "Hey, my APAP is at 8.2 cmH2O minimum and 8.5 cmH2O maximum"), well, then fine, I would think that that's getting pretty darn close to fixed CPAP.

Perhaps a better way to look at this would be that if you're having x-number of pressure increases per night (not "reported AHI"), then I would argue that you're having at least that many events.

Or even better, as far as this study goes, if there's no improvement in blood pressure or glucose control, then you gotta ask whether or not your therapy is optimal.

And again, it looks like AHI>5 is the magic number.
SAG

[ProfessorEd]

I must admit thieir result is puzzling.

If someone has the full article perhaps they could say if the people were randomly assigned to the two treatments, or if they merely took samples of patient some of which ended up with APAP machines and others with CPAP.

If it was the latter, it is possible those on auto machines were sicker (or differed in some other way) and this could produce thedr results. My impression is that in the US most doctors only try auto machines for the patients that need either higher pressures or those who ask for them (which are often those who have have a serious enough problem to research the issue or have a long standing problem and gradually learn there are better machines outs there.

[StillAnotherGuest]

If someone has the full article perhaps they could say if the people were randomly assigned to the two treatments, or if they merely took samples of patient some of which ended up with APAP machines and others with CPAP.

The patients were randomly assigned and did not differ in baseline measurements.

SAG: Have you got to play with any A-Flex yet?

Not yet, but "soon", trying to get that "other" new Respironics thing up and running.
SAG

[DreamStalker]

I must admit thieir result is puzzling.

If someone has the full article perhaps they could say if the people were randomly assigned to the two treatments, or if they merely took samples of patient some of which ended up with APAP machines and others with CPAP.

If it was the latter, it is possible those on auto machines were sicker (or differed in some other way) and this could produce thedr results. My impression is that in the US most doctors only try auto machines for the patients that need either higher pressures or those who ask for them (which are often those who have have a serious enough problem to research the issue or have a long standing problem and gradually learn there are better machines outs there.

Not seen full journal article text but here is their abstract -


Fixed and Autoadjusting Continuous Positive Airway Pressure Treatments Are Not Similar in Reducing Cardiovascular Risk Factors in Patients With Obstructive Sleep Apnea

Vincenzo Patruno, MD; Stefano Aiolfi, MD; Giorgio Costantino, MD; Rodolfo Murgia, MD; Carlo Selmi, MD, PhD; Alberto Malliani, MD and Nicola Montano, MD, PhD
* From the Division of Respiratory Rehabilitation (Drs. Patruno, Aiolfi, and Murgia), S. Marta Hospital, Rivolta d’Adda, "Ospedale Maggiore", Crema; and Department of Clinical Sciences (Drs. Costantino, Selmi, Malliani, and Montano), Internal Medicine II, L. Sacco Hospital, University of Milan, Milan, Italy.


Correspondence to: Nicola Montano, MD, PhD, Department of Clinical Sciences, L. Sacco Hospital, University of Milan, via GB Grassi 74, 20157 Milano, Italy; e-mail: nicola.montano@unimi.it

Abstract

Background: A strong association between obstructive sleep apnea (OSA) and the risk for cardiovascular and cerebrovascular diseases has been reported. Continuous positive airway pressure (CPAP) is the first-line therapy for OSA, able not only to reduce daytime sleepiness but also to improve cardiovascular and metabolic outcomes. Autoadjusting CPAP (APAP), an alternative treatment to CPAP, can reduce OSA symptoms while increasing long-term CPAP compliance without the high costs of CPAP titration. However, no data are available on the effects of APAP on cardiovascular risk factors

Methods: We performed standard full polysomnography; obtained plasma levels of glucose, insulin, and C-reactive protein (CRP); and measured systolic BP (SBP) and diastolic BP (DBP) in 31 patients with newly diagnosed, severe OSA. After standard CPAP titration, all subjects were randomized to CPAP or APAP treatment. Measurements were obtained at baseline and after 3 months of treatment.

Results: The two groups were similar in terms of age, sex, body mass index (BMI), and severity of OSA. SBP, DBP, heart rate (HR), homeostasis model assessment index (HOMA-IR), and CRP were similar in the two groups. After 3 months of treatment, BMI, HR, and compliance to therapy were also comparable. OSA indexes were significantly reduced in both groups. Significant reductions in SBP, DBP, and HOMA-IR were observed in the CPAP group but not in the APAP group, while CRP plasma levels were similarly reduced.

Conclusions: Our results suggest that CPAP and APAP, despite significant effects on OSA indexes and symptoms, do not improve cardiovascular risk factors in the same fashion.


Key Words: BP • continuous positive airway pressure • inflammation • insulin resistance • obstructive sleep apnea

[BrianRT]

According to the authors, both CPAP and APAP took care of the OSA appropiately. Therefore, it would stand to reason that the corresponding effect on the cardiovascular system would be similar, but in the study, it isn't. This seems almost counter-intuitive as we know the effects of untreated OSA on the CV system (hypertension being the most common).
But treated OSA still evidencing hypertension?? WTF??

Ok, so why the different results??

Here's my take on it....

When the mean airway pressure is increased (Paw) there is a corresponding increase in intrathoraic pressure (Itp). Now, this causes a decrease in both arterial systolic and distolic pressures. The effects of high positive end expiratory pressure causing hypotension are well documented in the literature.

It's possible that with a CPAP keeping your Paw constant (in relation to your normal ventilatory pressures of course), that you will see a measurable decrease in SBP and DBP versus a trolling APAP maintaing your Paw as low as feasible in the abscence of an apneic event.

I would love to know what kind of pressure numbers ALL of the PAPs were set at (fixed and the auto's range) to see if this theory is applicable (though it's my strong feeling this is the case)

[Snoredog]

[quote="BrianRT"]According to the authors, both CPAP and APAP took care of the OSA appropiately. Therefore, it would stand to reason that the corresponding effect on the cardiovascular system would be similar, but in the study, it isn't. This seems almost counter-intuitive as we know the effects of untreated OSA on the CV system (hypertension being the most common).
But treated OSA still evidencing hypertension?? WTF??

Ok, so why the different results??

Here's my take on it....

When the mean airway pressure is increased (Paw) there is a corresponding increase in intrathoraic pressure (Itp). Now, this causes a decrease in both arterial systolic and distolic pressures. The effects of high positive end expiratory pressure causing hypotension are well documented in the literature.

It's possible that with a CPAP keeping your Paw constant (in relation to your normal ventilatory pressures of course), that you will see a measurable decrease in SBP and DBP versus a trolling APAP maintaing your Paw as low as feasible in the abscence of an apneic event.

I would love to know what kind of pressure numbers ALL of the PAPs were set at (fixed and the auto's range) to see if this theory is applicable (though it's my strong feeling this is the case)