Volume 90%Press shift question mark to access a list of keyboard shortcutsKeyboard ShortcutsEnabledDisabledPlay/PauseSPACEIncrease Volume↑Decrease Volume↓Seek Forward→Seek Backward←Captions On/OffcFullscreen/Exit FullscreenfMute/UnmutemSeek %0-91x1.25x1.5xLive00:0000:0000:00 Chapters Transcript Video Obstructive Sleep Apnea and Cardiovascular Disease Dr. Joe Maglaya from Sentara Medical Group, PCCM and Sleep Specialists, reviews the associations between OSA and various cardiovascular disorders. I'd like to introduce joe Maguire, who many of you know, as a very effective critical care physician. Dr McGuire graduated from the University of santa thomas in the Philippines. He graduated cum laude. E he also graduated from medical school at the University of santo thomas. At this time, he was magna cum laude. He did his medicine residency at Beth Israel in new york, did his fellowship at Yale Norwalk Hospital in Norwalk and also fellowship at Yale, New Haven. He's had a number of honors to to settle out is at one point he was voted one of Delaware's best in pulmonary medicine by his peers, definitely a recognized honor. And actually as a fellow, he received the fellowship award, the norman brady. So he obviously has distinguished himself. And we're looking forward to his talk today about obstructive sleep apnea and cardiovascular disease, joe Thanks. Thank you john, good morning everyone. I'd like to thank you for inviting me to uh talk to you about a very timely topic. Um It is the Association of Obstructive Sleep apnea and cardiovascular disease. Now, uh this is a very broad topic and I actually had uh issues with editing my slides. So uh what I've decided to do is just present to you some of the highlights uh that uh uh of the associations between obstructive sleep pattern and various cardiovascular diseases diseases. And I apologize in advance if I am not able to get into more details as uh we start going over the slides. Um I'll try to see, I'll try to make sure to finish uh five uh 10 minutes uh before the end of the hours. So, you know, we can talk about some of your questions. Um I have no conflict of interest to declare the learning objectives for this morning. Um For the 1st 10 minutes we're gonna talk about the basics of obstructive sleep apnea, including its management. And this is meant uh as an introduction for those who may not be as familiar with this sleep disorder. And then for the rest of the hour, we're gonna talk about the associations between OS. A. And various cardiovascular disorders. And also talk about the impact of always say treatment on these disorders, primarily that of the CPAP. Since it's the one that has received the most uh studies in the literature, there's less on oral appliance therapy and and some of the surgical solutions to uh oh S. A. So for those of you who still remember your anatomy of the upper airway, uh the upper area actually from the the back of the hard palate to the larynx. Uh It's made of many different muscles and soft tissues. And uh the reason we evolved uh with such is so that we were able to speak, were able to breathe. We're able to swallow right. Um uh The problem though, is that uh this area here is also quite collapsible, so during sleep, when all these muscles begin to relax, uh then uh and and some of that uh muscle tone goes away. Uh then this area becomes highly collapsible. And when that happens uh sleep apnea is follow. So um with upper airway collapse which results from the increased collapse ability of the muscles and soft tissues of the upper airway. With that will follow hypoxia. Uh And uh and then an activation a cortical activation of the brain uh that leads to a respiratory effort related arousal and this repetitive arousal as you might imagine, lead to significant sleep disruption. Uh And thus most patients with obstructive sleep apnea will present with daytime sleepiness and fatigue. Those are some of the most common presenting symptoms of O. S. A. In addition to snoring. So what happens then because of the recurrent hypoxia and hyper cap nia and arousal associated with over say there is also an increase a recurrent increase in the sympathetic nervous activation. And uh and this is what leads to some of the card uh come some of its cardiovascular complications. Um And we're gonna talk more about this later. Uh When I look at a sleep study this is a typical epic uh that shows obstructive sleep pattern as you can see there is a flattening here of the airflow. These are just the E. G. S. And right here is the Jurassic channel and the abdominal channel. And you can see uh I'm sorry this is the thoracic and abdominal channel. And you can see that during that cessation of airflow. You see a paradoxical briefing pattern which is accompanied by a drop in the oxygen saturation and a cortical arousal. So this is your typical obstructive sleep apnea. Now. So the other term that you're you hear often from us is a hypothermia. And hypotheses are essentially uh I'd like to think of them as shallow breathing. So they don't really you don't really like have a complete cessation of the airflow. But because of the the drop in the airflow meaning there's still an obstruction happening. Uh It's also causes paradoxical briefing. It also causes a drop in oxygen saturation and a cortical arousal. And there they are pathologic as the obstructive sleep happiness. This is why the term we use to describe the severity of O. S. A. Is apnea. High partner index. We're gonna take a look at that in this next slide. So and remember this because a lot of the cardiovascular disorders are associated with the more severe cases of OS. A. So for the severity criteria, anyone with 5 to 14 Agnes and hypotheses per hour are categorized categorized as mild ethnics, moderate obstructive apnea is between 15 to 30 events per hour and severe is greater than 30 events per hour. And of course we also factoring the degree of sleep disturbance uh the oxygenation level. The associated arrhythmias and the duration of respiratory events when we're trying to categorize the severity of O. S. A. The major risk factors are obesity, snoring, Male Gender until about age 50. And when women turn into when women get into the post menopausal state. The uh the prevalence of always say is uh reaches the same as uh men. And we think that's because of the loss of some of the hormonal influences associated with the pre menopausal state and of course the presence of an upper airway and atomic obstruction. The typical signs and symptoms include snoring, daytime sleepiness, fatigue, and witness apnea. So those are the most common ones. But as you can see, sleep apnea can be associated with some other symptoms, including heart burns, nocturnal heart burns dr area which is actually a also a common symptoms seen in patients with hard issues. And then it can also affect the mood, the memory and it might be associated with learning problems. But the other thing to remember is that some of these patients may not even have any presenting symptoms. The quality of obstructive sleep apnea include neurocognitive impairment, daytime sleepiness and and drowsy driving is a big deal uh impaired quality of life metabolic effects and cardiovascular effects. Uh The treatment for obstructive sleep apnea is four polled. We have the you have the CPAP machine, the standard treatment you have the oral appliance. Uh There are some surgical solutions and behave medical behavioral solutions including weight loss. Again, um Mostly we're going to be talking about the impact of CPAP treatment on this cardiac disorders later. Uh This is just a picture of someone with obstructive sleep apnea there is the CPAP machine. Uh there is a host that attaches to a mask which is what the patient wears during the night. The biggest challenge for a lot of CPAP users is mask intolerance. Um And this just illustrates what happens when you put someone on CPAP. So the CPAP or positive airway pressure actually access an airway stand. And these are some uh corona M. R. I. Cuts uh And as you can see and that's the airway right there and as you can see as the CPAp pressure goes up or it's get it gets tight rated higher. You see an as an increase in the opening of the upper airways. So that's how the CPAP works. Very simple but highly effective uh oral appliances. I just want to give you an idea of what they do essentially. Uh There is an upper and a lower plate and what that and and this is made by dentists. And the way they work is by shifting the lower jaw forward thus increasing the size of the airway. It also kind of helps prevent the tongue from flopping back. Um They're also quite effective for especially for mild to moderate cases and then there's also a fair number of surgical procedures that have been looked at for treatment of obstructive sleep apnea in Children. The actually the treatment of choice is a consul ectomy. Um And the the problem with surgical procedures is that the literature as far as out measuring outcomes uh over time is is pretty limited. So and they're not as effective at reducing the A. H. I. So there's kind of a lot of these procedures have fallen out of favor. The most effective one is also the most invasive one. Which is the maxi maximum mandibular advancement surgery. For those with really severe sleep apnea who are morbidly obese. We might resort a tracheostomy. Uh Although we haven't I haven't done this in forever. Um Bariatric surgery also has a role because we all know that obstructive sleep apnea is made worse uh by weight gain. And then the one thing that you might hear advertised uh in the area is the inspired procedure. Uh Now this is a relatively new procedure for obstructive sleep apnea. So we don't know whether it will impact cardiovascular outcomes in the future. But think of it as sort of like a pacemaker like device similar to the cardiac pacemakers. It's got a sensor that the tax the patient's briefing. And when the patient inspires uh it sends a signal to the pulse generator which is usually which is located uh in um or situated below the clavicle. And then you have a stimulation lead. Uh that is uh uh um connected close to the hipaa glassell nerve. And by sending signals to this nerve it causes the tongue to protrude forward a bit. And by doing so it prevents the tongue from flopping back and is able to maintain the airway. The data on this is pretty promising as far as a significant reduction in H. I. And we do have some empty surgeons in the area that perform this procedure. All right. So uh sorry for a rush introduction. Uh So now let's start talking about uh the association of O. S. A. With various cardiovascular disorders. And amongst these disorders. The Literature is most robust when it comes to Os. A. And hypertension. It has been shown that they frequently coexist in up 30-50% of cases. Uh And autonomic dysfunction is uh what uh most likely causes hypertension in these patients. Um And there is evidence of and this automatic autonomic dysfunction is evidenced by elevated levels of plasma and urinary cata column means in in some studies. And also uh from perennial micro and geography uh studies uh as we all know, the blood pressure tends to be lower during sleep. But patients with obstructive sleep apnea might present with a non dipping blood pressure. And current population studies that looked at the prevalence of hypertension In patients with obstructive sleep apnea had shown an increased prevalence when compared to controls even after adjustment for confounding factors. Uh And for prospective and then there are prospective longitudinal studies that have also shown an increased risk of incident hypertension in patients with O. S. A. Who are normal intensive baseline. So uh this is a study uh from the uh the sleep heart health cohort uh sleep heart health cohort is made up of uh about 6100 subjects recruited from various population studies. As you can see most of them are middle age with women making uh slightly with their slightly more women uh in this patient population. And uh this is a cross sectional study that looked at the prevalence of hypertension in patients with obstructive sleep apnea. And the results essentially showed an increased uh prevalence of high blood pressure with increased S. D. B. Measures. By the way, when I say S. D. B. Or sleep disordered breathing. For now, assume I'm talking about obstructive sleep apnea. They're not synonymous but they almost are when we get to the topic of heart failure uh S. D. B. Will also include central sleep after. So ah in this uh study uh I would like you to focus your attention on on this column here um where they compare patients with severe obstructive sleep apnea, H. I more than 30 to those who don't have obstructive sleep apnea. And they calculated the odds ratios uh And one can really appreciate if you look at the fully adjusted odds ratios, meaning after adjustment to be M. I. Uh next size waist hip ratio smoking alcohol use one can see that the odds of having hypertension in someone with obstructive sleep apnea is Higher uh in both sexes with obstructive sleep apnea. And hiring men even compared to women. And you can also see that those patients who are younger than 65 have a higher odds of having hypertension. Uh and it also applies to every ethnicity out there and the highest odds is almost twice uh compared to controls when it comes to the american indian population. And what's also interesting is that the odds of having high blood pressure uh is present at. Anyway, so even patients who have normal weights have a 1.5 chances of having hypertension uh if they have obstructive sleep apnea, which in this case is uh severe um in the severe category. Uh And of course the more advanced patients tend to have higher odds of having hypertension. Uh The odds ratios are pretty normal when it comes to snoring, meaning snoring itself does not lead to uh snoring itself is not associated with hypertension. Uh and here's another uh cohort study, but this time it's a prospective population based study uh that followed 709 participants over a period of four years. Um And the patients uh at baseline had obstructive sleep apnea, but they were never hypertensive, right? There were normal. Tencent. But baseline and then what the authors did here was they looked at the incidence of hypertension over a period of four years. Um And hypertension is defined as uh blood pressure of 1 40/90 or someone who ends up taking anti hypertensive meds. And this is from the Wisconsin sleep cohort. Um And what they found was that those response association between sleep disordered breathing at baseline and the presence of hypertension four years later, independent of known confounding factors. And I just want to show you this table that look at the odds ratios of incident hypertension. And I would just have you pay attention to the last column here. This is these are the odds ratios uh after various adjustments to confounding factors. Uh And you can see that those patients with moderate obstructive sleep apnea, h I more than 15 have an almost threefold risk of developing hypertension over that period of four years. And uh there's all the risk is almost twice for those patients with mild obstructive sleep apnea. And even for those with almost normal or borderline obstructive sleep apnea, there's still an increased risk. But but you can see that those association here, that those response association, the higher the number of obstructive sleep apnea is the greater the chances of that patient developing atrial fibrillation. I'm sorry, hypertension over time. Um And this is a study uh that uh look at obstructive sleep apnea and resistant hypertension. Uh It's a case control study 63 patients had resistant hypertension defined us. Uh somebody who has a blood pressure of 1 40/90. even after you treatment with three blood uh lower pressure lowering drugs that includes a diuretic and controlled with Subject 63 patients who have controlled blood pressure on drug therapy. And as you can see in this table, uh the case patients and these are once again the patients who have persistent hypertension. Uh and the control subjects are the ones that have well controlled hypertension uh for those. But but when you compare those uh uh those patients with obstructive sleep apnea, right the case. And the control both of them have obstructive sleep apnea. But you can see that the incidence or the prevalence, I'm sorry, of obstructive sleep apnea is higher in patients with resistant hypertension. Uh In fact, it's uh for the case patients it's 71%. And for the control subjects it's 38%. So um what this shows is that uh resistant hypertension is highly associated with obstructive sleep apnea. And this is just to show you further the relationship between those two. Uh And as you can see uh as the as the OS A worsens uh you also see an increased prevalence of resistant hypertension. So meaning those patients with severe obstructive sleep apnea are more likely to also have resistant hypertension. And so uh so we know that so now that we are familiar with the relationships or the associations between always saying hypertension. What happens then with uh when you treat the OS A does have does it have an impact on the blood pressure. Right. Um And so this is a meta analysis of about 28 randomized controlled trials Represented 1948 patients. And in this meta analysis, the authors were able to show that those patients who go on CPAP treatment ah have a 2.58 millimeter a weighted mean difference, right? Of 2.58 millimeter mercury uh in the diurnal systolic blood pressure. And there's also uh a difference of 2.1 millimeter mercury in those for the diastolic blood pressure when compared to controls. Um And uh these results were also seen even in the nocturnal reading. So so uh this uh study clearly showed that there is some improvement uh in the blood pressure uh with CPAP treatment. And these studies also showed that those patients who were younger, sleepier had more severe O. S. A. And who are more compliant with CPAP treatment were the ones that showed this uh the most reduction in blood pressure in blood pressure. So what we know is that CPAP treatment leads to a modest reduction in the blood pressure. You know, I really thought that this would be higher because I've seen this pressure, the blood pressure improve more significantly than this anecdotally. Uh And the studies also showed that those patients with long standing systemic hypertension or those without symptoms like daytime sleepiness may not you may not see this response uh in this population. So it's best probably to start CPAP treatment when someone has uncontrolled hypertension uh diagnosed with obstructive sleep apnea. Though that is a good predictor of reduction in blood pressure. Note that a decrease of two millimeter mercury in blood pressure is enough to reduce cardiovascular risk. And once again, uh the greatest decrease in blood pressure are seen in those patients with more severe O. S. A. And hypoxia. So moving on to always say in atrial fibrillation. Um there are several path official logic features of OS a that kind of lead to the predisposed to atrial arrhythmia genesis and that includes the recurrent autonomic dysfunction and hypoxia that we talked about earlier, the hypercar apnea, recurrent high per capita and the exaggerated negative intra terroristic pressures that lead to increase just a cardiac and trance mural pressures affecting the thin walled atria. Uh And what we know of is that there's also a strong association between Os a and atrial fibrillation described in multiple studies and there's also limited observational data um or data that suggests that oS a maybe a modifiable risk factor for those patients with recurrent atrial fibrillation after cardioversion or ablation. So in once again, going back to the sleep health study cohort this time, uh these authors compared to 228 subjects with sleep disordered briefing to those uh 388 patients with no significant sleep disordered breathing. And they were essentially trying to look at the prevalence of arrhythmias uh in this to sample populations. And what we're able to show is that patients with obstructive sleep apnea have a higher that's the shaded bar have a higher prevalence of a re of atrial fibrillation complex ventricular activities and S. V. T. By Germany and quad reach Germany. So what this slide tells us is that if someone has obstructive sleep happier then that person may have an increased prevalence of uh they present with an increased prevalence of cardiac arrhythmias. And uh when we look at the odds ratios of the prevalence of uh arrhythmias, one can see that the for atrial fibrillation right here at the bottom there's almost a forceful uh risk of having um oh S. A. Uh And uh for N. S. V. T. It's 3.4 for complex ventricular activity. It's 1.7. So the odds of having arrhythmias. Um uh It is higher In patients with obstructive sleep apnea. And again a 4-fold risk in patients with atrial fibrillation. So this was another cohort study in western Australia. Uh that look at uh the association of incident atrial fibrillation this time with the severity of Os. A. And it's called 6800 patients um that were followed over a median Period of 12 years. Most of these are middle aged men as you can see. And uh during the period of follow up 455 developed atrial fibrillation. When you look at the table they presented in there in their article one can see and I would like you to focus on this section here. They look at the hazard ratio of developing incident af over a long period of time and when compared to patients with no obstructive sleep apnea. Those patients with mild, moderate and severe obstructive sleep apnea have a much higher risk of developing atrial fibrillation over time. And this uh is highest uh for those patients with severe obstructive sleep apnea. So there is a those response association. And again this is just to reiterate what I just said over a period of years in this case, let's look at 10 years, one can see that those patients with mild, moderate and severe obstructive sleep apnea have an increased frequency of atrial fibrillation occurrence. Well compared to those who did not have it. And of course the association is strongest for those patients with severe obstructive sleep. Again, this is why when followed over a long period of time. Uh so what about uh atrial fibrillation recurrence after catheter ablation. Again, for the interest of time, I'm not gonna get into the details of this sleep study but essentially uh in this meta analysis uh that involved 3900 patients, or almost 4000 patients. Uh The authors were able to show a 25% greater risk of af recurrence uh in those patients with with untreated obstructive sleep apnea. Uh even after catheter ablation and then with regards to treatment of atrial fibrillation. Um This is another meta analysis uh that this time showed a 42% decreased risk of atrial fibrillation uh when patients uh have uh when patients go on treatment with a CPAP machine and the benefits of CPAP were stronger for the younger the more obese patients. And also uh it looks like for for male patients. But this method analysis showed us uh that atrial fibrillation uh the risk of atrial fibrillation uh drops with CPAP treatment. And this is the the orbit registry which is probably familiar with our cardiologists. Um uh In this uh study, patients were followed over a period of two years. Uh They look at the prevalence of obstructive sleep apnea. Uh and uh and and the continuous uh and CPAP treatment culture that baseline. Uh and uh they look at 1800 patients and what they found was that patients with atrial with Os. A have more symptomatic atrial fibrillation, meaning they have more disabling symptoms. And those patients are more likely to be on some sort of rhythm control therapy. Those patients are also at a higher risk of hospitalization. But interesting enough, and this needs further studies, uh there there's no increase in mortality and major cardiovascular major cardiovascular outcome and hp progression rates. Um that was shown in this registry when these patients are followed over time. Uh what's interesting also is that they noted that the CPAP treatment was likely uh those who received CPAP treatment were less likely to progress to more permanent forms of atrial fibrillation. Again showing that's treatment does improve uh atrial fibrillation control. So in summary, the prevalence of O. S. A. In patients with aF is much higher estimates run between 30 to 80% patients with usa have more disabling symptoms uh and higher risks of hospitalization. We all from uh from one of the slides I showed you uh um showed an increased risk of incident atrial fibrillation. There's also accumulating data that usa is a risk factor for recurrent atrial fibrillation after cardioversion or ablation. And uh once again uh CPAP confers a 42% reduction in af recurrence. Um And that untreated obstructive sleep pattern is actually associated with the 57% increased risk of af recurrence. Um and prospective clinical trials that are required to confirm the impact of O. S. A. On a. F burden and and outcomes. Moving on. What about obstructive sleep apnea and coronary heart disease? Uh Studies also have shown that severe O. S. A. Is associated with an increased risk of coronary heart disease. Uh And those patients with coronary artery disease and obstructive sleep apnea have tend to have worse worse outcomes. And uh the association between O. S. A. And and heart and coronary heart disease may be explained on the basis of multiple vascular risk factors that include high blood pressure, decreased HDL increased crp increased home assisting elevated glucose and insulin resistance slash diabetes mellitus. It's also been shown that the concentrations of uh troponin I. And also coronary artery calcification has been associated with increasing severity of OS. A. Meaning when they look at the troponin level of this uh of patients with more severe O. S. A. They it showed a higher level when compared to controls. So once again going back to the Wisconsin sleep cohort study. Uh Now this time uh they followed uh about 1131 adults over a 24 year period of time. And uh these patients were free of coronary heart disease at baseline. Uh They were not treated with obstructive sleep apnea. And and followed over a long period of time. And just focus on this column here. Uh the right most column. And again, this shows us the hazard ratio of incident coronary heart disease, which is defined as uh bio cardinal in functions or coronary heart revascularization procedures, or even sudden cardiovascular debt. Right. And um once again, you can see at those response association, uh there's almost a 2.5 increase in uh incident coronary heart disease events for those patients with obstructive sleep apnea. But even those patients with mild obstructive sleep apnea have showed a 1.7 odds of having an incident event over when followed over a long period of time. Okay, so what about the effect of cPAP on patients with mild to moderate obstructive sleep apnea. Does it uh reduce cardiovascular risks. So um uh this uh study compared event free survival rates in treated versus untreated patients. And those events are described as M. I. Strokes, acute coronary syndromes and fatal cardiovascular events. Uh These patients uh there's two groups of patients that they followed over time. Uh One group received treatment, the other group did not uh and it involved 449 patients, most of them uh middle age uh subjects and that they were followed over a long period of time. Uh The median follow up was six years. And what they were able to show here is that when uh when followed over a long period of time. Ah The green the green line represents those who received CPAP treatment. The red line represented those who did not received CPAP treatment. And when followed over time. Uh One clearly sees that uh event free survival is much higher in those patients we treated versus untreated obstructive sleep apnea. And this uh graph, the big graph here is actually looks at Multi moderate ethnics. And you can see that the association also held true when uh when followed over time. In fact, the survival free event for those patients with treated Agnes uh was at the range of 80 percent compared to % 50 For those patients who received no treatment at all. And the absolute risk reduction was found to be at around 28%. So that's that's a very significant uh finding And income. And the conclusion of the study showed that there is indeed a cardiovascular risk reduction of 64%. When patients uh with coronary heart coronary artery disease are treated with cpap at least those who have obstructive sleep apnea. And that is a treatment should be considered for considered for primary and secondary cardiovascular prevention. Even in patients with milder O. S. A. What about sleep disordered breathing, Congestive heart failure? This actually requires another session because it's it's it's a broad topic. But when we talk about heart failure, we tend to see two thoughts of apnea. The obstructive sleep apnea and the central sleep apnea is associated with Kane Stokes briefing. Um Now it has been shown in various studies that the prevalence of sleep disordered iterations of sleep disordered briefing In patients with heart failure reaches a high of 50-75%,, especially for those with reduced ejection fraction. And what is felt to be the path of physiology behind this is that obstructive sleep apnea, increased the left ventricular trance mural pressures uh from from the, you know, the increase in the inter touristic pressure during the obstructive events which then lead to a left ventricular preload reduction and then after load increase. So that's what is felt to be the mechanism that uh involved for patients with obstructive sleep apnea who developed congestive heart failure and having O. S. A. In a patient with heart failure is a negative prognostic factor. And it's been shown that treatment especially with CPAP has led to an improvement in left ventricular ejection fraction walking distance and the cat cat a column and a column in levels. And that for those patients with uh morbid S. D. B. N. C. H. F. There has been an increased risk of adverse outcomes including progression of heart failure, hospitalizations and mortality. And patients without heart failure diagnosed with all S. A have an increased subsequent risk of incident heart failure uh in population studies. Uh And this is just a picture of a central sleep apnea with the uh with uh the cyclical hyperthermia. Uh This is characteristic of uh cane stalks briefing. The path of physiology is complex and requires at least five minutes worth of discussion. But due to time constraints. All I'm gonna say is that this uh the development of this type of briefing is associated with changes in the P. C. 02 level. Um uh In those patients with uh congestive heart failure. In other words, the the PCO two is more label in this population uh due to the slower circulation time and also due to pulmonary congestion. And so how do we manage patients with sleep disordered breathing and chf well, we always recommend to our uh cardiologists to try to optimize heart failure therapy because it's been shown that improvement in heart failure control also leads to an improvement in the sleep disordered breathing. What about the role of positive area pressure therapy? Well it's been shown or cPAP. Well it's been shown to improve cardiac function, blood pressure, exercise capacity and quality of life. There's also some limited data that suggest that treatment can reduce the burden of arrhythmias. Uh The impact on mortality remains unclear however, so more studies are needed that look at various subgroups of patients with CHF. Um uh So uh CPAP is still the standard treatment for anyone with sleep disordered breathing and CHF but for those who fail CPAP or who have predominantly central sleep apnea with Kane Stokes briefing. Uh The other treatment of choice is adaptive servo ventilation or a SV. And I do have a good number of patients uh using A S. V. And it is quite effective. The problem though is that in the serve heart failure trial Uh back around 2015. Uh it showed that for those patients with a lower ejection fraction meaning less than equal or less than 45% there is actually an increase in mortality. So I remember this because when this study came out we had to stop R. A. S. V. Treatments on our patients who have lower ejection fractions and we still need further confirmation of those results. And fortunately there is another trial that is going on. We still don't have the results from the advent heart failure trial and hopefully that can further define the association between a S. V. I'm sorry, between S. D. B. N. C. H. F. The other treatment choices are bypassed with a backup rate, nocturnal oxygen and free nick nerve stimulation which is FDA approved. I believe that dr chu foe is one of the early proponents of this procedure in this population. Perhaps he can give us a comment later. Uh This is essentially free nick nerve stimulation is diaphragmatic facing pacing which leads to stabilization of the C. 02 level uh thus leading to an improvement in the C. S. A. C. S. B. Uh in those patients with C. S. A. C. S. B. So uh the next two slides, I'm destroying this out with this lecture again. Sorry, We don't have enough time to go over all of these disorders. But I always say, and it's strongly associated with pulmonary hypertension. The reported prevalence is as high as 70-80%. The mechanism involved is thought to be hypoxia induced pulmonary arterial or basic constriction. Um uh In the absence though, of additional cardiopulmonary disease. Uh the pulmonary hypertension associated with USa is pretty mild. The main pulmonary artery pressure between it's usually between 25 and 30 Mercury. Um But it's been shown though that in those patients with severe pulmonary hypertension that's attributable to another primary cost who has who have coexisting or as a uh it's been shown that those patients are increased, there's an increased risk of mortality. So uh you know, it's probably best to treat uh this pulmonary hypertension, patients with cPAP. So we can we can see so we can see some improvement in the pulmonary arterial pressure. And of note that those patients with more severe pulmonary hypertension tend to respond greatest to CPAP treatment. And the available literature, although limited by sample size uh does suggest a potential benefit associated with CPAP treatment in anybody who's got coexistence OS. A. And pulmonary hypertension as for strokes. Um the prevalence of O. S. A. Has been found to be Up to 70% in those patients who have had strokes and the O. S. A. Has been shown to be an independent risk factor for incident stroke stroke, recurrence mortality and functional and cognitive outcomes. Um And CPAP trials had shown that uh some have shown that there is some uh improvement in the outcomes when it comes to stroke recovery and secondary prevention. But it the literature has yet to show the benefit of CPAP machine for primary stroke prevention. So right now uh the CPAP trial appears to be uh affected. Uh at least in those patients who already have had strokes or or we're trying to prevent the recurrence of another stroke. And I'm gonna end this presentation. I think we made it we still have eight minutes uh with uh the recommendations for always a screening by the american heart association. Uh This just came out last year in the journal circulation. And they are currently recommending that those patients with poorly controlled hypertension, pulmonary hypertension and recurrent atrial fibrillation. Be screened for OS A for other patients, such as those with heart failure symptoms. Arrhythmias. Uh, those who have those survivors of sudden cardiac death and strokes, uh, that they should also be screened for OS. A. If concerning signs and symptoms of O. S. A. Are present. Thank you for listening. I'm sorry for the rush presentation, but I had to cover a lot of grounds for this uh lecture. I appreciate your patience. Thank you. Published June 29, 2022 Created by Related Presenters Fernando Maglaya, M.D. Pulmonologist View full profile
BROADCASTMED