Why CPAP is not effective in treating resistant hypertension. Does CPAP fail to reduce stroke risk and myocardial risk?

I have reviewed several article recently on why CPAP doesn't seem overly helpful in treating hypertension. A new article in Sleep Medicine Review "A systematic review of CPAP adherence across age groups: Clinical and empiric insights for developing CPAP adherence interventions." clearly explains why CPAP is ineffective intreatment of hypertension. IT ISN'T USED or it isn't used enough. The article clearly states "Continuous positive airway pressure (CPAP) is a highly efficacious treatment for obstructive sleep apnea (OSA) but adherence to the treatment limits its overall effectiveness across all age groups of patients", in simple English, CPAP does not work because CPAP is not used!

Numerous studies have shown low CPAP compliance with only 23-42% of patients utilizing CPAP and a recent study showed 60% quit CPAP completely.

CPAP SUCCESS IS DESCRIBED AS USING CPAP 4-5 NIGHTS FOR 4-5 HOURS A NIGHT, THIS TYPE OF SUCCESS CAN KILL YOU OR LEAD TO CARDIOVASCULAR ACCIDENTS AND STROKES. More importantly this horrendous description of success lulls cardiologists into a false sense of security with treatment.

Studies have shown that most heart attacks and strokes occur between 3-5 AM. The typical patient only wears their CPAP for 4-5 hours/ night. Patients who go to sleep with their CPAP at 10 PM and wear it 4-5 hours will be untreated during the critical hours of 3-5 AM.

It is time for the sleep community to recognize that part-time CPAP use can result in deadly outcomes. An article in the Journal of Human Hypertension "Resistant hypertension, obstructive sleep apnoea and aldosterone." state that "CPAP studies do, however, indicate a wide variation in the BP effects of CPAP, with some patients manifesting a large antihypertensive benefit such that a meaningful BP effect can be anticipated in some individuals. OSA is particularly common in patients with resistant hypertension (RHTN)" The wide variation is likely based on CPAP use. CPAP used 4 hours a night is at best 50% effective, and totally ineffective during times of highest risk.

Treatment of Obstructive Sleep Apnea is essential for many reasons. A recent study showed that oral appliances and CPAP are equivlant when objectively titrated. Oral appliances show much higher compliance than CPAP in both time of use and frequency of use. This could correct hormonal changes that occur due to sleep disruption.

"Diagnosis and treatment of primary aldosteronism" is an article published in
Endocrinology Metabolism Clinics of North America (2011 Jun;40(2):313-32) states that "A few simple rules can allow physicians to successfully identify many patients with arterial hypertension caused by PA among the so-called essential hypertensive patients. The hyperaldosteronism and the hypokalemia can be cured with adrenalectomy in practically all of these patients.

The removal of the adrenal gland may cure the hypertension but the cause of adrenal excess is obstructive sleep apnea that is not effectively treated due to short time use of CPAP.

IF PATIENTS ARE NOT RESOLVING HYPERTENSION PROBLEMS AN ORAL APPLIANCE TRIAL SHOULD PRECEDE ADRENALECTOMY.

Many sleep physicians are "married" to CPAP and their blinders make them declare 70-90% success rates in their patients even though objective studies show that their success is due not to high patient compliance but rather success described as 4-5 hours of use.

Cardiologists, endocrinologists and vascular surgeons need to demand higher levels of success from the sleep community. Unfortunately CPAP is the fiscal engine that drives much of sleep medicine. The elimination of stage 4 sleep from sleep reports was due to the inability of CPAP to return a normal Delta Sleep percentage. Research at University of Chicago showed that Growth Hormone is produced during the first period of Delta Sleep as a quick example. Dumbing down of sleep medicine is inexcusable. Currently Sleep Labs Accredited by the AASM are not even allowed to break Slow Wave sleep into stage 3 and 4.


Sleep Med Rev. 2011 Jun 6. [Epub ahead of print]
A systematic review of CPAP adherence across age groups: Clinical and empiric insights for developing CPAP adherence interventions.
Sawyer AM, Gooneratne NS, Marcus CL, Ofer D, Richards KC, Weaver TE.
Source

University of Pennsylvania School of Nursing, Biobehavioral Health Sciences Division, USA; Philadelphia Veterans Affairs Medical Center, Philadelphia, PA, USA.
Abstract

Continuous positive airway pressure (CPAP) is a highly efficacious treatment for obstructive sleep apnea (OSA) but adherence to the treatment limits its overall effectiveness across all age groups of patients. Factors that influence adherence to CPAP include disease and patient characteristics, treatment titration procedures, technological device factors and side effects, and psychological and social factors. These influential factors have guided the development of interventions to promote CPAP adherence. Various intervention strategies have been described and include educational, technological, psychosocial, pharmacological, and multi-dimensional approaches. Though evidence to date has led to innovative strategies that address adherence in CPAP-treated children, adults, and older adults, significant opportunities exist to develop and test interventions that are clinically applicable, specific to sub-groups of patients likely to demonstrate poor adherence, and address the multi-factorial nature of CPAP adherence. The translation of CPAP adherence promotion interventions to clinical practice is imperative to improve health and functional outcomes in all persons with CPAP-treated OSA.

Copyright © 2011 Elsevier Ltd. All rights reserved.

J Hum Hypertens. 2011 Jun 9. doi: 10.1038/jhh.2011.47. [Epub ahead of print]
Resistant hypertension, obstructive sleep apnoea and aldosterone.
Dudenbostel T, Calhoun DA.
Source

Vascular Biology and Hypertension Program, Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, AL, USA.
Abstract

Obstructive sleep apnoea (OSA) and hypertension commonly coexist. Observational studies indicate that untreated OSA is strongly associated with an increased risk of prevalent hypertension, whereas prospective studies of normotensive cohorts suggest that OSA may increase the risk of incident hypertension. Randomized evaluations of continuous positive airway pressure (CPAP) indicate an overall modest effect on blood pressure (BP). Determining why OSA is so strongly linked to having hypertension in cross-sectional studies, but yet CPAP therapy has limited BP benefit needs further exploration. The CPAP studies do, however, indicate a wide variation in the BP effects of CPAP, with some patients manifesting a large antihypertensive benefit such that a meaningful BP effect can be anticipated in some individuals. OSA is particularly common in patients with resistant hypertension (RHTN). The reason for this high prevalence of OSA is not fully explained, but data suggest that it may be related to the high occurrence of hyperaldosteronism in patients with RHTN. In patients with RHTN, it has been shown that aldosterone levels correlate with severity of OSA and that blockade of aldosterone reduces the severity of OSA. Overall, these findings are consistent with aldosterone excess contributing to worsening of underlying OSA. We hypothesize that aldosterone excess worsens OSA by promoting accumulation of fluid within the neck, which then contributes to increased upper airway resistance.Journal of Human Hypertension advance online publication, 9 June 2011; doi:10.1038/jhh.2011.47.

PMID:
21654850
[PubMed - as supplied by publisher]

Prog Cardiovasc Dis. 2009 Mar-Apr;51(5):371-80.
Sleep apnea, aldosterone, and resistant hypertension.
Pimenta E, Calhoun DA, Oparil S.
Source

Department of Hypertension and Nephrology, Dante Pazzanese Institute of Cardiology, Sao Paulo, SP, Brazil. espimenta@hotmail.com
Abstract

Obstructive sleep apnea, aldosterone excess, and resistant hypertension are common comorbidities in obese patients. The mechanisms that link these conditions are not fully elucidated, but sympathetic nervous system activation, sodium retention, renin-angiotensin-aldosterone system stimulation, endothelial dysfunction, and increased production of reactive oxidative species may be contributing factors. Patients diagnosed with this triad should be treated with low-salt diet, weight-loss counseling, and continuous positive airway pressure, as well as aggressive antihypertensive therapy, usually with multiple agents, including a mineralocorticoid receptor antagonist. Patients with aldosterone-producing adenoma may require adrenalectomy.

PMID:
19249443
[PubMed - indexed for MEDLINE]

Endocrinol Metab Clin North Am. 2011 Jun;40(2):313-32.
Diagnosis and treatment of primary aldosteronism.
Rossi GP.
Source

Molecular Hypertension Laboratory, Dipartimento di Medicina Clinica e Sperimentale (DMCS) 'G. Patrassi' - Internal Medicine 4, University of Padua, University Hospital Padua, Via Giustiniani, 2, 35126 Padua, Italy.
Abstract

Moreover, in a substantial proportion of them, the blood pressure can be normalized or markedly lowered if a unilateral cause of PA is discovered. Hence, the screening for PA can be rewarding both for the patient and for the clinician, particularly in those cases where hypertension is severe and/or resistant to treatment, in which the removal of an APA can allow blood pressure to be brought under control despite withdrawal of, or a prominent reduction in, the number and doses of antihypertensive medications.

Copyright © 2011 Elsevier Inc. All rights reserved.

PMID:
21565669
[PubMed - in process]