The “Day Dreamer” - Sleep Apnea
Obstructive Sleep Apnea: The Cardiometabolic Bad Actor
A CardioAdvocate Phenotype
Case Presentation
Marcus is 47 years old. He drives a delivery truck. He has been told he has "borderline" blood pressure, and his doctor started him on one medication about two years ago. His BMI is 34. He snores — loudly — and his wife sometimes sleeps in another room. He wakes up tired. He drinks three cups of coffee before noon just to function. He falls asleep during meetings. He once nodded off at a stoplight.
His doctor has never asked him about his sleep.
At his last visit, his blood pressure was 152/94 despite medication. His doctor added a second antihypertensive. Still no mention of sleep.
Marcus mentions the snoring to a friend, who had a procedure — a UPPP (uvulopalatopharyngoplasty) — that "fixed" his snoring. Marcus sees an ENT, gets the surgery. The snoring improves. His wife is happier. He assumes the problem is solved.
It is not.
Six months later, Marcus is in the emergency department. His blood pressure is 198/112. His legs are swollen. He is short of breath lying flat. An echocardiogram shows a preserved ejection fraction but elevated filling pressures and an enlarged right ventricle with estimated pulmonary artery pressures of 52 mmHg. His BNP is 840. He has heart failure with preserved ejection fraction (HFpEF). He has pulmonary hypertension. And he has had obstructive sleep apnea all along — untreated, unrecognized, and now responsible for years of silent damage.
Marcus is not unusual. He is a pattern. And the pattern is everywhere.
Flying Under the Radar
More than 80% of people with obstructive sleep apnea (OSA) are undiagnosed. An estimated 83.7 million adults in the United States alone are living with OSA — roughly one in three adults over age 20. The vast majority have never been tested.
Why? Because OSA does not announce itself the way a heart attack does. It creeps. It accumulates. It hides behind symptoms that get attributed to aging, stress, weight, or just "being tired." Clinicians often do not screen for it because it falls between specialties — too "sleep" for cardiologists, too "cardiac" for sleep specialists, and too easy to overlook in primary care where visits are short and checklists are long. The American Academy of Sleep Medicine (AASM) has published updated quality measures for OSA screening in primary care (2024), yet adoption remains inconsistent.
And here is the deeper problem: even when symptoms are obvious — loud snoring, witnessed apneas, daytime somnolence, resistant hypertension — the connection to cardiovascular risk is frequently underestimated. According to the AHA Scientific Statement on OSA and Cardiovascular Disease, OSA is not just about being sleepy. It is a systemic inflammatory, sympathetic, and hemodynamic disease that touches nearly every organ system in the body.
The Screening Gap
Validated questionnaires like the STOP-BANG take less than two minutes. The Epworth Sleepiness Scale is a simple self-assessment. Home sleep apnea testing has made diagnosis more accessible than ever. Yet millions continue to fly under the radar — particularly in rural and underserved communities. Women are underdiagnosed because their symptoms often differ from the classic male presentation — they may present with insomnia, fatigue, or mood changes rather than loud snoring.
The Cardiometabolic Web: Why OSA Is a Bad Actor
OSA does not exist in isolation. As outlined in a 2025 Circulation Research review on OSA and cardiometabolic disease, it is embedded in a web of cardiometabolic disease, both as a cause and as a consequence.
OSA and Hypertension: The Resistant Blood Pressure Problem
Among patients with resistant hypertension — blood pressure that remains uncontrolled despite three or more medications — the prevalence of OSA exceeds 70%. In patients with truly refractory hypertension, the numbers are even more striking: 80–90% have OSA, and more than half have severe disease (Hypertension Reviews, Nature 2024).
The mechanisms are well understood. Repeated episodes of airway collapse during sleep trigger surges in sympathetic nervous system activity. Intermittent hypoxia activates the renin-angiotensin-aldosterone system (RAAS), driving aldosterone and angiotensin II levels upward — independent of obesity. Endothelial dysfunction, systemic inflammation, and vascular remodeling follow. The result is a pattern of resistant hypertension, nocturnal hypertension, and abnormal blood pressure variability that is difficult to control with medication alone.
OSA and Obesity: A Bidirectional Relationship
A meta-analysis across four community-based cohorts confirms: among people with obesity, approximately 74% have OSA. A landmark longitudinal study (Peppard et al., JAMA 2000) found that a 10% weight gain predicts a 32% increase in the apnea-hypopnea index (AHI) and a six-fold increase in the risk of moderate-to-severe disease.
But here is what many people miss: 44% of adults with OSA are not obese. You do not have to be heavy to have sleep apnea (JCEM Clinical Approach, 2024).
Excess fat deposition in and around the upper airway narrows the pharynx. Abdominal adiposity alters respiratory mechanics and impairs ventilatory drive. Meanwhile, OSA itself promotes weight gain through sleep fragmentation, hormonal disruption (reduced leptin, increased ghrelin), insulin resistance, and fatigue-driven sedentary behavior. It is a vicious cycle.
The Relative Fat Mass Signal: A Better Measure Than BMI?
New research published in the Journal of Clinical Lipidology (October 2025) brings a fresh perspective. An NHANES analysis of 21,115 U.S. adults found that Relative Fat Mass (RFM) — a waist-to-height derived measure originally developed by Woolcott and Bergman (2018) — is strongly and independently associated with physician-diagnosed sleep disorders.
The RFM Formula: 64 – (20 × height / waist circumference) + (12 × sex), where sex = 0 for men and 1 for women.
Proposed obesity cutoffs: ≥40% for women and ≥30% for men.
The study revealed a nonlinear relationship: sleep disorder risk rose steeply as RFM increased, up to an inflection point around RFM of approximately 39.3, after which the risk curve began to flatten. This pattern held across age, sex, smoking, alcohol use, and comorbidity subgroups. A separate Frontiers in Nutrition analysis (2024) corroborated the RFM-sleep disorder association and explored its intersection with dietary patterns.
Why does this matter? Because BMI is a blunt instrument. It does not distinguish between muscle and fat, and it does not capture where fat is distributed. RFM may more accurately identify individuals at risk for both sleep disorders and the cardiometabolic consequences that follow. It is a simple calculation that could become part of routine screening.
OSA and Chronic Kidney Disease: A Two-Way Street
A 2024 systematic review and meta-analysis of 63 studies (Clinical Kidney Journal) involving over 26 million participants confirmed that the relationship between OSA and chronic kidney disease (CKD) is bidirectional. Additional support comes from a bidirectional Mendelian randomization study (Frontiers in Neurology, 2024) that strengthened the causal inference.
- OSA is associated with a 77% increased risk of developing CKD (RR 1.77, 95% CI 1.56–2.01)
- CKD is associated with a 60% increased risk of developing OSA (RR 1.60, 95% CI 1.35–1.89)
- In CKD patients, the prevalence of OSA is approximately 39%, rising to 47% in those over age 60
- OSA is associated with a 26.5% higher mortality risk in CKD patients
The shared pathways include renal hypoxia from intermittent oxygen desaturation, sympathetic overdrive, RAAS activation, endothelial dysfunction, and oxidative stress. Fluid shifts during sleep in CKD patients can worsen upper airway edema and obstruction, fueling the cycle.
OSA and Heart Failure: The Path to HFpEF, Right Heart Failure, and Pulmonary Hypertension
This is where the story gets serious. The prevalence of OSA in heart failure populations ranges from 20–60% (Heart Failure Review, 2018), and it is even higher in heart failure with preserved ejection fraction (HFpEF). In one prospective study, 70% of HFpEF patients had sleep apnea — approximately 40% obstructive, 30% central.
How OSA Causes Heart Failure
Every obstructive event is a hemodynamic stress test. The negative intrathoracic pressure generated by breathing against a closed airway increases venous return to the right heart while simultaneously increasing left ventricular afterload. Meanwhile, intermittent hypoxia triggers sympathetic surges, RAAS activation, and systemic inflammation. Night after night, year after year, this produces:
- Left ventricular hypertrophy and diastolic dysfunction — the hallmarks of HFpEF
- Pulmonary vasoconstriction and remodeling, leading to pulmonary hypertension
- Right ventricular dilation and failure from chronic pressure overload
Pulmonary Hypertension: The Right Heart Under Siege
OSA prevalence in patients with pulmonary hypertension ranges from 40–80%. Chronic intermittent hypoxia causes pulmonary arteriolar vasoconstriction and, over time, vascular remodeling. The right ventricle — a thin-walled chamber not designed for sustained pressure overload — dilates, becomes dysfunctional, and eventually fails.
OSA and Sudden Cardiac Death: Even in Young People
Perhaps the most alarming data: OSA independently increases the risk of sudden cardiac death. The landmark study by Gami et al. (JACC, 2013) followed 10,701 consecutive adults who underwent polysomnography over an average of 5.3 years. Among 142 who experienced resuscitated or fatal sudden cardiac death, the risk was independently and significantly associated with OSA severity.
The strongest predictors of sudden cardiac death:
- Age greater than 60 years
- Apnea-hypopnea index (AHI) greater than 20
- Mean nocturnal oxygen saturation below 93%
- Lowest nocturnal oxygen saturation below 78%
The mechanism is sobering. Obstructive events generate extreme intrathoracic pressure swings that alter ventricular repolarization. Combined with sympathetic surges and hypoxia, these events create a substrate for fatal arrhythmias. An earlier study by Gami et al. (NEJM, 2005) showed that OSA reverses the normal circadian pattern of sudden death — shifting the peak risk from the morning hours into the nighttime sleeping hours.
This is not limited to the elderly. Young adults with severe, unrecognized OSA face arrhythmia risk during every hour of every night of untreated sleep. This is a preventable cause of catastrophic events in people who may otherwise appear healthy. The AHA Scientific Statement emphasizes that OSA should be considered in the evaluation of unexplained arrhythmias and sudden cardiac events, particularly in younger patients.
The CPAP Problem: When Treatment Fails the Patient
Even when OSA is diagnosed, effective treatment remains a challenge. Continuous positive airway pressure (CPAP) is the gold standard therapy — but adherence is dismal. Manufacturers like ResMed have made significant advances in comfort and connectivity, yet the fundamental compliance crisis persists.
The Compliance Crisis
CMS (Medicare) defines "compliance" as using CPAP for at least 4 hours per night on at least 70% of nights within a 30-day period (CMS PAP Adherence Criteria). That 4-hour threshold originated from a 1993 manuscript based on expert opinion — not empirical evidence. The American Thoracic Society issued a 2023 policy statement calling for CMS to eliminate this arbitrary threshold and adopt patient-oriented outcomes instead.
Yet even by this low bar, nearly half of patients discontinue CPAP treatment during the first few years. Approximately 25% fail by about 38 months. Half of those who quit do so within the first 12 months.
Why Patients Stop
- Device discomfort: nasal irritation, mask leaks, noise, claustrophobia (23% of discontinuers)
- Perceived lack of benefit (20%)
- Psychological barriers: anxiety, inconvenience, partner complaints
- Financial constraints (10%)
- Higher BMI and low initial utilization predict long-term dropout
The result is a treatment that works when used but is abandoned by a staggering number of the people who need it most. Patients need better mask fitting, more follow-up, and alternative therapies when CPAP is intolerable — including oral appliance therapy, positional therapy, and hypoglossal nerve stimulation (Inspire).
The UPPP Trap: When Quiet Snoring Is Not a Cure
Uvulopalatopharyngoplasty (UPPP) is one of the most commonly performed surgeries for snoring and OSA. It involves removing or reshaping tissue in the throat — typically the uvula, soft palate, and sometimes the tonsils — to widen the upper airway.
The problem is that UPPP is very good at reducing snoring but significantly less effective at treating the apnea itself.
The Numbers
- Short-term snoring reduction: 75–95% of patients report improvement
- Strict OSA cure (postoperative AHI ≤5): only about 24% in a Mayo Clinic analysis
- 50% or greater AHI reduction: approximately 51% of patients
- Success rates vary enormously depending on patient anatomy (Stage I: 80.6% vs. Stage II: 37.9%)
- Long-term snoring success declines over time
The Dangerous Misconception
Here is the critical point for patients: the snoring and the apnea are not the same thing. Snoring is the noise. Apnea is the obstruction, the oxygen desaturation, the sympathetic surge, the hemodynamic stress. You can silence the snoring and leave the apnea completely untreated.
Marcus had a UPPP. His wife stopped complaining. His bedroom was quieter. But his airway was still collapsing dozens of times per hour. His oxygen was still plummeting. His sympathetic nervous system was still firing. His heart was still under siege. The only thing that changed was the sound.
If you or someone you know has had a procedure for snoring and has not had a follow-up sleep study to confirm that the apnea is actually resolved, the disease may still be there — silent, dangerous, and progressing.
The Sedentary Spiral: Lifestyle, Diet, and Exercise
OSA does not develop in a vacuum. It thrives in the context of modern sedentary life.
Physical Inactivity and OSA
Research from three large prospective U.S. cohorts has shown that higher physical activity levels and fewer sedentary hours are associated with lower OSA incidence. Specific sedentary behaviors carry measurable risk: watching television 28 or more hours per week is associated with a 78% increased risk of OSA compared to fewer than 4 hours per week.
The mechanisms linking inactivity to OSA include increased adiposity (particularly upper airway and visceral fat deposition), inflammation, insulin resistance, and fluid retention that worsens nocturnal upper airway edema.
Exercise as Treatment
Multiple randomized trials have demonstrated that exercise-based interventions — even without significant weight loss — can improve OSA severity. The ATS Clinical Practice Guideline on Weight Management in OSA recommends comprehensive lifestyle interventions combining diet and physical activity for improvements in AHI, cardiometabolic comorbidities, and quality of life.
A 10% weight loss predicts a 26% decrease in AHI (Peppard et al., JAMA 2000). That is not a cure, but it is clinically meaningful — particularly when combined with other therapies.
Diet and Metabolic Health
There is no single "OSA diet," but dietary patterns that reduce visceral adiposity, inflammation, and insulin resistance are relevant. Mediterranean-style dietary patterns, which emphasize whole foods, healthy fats, and anti-inflammatory nutrients, align well with the metabolic goals for OSA patients. Reducing processed food, excess alcohol (which relaxes upper airway muscles and worsens apnea), and excessive caloric intake are all part of the conversation.
The bottom line: OSA is not just a breathing problem that needs a machine. It is a metabolic and lifestyle problem that demands a comprehensive approach — and patients deserve to know this.
CardioAdvocate Checklist
This is not a prescription. This is navigation — a guide for what to assess, what to ask, and what not to assume.
Questions to Ask Your Clinician
What Clinicians Should Assess
Deep Dive
This section is a living, expandable knowledge layer — designed to evolve over time as new evidence emerges. It links directly to primary literature, explains nuance and controversy, separates population data from individual risk, and explicitly acknowledges uncertainty. Think of it as a Wiki for this phenotype.
Pathophysiology: How Airway Collapse Becomes Organ Damage
The core mechanism of OSA is repetitive upper airway obstruction during sleep. During each obstructive event, the pharynx collapses, airflow ceases, oxygen saturation drops, and carbon dioxide rises. The body responds with progressively forceful respiratory efforts against the closed airway, generating extreme negative intrathoracic pressures (sometimes exceeding −65 cmH₂O). These events typically end with a cortical arousal that restores airway patency but fragments sleep architecture.
The downstream consequences are multisystem:
- Sympathetic Nervous System Activation: Intermittent hypoxia and arousals trigger repeated surges in catecholamines. Over time, this produces sustained sympathetic hyperactivity that persists into waking hours — driving hypertension, tachycardia, and vascular tone abnormalities (Hypertension 2021)
- RAAS Activation: Intermittent hypoxia directly stimulates renin release and aldosterone production, independent of obesity or volume status. This contributes to fluid retention, nocturnal hypertension, and may explain the high prevalence of hyperaldosteronism in OSA patients (Nature Reviews, 2024)
- Endothelial Dysfunction and Inflammation: Cycles of hypoxia-reoxygenation mirror ischemia-reperfusion injury, generating reactive oxygen species (ROS), activating NF-κB signaling, and elevating inflammatory markers (CRP, IL-6, TNF-α). This accelerates atherosclerosis (AHA Scientific Statement)
- Metabolic Disruption: Sleep fragmentation and hypoxia impair glucose metabolism, reduce insulin sensitivity, disrupt leptin/ghrelin signaling, and promote visceral fat deposition — creating a feed-forward loop with obesity (Circ Res 2025)
- Cardiac Mechanical Stress: Negative intrathoracic pressure increases right ventricular preload and left ventricular afterload simultaneously. Chronic repetition leads to ventricular remodeling, diastolic dysfunction, and heart failure (Heart Failure Review)
Diagnosis: More Than a Questionnaire
The American Academy of Sleep Medicine (AASM) recognizes two primary diagnostic pathways:
Level 1: In-Laboratory Polysomnography (PSG)
The traditional gold standard. Monitors EEG, EOG, EMG, airflow (nasal pressure + thermistor), respiratory effort (chest/abdominal belts), pulse oximetry, body position, and snoring. Allows differentiation between obstructive and central events, identifies UARS (upper airway resistance syndrome), and captures REM-related vs. positional OSA.
Level 3: Home Sleep Apnea Testing (HSAT)
Increasingly used for patients with high pretest probability and no significant comorbidities. Measures airflow, respiratory effort, and oximetry. Advantages: lower cost, patient comfort, greater accessibility. Limitations: may underestimate AHI because total recording time (not total sleep time) is the denominator; does not capture sleep staging; may miss positional or REM-related predominance.
Severity Classification
| Severity | AHI (events/hr) | Clinical Significance |
|---|---|---|
| Mild | 5–14 | Often undertreated; may still carry CV risk if symptomatic |
| Moderate | 15–29 | Significant hemodynamic and sympathetic burden |
| Severe | ≥30 | Highest arrhythmia, HF, and sudden death risk; urgent treatment needed |
The Treatment Landscape: Beyond CPAP
CPAP remains the first-line therapy for moderate-to-severe OSA, but a comprehensive treatment approach requires understanding the full spectrum of options:
Positive Airway Pressure (PAP) Therapy
CPAP delivers a continuous stream of pressurized air to splint the airway open. Auto-titrating PAP (APAP) adjusts pressure breath-by-breath. Bilevel PAP (BiPAP) provides different inspiratory and expiratory pressures and is used for patients with comorbid hypoventilation or central apneas. Device manufacturers (ResMed) now incorporate Bluetooth connectivity, cloud-based monitoring, and heated humidification to improve comfort and tracking.
Oral Appliance Therapy (OAT)
Mandibular advancement devices reposition the lower jaw forward to widen the retroglossal airway. Appropriate for mild-to-moderate OSA and for patients who cannot tolerate CPAP. Custom-fitted devices from a dental sleep medicine specialist are preferred over over-the-counter options. Efficacy is lower than CPAP for severe disease, but adherence is often better.
Hypoglossal Nerve Stimulation
The Inspire system is an implantable device that stimulates the hypoglossal nerve to protrude the tongue during sleep, preventing airway collapse. FDA-approved for moderate-to-severe OSA in patients who have failed CPAP. The STAR trial demonstrated significant reductions in AHI and oxygen desaturation index at 12 months, with durable outcomes at 5 years. Candidacy requires drug-induced sleep endoscopy (DISE) to rule out concentric collapse at the velopharynx.
Surgical Options
Beyond UPPP, options include maxillomandibular advancement (MMA), which has the highest reported surgical success rate for OSA (~85–90% for AHI reduction); transoral robotic surgery (TORS) for tongue base reduction; and bariatric surgery for patients with severe obesity and OSA. The key message: any surgical intervention for snoring or OSA must be followed by a post-operative sleep study to confirm that the apnea — not just the snoring — has been resolved.
Positional Therapy
For patients whose OSA is predominantly positional (significantly worse in the supine position), positional therapy devices that encourage lateral sleep can reduce AHI. These range from simple tennis-ball techniques to vibrotactile devices worn around the chest. Positional OSA is more common in mild-to-moderate disease and in non-obese patients.
Weight Management
Per the ATS Clinical Practice Guideline, comprehensive lifestyle interventions are recommended. GLP-1 receptor agonists (semaglutide, tirzepatide) are showing promise not just for weight loss but for direct effects on OSA severity — the SURMOUNT-OSA trial demonstrated significant AHI reductions with tirzepatide. Bariatric surgery remains the most effective weight loss intervention for severe obesity with OSA.
Controversies and Evolving Evidence
The CPAP-Cardiovascular Outcomes Debate
The SAVE trial (NEJM 2016) randomized 2,717 patients with moderate-to-severe OSA and established cardiovascular disease to CPAP plus usual care vs. usual care alone. It found no significant reduction in the composite cardiovascular endpoint. However, mean CPAP use was only 3.3 hours/night — below the CMS compliance threshold. Post-hoc analyses suggested benefit in those using CPAP >4 hours. The debate continues: is it that CPAP does not help, or that we have not achieved adequate adherence?
OSA in Women: An Underrecognized Epidemic
OSA prevalence in women has historically been underestimated due to sex-biased diagnostic criteria and symptom presentation. Women more often present with insomnia, fatigue, morning headaches, and mood disturbances rather than the classic triad of snoring, witnessed apneas, and daytime sleepiness. Hormonal transitions (pregnancy, menopause) significantly modulate risk. Post-menopausal women approach male prevalence rates.
Central Sleep Apnea vs. Obstructive: The Overlap in Heart Failure
In heart failure patients, distinguishing between obstructive and central sleep apnea (CSA) is critical because treatment differs. CSA — characterized by Cheyne-Stokes breathing — is driven by ventilatory control instability and low cardiac output. The SERVE-HF trial (NEJM 2015) found that adaptive servo-ventilation (ASV) for CSA in HFrEF increased cardiovascular mortality. This makes accurate diagnosis essential: ASV is contraindicated in HFrEF with CSA but may be appropriate for treatment-emergent central apnea.
Emerging Pharmacotherapy
Drug-based approaches to OSA are in active development. Combinations targeting upper airway muscle tone (atomoxetine + oxybutynin) have shown promise in small trials. Carbonic anhydrase inhibitors (acetazolamide) may reduce AHI at altitude and in specific phenotypes. The GLP-1 agonist class is emerging as potentially game-changing given their effects on both weight and possibly direct airway/respiratory physiology. However, none have yet replaced mechanical therapy as first-line treatment.
Medical Societies and Resources
The following organizations provide authoritative guidelines and patient resources:
- American Academy of Sleep Medicine (AASM) — Clinical practice guidelines, quality measures, screening standards
- American Heart Association (AHA) — Scientific statements on OSA and cardiovascular disease
- American College of Cardiology (ACC) — Expert consensus decisions, imaging guidelines
- American Thoracic Society (ATS) — CPAP policy advocacy, weight management guidelines
Key References and Landmark Studies
- Gami AS et al. Obstructive Sleep Apnea and the Risk of Sudden Cardiac Death: A Longitudinal Study of 10,701 Adults. JACC 2013
- Gami AS et al. Day-Night Pattern of Sudden Death in Obstructive Sleep Apnea. NEJM 2005
- AHA Scientific Statement. Obstructive Sleep Apnea and Cardiovascular Disease. Circulation 2021
- ATS Policy Statement. Moving Toward Equitable Care: PAP Adherence Thresholds. AJRCCM 2023
- RFM-Sleep Disorder Association. NHANES 2007–2014 Analysis. J Clin Lipidol 2025
- Woolcott OO, Bergman RN. Relative Fat Mass as an Estimator of Whole-Body Fat Percentage. Sci Rep 2018
- Bidirectional Association of Sleep Disorders with CKD. Systematic Review and Meta-Analysis. Clin Kidney J 2024
- OSA-Related Hypertension. Review of Literature and Clinical Management Strategy. Hypertension Research (Nature) 2024
- Woolson SA et al. UPPP in the Management of OSA: The Mayo Clinic Experience. Mayo Clin Proc 2009
- OSA and Cardiometabolic Disease. Comprehensive Review. Circ Res 2025
- Peppard PE et al. Longitudinal Study of Moderate Weight Change and Sleep-Disordered Breathing. JAMA 2000
- Physical Activity, Sedentary Behavior, and OSA Incidence. Three Prospective U.S. Cohorts. Eur Respir J 2022
- SAVE Trial. CPAP for Prevention of CV Events in OSA. NEJM 2016
- SERVE-HF Trial. ASV for Central Sleep Apnea in Heart Failure. NEJM 2015
- OSA Neurogenic Nocturnal Hypertension. Mechanisms and Management. Hypertension 2021
- HFpEF Risk and OSA Prevalence/Severity. Prospective Analysis. JCSM 2022
- ATS Clinical Practice Guideline. Role of Weight Management in OSA Treatment. AJRCCM 2018
- AASM Quality Measure. Screening for Adult OSA by Primary Care Providers: 2024 Update. JCSM 2024
Obstructive sleep apnea is not a nuisance. It is a systemic cardiometabolic disease that drives hypertension, heart failure, pulmonary hypertension, chronic kidney disease, and sudden cardiac death.
More than 80% of cases are undiagnosed. Screening takes two minutes. There is no excuse for this gap.
Reducing snoring is not the same as treating sleep apnea. If you have had a procedure for snoring, demand a follow-up sleep study.
CPAP works when used — but adherence is a crisis. Patients deserve better support and better alternatives when CPAP fails.
Relative Fat Mass may be a more useful screening signal than BMI alone. Ask about it.
Diet, exercise, and addressing sedentary behavior are not optional add-ons. They are core components of OSA management.
CardioAdvocate helps people understand what matters — and how to speak up about it.
CardioAdvocate helps people understand what matters — and how to speak up about it.
