Can obstructive sleep apnea (OSA) cause an elevated B‑type natriuretic peptide (BNP) level?

Can Obstructive Sleep Apnea Cause Elevated BNP?

Obstructive sleep apnea (OSA) can cause modest elevations in BNP, particularly in patients with severe OSA, coexisting hypertension, or left ventricular hypertrophy, but OSA alone in otherwise healthy individuals typically does not produce clinically significant BNP elevation during waking hours. 1, 2

Evidence from Guidelines

The most authoritative guidance comes from major cardiovascular societies, which explicitly recognize OSA as a condition that may elevate natriuretic peptides:

• The 2024 American Diabetes Association guidelines list obstructive sleep apnea among conditions that may lead to increased levels of natriuretic peptide when screening for cardiac abnormalities, alongside renal insufficiency, pulmonary disease, and stroke. 1

• The 2024 European Society of Cardiology hypertension guidelines note that up to 60% of patients with resistant hypertension have features of OSA, and recommend screening for OSA in patients with hypertension, particularly those with non-dipping blood pressure patterns—a population in which BNP interpretation becomes more complex. 1

• Praxis Medical Insights (synthesizing American Heart Association, American College of Cardiology, and European Society of Cardiology guidance) explicitly lists obstructive sleep apnea among pulmonary conditions that can increase proBNP levels. 2

Magnitude and Clinical Context of BNP Elevation in OSA

The research evidence clarifies the degree and circumstances under which OSA raises BNP:

In Otherwise Healthy OSA Patients

• Baseline BNP levels in normotensive OSA patients without cardiovascular disease are typically NOT significantly elevated compared to controls during waking hours (mean 43.2 pg/mL in normotensive OSA vs. 36.5 pg/mL in controls, not statistically significant). 3

• OSA does not elicit acute overnight changes in BNP, even in patients with coexisting cardiovascular disease including chronic heart failure. 4

• Atrial natriuretic peptide (ANP) increases overnight in untreated OSA, but BNP remains stable, suggesting different regulatory mechanisms. 4

In Severe OSA with Comorbidities

• Patients with severe OSA (AHI ≥30/h) show significantly higher BNP levels (mean 22.3 pg/mL) compared to controls (9.2 pg/mL, p=0.0001), particularly when left ventricular hypertrophy is present. 5

• Hypertensive OSA patients have the highest baseline BNP levels (mean 27.7 pg/mL), significantly higher than normotensive OSA patients (18 pg/mL, p=0.001) and controls (9.2 pg/mL, p=0.039). 5

• All patients with markedly elevated BNP (≥37 pg/mL) had moderate or severe OSA (11/43 OSA patients), and the difference between severe and mild OSA was statistically significant (p=0.029). 5

• BNP levels correlate with severity of nocturnal hypoxemia: increased BNP is significantly associated with mean oxygen saturation (p<0.0001), minimal oxygen saturation (p=0.002), oxygen desaturation index (p=0.001), and total sleep time with SpO₂ <90% (p=0.002). 5

Left Ventricular Hypertrophy as the Key Mediator

• The quintile value of BNP is an independent predictor of left ventricular hypertrophy in OSA patients (adjusted odds ratio 4.01,95% CI 1.18–13.70, p<0.01), even after adjusting for obesity and other risk factors. 6

• 80% of patients with severe OSA had LVH compared to 35% with mild-to-moderate OSA (p<0.01), and BNP elevation reflects this structural cardiac change rather than OSA per se. 6

Effect of CPAP Treatment on BNP

The therapeutic response to CPAP provides mechanistic insight into the OSA-BNP relationship:

• CPAP significantly decreases NT-proBNP levels in hypertensive OSA patients (from 60.8 to 47.6 pg/mL, p=0.023) and normotensive OSA patients (from 43.2 to 29.6 pg/mL, p=0.0002), while controls show no change. 3

• The effect of CPAP on BNP is more marked in patients with higher baseline BNP levels and those with the most prolonged nocturnal desaturation (p=0.001, r=0.65). 5

• In patients with severe OSA and coexisting coronary artery disease, elevated NT-proBNP levels are significantly reduced by CPAP, and NT-proBNP levels correlate with AHI and show negative correlation with ST-segment depression. 7

Clinical Algorithm for Interpreting Elevated BNP When OSA Is Present

When evaluating a patient with both OSA and elevated BNP, apply this stepwise approach:

Step 1: Quantify the BNP Elevation

• BNP <100 pg/mL or NT-proBNP <300 pg/mL: OSA alone is unlikely to account for this level; heart failure is effectively ruled out. 2, 8

• BNP 100–400 pg/mL or NT-proBNP 300–900 pg/mL: OSA may contribute modestly, particularly if severe OSA with hypertension or LVH is present; echocardiography is mandatory. 2, 9

• BNP >400 pg/mL or NT-proBNP >900 pg/mL: OSA alone cannot explain this elevation; primary cardiac pathology (heart failure, valvular disease, acute coronary syndrome) must be present. 2, 8

Step 2: Assess OSA Severity and Comorbidities

• Mild OSA (AHI <15) in normotensive patients: BNP elevation is NOT attributable to OSA; pursue alternative cardiac diagnoses. 5

• Severe OSA (AHI ≥30) with hypertension: OSA may contribute 10–30 pg/mL to baseline BNP; adjust interpretation accordingly. 5, 3

• Severe OSA with LVH on echocardiography: BNP elevation reflects structural cardiac disease triggered by OSA; both conditions require treatment. 6

Step 3: Evaluate for Confounding Factors

• Renal function: Even mild renal impairment (eGFR <60 mL/min/1.73 m²) elevates BNP independent of OSA; adjust thresholds upward. 1, 2

• Obesity (BMI ≥30 kg/m²): Suppresses BNP by 20–30%; a "normal" BNP in an obese OSA patient may underestimate cardiac dysfunction. 2, 9

• Atrial fibrillation: Independently raises BNP by 20–30%; common in OSA patients and must be identified on ECG. 1, 2

Step 4: Obtain Echocardiography

• Mandatory in all OSA patients with BNP ≥100 pg/mL to assess for left ventricular hypertrophy, diastolic dysfunction, reduced ejection fraction, or valvular disease. 2, 9

• Focus on diastolic parameters (E/A ratio, e′ velocity, left atrial volume), as OSA primarily affects diastolic function before systolic dysfunction develops. 6

Common Pitfalls to Avoid

• Do not dismiss BNP >400 pg/mL as "just OSA": This level of elevation requires primary cardiac pathology and warrants full heart failure workup regardless of OSA severity. 2, 8

• Do not overlook obesity: Obese OSA patients with BNP 100–200 pg/mL may have significant cardiac dysfunction masked by adiposity-related BNP suppression; lower diagnostic thresholds by 20–30%. 2, 9

• Do not assume OSA treatment alone will normalize markedly elevated BNP: While CPAP reduces BNP by 10–20 pg/mL in severe OSA, persistent elevation after CPAP initiation indicates coexisting cardiac disease requiring guideline-directed medical therapy. 5, 3

• Do not ignore left ventricular hypertrophy: BNP elevation in OSA is mediated primarily through LVH; if echocardiography confirms LVH, both OSA treatment (CPAP) and antihypertensive therapy are required. 6