PURPOSE: To evaluate the effects of OSA as well as CPAP therapy on serum level of brain natriuretic peptide (BNP).
METHODS: Subjects referred for evaluation of OSA were evaluated. Subjects with history of systolic or diastolic ventricular dysfunction, or pulmonary hypertension were excluded. Patients older than 40 years of age with cardiac risk factors underwent a 2-D echocardiogram. Those found to have left ventricular hypertrophy, or systolic or diastolic dysfunction were also excluded. Cardiac risk factors were defined as active smoking, DM, HTN, or CAD. Patients underwent nocturnal polysomnography (NPSG). Blood was drawn for night BNP (N BNP), and for morning BNP (M BNP). OSA was defined as an Apnea/Hypopnea Index (AHI)>10. Patients with OSA underwent CPAP titration. Two sets of blood were also drawn.
RESULTS: 59 subjects were included. In subjects with cardiac risk factors, those with OSA had higher levels of N BNP compared to those with no OSA. (44.1 and 11.1 p=0.02). The M BNP levels were higher than the N BNP levels in subjects with OSA and cardiac risk factors (55.59 and 44.09 p=0.007) whereas in subjects with OSA but no cardiac risk factors the M BNP and N BNP levels were similar (10.70 and 11.11 p=0.69). A total of 13 patients with OSA and cardiac risk factors underwent CPAP titration. The M BNP levels were similar to the N BNP levels while on CPAP therapy (42.4 + 14 and 43.8 + 16 respectively).
CONCLUSION: In subjects with cardiac risk factors, the presence of OSA significantly raises the level of BNP after sleep. This is probably due to cardiac stress and diastolic heart failure that develop during sleep. This elevation of BNP levels persists throughout the day signaling cardiac stress that persists even during wake. CPAP therapy during sleep eleminates the rise of BNP levels.
CLINICAL IMPLICATIONS: CPAP therapy reverses heart failure that occurs in patients with OSA and cardiac risk factors.
DISCLOSURE: Michael Chalhoub, No Financial Disclosure Information; No Product/Research Disclosure Information