Introduction: Obstructive sleep apnea (OSA) is cha-racterized by repetitive collapse of upper airways, indu-cing both sympathetic and renin-angyotensin-aldoste-rone system overactivation. Thus, cardiac arrhythmias, especially atrial fibrillation are common among sub-jects with OSA.
Methods: We present the case of a 60-year-old male with cardiovascular risk factors (obesity, arterial hyper-tension, impaired fasting glucose and chronic alcohol consumption 30 IU/week), presenting with excessive daytime sleepiness (Epworth schore=12) along with dyspnea upon moderate exertion. Blood pressure (BP) was 110/80 mmHg upon admission, and ECG showed atrial fibrillation 85/min, with normal QRS morpho-logy. The subject presented grade II abdominal obesity (BMI 35, WC=124 cm). ABPM showed controlled BP values under treatment with indapamide, angiotensin receptor blocker and calcium blocker (medium BP/24 h=111/73 mmHg), but a riser cicardian pattern. Hol-ter ECG monitored atrial fibrillation 54/min (32-120/ min), 3233 pauses >2 s (maximum RR 4226 ms), in the absence of dizziness or syncope. Echocardiography showed borderline LV ejection fraction (50%), mild atrial dilation with indirect pulmonary hypertensi-on signs (pulmonary artery acceleration time 70 ms, RVEDD 36 mm, RVW 9 mm).
Results: As the Berlin questionnaire indicated a high risk for sleep apnea, we conducted a cardiorespiratory polygraphy which confirmed a severe form of sleep ap-nea (apnea-hypopnea index 31,5/h, medium nocturnal O2 saturation 92%, minimal nocturnal O2 saturation 75%), requiring continuous positive airway pressure (CPAP) therapy 4-12 cmH20. We included our patient in a cardiovascular rehabilitation program including psychological support for alcohol dependence, nutri-tional counseling and adherence to an exercise plan elaborated by the kinesiotherapist-cardiologist team. Our subject was readmitted after 4 months, and repor-ted a 20 kg weight-loss (current BMI 31,1, WC 117 cm) and a reduction of BP values with a dipper cicardian pattern, allowing diuretic withdrawal. Furthermore, Holter ECG monitoring showed a reduction in number of significant pauses (1974 pauses >2 s, maximum RR 3930 ms) along with the reduction of sleep apnea seve-rity to a mild form, with no indication of CPAP thera-py. Our patient refused electrical cardioversion of the arrhythmia as well as permanent cardiac pacing, thus we opted for conservative treatment and biannual Hol-ter monitoring.
Conclusions: T he multidisciplinary cardiac rehabili-tation program, along with appropriate CPAP therapy are indispensable for patients with OSA. Together they can lead to a reduction in both the need of noninvasive ventilation therapy and antihypertensive medication. Obesity is a major risk factor for obstructive sleep ap-nea, which predisposes to supplementary weight gain, thus closing a vicious circle.