At least every other patient I see as a cardiologist has obstructive sleep apnea (OSA). They come to see me for their atrial fibrillation, hypertension or coronary artery disease, and many struggle with obesity and diabetes1-3. I tend to look them in the eye and tell them they look tired. They don't always realize they haven‘t been sleeping well for ages; they just know something isn't right. Often, this is the first time a doctor has asked them about their sleep, and they certainly didn't expect that at a cardiology clinic. Further questioning then usually reveals some other sleep-related health issues: memory impairment, anxiety, attention deficit, nocturia and erectile dysfunction, for which they might have been prescribed antidepressants, anxiolytics, testosterone or even central stimulants (that are, in essence, cardiotoxic) to keep them functioning.4,5
Sleep is not an integral part of cardiology practice in most places. And as a cardiologist in Scandinavia, you are unlikely to know much about sleep apnea. You have probably never reviewed or analyzed a sleep study, or given much thought to what a sleep report actually tells you. What are we measuring, and what does it imply for the cardiovascular system?
A standard sleep apnea study focuses on respiratory parameters and reports the number (and duration, if you dive into the report) of airway occlusions (apneas) and airway narrowings (hypopneas) per hour, as well as oxygen saturation. It may also include an electrocardiogram (ECG), though that is not always the case. If included, the ECG analysis may reveal premature beats or clinically relevant pauses or arrhythmias, such as atrial fibrillation, which would, of course, raise a cardiologist’s eyebrow.
The stress of repeated airway occlusions and hypoxia directly affects the cardiovascular system,5 and measuring continuous blood pressure in a patient with OSA would be very exciting. However, this would require invasive arterial cannulation, which is not feasible in the clinical setting. Therefore, momentary surges in blood pressure after longer apneas, as described in the research setting, are overlooked.1 Recognizing this association is imperative. For example, one would be very eager to treat sleep apnea in a patient with a dilated aorta, where surges in blood pressure increase the risk of dissection or rupture.
I have seen quite a few patients with undiagnosed sleep apnea, severe hypertension and a dilated aorta. The youngest was 37. His blood pressure was 198/110. Central stimulants had made the situation worse. He is now doing well on positive airway pressure (PAP) therapy, the appropriate treatment for his sleep apnea, as an essential component. His 24-hour blood pressure is ideal and his aorta is stable on routine check-ups. His attention deficit is long gone.
Sleep was also central to the case of a young man who fainted behind the wheel. The monitor in the cardiology department alarmed repeatedly. The longest pause was eight seconds, so he was scheduled for urgent pacemaker implantation (not a trivial matter for a young man) given the lifetime risks of complications. He looked exhausted. When asked, he said he hadn’t been sleeping for weeks. If he fell asleep, he would wake up after an hour or so feeling as if he were suffocating. He received PAP at the hospital and was discharged home. Two weeks later, a follow-up Holter monitor showed no pauses, and he had a glimpse of hope in his eyes.
These are the kind of follow-up visits I like. In fact, seeing someone who has received therapy for sleep apnea is among the most rewarding parts of my work as a cardiologist. The blood pressure is finally under control, the fasting blood sugar has markedly improved and the atrial fibrillation is no longer troubling. Of course, some may have difficulty initiating or maintaining therapy, but those are the ones who need our attention and encouragement the most, preferably as part of comprehensive cardiology care.6,7
