Mr. L is a 67-year-old man with dyslipidemia and stable CAD. He was recently treated at an outside facility for recurrent persistent atrial fibrillation (AF) before requesting to be seen in our clinic for a second opinion of his management. At this point, he has been taking dabigatran and carvedilol for anticoagulation and rate control, but he questioned whether he could have a curative ablation procedure. He has had direct current cardioversion in the past and is unclear what precipitated this recurrence. He leads an active lifestyle through yard work, chores, community activities, but notes he has been limited more than usual by fatigue. An echocardiogram report (he provided) demonstrated normal systolic, diastolic and valvular function without evidence of pericardial disease. By the time of his physical evaluation, his blood pressure was 116.70, HR 65. He was 5'8" 165lbs in no acute distress. His heart and lung evaluation was unremarkable and his abdominal exam was benign. His laboratory data was within normal limits except for dyslipidemia. The lipid panel showed LDL 130, HDL 30 and Triglycerides of 170. An ECG was performed (Figure 1). Aware of the association of AF with OSA, the decision was made to perform the sleep study shown (Figure 2). Mr. L asked if there was any way one could estimate how long he had sleep apnea. He was informed that OSA may have been present since his diagnosis of dyslipidemia.
All are postulated mechanisms in OSA-related dyslipidemia, except:
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The correct answer is: E. Hypoxic microatherothrombosis.
Most commonly, dyslipidemia and Obstructive Sleep Apnea (OSA) are associated with patients who are obese, have hypertension, coronary heart disease, cerebrovascular accidents, and/or diabetes mellitus and overall cardiovascular risk.1 However, it was not until recently that mechanisms elucidating OSA-induced dyslipidemia became evident. While data to stratify the relative impact across races and socioeconomic class is pending, it seems clear the common factor is chronic intermittent hypoxia (CIH). Repeated nocturnal CIH activated hypoxic inhibitory factor (HIF-1) which, in turn, alters fatty acid metabolic pathways that involve SREB1 overexpression. The metabolic perturbation results in dyslipidemia and contributes to the development of atherosclerosis.1,2,3 The resultant mixed dyslipidemia pattern is one of low and dysfunctional HDL with hypertriglyceridemia. However, LDL levels are also elevated, distinguishing the OSA pattern from the metabolic syndrome. Ongoing studies to elucidate the basic pathophysiologic pathways and mechanisms are being done.
The case underscores the importance of early evaluation of OSA. Beyond the more commonly recognized overall cardiovascular risk, OSA seems to exert its cardiovascular damage much earlier than previously recognized. Moreover, recognition may drastically reduce overall atherosclerotic burden in susceptible individuals. As such, the potential for more widespread screening and management in patients with dyslipidemia may raise the profile of OSA as an important component of primary prevention of atherosclerotic coronary vascular disease.
References
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