There is a certain patient type that becomes a frequent point of focus in cardiology — Patients with a constellation of clinical problems brought on by obesity and its associated findings of worsening insulin resistance triggered by so called “central adiposity,” where fat is stored primarily in the abdomen, that can lead to diabetes, hyperlipidemia, and increased progression of coronary and vascular disease. This very process of storing fat cells centrally, increasing these cell’s resistance to the hormone insulin, thus triggering the diabetes, is aggravated by Sleep Apnea. The lack of good quality ventilation and oxygenation at night — the “snore” or “gasp” we hear is a sign of airways closing down — puts us almost in a nighttime “hibernation” physiology, wherein our metabolism slows down, reducing our caloric burn even more so as to further exacerbate the obesity and thus further worsen this vicious cycle. The physiologic chain reaction of weight gain leading to worsening sleep apnea, more insulin resistance and ultimately diabetes is unfortunately extremely common in our patient population. During this process your body initially tries to compensate for increased insulin resistance by just secreting more insulin and “upping the ante in this high stakes poker game,” via the pancreas. That works for a time but eventually the pancreas begins to fail and blood sugars start to rise leading to diabetes.
Sleep Apnea leads not only to more obesity and possible diabetes, but also to more difficult blood pressure problems, increased vascular complications and troubles with heart rhythm and stroke.
So, how does this tie in to our cardiology patient? Well, reduced nighttime oxygenation leads to greater secretion of adrenalin as your body fights the stress of smothering due to poor ventilation as well as increased levels circulating insulin from the ever increasing tissue insulin resistance. Increased blood pressure develops as well (>70% of resistant hypertension has associated Sleep Apnea). These hormonal and hemodynamic effects lead to more progressive laying down of cholesterol plaque in our arteries which results in coronary and peripheral vascular disease. Premature aging and fibrosis of electrical pathways within heart tissue also arises along the way leading to electrophysiologic problems such as atrial fibrillation, slow heart rates that might require a pacemaker and even life-threatening ventricular arrhythmias. The development of atrial fibrillation is particular telling because in greater than (>) 70% of A fib cases there is associated Sleep Apnea, with increasing risk as we age. With atrial fibrillation comes a tendency for clots to form in the heart due to stagnant blood in our left atrium when it is not in sync with our ventricle. These clots can break off and cause very dangerous and/or life-threatening strokes.
There you have it — the tie in between obesity and Sleep Apnea. Sleep Apnea leads not only to more obesity and possible diabetes, but also to more difficult blood pressure problems, increased vascular complications and troubles with heart rhythm and stroke. Understanding and treating this “perfect storm” of physiologic abnormalities has become the cornerstone of primary and secondary prevention efforts in cardiology. Knowing the impact of something like sleep apnea on this physiology thus becomes fundamental and necessary in protecting a patient from the ravages of diabetes, hypertension, obesity, coronary disease, atrial fibrillation, ventricular arrhythmias, and stroke.
Do you believe you are currently suffering from symptoms of Sleep Apnea? Contact us! We can help you find the sleep resources you need.
Dr. Ajluni is a fellow of the American College of Cardiology and a member of the Oakland County Medical Society, Michigan State Medical Society, and the American Heart Association. He is on staff at William Beaumont Hospital in Royal Oak and Troy. He practices at both Michigan Heart Group and Western Wayne Heart Group where he is also the CEO.