People who smoke tobacco have sleep apnea at three times the rate of people who have never done so.Central sleep apnea is more often associated with any of the following risk factors:

being male
an age above 65
having heart disorders such as atrial fibrillation or atrial septal defects such as PFO
strokeHigh blood pressure is very common in people with sleep apnea. Mechanism
When breathing is paused, carbon dioxide builds up in the bloodstream. Chemoreceptors in the bloodstream note the high carbon dioxide levels. The brain is signaled to awaken the person, which clears the airway and allows breathing to resume. Breathing normally will restore oxygen levels and the person will fall asleep again. This carbon dioxide build-up may be due to the decrease of output of the brainstem regulating the chest wall or pharyngeal muscles, which causes the pharynx to collapse. People with sleep apnea experience reduced or no slow-wave sleep and spend less time in REM sleep. Complication
It is considered that OSA is a serious medical condition. Daytime fatigue and sleepiness, cardiovascular problems and eye problems are also be considered as a potential complications of OSA. OSA may also be a risk factor of COVID-19. It is found that people with OSA have a higher risk of developing severe complications of COVID-19. Diagnosis
Despite this medical consensus, the variety of apneic events (e.g., hypopnea vs apnea, central vs obstructive), the variability of patients physiologies, and the inherent shortcomings and variability of equipment and methods, this field is subject to debate.
These drugs work by increasing nitric oxide levels in the blood and inducing coronary vasodilation which will allow for more coronary blood flow due to a decreased coronary resistance, allowing for increased oxygen supply to the vital organs (myocardium). The nitric oxide increase in the blood resulting from these drugs also causes dilation of systemic veins which in turn causes a reduction in venous return, ventricular work load and ventricular radius. All of these reductions contribute to the decrease in ventricular wall stress which is significant because this causes the demand of oxygen to decrease. In general organic nitrates decrease oxygen demand and increase oxygen supply. It is this favourable change to the body that can decrease the severity of ischemic symptoms, particularly angina. Other medications used to reduce the occurrence and severity of vasospasm and ultimately ischemia include L-type calcium channel blockers (notably nimodipine, as well as verapamil, diltiazem, nifedipine) and beta-receptor antagonists (more commonly known as beta blockers or β-blockers) such as propranolol. L-type calcium channel blockers can induce dilation of the coronary arteries while also decreasing the hearts demand for oxygen by reducing contractility, heart rate, and wall stress. The reduction of these latter three factors decreases the contractile force that the myocardium must exert in order to achieve the same level of cardiac output. Beta-receptor antagonists do not cause vasodilation, but like L-type calcium channel blockers, they do reduce the hearts demand for oxygen. This reduction similarly results from a decrease in heart rate, afterload, and wall stress.