Obstructive sleep apnea (OSA) is a newly recognized risk factor for the development of systemic hypertension, ischemic heart disease, and congestive heart failure. Mechanisms responsible for these links include OSA-related hypoxemia and arousal from sleep-induced increased sympathetic activity, large negative intrathoracic pressure-induced increased left ventricular transmural pressure gradient and impaired vagal activity, plus formation of oxygen radicals. Secondary phenomena include increased platelet aggregability, insulin resistance, and endothelial dysfunction with reduced endogenous nitric oxide production. Safe, nonpharmacologic, nonsurgical therapy, namely continuous positive airway pressure, can attenuate OSA and improve cardiac function and quality of life. Searching for signs or symptoms of OSA from the patient (or bed partner), namely loud habitual snoring, apneas, nocturnal choking, orthopnea, paroxysmal nocturnal dyspnea, excessive daytime sleepiness, or cardiovascular disease which is difficult to control, may reward the curious physician with another treatment avenue.