Medical attention to uric acid (UA) has been increasing in recent years, mainly because this molecule has been shown to be associated with increased cardiovascular risk, both in the general population and in the hypertensive patients. A growing body of clinical and experimental data supports this view and prompts reconsideration of the role of UA in the development of atherosclerosis and the genesis of cardiovascular disease. It is known that this substance, in certain plasma concentrations, induces increased oxidative stress, a chronic inflammatory state, and a whole series of other modifications that are potentially deleterious at the cardiovascular level leading to hypertension, atherosclerosis, atrial fibrillation (AF), and other metabolic changes such as diabetes, metabolic syndrome, non-alcoholic fatty liver disease and kidney failure. Despite this epidemiologic and mechanistic evidence, the current guidelines from international cardiology scientific societies do not give precise indications in this regard, and some of them only suggest UA evaluation as part of an initial screening of the hypertensive patient. The purpose of this review is to briefly describe the main clinical and epidemiological evidence supporting the role of hyperuricemia as a possible emerging cardiovascular risk factor and to analyze the potential pathophysiological mechanisms through which elevated UA levels may exert a detrimental effect on the cardiovascular system.

Hyperuricemia is known to be a necessary and causal condition for gout, but much more prevalent than gout. Medicine has standardized treatments for gout, but has no such determination for asymptomatic hyperuricemia. Nevertheless, people with hyperuricemia, gouty or not, too often continue to be at risk for shortened lifespans from life-threatening comorbidities, all of which are known to be consequences of obstructive sleep apnea (OSA), which is shown herein to cause most hyperuricemia. This review also presents the wide variety of OSA consequences, many of which are irreversible and life-threatening, as the rationale for treating all hyperuricemia (gouty and asymptomatic) by diagnostic testing and effective treatment for OSA as soon as hyperuricemia is detected. It advocates frequent ultrasonic screening for aggregated urate crystals. Multiple epidemiological studies have found OSA to be significantly more prevalent in those people with gout diagnosed with OSA than it is in those never diagnosed with it. A clinical study shows an even higher prevalence of OSA in people with gout. The pathophysiology of hypoxia from OSA explains how it would lead to both the overproduction and the underexcretion of uric acid, leading to hyperuricemia and the precipitation of monosodium urate crystals which cause a gout flare. Resolving OSA has been shown to prevent or even reverse life-threatening diseases that are recognized comorbidities of hyperuricemia and gout, and can prevent further gout flares. In order to extend the length and quality of life of people with gout or hyperuricemia, when either first manifests a patient sleep study is recommended, followed by effective OSA treatment as warranted.