The relationship between sleep-disordered breathing and cardiovascular disease has now been clearly identified.1 Part of the cardiovascular impact is attributable to chronic intermittent hypoxia2 generating oxygen free radicals which trigger the inflammatory cascade by promoting a state of systemic inflammation that leads to widespread endothelial damage, thus predisposing toward atherosclerosis.

The severity of these disorders is evaluated using the apnea–hypopnea index (AHI), defined by the number of apnea and hypopnea events per hour of sleep using polysomnography as a diagnostic method, and per hour of recording, if respiratory polygraphy is used. Apneas are defined by a reduction in airflow of at least 90% with a duration of at least 10s. Hypopnea occurs when airflow is reduced by at least 30% for at least 10s, in association with arterial oxygen desaturation of 3% or more.3 This raises the first question: is the pathophysiological impact of both parameters the same? Do they represent the same thing? Is it acceptable to combine them in the same index?

In a cohort of 963 patients with stable heart failure, 58% had moderate to severe apnea, and mortality during a follow-up of 7.3 years was 50%. The percentage of time during sleep with an oxygen saturation below 90% (T90) was significantly associated with mortality, which increased by 16% for every hour that the patient showed a saturation of less than 90%. This relationship was not observed with the AHI.4 Obviously, the presence of apnea and hypopnea define the presence of the disease, but is this ratio useful for stratifying their severity? Is it an appropriate representation of the pathophysiological mechanisms that potentially contribute to the increased risk of cardiovascular disease in these patients? Probably not, since a higher degree of hypoxemia will surely have greater negative effects; but the AHI ignores this, and does not reflect either the depth or the duration of desaturations and therefore would classify patients with different T90 values, desaturations or comorbidities but with the same AHI in the same severity group.

It was recently reported that the severity of obstructive sleep apnea, quantified by the hypoxic burden associated with the respiratory event, was independently associated with cardiovascular mortality. In contrast, there was no association between this and AHI when it was evaluated as an independent predictor.5

Excessive daytime sleepiness, on the other hand, is a symptom that indicates the clinical severity of obstructive sleep apnea. However, patients may have worse oxygenation indices and longer apneas than those without this symptom, despite having a similar AHI.6

This evidence suggests that when stratifying disease severity, we must set aside our one-dimensional vision that only considers AHI, and instead take into account other parameters that reflect the overall status of the patient, and include those that reflect the hypoxemic burden of the disease, which is ultimately responsible for cardiovascular morbidity and mortality. It would be interesting to combine efforts to develop a similar tool to the BODE index in COPD that would provide an overall assessment of patients with sleep disordered breathing.