Abstract
The acute cardiogenic pulmonary edema (ACPE) is a common condition in Emergency Units and it is associated with high hospital costs, high cardiovascular morbidity and mortality. In fact, it is estimated that the mortality rate of the ACPE is around 12 and 20% reaching 40% in the long term follow-up. Despite the advances in the treatment of potential risk factors for ACPE (such as the improvements of blood pressure control) the readmissions rates and cardiovascular events remain very high. In this context, it is possible that other potential risk factors may be contributing to this unfavorable scenario of the ACPE. One of these potential candidates is Obstructive Sleep Apnea (OSA), a clinical condition characterized by partial or complete obstruction of the upper airways, promoting abrupt reduction in intrathoracic pressure, sleep fragmentation and intermittent hypoxemia. Evidence from the literature consistently describes sympathetic hyperactivation and elevations in blood pressure associated with OSA. Preliminary data from our group comprising consecutive patients with ACPE from two Cardiology Centers showed the following: 1) OSA is very common (62%) and underdiagnosed; 2) patients with OSA had a higher frequency of ACPE due to hypertension than patients without OSA; 3) OSA was associated with increased rates of acute myocardial infarction (AMI), cardiovascular death, new ACPE event and increased rates of hospital readmission in the mean follow-up of 9 months. Although it cannot be proven that OSA is a cause of ACPE, these data provide substrate for conducting a randomized trial to clarify this relationship and evaluate preventive strategies to reverse this unfavorable scenario of the ACPE. Therefore, we propose a randomized clinical trial involving two Brazilian regions (3 Cardiologic University Centers) with expertise in the management of Sleep Disorders. After the diagnosis of hypertensive ACPE (the most common cause of ACPE) and clinical stabilization, we will perform a sleep study to assess the presence or absence of OSA (defined by an apnea-hypopnea index e15 events / hour of sleep). OSA patients will be randomized to use continuous positive airway pressure (CPAP), the standard treatment for OSA, or continuing in the routine medical treatment post ACPE (control group). In addition to clinical and laboratory assessment at baseline, we will perform a follow up at 30 days, 3 months, 6 months and 12 months after randomization to assess outcomes (primary endpoint: combined outcome of fatal and nonfatal MI, fatal and nonfatal stroke, new episode of ACPE and hospital admissions). With a significance level of 5% and study power of 85%, two-tailed hypothesis test, 48 OSA patients per group will be necessary, i.e., 96 patients total. Patients without OSA will also be followed for assessing outcomes described above. Some sub-studies are being proposed, including the analysis of blood pressure control overtime and a cost-effectiveness analysis of OSA treatment. We hypothesized that treatment of OSA will reduce the rate of cardiovascular events, ACPE recurrence and hospital admissions. If so, we strong believe that this study may impact the quality and quantity of life for patients and reducing hospital costs for our Public Health System.
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