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Author Topic: Untreated Obstructive Sleep Apnea May Worsen Survival in Heart Failure  (Read 1333 times)
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« on: May 10, 2007, 09:22:21 am »

April 6, 2007 (Toronto, ON) - The presence of obstructive sleep apnea (OSA) in patients with heart failure significantly raises their risk of death, independent of ventricular function and HF severity, suggests a prospective single-center observational study that emphasizes the importance of looking for--and maybe treating--the breathing disorder when it accompanies heart failure [1].

Of 164 patients with systolic HF but no prior diagnosis of sleep apnea, those with OSA discovered by polysomnography but who declined continuous positive airway pressure (CPAP) therapy had more than twice the adjusted risk of death over an average of three years than those found to be without OSA, write Dr Hanqiao Wang and associates (University of Toronto, ON). None of the OSA patients who agreed to receive CPAP therapy died, but the apparent treatment-related risk reduction failed to reach significance, according to their report published online March 30, 2007 by the Journal of the American College of Cardiology.

"These findings, although not unexpected and somewhat optimistic, are of great importance," write Dr Thierry H Le Jemtel (Tulane University School of Medicine, New Orleans, LA) and Dr Sanja Jelic (Columbia University, New York, NY) in an accompanying editorial [2]. OSA might be present in one third to one half of patients with HF but often goes unrecognized, they observe and, even when detected, it's often not treated. "Hopefully, the positive findings [from Wang et al] will encourage physicians and nurse practitioners who care for patients with congestive heart failure to be more vigilant about the diagnosis and treatment of OSA."

As noted by the editorialists and study authors, and as previously covered by heartwire, OSA is a recognized risk factor for hypertension and stroke and can have adverse physiologic effects that worsen HF severity, including hypoxia with related LV wall-motion disturbances, endothelial dysfunction, ventricular hypertrophy, and proarrhythmia.

The study by Wang et al enrolled consecutive patients with ischemic or nonischemic HF characterized by dyspnea and LVEF <45% who were stable on medical therapy and in whom primarily central sleep apnea had been ruled out by polysomnography. The analysis encompassed 113 people with an apnea-hypopnea index (AHI) <15 who were classified as having "mild or no sleep apnea" (MNSA) and 51 with OSA, defined by an AHI >15. All of the latter group were offered CPAP therapy but only 14 accepted and continued the treatment until at least the first three-month follow-up.

Mortality over an average follow-up of 2.9 years (but range of more than seven years) was 12% in the MNSA group and 24% and nil in the untreated- and treated-OSA groups, respectively. The mortality hazard ratio for untreated OSA, compared with MNSA, adjusted for LVEF, NYHA class, and age, was 2.81 (p=0.029).

As both Wang et al and the editorialists note, the nonsignificant mortality difference between the two OSA groups (p=0.07) prevents a conclusion that CPAP can prolong survival in patients with both heart failure and OSA. Also, the trial's nonrandomized design limits what it can show authoritatively--although Le Jemtel and Jelic contend that multivariate analysis of outcomes in a prospective registry is the only practical and even ethical way to test the issue, given the abundant evidence supporting CPAP in moderate-to-severe OSA.

Moreover, according to the editorialists, there is abundant evidence that CPAP can attenuate or prevent the adverse cardiovascular effects of OSA and that "effective CPAP therapy may halt progression of the underlying cardiovascular condition. Therefore, early diagnosis of OSA and initiation of effective CPAP therapy are of paramount importance in patients with coexistent congestive heart failure and OSA."

http://www.medscape.com/viewarticle/554749?src=mp
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