Sleep apnea in 81 ambulatory male patients with stable heart failure. Types and their prevalences, consequences, and presentations.

BACKGROUND: Heart failure is a highly prevalent disorder that continues to be associated with repeated hospitalizations, high morbidity, and high mortality. Sleep-related breathing disorders with repetitive episodes of asphyxia may adversely affect heart function. The main aims of this study were to determine the prevalence, consequences, and differences in various sleep-related breathing disorders in ambulatory male patients with stable heart failure. METHODS AND RESULTS: This article reports the results of a prospective study of 81 of 92 eligible patients with heart failure and a left ventricular ejection fraction < 45%. There were 40 patients without (hourly rate of apnea/hypopnea, 4 +/- 4; group 1) and 41 patients with (51% of all patients; hourly rate of apnea/hypopnea, 44 +/- 19; group 2) sleep apnea. Sleep disruption and arterial oxyhemoglobin desaturation were significantly more severe and the prevalence of atrial fibrillation (22% versus 5%) and ventricular arrhythmias were greater in group 2 than in group 1. Forty percent of all patients had central sleep apnea, and 11% had obstructive sleep apnea. The latter patients had significantly greater mean body weight (112 +/- 30 versus 75 +/- 16 kg) and prevalence of habitual snoring (78% versus 28%). However, the hourly rate of episodes of apnea and hypopnea (36 +/- 10 versus 47 +/- 21), episodes of arousal (20 +/- 14 versus 23 +/- 11), and desaturation (lowest saturation, 72 +/- 11% versus 78 +/- 12%) were similar in patients with these different types of apnea. CONCLUSIONS: Fifty-one percent of male patients with stable heart failure suffer from sleep-related breathing disorders: 40% from central and 11% from obstructive sleep apnea. Both obstructive and central types of sleep apnea result in sleep disruption and arterial oxyhemoglobin desaturation. Patients with sleep apnea have a high prevalence of atrial fibrillation and ventricular arrhythmias.

Association of low PaCO2 with central sleep apnea and ventricular arrhythmias in ambulatory patients with stable heart failure.

BACKGROUND: Central sleep apnea frequently occurs in patients with heart failure. Because it is not practical to perform sleep studies on all patients, readily available laboratory tests that predict sleep apnea would be clinically useful. Arterial PCO2 has a profound influence on breathing during sleep: When it decreases below a certain threshold, apnea occurs. OBJECTIVE: To study the value of a low PaCO2 while patients are awake in predicting central sleep apnea in patients with stable, treated heart failure. DESIGN: Prospective study. SETTING: Referral sleep laboratory of a Department of Veterans Affairs Medical Center. PARTICIPANTS: 59 patients with left ventricular ejection fractions of 45% or less. MEASUREMENTS: Arterial blood gases and hydrogen ion concentrations were measured, and cardiac radionuclide ventriculography, Holter monitoring, and polysomnography were done. RESULTS: Patients were classified as eucapnic (PaCO2 > 35 and < 44 mm Hg [n = 41]) or hypocapnic (PaCO2 < or = 35 mm Hg [n = 18]). The mean (+/- SD) hourly episodes of apnea or hypopnea (36 +/- 25 and 20 +/- 27; P = 0.015), the prevalence of central sleep apnea (78% and 39%; P = 0.01), and the mean hourly occurrences of ventricular tachycardia (2 +/- 3 and 0.1 +/- 0.1; P = 0.003) were significantly greater in hypocapnic patients than in eucapnic patients. CONCLUSION: Data on patients with heart failure in this study are consistent with the physiologic notion that a low PaCO2 results in ventilatory instability and central apnea during sleep. The positive predictive value of a low PaCO2 for central sleep apnea is 78%. The prevalence of ventricular tachycardia was 20 times greater in hypocapnic patients than in eucapnic patients.

Different effects of omeprazole and Sch 28080 on canine cerebrospinal fluid production.

We investigated the effects of omeprazole and Sch 28080, a more specific and a more potent inhibitor of K+,H+-ATPase than omeprazole, in canine cerebrospinal fluid (CSF) production. CSF production was measured by ventriculocisternal perfusion (VCP) technique in three groups (n = 10 in each group) of anesthetized, paralyzed and mechanically ventilated dogs. Group I served as control, Sch 28080 (10(-4) mol/l of synthetic CSF) was added to VCP in group II, and omeprazole (10(-5) mol/l of synthetic CSF) was added to VCP in group III, after baseline control CSF production had been determined at 15, 30, 45, and 60 min. Comparing the three groups, the mean baseline values for CSF production did not differ significantly. However, the percent decreases in CSF production in the omeprazole treated group were 26 +/- 17 and 24 +/- 13 at 210 and 225 min, which were significantly more than the respective values in the control group. Percent decrease in CSF production in Sch 28080 was not significantly different from that in the control group. We conclude that in the canine model, physiological doses of omeprazole decrease CSF production by about 26%. However, the effect is independent of the K+,H+-ATPase activity, since Sch 28080 which is more potent than omeprazole did not significantly affect CSF production.