[Sleep apnea syndrome and heart failure].

More than half of all patients with stable heart failure are affected by sleep apnea syndrome. The mechanism of apnea may be either obstructive, by collapse of the upper airways, or central with nocturnal Cheyne-Stokes respiration. Changes in intrathoracic pressure, awakening and hypoxemia all lead to an increase in left ventricular afterload and to sympathetic activation, which can aggravate heart failure and prognosis.

Different effects of ambulatory blood pressure monitoring on subjective and objective sleep quality.

Objective: To determine whether ambulatory blood pressure monitoring affects objective and subjective sleep quality in patients tested at home.

Methods: Seventy consecutive patients (40 women and 30 men, aged 53+/-15 years), having ambulatory blood pressure monitoring to monitor the efficacy of antihypertensive treatment or to distinguish between hypertension or white-coat hypertension had an evaluation of their sleep quality on a first night with ambulatory blood pressure monitoring and the three following nights without ambulatory blood pressure monitoring. Ambulatory blood pressure monitoring was performed with an auscultatory device with a measure every 15 min during 24 h.

[Sleep apnoea syndrome and cardiac failure].

Despite recent therapeutic advances, chronic cardiac failure is still associated with a significant morbidity and mortality. Sleep apnoea syndrome is common in this population, affecting almost half of these patients. However, it is rarely diagnosed and treated.

N-acetylcysteine treatment normalizes serum tumor necrosis factor-alpha level and hinders the progression of cardiac injury in hypertensive rats.

Background: Studies in isolated cardiomyocytes showed that replenishment in cellular glutathione, achieved with the glutathione precursor N-acetylcysteine (NAC), abrogated deleterious effects of tumor necrosis factor-alpha (TNF-alpha).

Methods And Results: We examined the ability of NAC to limit the progression of cardiac injury in the rat model of hypertension, induced by the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) (50 mg/kg per day SC) and high-salt diet (HS) (8% NaCl). Four-week HS/L-NAME administration induced hypertension (193+/-8 versus 122+/-4 mm Hg for low-salt diet [LS] group) and left ventricular (LV) dysfunction, revealed by echocardiography and characterized by decreased LV shortening fraction (38+/-2% versus 49+/-4% for LS group; P<0.