Cardiovascular variability characteristics in obstructive sleep apnea

Patients with obstructive sleep apnea (OSA) are at increased risk for cardiovascular disease. Altered cardiovascular variability is a prognostic indicator for cardiovascular events. This review examines the evidence that OSA is accompanied by alterations in cardiovascular variability. This alteration is evident even in the absence of hypertension, heart failure or other disease states, and may be linked to the severity of OSA. The presence of clear-cut abnormalities in time and frequency-domain measures of blood-pressure and heart-rate variability in normotensive OSA patients provides intriguing evidence for the concept of an etiologic interaction between sleep apnea and cardiovascular disease. Mechanisms that could contribute to altered cardiovascular variability in patients with sleep apnea include abnormalities in chemoreflex, baroreflex and endothelial function.     

Purines, lactate and phosphate release from child and adult heart during cardioplegic arrest

The release of lactate, phosphate and purine catabolites from the heart in adult and children undergoing cardiac surgery was recorded. The compounds were determined in the coronary effluent collected during subsequent infusions of cardioplegic solution into the coronary root. As compared to the infusion just after onset of ischemia, both in adults and children manifold increase of the release was observed during subsequent infusions. The rates of release of lactate, phosphate and purines (adenosine + inosine + hypoxanthine) were 1.5 to 2.5 times higher in children than in adult hearts during the second cardioplegic infusion and 3 to 7 times higher during the third cardioplegic infusion in spite of a more frequent infusion of cardioplegic solution in children. A much greater increase of the release of lactate, phosphate and purines provides evidence for more severe metabolic injury during cardioplegic arrest to the heart in children than in adults.