Disturbances in pulmonary gaseous exchange in primary hyperlipoproteinemias.

Carbon monoxide diffusion (DLCO), blood gas analysis at rest and after exercise, distribution of ventilation and perfusion by Xenon 133 were carried out in 43 hyperlipidemic patients, Fredrickson's types I, IIA, IIB, and IV. DLCO was significantly reduced in hypertriglyceridemic and to a lesser degree in hypercholesterolemic patients. A significant negative correlation was found between DLCO and triglyceride values. Significantly lower basal PaO2 values, which improved after exercise, were observed in both type IIA and type IV hyperlipemic patients. The ventilation/perfusion ratio distribution (V/Q) did not increase from the basal to the apical segments of the lungs in hyperlipidemic patients as it did in normals. The hypothesis of an alteration in pulmonary surface-active lipoprotein, directly related to hyperlipoproteinemia or indirectly caused by fat microembolism, may explain the reduced DLCO, the loss of V/Q gradient, and the decrease in PaO2 (which improves after exercise) observed in hyperlipemic patients. Disturbances in pulmonary gas exchange and PaO2 reduction could play an important role in the pathogenesis of both angina pain due to ischaemic heart disease, which is frequently observed in hyperlipemic patients, and the postprandial angina syndrome.