DECREASED FECAL BILE-ACID OUTPUT IN PATIENTS WITH CORONARY ATHEROSCLEROSIS

In most patients with atherosclerosis, the underlying metabolic derang ement remains undefined. Animal experiments have suggested that the ab ility to produce and excrete large amounts of bile acids may be an ada ptation mechanism to cholesterol overload protecting against the ather ogenic effects of cholesterol. However, there are very few data on bil e acid excretion in human atherosclerosis. In the present study, we ha ve investigated fecal bile acid secretion in subjects with and without coronary artery disease. The target group consisted of 30 patients wi th proven coronary artery disease and the control group consisted of 2 7 matched subjects without clinical or laboratory evidence of coronary atherosclerosis. Fecal bile acids were measured by gas-liquid chromat ography from 24-hr stool collections under a controlled diet. The pati ents excreted significantly less bile acids than the controls (325 +/- 135 vs. 592 +/- 223 mg/day, respectively, p < 0.0001). The difference was primarily due to a reduced excretion of secondary bile acids. Les s than 50% of deoxycholate was excreted by patients (180 +/- 81 mg/day ) as compared to controls (367 +/- 168 mg/day, p < 0.0002), while lith ocholic acid excretion was 111 +/- 62 mg/day in patients vs. 190 +/- 7 0 mg/day in controls (p < 0.005). The fecal output of the two primary bile acids, cholic and chenodeoxycholic acid, did not differ significa ntly between patients and controls. The fecal output of total bile aci ds correlated with that of both secondary bile acids in patients as we ll as in controls. These findings suggest that patients with coronary heart disease are unable to excrete adequate amounts of bile acids to rid themselves of excess cholesterol, even if they are able to maintai n a plasma cholesterol level comparable to that of healthy controls.