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Published on: August 9, 2024
Diminished bile acids excretion is a risk factor for coronary artery disease: 20-year follow up and long-term outcome
Gideon Charach1, Ori Argov2, Karyn Geiger2
1Department of Internal Medicine 'C', Tel Aviv Sourasky Medical Center, Affiliated to Tel Aviv University, Sackler Medical School, 6 Weizman Street, Tel Aviv 6423906, Israel.
Insights
Patients with coronary artery disease (CAD) showed significantly lower bile acid excretion (BAE). Impaired BAE is linked to increased CAD mortality, suggesting it
Area of Science:
- Cardiovascular Medicine
- Metabolic Disorders
- Gastroenterology
Background:
- Coronary artery disease (CAD) patients exhibit reduced bile acid excretion (BAE) compared to controls.
- This suggests a potential link between impaired BAE and the development of coronary atherosclerosis.
Purpose of the Study:
- To investigate the long-term role of BAE in CAD development.
- To assess the association between BAE and mortality in CAD patients.
Main Methods:
- A cohort of 50 CAD patients and 50 controls (chest pain, no CAD) were studied.
- Subjects consumed a standard diet with ~500 mg cholesterol for 4 days.
- Fecal bile acids were quantified using gas liquid chromatography from 24-hour stool collections.
Main Results:
- CAD patients demonstrated significantly lower total bile acid excretion (p < 0.001).
- Reduced excretion of deoxycholic acid (p < 0.0001) and lithocholic acid (p < 0.01) was observed in CAD patients.
- BAE emerged as the strongest independent laboratory predictor of CAD (p < 0.05).
- Controls experienced significantly lower mortality and CAD development rates over 20 years.
Conclusions:
- CAD patients exhibit markedly decreased BAE levels compared to non-CAD controls.
- BAE below 415 mg/day was associated with increased long-term CAD mortality.
- Impaired cholesterol excretion via BAE may represent an independent risk factor for CAD development.
Background:
Patients with coronary artery disease (CAD) had significantly lower bile acid excretion (BAE) compared with non-CAD patients, leading to the hypothesis that the inability to efficiently excrete bile acids leads to coronary atherosclerosis development. We investigated the long-term role of BAE in CAD development and related mortality in 50 patients with proven CAD compared with that of 50 patients with chest pain and no CAD (controls) matched for clinical and laboratory characteristics.
Methods:
All subjects received a 4-day standard diet that included ~500 mg of cholesterol. Fecal bile acids from 24-h stool collections were measured by gas liquid chromatography.
Results:
CAD patients excreted lower amounts of total bile acids than controls (p < 0.001), less deoxycholic acid (p < 0.0001) and less lithocholic acid (p < 0.01). BAE was the best significant independent laboratory factor that predicted CAD (p < 0.05). Mortality and CAD development rates were significantly lower for the controls at the 20-year follow up.
Conclusions:
These results showed that CAD patients had markedly decreased BAE levels compared with non-CAD controls. BAE <415 mg/day was associated with increased CAD long-term mortality. Impaired ability to excrete cholesterol might be considered an additional independent risk factor for CAD development.
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