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Published on: March 25, 2020
Cholesterol metabolism in cardiac sarcoidosis
Piia Simonen1, Jukka Lehtonen1, Helena Gylling2
1University of Helsinki and Helsinki University Central Hospital, Heart and Lung Center, Division of Cardiology, P.O. BOX 340, FI-00029 HUS, Helsinki, Finland.
Insights
Patients with cardiac sarcoidosis show increased cholesterol absorption, a potential risk factor for atherosclerosis. This heightened absorption correlates with markers of hemodynamic load, suggesting a link between cholesterol metabolism and inflammation.
Area of Science:
- Cardiology
- Metabolic Research
- Immunology
Background:
- Cardiac sarcoidosis (CS) involves myocardial inflammation.
- Atherosclerosis is common in CS patients, but its risk factors are unclear.
- Cholesterol metabolism in CS remains poorly understood.
Purpose of the Study:
- To investigate cholesterol metabolism in patients with cardiac sarcoidosis.
- To assess serum non-cholesterol sterols as biomarkers of cholesterol synthesis and absorption.
- To explore correlations between cholesterol metabolism and hemodynamic load markers.
Main Methods:
- Gas-liquid chromatography was used to analyze serum non-cholesterol sterols.
- 39 patients with verified CS were compared to 124 age-adjusted controls.
- Cholesterol synthesis and absorption markers were measured.
Main Results:
- CS patients exhibited higher cholesterol absorption efficiency compared to controls.
- CS patients showed lower cholesterol synthesis markers than controls.
- Cholesterol absorption markers correlated with plasma prohormone brain natriuretic peptide (proBNP).
Conclusions:
- The cholesterol metabolic profile in CS is characterized by high cholesterol absorption efficiency.
- This suggests a potential atherogenic risk in CS patients.
- The link between cholesterol absorption, inflammation, and hemodynamic load requires further investigation.
Background And Aims:
Patients with cardiac sarcoidosis (CS) suffer from myocardial inflammation, but atherosclerosis is not infrequent in these patients. However, the classical atherosclerotic risk factors, such as perturbed serum lipids and whole-body cholesterol metabolism, remain unravelled in CS.
Methods:
We assessed serum non-cholesterol sterols, biomarkers of whole-body cholesterol synthesis and cholesterol absorption efficiency, with gas-liquid chromatography in 39 patients with histologically verified CS and in an age-adjusted random population sample (n = 124).
Results:
CS was inactive or responding to treatment in all patients. Concentrations of serum, LDL, and HDL cholesterol and serum triglycerides were similar in CS patients and in control subjects. Cholesterol absorption markers were higher in CS patients than in controls (eg serum campesterol to cholesterol ratio in CS 246 ± 18 vs in controls 190 ± 8 10(2) x μmol/mmol of cholesterol, p = 0.001). Cholesterol synthesis markers were lower in CS patients than in controls (eg serum lathosterol to cholesterol ratio in CS 102 ± 8 vs in controls 195 ± 5 10(2) x μmol/mmol of cholesterol, p = 0.000). In CS patients, cholesterol absorption markers significantly correlated with plasma prohormone brain natriuretic peptide (proBNP), a marker of hemodynamic load.
Conclusion:
High cholesterol absorption efficiency, which is suggested to be atherogenic, characterized the metabolic profile of cholesterol in CS patients. The association between cholesterol absorption efficiency and plasma proBNP concentration, which suggests a link between inflammation, cholesterol homeostasis, and hemodynamic load, warrants further studies in order to confirm this finding and to reveal the underlying mechanisms.
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