Acute heart failure and cardiogenic shock are associated with an impaired intestinal perfusion, which may lead to a release of cytoplasmatic proteins by hypoxic epithelial injury. Intestinal fatty acid binding protein (iFABP), highly specific for the small bowel enterocyte, may pose a useful novel and very sensitive biomarker for predicting outcome of these patients.
The aim of this study was to investigate whether circulating levels of iFABP are associated with mortality in patients with acute heart failure or cardiogenic shock requiring intensive care unit (ICU) admission.
We included 90 consecutive patients with cardiogenic shock (74.4%) or severe acute heart failure (25.6%) admitted to a cardiac ICU. Blood samples were taken at day 0 and day 3. Median age was 64.7 (49.4–74.3), 76.7% of patients were male and median NT-proBNP levels were 4,986 (1,525–23,842) pg/mL. 30-day survival was 64.4%.
Patients with serum levels of iFABP at day 0 in the highest quartile (iFABP ≥ 588.4 pg/mL) had a 2.5-fold risk (P = 0.02) of dying independent of demographics, NT-proBNP levels, and vasopressor use. Extensively elevated admission levels of iFABP above the 90th percentile (iFABP ≥ 10208.4 pg/mL) were associated with an excessive mortality rate of 88.9%. In contrast, iFABP levels at day 3 were not associated with outcome.
Circulating levels of iFABP at admission predict mortality. This suggests that early inadequate perfusion of the small intestine may be associated with a dramatically decreased survival in patients with cardiogenic shock or severe acute heart failure.
*Department of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Vienna, Austria
†Ludwig Boltzmann Cluster for Cardiovascular Research, Vienna, Austria
‡3rd Medical Department, Wilhelminen Hospital, Vienna, Austria
§Core Facilities, Medical University of Vienna, Vienna, Austria
Address reprint requests to Gottfried Heinz, MD, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria. E-mail: email@example.com
Received 17 February, 2018
Revised 26 February, 2018
Accepted 22 May, 2018
This work was supported by a scientific grant by the Medical Scientific Fund of the Mayor of the City of Vienna (Grant No. 15146 to KAK), the Association for the Promotion of Research on Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB), and the Ludwig Boltzmann Cluster for Cardiovascular Research.
The authors report no conflicts of interest.