Relationship between non-invasively detected liver fibrosis and in-hospital outcomes in patients with acute coronary syndrome undergoing PCI

Abstract

Background Patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI) still experience a high rate of in-hospital complications. Liver fibrosis (LF) is a risk factor for mortality in the general population. We investigated whether the presence of LF detected by the validated fibrosis 4 (FIB-4) score may indicate ACS patients at higher risk of poor outcome. Methods In the prospective ongoing REAl-world observationaL rEgistry of Acute Coronary Syndrome (REALE-ACS), LF was defined by a FIB-4 score > 3.25. We repeated the analysis using an APRI score > 0.7. The primary endpoint was in-hospital adverse events (AEs) including a composite of in-hospital cardiogenic shock, PEA/asystole, acute pulmonary edema and death. Results A total of 469 consecutive ACS consecutive patients were enrolled. Overall, 21.1% of patients had a FIB-4 score > 3.25. Patients with LF were older, less frequently on P2Y12 inhibitors (p = 0.021) and admitted with higher serum levels of white blood cells (p < 0.001), neutrophils to lymphocytes ratio (p < 0.001), C-reactive protein (p = 0.013), hs-TnT (p < 0.001), creatine-kinase MB (p < 0.001), D-Dimer levels (p < 0.001). STEMI presentation and higher Killip class/GRACE score were more common in the LF group (p < 0.001). 71 patients experienced 110 AEs. At the multivariate analysis including clinical and laboratory risk factors, FIB-4 > 3.25 (OR 3.1, 95%CI 1.4–6.9), admission left ventricular ejection fraction% below median (OR 9.2, 95%CI 3.9–21.7) and Killip class ≥ II (OR 6.3, 95%CI 2.2–18.4) were the strongest independent predictors of in-hospital AEs. Similar results were obtained using the APRI score. Conclusion LF detected by FIB-4 score > 3.25 was associated with more severe ACS presentation and worse in-hospital AEs irrespective of clinical and laboratory variables. Graphical abstract

Hepatic steatosis and advanced hepatic fibrosis are independent predictors of long‐term mortality in acute myocardial infarction

“…In addition, the increased prevalence of NSTEMI in individuals with hepatic steatosis and STEMI in those with advanced fibrosis appears to be consistent with previous studies 54,55 . A growing body of evidence has shown that gut‐derived lipopolysaccharides found in advanced liver disease 56,57 are also seen in atherosclerotic plaque that may potentially result in plaque vulnerability and plaque rupture 58,59 .…”

“…58,59 One may postulate that the higher metabolic burden of hepatic steatosis is associated with accelerated coronary artery narrowing and its resultant increased NSTEMI risk; however, the lipopolysaccharide hypothesis, associated with advanced liver disease, may further modify vulnerable coronary plaque characteristics and eventual plaque rupture that lead to acute coronary artery occlusion and STEMI risk. 54 Importantly, this association deserves deeper investigations with further mechanistic studies. Similar to most metabolic diseases, clinicians need to be cognizant that the impact of fatty liver on CVD is a continuum that should not be limited to the binary categorization of hepatic steatosis.…”

“…This is in line with other studies that portray the increasingly adverse metabolic burden as associated with increasing severity of fatty liver disease, 17 including an increased incidence of hypertension, 46 diabetes, 47,48 appears to be consistent with previous studies. 54,55 A growing body of evidence has shown that gut-derived lipopolysaccharides found in advanced liver disease 56,57 are also seen in atherosclerotic plaque that may potentially result in plaque vulnerability and plaque rupture. 58,59 One may postulate that the higher metabolic burden of hepatic steatosis is associated with accelerated coronary artery narrowing and its resultant increased NSTEMI risk; however, the lipopolysaccharide hypothesis, associated with advanced liver disease, may further modify vulnerable coronary plaque characteristics and eventual plaque rupture that lead to acute coronary artery occlusion and STEMI risk.…”

“…A growing body of evidence has shown that gut‐derived lipopolysaccharides found in advanced liver disease 56,57 are also seen in atherosclerotic plaque that may potentially result in plaque vulnerability and plaque rupture 58,59 . One may postulate that the higher metabolic burden of hepatic steatosis is associated with accelerated coronary artery narrowing and its resultant increased NSTEMI risk; however, the lipopolysaccharide hypothesis, associated with advanced liver disease, may further modify vulnerable coronary plaque characteristics and eventual plaque rupture that lead to acute coronary artery occlusion and STEMI risk 54 . Importantly, this association deserves deeper investigations with further mechanistic studies.…”

De Ritis ratio and long‐term major cardiovascular adverse events in patients undergoing elective percutaneous coronary intervention

“…First , although patients with known advanced liver disease (cirrhosis) were excluded, an elevated De Ritis ratio still may be a marker of liver disease and fibrosis 30 . Liver fibrosis detected by FIB‐4 score was associated with more severe presentation of acute coronary syndromes and a worse clinical outcome regardless of other clinical or laboratory variables 31 and a higher risk of cardiovascular events including cardiovascular mortality and all‐cause mortality in patients with cardiovascular disease 32 . Second , previous studies, 15,27 and current analysis showed that an elevated De Ritis ratio was associated with a number of cardiovascular risk factors.…”