Published online Aug 21, 2018. doi: 10.3748/wjg.v24.i31.3547
Peer-review started: April 19, 2018
First decision: June 6, 2018
Revised: July 11, 2018
Accepted: July 16, 2018
Article in press: July 16, 2018
Published online: August 21, 2018
Processing time: 120 Days and 7.2 Hours
The risk of mortality in nonalcoholic liver cirrhosis (LC) patients with coronary artery disease (CAD) is unclear. Previous case-control studies demonstrated conflicting results potentially due to the different etiologies of LC. LC patients with alcoholic and nonalcoholic fatty liver disease-related metabolic disorders exhibit an increased risk of CAD. In contrast, hemostatic defects that occur in LC, such as thrombocytopenia, coagulopathy, and low blood pressure, are not considered as potential protective factors of cirrhosis against atherosclerotic events.
The results of CAD risk in LC patients are controversial. In contrast to the present study, previous works using alcoholic LC-based cohorts may have been confounded by the increased risk of metabolic syndrome in heavy drinkers. To the best of our knowledge, the risk of CAD in nonalcoholic cirrhotic patients is not well established.
The aim of the study was to elucidate the prevalence and risk of mortality in nonalcoholic cirrhotic patients. The comorbidities and LC-related complications were also important prognostic factors among cirrhotic patients. The result of this study can provide a better understanding of CAD risk in LC patients.
We collected 10142 LC patients diagnosed from 2004 to 2011 using the Taiwanese National Health Insurance research database. After exclusion of subjects who were treated before the end of 2005, had alcoholic or biliary cirrhosis, had LC occurring after CAD, and were younger than 40 years old, a total of 3409 LC patients were enrolled in the study. The comorbidities and complications of LC were collected. The first-time diagnosis of CAD was identified as the primary end point, and the death of the subject served as the secondary end point. All-cause mortality was analyzed in both the study and control cohorts. A Cox proportional hazards model was developed to calculate the overall mortality hazard ratios of all comorbidities and complications in cirrhotic patients. The six-year cumulative survival and survival curve were calculated using the Cox regression method and the Kaplan-Meier method.
CAD was less prevalent in nonalcoholic LC patients than in controls. Nonalcoholic LC patients with CAD were associated with a reduced risk of mortality. The six-year survival rates were increased in patients with CAD compared to patients without CAD in the nonalcoholic LC cohort. As this is a retrospective cohort study, further prospective studies are needed to confirm this finding.
In this study, we demonstrate that CAD is less prevalent and associated with a reduced risk for mortality in nonalcoholic LC patients. This result confirms previous studies regarding the lower risk for atherosclerotic events (i.e. ischemic stroke and coronary artery disease) in alcohol-related and nonalcohol-related LC cohorts. Although viral hepatitis can cause endothelial dysfunction, which correlates with atherosclerotic disease progression, we propose that LC has a more powerful protective effect against atherosclerotic events based on the favorable cardiovascular risk profiles, such as thrombocytopenia, coagulopathy, and low blood pressure. The strengths of the study include the large sample size cohort and risk adjustments for comorbidities and complications. Finally, we conclude that nonalcoholic LC patients with CAD exhibit a favorable outcome.
Future prospective research should focus on the advantages and disadvantages of antiplatelet therapy in the prevention of CAD in nonalcoholic LC patients. Additionally, it is advised that future studies should compare alcoholic and nonalcoholic LC cohorts and evaluate the effect of viral treatment.