Accelerated atherosclerosis post liver transplant associated to MetALD: atherogenic dyslipidemia post-transplant as a forgotten risk marker.

Abstract

Background/Synopsis

The impact of liver transplant in the change of lipids metabolism is well known. However, primary prevention strategies are not implemented as aggressively in this population.

Objective/Purpose

To illustrate accelerated atherosclerosis post-liver transplant and a gap of care.

Methods

Case Presentation: The patient is a 65-year-old male with a history of Metabolic Dysfunction- and Alcohol-Associated Liver Disease (MetALD) status post orthotopic liver transplant one year before this presentation, came to the emergency department (ED) complaining of severe chest pain, an ECG was obtained noting ST-Elevation Myocardial Infarction (STEMI) of the inferior leads (Figure 1) and was taken emergently to the cardiac catheterization laboratory where he underwent percutaneous coronary intervention (PCI) to the right coronary artery (RCA) and also noted to have severe multivessel disease of the left system (Figure 2) which compared with his coronary angiogram a year prior represented significant accelerated atherosclerotic disease.

Results

During admission to the ED, lipid profile was obtained showing total cholesterol of 225 mg/dL, high-density lipoprotein (HDL) of 37 mg/dL, Calculated low-density lipoprotein (LDL- C): 157 mg/dL, triglycerides: 168 mg/dL, non-HDL C: 188 mg/dL, Apolipoprotein B: 122 mg/dL, Apolipoprotein A1 103 mg/dL, Lipoprotein (a): 7 nmol/L. The patient was not on any lipid-lowering therapy before this event. During his pre-transplant workup one year prior, the patient had coronary angiography, which only revealed mild nonobstructive disease in his right and left coronary system (Figure 3). Interestingly, his lipid panel concomitantly was not abnormal, as illustrated in Table 1.

The patient was discharged with a plan for possible coronary artery bypass grafting evaluation and with aggressive lipid-lowering therapy, including high-intensity statin and a PCSK9 inhibitor, in addition to his guideline-directed therapy post-myocardial infarction.

Conclusions

Atherogenic dyslipidemia post-liver transplant has been a described mechanism that contributes to the higher risk of cardiac-associated adverse events; this case of accelerated atherosclerosis in a patient with a history of MetALD-associated liver disease illustrates the need for early aggressive primary prevention strategies post-transplant that include the use of evidence-based lipid-lowering therapies.