Cardiac MRI Identifies Heart Disease Risk in Individuals with Hepatitis C Regardless of Myocardial Damage Markers or Fibrosis Stage  - European Medical Journal

Cardiac MRI Identifies Heart Disease Risk in Individuals with Hepatitis C Regardless of Myocardial Damage Markers or Fibrosis Stage 

Authors:
*Aaron D'Amore,1,2 Arlene Sirajuddin,3 Nivya George,2 Ahmed Gharib,3 Poonam Mathur2
  • 1. Harvard Affiliated Emergency Medicine Residency, Mass General Brigham, Boston, Massachusetts, USA
  • 2. Institute of Human Virology, University of Maryland School of Medicine, Baltimore, Maryland, USA 
  • 3. National Institutes of Health (NIH), Bethesda, Maryland, USA
*Correspondence to [email protected]
Disclosure:

D’Amore disclosed provision of a PRISM grant to their institution to fund this project. Mathur disclosed payment from the Merck Investigator Studies Program to their institution and hepatitis C medications for this abstract review. Sirajuddin, George, and Gharib have declared no conflicts of interest.

Citation:
Microbiol Infect Dis AMJ. ;2[1]:59-61. https://doi.org/10.33590/microbiolinfectdisam/FHYN5850.
Keywords:
Cardiac magnetic resonance (CMR), extracellular volume (ECV), hepatitis C, MRI.

Each article is made available under the terms of the Creative Commons Attribution-Non Commercial 4.0 License.

BACKGROUND

Infection with hepatitis C virus (HCV) increases the risk of extrahepatic manifestations, including cardiovascular disease (CVD).1 Cardiac magnetic resonance (CMR) remains the gold standard test for non-invasive structural and functional assessment of the heart, and can be used to detect CVD. Using CMR, the authors sought to determine the CVD risk in patients with HCV prior to therapy.2

METHODS

Individuals with chronic HCV infection were prospectively enrolled in the CHROME study (NCT03823911).3 A subset of 10 individuals infected with HCV were enrolled in the MRI sub-study from March–September 2019.  HCV antibody assays, HCV RNA levels, liver fibrosis scores, and markers of inflammation and myocardial damage were obtained.

CMR was performed prior to the initiation of direct-acting antiviral treatment. Extracellular volume (ECV) fraction was calculated using the equation: ECV=100% x (1-hematocrit) x [(1/T1myocardium post-contrast) – (1/T1myocardium pre-contrast)]/[(1/T1blood post-contrast) – (1/T1 blood pre-contrast)]. An ECV fraction >30% was considered abnormally increased. Ten age-matched, HCV-negative volunteers were included in the analysis so that T-test was used to compare ECV fraction in both groups.

RESULTS

Demographics are shown in Table 1. CMR showed that 8/10 individuals infected with HCV had an abnormal ECV fraction (>30%;4 average=0.30; range 29–38%). When compared with age-matched healthy volunteers, ECV fraction in the individuals infected with HCV was significantly increased (0.30±0.03 versus 0.26±0.03; p=0.0036; Figure 1). Three of the 10 individuals infected with HCV had non-ischemic patterns of gadolinium enhancement on the late gadolinium enhancement images (Figure 2). For individuals infected with HCV, markers of inflammation and myocardial damage were within laboratory reference ranges for all subjects in the CMR cohort, and ECV fraction was elevated regardless of myocardial damage markers or liver fibrosis stage.

Table 1: Baseline demographic features of hepatitis C virus cardiac magnetic resonance cohort.
IQR: interquartile range.

Figure 1: Extracellular volume of individuals infected with hepatitis C virus and healthy volunteers.

Figure 2: Inflammatory changes seen on cardiac magnetic resonance in patient with hepatitis C.
A) Short axis late gadolinium enhancement image shows a midwall pattern of enhancement within the basal septal wall (arrow), compatible with an area of midwall fibrosis. B) Native T1 map, and C) Post-contrast T1 mapshow a corresponding area of abnormal T1 measurements within the basal septum (arrows).

CONCLUSIONS

The findings suggest that myocardial changes secondary to HCV infection can occur without measurable changes in inflammatory or myocardial biomarkers, and that ECV fraction via CMR may be a sensitive screening tool to detect these changes. This has important implications for the necessity of early HCV treatment, since cardiovascular changes can precede the development of advanced liver fibrosis in individuals infected with HCV.

References
Revuelto Artigas T et al. Antiviral treatment does not improve subclinical atheromatosis in patients with chronic hepatitis caused by hepatitis C virus. Gastroenterol Hepatol. 2019;42(6):362-71. Kramer CM. Role of cardiac MR imaging in cardiomyopathies. J Nucl Med. 2015;56(Suppl 4):39S-45S. University of Maryland, Baltimore. Cardiovascular Disease in HIV and hepatitis C: risk outcomes after hepatitis C eradication (CHROME). NCT03823911. https://www.clinicaltrials.gov/study/NCT03823911?term=NCT03823911&rank=1. Marques MD et al. Myocardial fibrosis by T1 mapping magnetic resonance imaging predicts incident cardiovascular events and all-cause mortality: the Multi-Ethnic Study of Atherosclerosis. Eur Heart J Cardiovasc Imaging. 2022;23(10):1407-16.

Rate this content's potential impact on patient outcomes

Average rating / 5. Vote count:

No votes so far! Be the first to rate this content.