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Myocardial perfusion reserve in patients with chronic hepatitis C before and after direct-acting antiviral
Christina Sølund1, Philip Hasbak2, Andreas Knudsen1
1Department of Infectious Diseases, Copenhagen University Hospital, Hvidovre, Denmark.
Insights
Curing chronic hepatitis C with direct-acting antivirals did not improve coronary microvascular function or reduce cardiovascular risk markers in this pilot study. Further research is needed to explore long-term effects.
Area of Science:
- Cardiology
- Hepatology
- Nuclear Medicine
Background:
- Patients with chronic hepatitis C (CHC) face elevated risks of atherosclerotic cardiovascular disease.
- Inflammation and endothelial dysfunction from CHC infection are potential contributors to this risk.
- Direct-acting antiviral (DAA) therapies offer a cure for CHC, but their impact on cardiovascular health requires investigation.
Purpose of the Study:
- To evaluate myocardial perfusion reserve (MPR) using Rubidium-82 (82Rb) positron emission tomography (PET)/computed tomography (CT) before and after DAA treatment in CHC patients.
- To compare MPR with systemic inflammation and endothelial dysfunction biomarkers post-treatment.
- To assess the effect of viral clearance on cardiovascular risk markers.
Main Methods:
- A prospective pilot study involving 10 CHC patients undergoing 8 or 12 weeks of DAA treatment.
- Cardiac 82Rb PET/CT scans were performed at baseline and 12–24 weeks post-treatment to measure MPR.
- Markers of endothelial dysfunction and inflammation were measured at baseline and 12 weeks after DAA treatment.
Main Results:
- All 10 patients achieved viral cure.
- No significant improvement in MPR was observed after DAA treatment (median 3.1 pre-treatment vs. 2.9 post-treatment, p=0.63).
- DAA treatment cure did not significantly decrease markers of endothelial dysfunction or systemic inflammation within the study timeframe.
Conclusions:
- Viral clearance achieved through DAA treatment did not significantly improve coronary microvascular function or reduce soluble cardiovascular risk markers in the short term.
- MPR was within the normal range before treatment.
- Further studies with larger sample sizes and longer follow-up are necessary to determine the long-term effects of viral clearance on coronary microvascular function and endothelial dysfunction in CHC patients.
Introduction:
Patients with chronic hepatitis C (CHC) have an increased risk of atherosclerotic cardiovascular disease which may be due to inflammation and endothelial dysfunction caused by the chronic infection. In this prospective pilot study, we assessed, for the first time among patients with CHC the myocardial perfusion reserve (MPR) by Rubidium-82 (82 Rb) positron emission tomography (PET)/computed tomography (CT) before and after direct-acting antiviral (DAA) treatment and compared them with biomarkers of systemic inflammation and endothelial dysfunction.
Methods:
We included 10 patients with CHC who received 8 or 12 weeks of DAA treatment. To obtain the MPR, a cardiac 82 Rb PET/CT scan at rest and adenosine-induced stress was performed at baseline and between 12 and 24 weeks post DAA treatment. Additionally, markers of endothelial dysfunction and inflammation were measured at baseline and 12 weeks after DAA treatment.
Results:
All 10 patients achieved cure and the median age was 50 (range: 40-62 years). The median MPR before treatment was 3.1 (range: 2.3-4.8) compared to 2.9 (range: 2.2-4.1) after DAA treatment p = 0.63. Also, cure after DAA treatment was not associated with an overall significant decrease in markers of endothelial dysfunction and inflammation.
Discussion:
Cure after DAA treatment in patients with CHC did not improve coronary microvascular function nor did it lead to a decrease in soluble markers of cardiovascular risk in the given time frame where the patients were followed. It should be noted, that MPR before DAA treatment was in the normal range. Considering the small sample size and short follow-up time, further studies are warranted to determine if viral clearance has an effect on coronary microvascular function and endothelial dysfunction.
