# Novel Mechanisms Driving Excess Atherosclerotic Cardiovascular Disease Risk in the Context of HIV: The Role of Liver Injury

> **NIH NIH K01** · BOSTON MEDICAL CENTER · 2020 · $129,573

## Abstract

Project Summary
Human immunodeficiency virus (HIV) infected (HIV+) people have up to 50% excess risk of atherosclerotic
cardiovascular disease (ASCVD, i.e. acute myocardial infarction, ischemic stroke) compared to uninfected
people. This excess ASCVD risk is not explained by traditional cardiovascular disease (CVD) risk factors (e.g.
smoking, hypertension). Liver disease is common among HIV+ people, and the liver regulates immuno-
metabolic processes associated with atherosclerosis (e.g. inflammation, dyslipidemia and microbial
translocation). Whether liver injury is in the causal pathway between HIV and incident ASCVD is unknown. The
objective of this application is to understand whether liver injury contributes to the excess risk of ASCVD
among HIV+ compared to uninfected people. The knowledge gained will be used to assess ways to improve
existing ASCVD risk prediction tools in HIV+ populations. For these objectives, we will leverage existing
NHLBI/NIAAA-funded cohorts to: 1) assess whether liver injury mediates the relationship between HIV
infection and excess ASCVD risk; 2) investigate associations between liver injury and biomarkers of a)
subclinical CVD, b) immuno-metabolism by HIV status; and 3) assess whether accounting for liver injury
improves ASCVD risk prediction in HIV. If liver injury explains some of the excess ASCVD risk observed
among HIV+ people, this would have important implications: It would reveal a novel, preventable, potentially
reversible ASCVD risk factor (liver injury) that results in worse clinical outcomes for HIV+ compared to
uninfected people. Two innovations in this study are: 1) the use of existing data from the Veteran's Aging
Cohort Study (VACS), a large (N~150,000), national sample of HIV+ and uninfected Veterans with a rich
collection of longitudinal clinical data; and 2) a causal inference strategy combining epidemiological studies of
clinical ASCVD events, mechanistic studies of subclinical atherosclerosis risk and ASCVD risk prediction. Dr.
So-Armah has a PhD in Epidemiology, experience designing and conducting biostatistical analyses, and a
strong publication and collaboration record in the field of HIV, comorbid diseases and CVD. To successfully
complete this career development award, he will pursue further didactic, experiential (clinical rotations), and
professional training. With the activities proposed in this application, he will transition to an independent
investigator, with expertise in novel potential mechanisms of CVD (e.g. liver injury), in the setting of HIV. He
will be able to combine 1) population and clinical science, 2) understanding of pathology at the molecular level,
3) causal inference epidemiology and biostatistics methods, and 4) big data analytics to answer questions of
public health importance in HIV and CVD. This inter-disciplinary K01 application is supported by a multi-
disciplinary mentorship team that has a history of successful collaboration and expertise spanning HIV,
hepato...

## Key facts

- **NIH application ID:** 9982396
- **Project number:** 5K01HL134147-05
- **Recipient organization:** BOSTON MEDICAL CENTER
- **Principal Investigator:** Kaku So-Armah
- **Activity code:** K01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $129,573
- **Award type:** 5
- **Project period:** 2016-08-01 → 2022-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9982396

## Citation

> US National Institutes of Health, RePORTER application 9982396, Novel Mechanisms Driving Excess Atherosclerotic Cardiovascular Disease Risk in the Context of HIV: The Role of Liver Injury (5K01HL134147-05). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/9982396. Licensed CC0.

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