# Integrated proteomic and metabolomics analysis of thrombotic myocardial infarction

> **NIH NIH SC1** · NEW MEXICO STATE UNIVERSITY LAS CRUCES · 2022 · $222,000

## Abstract

Project Summary / Abstract:
Acute myocardial infarction (MI) is defined as myocardial ischemia, the inadequate supply of blood to heart
muscle, followed by myocardial cell death. Multiple causes of acute MI are widely recognized and can be
categorized as thrombotic, non-thrombotic, and acute MI secondary to coronary procedures. The mechanistic
cause of a thrombotic MI is the rupture or erosion of an atherosclerotic plaque that results in the formation of a
thrombus, or blood clot, which occludes the flow of blood. In contrast, non-thrombotic MI occurs secondary to
mechanisms which create an oxygen supply and demand imbalance, but are not associated with atherosclerotic
plaque rupture or disruption. Given that myocardial cell death is the pathological characteristic that is common
to all acute MI, non-invasive diagnostics for acute MI are based on the detection of myocardial cell death.
Currently non-invasive diagnostics for differentiating thrombotic MI from non-thrombotic MI do not exist which
results in sub-optimal treatment and diminished patient safety. Further, it is not known how the impacts on
metabolism and biological processes differ between thrombotic and non-thrombotic MI. In this project, we will
address both of these problems. We will develop a diagnostic method for the non-invasive differentiation of
thrombotic MI versus non-thrombotic MI that will enable earlier, safer, and more precise targeting of therapeutics
to patients suffering from acute MI. We will determine biological processes that differ between thrombotic and
non-thrombotic MI, which will suggest targets for therapeutic intervention that are specific to the underlying cause
of an acute MI. In Aim 1 we will utilize high resolution mass spectrometry to determine the absolute concentration
of over 500 proteins in previously collected plasma samples from human subjects who were experiencing an
acute MI for which the cause (thrombotic versus non-thrombotic) was determined. This will enable us to
determine which proteins report on the cause of the acute MI as opposed to the presence of myocardial cell
death. A critical advantage of our study design is that we have repeated measures from the same human
subjects: at the time of presentation, 6 hours post-presentation, and at a stable event-free follow-up timepoint 3
months after the acute MI. In Aim 2 we will integrate this data with our existing data on the abundances of
metabolites and lipids generated from the same human subject samples. This integrated data will facilitate an
in-depth analysis of the differences between thrombotic and non-thrombotic MI in the activities of metabolic
pathways, receptor-ligand binding events, and other biochemical reactions. Further we will conduct data-
dependent systems biology analyses that will highlight proteins, metabolites, and lipids that are co-abundant in
plasma and will evaluate how the topology of these related entities differs between thrombotic and non-
thrombotic MI. In Aim 3 w...

## Key facts

- **NIH application ID:** 10337207
- **Project number:** 5SC1GM139730-02
- **Recipient organization:** NEW MEXICO STATE UNIVERSITY LAS CRUCES
- **Principal Investigator:** Patrick J Trainor
- **Activity code:** SC1 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $222,000
- **Award type:** 5
- **Project period:** 2021-02-01 → 2025-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10337207

## Citation

> US National Institutes of Health, RePORTER application 10337207, Integrated proteomic and metabolomics analysis of thrombotic myocardial infarction (5SC1GM139730-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10337207. Licensed CC0.

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