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| Funder | NATIONAL HEART, LUNG, AND BLOOD INSTITUTE |
|---|---|
| Recipient Organization | University of Pennsylvania |
| Country | United States |
| Start Date | Aug 01, 2024 |
| End Date | Jul 31, 2029 |
| Duration | 1,825 days |
| Number of Grantees | 2 |
| Roles | Principal Investigator; Co-Investigator |
| Data Source | NIH (US) |
| Grant ID | 10981906 |
Myocardial infarction (MI) from coronary artery obstruction affects more than 1 million people annually in the United States resulting in symptoms, reduced quality of life, and substantially increased risk of heart failure and sudden death. Rapid diagnosis on electrocardiography and treatment with percutaneous intervention (PCI) are
essential to minimize the risk and size of permanent myocardial injury as well as the risks of ischemia or reperfusion triggered malignant arrhythmia. Ironically, restoration of blood flow to infarcting myocardium can result in reperfusion injury and expand infarct size. Recent data from animal studies suggest that reperfusion
injury may promote lipomatous metaplasia (LM) or intra-myocardial fat deposition. LM has been shown to associate with negative cardiac remodeling, leading to worsening heart function and higher chances for congestive heart failure. We have shown that LM is prevalent but highly variable in distribution among patients
with prior MI and ubiquitous among those presenting with ventricular tachycardia (VT). We have also shown that corridors critical to VT circuitry traverse infarcted tissue through or near LM. The latter association appears to be mediated by prolonged local action potential duration, reduced conduction velocity, as well as increased
regional resistance and reduced current loss as impulses traverse corridors adjacent to LM. In prior studies, we have also shown that reperfusion injury, the apparent precursor to LM, can be quantified by cardiac magnetic resonance (CMR) as pathologic iron deposition, and is present in most patients despite nominally successful
reperfusion. However, the association of reperfusion injury with LM incidence and progression in humans have not yet been defined. Additionally, no prospective study has evaluated the longitudinal evolution of scar, LM, and viable tissue architecture with the incidence of VT. Thus, we propose a prospective observational study of
175 patients
University of Pennsylvania
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