Rapid Fire Abstracts
Xingmin Guan, PhD
Postdoctorral Fellow
Indiana University
Xingmin Guan, PhD
Postdoctorral Fellow
Indiana University
Xinheng Zhang, MSc
Graduate Researcher
University of California, Los Angeles
Yinyin Chen, MD
Attending Radiologist
Zhongshan Hospital, Fudan University and Shanghai Institute of Medical Imaging, Shanghai, China, China (People's Republic)
Keyur P. Vora, MD, MS, FACC
Cardiologist, Assistant Professor of Medicine
Indiana University School of Medicine
Diego Hernando, PhD
University of Wisconsin
Scott Reeder, MD, PhD
University of Wisconsin-Madison
Rohan Dharmakumar, PhD
Executive Director
Indiana University School of Medicine
Rohan Dharmakumar, PhD
Executive Director
Indiana University School of Medicine
Among reperfused ST-elevation myocardial infarction (MI) patients, those who develop intramyocardial hemorrhage (IMH) following reperfusion carry the highest risk for major adverse cardiovascular events (MACE). In addition, clinical studies have demonstrated that MIs which become fatty contribute to fatal arrhythmias and poor left ventricular function. Preclinical studies are starting to yield pathophysiological insight into how IMH promotes fatty remodeling but whether these observations are germane to hemorrhagic MI patients is not clear. Specifically, whether IMH promotes fatty remodeling of MI zones of hemorrhagic MI patients has not been invested. We investigated whether hemorrhagic MI patients are at greater risk for fatty remodeling of MI zones than non-hemorrhagic patients at 6 months follow up.
Methods:
We investigated the temporal evolution of fat deposition and its relation to iron within MI using serial CMR in revascularized STEMI patients (n=32) with and without IMH. All patients underwent CMR at 7 days and at 6 months, post reperfusion. Among patients with diagnostic T2* images (n=26), 18 patients were positive for IMH (IMH+) and 8 were negative for IMH (IMH-). Confounder-corrected R2* (=1/T2*) and Proton Density Fat Fraction (PDFF) maps from multi-Gradient Echo (mGRE) acquisitions were computed. Late Gadolinium Enhancement (LGE) CMR were used to identify MI and remote zones.
Results:
Example R2* and PDFF maps from IMH+ and IMH- patients from the 7-day and 6-month CMR are shown (Figure 1). Figure 2 shows the aggregate data across all patients over 6 months post MI. Our findings show that reperfused hemorrhagic MI patients indeed demonstrate an elevation of iron as well as fat within the MI zone compared to those without IMH at 6-month follow up.
Conclusion:
Hemorrhagic STEMI patients are prone to both iron deposition and fat infiltration at 6-months post MI. Our findings suggest that fatty remodeling of MI is rooted in the development of intramyocardial hemorrhage. Hence, novel therapies that can reduce iron within hemorrhagic MI zones may have the potential to mitigate fatty remodeling of MI zones and reduce MACE in revascularized STEMI patients.