CAD: Acute Coronary Syndromes
Ting Liu, PhD
professor
The First Hospital of China Medical University, China (People's Republic)
Ting Liu, PhD
professor
The First Hospital of China Medical University, China (People's Republic)
Andrew G. Howarth, MD, PhD
Clinical Co-director
Libin Cardiovascular Institute of Alberta, University of Calgary
Calgary, Alberta, Canada
Yinyin Chen, MD
Attending Radiologist
Zhongshan Hospital, Fudan University and Shanghai Institute of Medical Imaging, Shanghai, China
LOS ANGELES, California, China (People's Republic)
Hsin-Jung Yang, PhD
Assistant Professor
Cedars-Sinai Medical Center
Los Angeles, California, United States
Richard LQ. Tang, MD
Faculty
Indiana University School of Medicine, California, United States
Damini Dey, PhD
doctor
Cedars-Sinai Medical Center, Los Angeles, California, USA, California, United States
Piotr J. Slomka, PhD
Director of Innovation in Imaging, Professor of Medicine and Cardiology
Cedars-Sinai
Los Angeles, California, United States
John C. Wood, MD, PhD
Professor
Children's Hospital Los Angeles
Los Angeles, California, United States
Daniel S. Berman, MD
doctor
Cedars-Sinai Medical Center, Los Angeles, California, USA, United States
Andreas Kumar, MD
doctor
Northern Ontario School of Medicine, Sudbury,Ontario, Canada
Sudbury, Ontario, Canada
Rohan Dharmakumar, PhD
Professor of Medicine, Radiology & Imaging Sciences, Anatomy, Cell Biology & Physiology
Krannert Cardiovascular Research Center, Indiana University School of Medicine
Indianapolis, Indiana, United States
We studied cardiac troponin kinetics (cTn) of ST-segment elevation MI patients (n = 70) classified by cardiovascular magnetic resonance to be hemorrhagic (70%) or nonhemorrhagic following primary percutaneous coronary intervention. To isolate the effects of hemorrhage from ischemic burden, we performed controlled canine studies (n = 25), and serially followed both cTn and MI size with time-lapse imaging.
Results: CTn was not different before reperfusion; however, an increase in cTn following primary percutaneous coronary intervention peaked earlier (12 hours vs 24 hours; P < 0.05) and was significantly higher in patients with hemorrhage (P < 0.01). In hemorrhagic animals, reperfusion led to rapid expansion of myocardial necrosis culminating in epicardial involvement, which was not present in nonhemorrhagic cases (P < 0.001). MI size and salvage were not different at 1 hour postreperfusion in animals with and without hemorrhage (P = 0.65). However, within 72 hours of reperfusion, a 4-fold greater loss in salvageable myocardium was evident in hemorrhagic MIs (P < 0.001). This paralleled observations in patients with larger MIs occurring in hemorrhagic cases (P < 0.01).
Conclusion:
Myocardial hemorrhage is a determinant of MI size. It drives MI expansion after reperfusion and compromises myocardial salvage. This introduces a clinical role of hemorrhage in acute care management, risk assessment, and future therapeutics.