Type 2 myocardial infarction (MI) is defined as myocardial necrosis that results from an imbalance of myocardial oxygen supply and demand. Although type 2 MI is highly prevalent in patients with critical illness and strongly associated with mortality, the pathophysiology remains poorly understood. Inflammation is central to the development of atherosclerosis, plaque rupture, and other subtypes of MI, but the role of inflammation in type 2 MI and myocardial necrosis has not been defined. The investigators aim to to delineate the mechanistic role of inflammation in myocardial necrosis and type 2 MI complicating critical medical illness.
Study Type
OBSERVATIONAL
Bellevue Hospital Center
New York, New York, United States
Leukocyte-platelet aggregates
Time frame: Day 1
Leukocyte-platelet aggregates
Participants will be followed for the duration of hospital stay, an expected average of 10 days.
Time frame: Day 10
Monocyte-platelet aggregates
Time frame: Day 1
Monocyte-platelet aggregates
Participants will be followed for the duration of hospital stay, an expected average of 10 days.
Time frame: Day 10
Neutrophil-platelet aggregates
Time frame: Day 1
Neutrophil-platelet aggregates
Participants will be followed for the duration of hospital stay, an expected average of 10 days.
Time frame: Day 10
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