Abstract
Acute myocardial infarction (AMI) is currently further diagnosed as being a type 1 (T1), caused by coronary artery atherosclerosis with thrombosis or a type 2 (T2), resulting from cardiac oxygen supply and demand imbalance. It is hypothesized that patients with T2 might develop earlier and increased cardiac wall stressing before the development of AMI as compared to those with T1, resulting in higher N- terminal pro B-type natriuretic peptide (NT-proBNP)/high sensitivity cardiac troponin T (hs-cTnT) ratios.
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