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The quantification of infarct size

Raymond J. Gibbons, MD^*,*, Uma S. Valeti, MD^*, Philip A. Araoz, MD and Allan S. Jaffe, MD^*

^* Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota
Department of Radiology, Mayo Clinic and Foundation, Rochester, Minnesota

View larger version (19K): [in a new window]   Figure 1 Relationship between commutative release of hydroxybutyrate dehydrogenase (HBDH) during the course of 120 h and ejection fraction in 54 patients. Although there was a highly significant correlation, there is considerable scatter in data with a wide range of enzyme release for ejection fraction between 50% and 55% and a wide range in ejection fraction for cumulative enzyme release of between 1,500 and 2,000. Reprinted, with permission, from Dissman et al. (17).

View larger version (31K): [in a new window]   Figure 2 Association between single troponin T (TnT) measurement at 72 h and peak creatine kinase (CK) with estimated thallium infarct size in non-reperfused (A) and reperfused (B) patients. Reprinted, with permission, from Licka et al. (23).

View larger version (13K): [in a new window]   Figure 3 Relationship between the perfusion defect measured by single-photon emission computed tomography and the amount of scarring measured by pathology in human hearts explanted at the time of cardiac transplantation. Reprinted, with permission, from Medrano et al. (32).

View larger version (14K): [in a new window]   Figure 4 Six-month mortality in 1,122 patients in the Collaborative Organization for RheothRX Evaluation (CORE)trial, according to the single-photon emission computed tomography infarct size measured at discharge. The groupings of infarct size were chosen on the basis of previous studies. LV = left ventricle. Modified from Burns et al. (39).

View larger version (14K): [in a new window]   Figure 5 Infarct size and myocardial salvage measured by single-photon emission computed tomography sestamibi imaging in patients treated with tissue plasminogen activator (tPA) and patients treated with stenting and a glycoprotein IIb/IIIa inhibitor. The stent group had a smaller infarct size and greater myocardial salvage. LV = left ventricle. Based on data from Schomig et al. (40).

View larger version (15K): [in a new window]   Figure 6 Clinical outcome in patients from the same randomized trial shown in Figure 5. The cumulative incidence of death, infarction, and stroke was significantly lower in the stent group compared with the tissue plasminogen activator group. Reprinted, with permission, from Schomig et al. (40).

View larger version (34K): [in a new window]   Figure 7 Relationship between the transmural extent of hyperenhancement by magnetic resonance imaging before revascularization and the likelihood of improved function after revascularization in 804 dysfunctional segments in 41 patients. There was a clear inverse relationship between the transmural extent of hyperenhancement and the likelihood of improved function. Reprinted, with permission, from Kim et al. (85).

View larger version (16K): [in a new window]   Figure 8 Survival free of reinfarction, congestive heart failure, stroke, or unstable angina requiring hospitalization for 43 patients grouped by infarct size obtained by magnetic resonance imaging. There was a significant association of infarct size with subsequent outcome.However, if unstable angina was removed from the definition of events, the relationship was no longer significant. Reprinted, with permission, from Wu et al. (90).