2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction

Antman, Elliott M.; Armstrong, Paul W.; Green, Lee A.; Halasyamani, Lakshmi; Hochman, Judith S.; Krumholz, Harlan M.; Lamas, Gervasio A.; Smith, Sidney C.; Hand, Mary M.; Bates, Eric R.; Mullany, Charles J.; Pearle, David L.; Sloan, Michael A.

doi:10.1016/j.jacc.2007.10.001

Cited by 776 publications

(173 citation statements)

References 93 publications

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“…Post-infarction ventricular remodeling occurs over the weeks and months following an acute ischemic event. This contrasts with the narrow therapeutic window of only 90 min after hospital presentation (or B6 h from infarction) for coronary reperfusion therapy to reduce myocardial necrosis and infarct size (Antman et al, 2008). Second, anti-BNIP3 therapy might not necessarily need to be given specifically to the myocardium.…”

Section: Transgenic Cardiac Overexpression Studies Of Bnip3 and Nix/bmentioning

confidence: 99%

Cardiac reanimation: targeting cardiomyocyte death by BNIP3 and NIX/BNIP3L

Dorn

Kirshenbaum

2008

Oncogene

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Programmed cardiac myocyte death contributes to pathological ventricular remodeling and the progression of myocardial infarction or pressure overload hypertrophy to dilated cardiomyopathy. Recent work has identified importance of stress-mediated transcriptional induction of BNIP3 (BCL2 and 19-kDa interacting protein-3) and NIX/BNIP3L in cardiac remodeling. Here, the regulatory mechanisms for these two factors in the heart and their effects on programmed cardiomyocyte death are reviewed, with a focus on information derived from studies using mouse models of cardiac BNIP3 and NIX/BNIP3L overexpression and gene ablation.

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Section: Transgenic Cardiac Overexpression Studies Of Bnip3 and Nix/bmentioning

confidence: 99%

Cardiac reanimation: targeting cardiomyocyte death by BNIP3 and NIX/BNIP3L

Dorn

Kirshenbaum

2008

Oncogene

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“…1) PCI performed early after admission (within 4 h) [11,12] according to risk stratification gauged on ECG findings and clinical evaluation reported by running guidelines [12,13]. The resting 12-lead ECG was obtained within 10 min after first medical contact upon arrival of the patient in the emergency room and immediately interpreted by a qualified physician.…”

Section: Patientsmentioning

confidence: 99%

New insights in the pathophysiology of acute myocardial infarction detectable by a contemporary troponin assay

Ferraro

Biganzoli

Marano

et al. 2013

Clinical Biochemistry

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Objectives: ST-elevation and non-ST-elevation myocardial infarction (STEMI, NSTEMI) are considered two distinct pathophysiologic entities. We evaluated cardiac troponin I (cTnI) release in STEMI and NSTEMI using a "contemporary" (CV > 10 to 20% at the 99th percentile concentration) cTnI assay for patients undergoing early percutaneous coronary intervention (PCI).Design and methods: 856 patients with suspected acute coronary syndrome consecutively admitted to the Emergency Department of the Maggiore Hospital of Novara (225 STEMI and 135 NSTEMI) were selected according to: 1) early (≤4 h from admission) and successful PCI; and 2) cTnI measurements at ED presentation and within 24 h. The influence of the MI type on cTnI concentrations at baseline and after PCI as well as the velocity of cTnI [cTnI V = absolute increase (after log conversion of cTnI measurements) / delay between the two measurements] was studied by multiple regression analysis, adjusting for patient parameters.Results: A statistically significant interaction between MI type and time from symptoms was reported on cTnI concentrations (p b 0.0001): STEMI and NSTEMI differed for cTnI releases at admission and after revascularization. Higher cTnI V in STEMI was detectable in patients admitted within 6 h from symptoms. Baseline cTnI concentrations were lower in patients with a history of coronary artery disease (CAD) and increased with aging (p b 0.0001). In the elderly (>75 years), the cTnI V was significantly increased.Conclusion: STEMI and NSTEMI patients have different patterns and dynamics of cTnI release influenced by the interaction with time from symptoms, by aging and history of CAD.

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“…Few pathologies had their evolution altered so radically as the AMI, with an accentuated decrease in mortality due to the changes regarding its treatment in the last 30 years 1,2 . The change in the treatment was the result of advances obtained in the study of the pathogenesis of the AMI and its complications.…”

Section: Introductionmentioning

confidence: 99%