1,721,581 research outputs found
Letter by Lippi and Cervellin Regarding Article, "High-sensitivity Cardiac Troponin in the Distinction of Acute Myocardial Infarction From Acute Cardiac Noncoronary Artery Disease".
No full textHigh-sensitivity Cardiac Troponin in the Distinction of Acute Myocardial Infarction From Acute Cardiac Noncoronary Artery Disease
Letter by Lippi and Cervellin regarding article, "High-sensitivity troponin T concentrations in acute chest pain patients evaluated with cardiac computed tomography".
No full textHigh-sensitivity troponin T concentrations in acute chest pain patients evaluated with cardiac computed tomography
Letter by Lippi and Cervellin Regarding Article, "Optimal Cutoff Levels of More Sensitive Cardiac Troponin Assays for the Early Diagnosis of Myocardial Infarction in Patients With Renal Dysfunction"
No full textOptimal Cutoff Levels of More Sensitive Cardiac Troponin Assays for the Early Diagnosis of Myocardial Infarction in Patients With Renal Dysfunctio
Letter by Cervellin et al Regarding Article, "Allergic Inflammation Is Associated With Coronary Instability and a Worse Clinical Outcome After Acute Myocardial Infarction"
No full textWe read with interest the article of Niccoli et al,who demonstrated a significant in vivo eosinophil degranulation and basophils activation during acute coronary syndrome along with a prognostic role of eosinophil cationic protein in ST-segment–elevation myocardial infarction. Indeed, the interplay between ischemic heart disease and atopy/allergy is complex and not completely revealed to date because the first report of acute coronary syndrome during a prolonged allergic reaction to penicillin was published more than half a century ago,followed by several studies supporting a role for allergic mediators in ischemic heart disease. In 1998, Eugene Braunwald described that vasospastic angina may be triggered by allergic reactions with mediators, such as histamine or leukotrienes, acting on coronary vascular smooth muscle. The results of Niccoli et al are consistent with both activation of eosinophil and basophil (both cells involved in allergic reactions) after an acute coronary event, with the additional finding of the prognostic role of elevated eosinophil cationic protein in patients with ST-segment–elevation myocardial infarction. Despite these important evidences, a causality dilemma remains. In fact, it is still unclear as to whether allergic pathway activation anticipates plaque disruption and subsequent acute thrombus formation during myocardial ischemia or, conversely, it just follows the ischemic/necrotic process. The answer to this intriguing issue would permit to recognize whether allergic reactions may be considered simple bystanders or active players in the challenging pathophysiology of myocardial ischemia
Diagnostic Criteria for Percutaneous Coronary Intervention-Related Myocardial Infarction Time for Revision?
No full textDiagnostic criteria for percutaneous coronary intervention-related myocardial infarction: time for revision
The Latest Generation of Troponin Immunoassays The “Cholesterol” of the Third Millennium?
No full textThe latest generation of troponin immunoassays: the "cholesterol" of the third millennium
The Predictive Value of Plasma Neutrophil Gelatinase-Associated Lipocalin on Cardiovascular Death and All-Cause Mortality Might Be Mediated by Leukocytosis
No full textThe predictive value of plasma Neutrophil Gelatinase-Associated Lipocalin on cardiovascular death and all-cause mortality might be mediated by leukocytosis
Risk assessment of post-infarction heart failure. Systematic review on the role of emerging biomarkers.
No full textThe prognostic significance of cardiospecific troponins and natriuretic peptides in patients with myocardial ischemia is well established, and their measurement is now endorsed by the most important guidelines and recommendations for diagnosis and management of heart failure (HF). Additional biomarkers have also been investigated to support clinical judgment and diagnostic imaging in the stratification of risk of cardiac dysfunction in patients with myocardial infarction (MI). We have performed a systematic analysis of the current scientific literature regarding the most important biomarkers of HF, selecting all prospective studies with adequate sample size (i.e. >100 patients) that have assessed, during the early phase of myocardial ischemia, the prognostic value of emergent biomarkers for new-onset HF or deterioration of cardiac function in patients with MI. This analysis has provided some good evidence suggesting that, in most cases, the use of diagnostic biomarkers of cardiac dysfunction does not translate into efficient risk prediction of HF. However, some notable exceptions were found, including biomarkers of cardiac fibrosis (especially galectin-3), growth differentiation factor-15 (GDF-15), osteoprotegerin, C-reactive protein (CRP), and red blood cell distribution width (RDW). Nevertheless, future studies with well-defined characteristics including the use of larger sample sizes, standardized end points, and replication populations, along with benchmark analyses against other consolidated biomarkers (i.e. cardiospecific troponins and natriuretic peptides), should be planned. Such evaluations will help to establish whether an integrated approach including biomarkers of different pathogenetic pathways - for example, apoptosis, stress of cardiomyocytes, cardiac fibrosis, inflammation, and extra-cardiac involvement - may be cost effective for identifying patients at increased risk of developing HF, and who, therefore, may benefit from a tailored therapeutic strategy
Counterpoint: highly-sensitive troponin immunoassays in the emergency department
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