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Myocardial necrosis

Wagner et. al (46) studied 376 patients to evaluate the importance of identification of the myocardial-specific MB isoenzyme in the diagnosis of acute myocardial infarction. An attempt was made to determine the incidence of falsely positive (mb). No acute infarction was diagnosed in all patients in whom neither total CK nor the isoenzymes of LD indicated myocardial necrosis. Incidence of falsely negative (MB) was zero in 33 patients. They concluded that determination of the isoenzymes of CK provides both a sensitive and specific indication of acute myocardial infarction. [Pg.200]

ECG. Therefore, it is important to review findings from the ECG in conjunction with biochemical markers of myocardial necrosis, such as troponin I or T, and other risk factors for CHD to determine the patient s risk for experiencing a new MI or having other complications. [Pg.86]

VSMCs 4. Angiogenesis. 5. Dysregulation of MMPs myocardial necrosis. [Pg.202]

Beyer et al. (1998c) aver that the most reliable indicators of lead poisoning in waterfowl include impactions of the upper alimentary tract, submandibular edema, myocardial necrosis, biliary discoloration of the liver, and hepatic lead concentrations of at least 38 mg/kg DW or 10 mg/kg FW. [Pg.300]

NSTEMI differs from UA in that ischemia is severe enough to produce myocardial necrosis, resulting in release of detectable amounts of biochemical markers, primarily troponin I or T and creatine kinase myocardial band (CK-MB) from the necrotic myocytes into the bloodstream. [Pg.56]

Effect of D-003 on isoproterenol-induced myocardial necrosis in rats. J... [Pg.455]

PLATE LETS-lb studies, a 600 mg loading dose was associated with increased platelet inhibition compared to a 300 mg loading dose, In turn, increased platelet inhibition was accompanied by a decrease in the release of myocardial necrosis and inflammation (19,20). In a very recent study of 106 patients undergoing stenting, high post-treatment platelet reactivity was asso-ciated with an increased risk of recurrent cardiovascular events (22). [Pg.149]

Biomarkers help establish the presence of myocardial necrosis. There are nearly two dozen biomarkers currently under study Most experience is with creatinine kinase, creatinine kinase MB, troponin I or 7) and myoglobin, Others are under study (Fig. I) (3). Two other biomarkers currently available are C-reactive protein (CRP) and brain natriuretic peptide (BNP), Even minor elevations of troponin I orT have had prognostic importance, In the tactics TIMI 18 study, troponin levels between 0,1 ng/mL and more than 1,5 ng/mL were found in 60% of the 1821 patients (9), In this study, troponin... [Pg.466]

More recent series have also documented a survival advantage (7-9). Hoye et al. in 874 consecutive patients with a CTO found a five-year survival in 93.5% of patients with successful revascularization versus 88.0% in these patients with failed revascularization (p = 0.02). In a Canadian registry of 1458 patients at seven year, successful recanalization of a chronic total occlusion was associated with improved survival as well as lower rates of PCI and/or CABG (9). In addition to survival advantage, both regional and global left ventricular function is improved in patients with successful treatment of a chronic total occlusion (10). This improvement may depend on whether the patient had a prior infarction in the distribution of the occlusion (II). If prior infarction resulted in frank myocardial necrosis, then recanalization may not improve the function however, many patients with chronic occlusion have preservation of regional wall function. [Pg.537]

Li C. 1982. [Experimental studies on the pathogenesis of barium chloride- induced myocardial necrosis in conditions of potassium deficiency], Yingyang Xuebao 4 341-347. (Chinese)... [Pg.119]

Cardiac imaging agent for detection of myocardial necrosis Mammalian cells... [Pg.1424]

Based on a retrospective study of 344 patients with cocaine-associated chest pain, it has been suggested that patients who do not have evidence of ischemia or cardiovascular complications over 9-12 hours in a chest-pain observation unit have a very low risk of death or myocardial infarction during the 30 days after discharge (59). Nevertheless, patients with cocaine-associated chest pain should be evaluated for potential acute coronary syndromes those who do not have recurrent symptoms, increased concentrations of markers of myocardial necrosis, or dysrhythmias can be safely discharged after 9-12 hours of observation. A protocol of this sort should incorporate strategies for treating substance abuse, since there is an increased likelihood of non-fatal myocardial infarction in patients who continue to use cocaine. [Pg.492]

Fletcher SE, Fyfe DA, Case CL, Wiles HB, Upshur JK, Newman RB. Myocardial necrosis in a newborn after long-term maternal subcutaneous terbutahne imusion for suppression of preterm labor. Am J Obstet Gynecol 1991 165(5 Pt 1) 1401. ... [Pg.452]


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See also in sourсe #XX -- [ Pg.103 ]

See also in sourсe #XX -- [ Pg.163 ]




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