Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac troponin I levels are frequently above normal values in several disease states in which myocardial necrosis is not a prominent aspect, particularly in pulmonary embolism, heart failure, liver cirrhosis, septic shock, renal failure and arterial hypertension. Sub-clinical myocardial necrosis has been postulated to be the cause of the phenomenon. Studies performed so far have not included pathological data to confirm this hypothesis. Increased troponin I plasma levels may be the result of myocardial strain, especially the type of strain that accompanies some forms of cardiac dilatation or hypertrophy. Troponin I may act as a marker of myocardial strain, either acute (in pulmonary embolism, septic shock and acute heart failure) or chronic (in chronic cardiac, renal and hepatic failure, as well as in arterial hypertension). The apparent paradox of elevated levels of troponin I without elevated levels of creatine kinase in several disease states might be solved if troponin I could be released from myocardial cells without the disruption of myocardial cell plasma membranes. Precise pathological studies are needed to elucidate whether increased troponin I with normal CK is associated with myocyte death, and, if so, with necrosis or with apoptosis.
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PMID:Cardiac troponin I in systemic diseases. A possible role for myocardial strain. 1158 28

Cardiac troponin I levels were increased in 24 of 147 patients (16%) with documented acute pulmonary embolism and in 20 of 594 patients (3%) without pulmonary embolism (p <0.001). In patients with acute pulmonary embolisms, 8 of 24 (33%) with increased cardiac troponin I levels and 9 of 123 (7%) with normal cardiac troponin I levels died during hospitalization (p <0.001).
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PMID:Prevalence of increased cardiac troponin I levels in patients with and without acute pulmonary embolism and relation of increased cardiac troponin I levels with in-hospital mortality in patients with acute pulmonary embolism. 1471 66

Although the incidence and prognostic significance of elevated cardiac troponins are known in patients with massive pulmonary embolism (PE), few studies have addressed this issue in patients with hemodynamically stable, submassive PE, who comprise the majority of patients presenting with PE. This prospective cohort study was, therefore, designed to determine the incidence and prognostic significance of elevated cardiac troponins in patients with submassive PE. Consecutive patients with acute, symptomatic, submassive PE that was confirmed by objective diagnostic testing were studied. All patients received treatment with either unfractionated heparin or fondaparinux followed by a coumarin derivative and underwent clinical follow-up for 3 months. Cardiac troponin I (cTnI) levels were measured within 24 h of clinical presentation. An elevated cTnI was defined as > 0.5 microg L(-1) and indicated myocardial injury. Major myocardial injury, that is associated with myocardial infarction, was defined by a cTnI > 2.3 microg L(-1). The clinical outcomes were recurrent venous thromboembolism and all-cause death. In 458 patients with submassive PE, the incidence of cTnI > 0.5 microg L(-1) was 13.5%[95% confidence interval (CI): 10.4-16.7], and the incidence of cTnI > 2.3 microg L(-1) was 3.5% (95% CI: 2.0-5.6). An elevated cTnI > 0.5 microg L(-1) was associated with an increased risk of all-cause death [odds ratio (OR) = 3.5; 95% CI: 1.0-11.9], but did not appear to confer an increased risk of recurrent venous thromboembolism (OR = 1.1; 95% CI: 0.2-4.9). In patients who present with submassive PE, an elevated cTnI occurs in about one in seven patients and is associated with a 3.5-fold increased risk of all-cause death.
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PMID:The incidence and prognostic significance of elevated cardiac troponins in patients with submassive pulmonary embolism. 1574 41

Cardiac troponin I (cTnI) and cardiac troponin T (cTnT) are valuable heart markers in patients presenting with symptoms of ischaemic heart disease. A number of categories of patients frequently have raised concentrations of cardiac troponin (cTn) without having ischaemic heart disease. These include patients with heart diseases such as heart failure, myocarditis and valvular disease but also those with lung emboli, renal failure and sepsis. Possible underlying mechanisms are diffuse necrosis, cTn proteolysis or leakage of cytoplasmatic cTn with no irreversible damage to the contraction complex of heart-muscle cells. It is possible that cTn-measurement in patients with non-cardiac conditions is of prognostic value but so far this has only been demonstrated in dialysis patients and patients with pulmonary embolism.
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PMID:[The significance of elevated troponin levels in the absence of acute cardiac ischaemia]. 1661 May 13