Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since the introduction of cardiac plasma troponin measurements, a significant number of patients were seen with chest pain, elevated troponin levels but no significant coronary artery disease. Pulmonary embolism, aortic valve disease, myocarditis, sepsis, trauma, arrythmias, stress cardiomyopathy and dilated cardiomyopathy stand among possible causes for this syndrome. In some cases, myocardial strain could be the mechanism underlying this phenomenon, since it is known that the stimulation of stretch-responsive integrins may lead to the release of cardiac troponin I. In the present text, a case is made in favour of classifying this syndrome, of chest pain with increased values for plasma cardiac troponin, with or without ECG changes, in the absence of definite myocardial infarction or coronary artery disease, as pseudo myocardial infarction (PMI). This constitutes a new definition for a concept with decades, formerly centered on clinical and electrocardiographic changes mimicking infarct. The case is based on the search of scientific truth, on avoidance of unnecessary cardiac examinations, on avoidance of unnecessary drug therapy and on avoidance of unnecessary legal liability. PMI should be seen as a working diagnosis, since a more definitive diagnosis can be reached at all time. It should also be seen as a heterogeneous group of patients - several different diseases and conditions can lead to this phenomenon. But it must certainly not be seen as a benign condition, since published studies point in a totally different direction.
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PMID:Pseudo myocardial infarction - a condition in need to be redefined? 1985 81

The mortality and morbidity of salmonella infections is seriously underestimated. Salmonella myocarditis is an unusual complication of salmonella sepsis in adults. Cases that do occur may be associated with high morbidity and mortality. We present a rare case of salmonella myocarditis with multi-organ failure in a previously healthy young adult man who was brought to the emergency room with fever, diarrhea, shortness of breath, and altered sensorium, discovered to have acute pulmonary edema and respiratory compromise for which he was assisted with mechanical ventilation for 8 days. Blood culture grew Salmonella typhi. Biochemically he exhibited myocardial, hepatic, and muscular enzymatic surge with renal failure, features of rhabdomyolysis, and disseminated intravascular coagulation. The patient showed a progressive improvement on treatment with ceftriaxone for 2 weeks in addition to decongestive therapy. He was discharged in good condition afterward.
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PMID:Salmonella myocarditis in a young adult patient presenting with acute pulmonary edema, rhabdomyolysis, and multi-organ failure. 1994 25

For years, cardiac troponins (cTn) have been regarded as the preferred biomarkers for the diagnosis of myocardial infarction and for the risk stratification of patients with acute coronary syndromes, as well as for the selection of patients who need an early invasive strategy, and for the guidance of adjunctive pharmacological therapy. In addition, measurement of cTn has been found useful for detection of myocardial necrosis in conditions unrelated to myocardial ischemia including acute pulmonary embolism, myocarditis, heart failure, sepsis, and end-stage renal disease. In these conditions, an unfavorable prognosis is unequivocally associated with detectable concentrations of cTn.A major limitation of most currently available cTn assays is the lack of adequate precision, i.e., to measure cTn concentrations at the 99th percentile value with a coefficient of variation < 10%. As a consequence, many manufacturers have developed more sensitive cTn assays that now comply with precision criteria required by the Joint European Society of Cardiology/ American College of Cardiology/American Heart Association/World Heart Federation Task Force for the Redefinition of Acute Myocardial Infarction.Using assays with higher analytic sensitivity more patients will be seen in clinical practice with the high-sensitivity cardiac troponin T (TnThs) above the 99th percentile discriminator. The causes of these elevations may be due to acute, subacute and chronic cardiac disease such as heart failure or cardiomyopathies.
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PMID:Troponins and high-sensitivity troponins as markers of necrosis in CAD and heart failure. 2002 39

Human enteroviruses are associated with various clinical syndromes from minor febrile illness to severe, potentially fatal conditions like aseptic meningitis, paralysis, myocarditis, and neonatal enteroviral sepsis. Between June 2000 and August 2008 echovirus (E) type 2, 4, 6, 7, 9, 11, 13, 25, 30, coxsackievirus (CV) -A16, -A19, -B5, and enterovirus 71 (EV71) were reported in Hungary. In this study, 29 previously enterovirus positive samples from 28 patients diagnosed with hand, foot and mouth disease, meningitis and encephalitis, were molecularly typed. The genetic relationships of identified serotypes CV-A16, EV71, and E30 were assessed by direct sequencing of genomic region encoding the capsid protein VP1. The sequences were compared to each other and sequences from other geographical regions possessed in Genbank. The phylogenetic analysis of CV-A16 revealed that the viruses were mostly of Far-Eastern or Asia-Pacific origin. Typing of EV71 showed that one virus from 2000 belonged to genotype C1 and five viruses observed in 2004 and 2005 were identified as genotype C4. The 11 echovirus 30 strains showed homology with those of neighbor European countries. The molecular examination of E30 revealed that three separate lineages circulated in 2000, 2001, and 2004-2006 in Hungary.
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PMID:Detection of non-polio enteroviruses in Hungary 2000-2008 and molecular epidemiology of enterovirus 71, coxsackievirus A16, and echovirus 30. 2004 91

Myocarditis is defined clinically as inflammation of the heart muscle, which can be caused by infectious agents, toxins or immunologic reactions. Most recognized cases of acute myocarditis are secondary to cardiotropic viral infections. Escherichia coli rarely cause myocarditis. The authors report a 25-year-old woman with E coli-induced acute pyelonephritis and septic shock that was complicated with acute myocarditis. Her symptoms mimicked acute myocardial infarction. The authors discuss the possible mechanism of bacterial sepsis-induced myocarditis.
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PMID:Escherichia coli urosepsis complicated with myocarditis mimicking acute myocardial infarction. 2060 56

The typical symptoms and signs of myocardial infarction are well known. Alterations in electrocardiogram (ECG), echocardiography or biochemical markers of myocardial necrosis are usually helpful to confirm the diagnosis. Some of these features, however, also occur in myocarditis, which is a potential differential diagnosis. We describe an unusual case of bacterial sepsis due to Escherichia coli that caused myocardial damage (myocarditis) with ECG changes mimicking acute myocardial infarction. The possible pathophysiological mechanisms of myocardial injury in sepsis are also reviewed.
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PMID:Unusual case of myocardial injury induced by Escherichia coli sepsis. 2092 78

The diagnosis of stress-induced cardiomyopathy requires wall motion abnormality, most typically apical ballooning. The authors report 3 cases of transient global left ventricular systolic dysfunction that developed over the course of severe medical illnesses. The cardiomyopathy that developed in each patient had all the features of takotsubo cardiomyopathy, including reversibility, mild troponin elevation, nonspecific electrocardiographic abnormalities, and a negative work-up for ischemia. The only difference was the absence of regional wall motion abnormalities. No patients developed sepsis or myocarditis. Stress-induced cardiomyopathy may present in different forms, including regional or global left ventricular dysfunction. Classic takotsubo syndrome may represent only part of the spectrum of this reversible condition.
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PMID:Not takotsubo: a different form of stress-induced cardiomyopathy--a case series. 2127 26

Systemic lupus erythematosus is an autoimmune connective tissue disorder that affects multiple organs. While the clinical manifestations may vary in intensity over time and be associated with chronic disease, occasional cases occur where sudden and unexpected death has occurred. Cardiovascular disease is common, with accelerated atherosclerosis, intravascular thrombosis associated with antiphospholipid syndrome, and hypertensive cardiomegaly. Vasculitis with superimposed thrombosis may result in critical reduction in blood to vital organs, such as the heart and brain with infarction. Mesenteric ischemia may be caused by vasculitis, thrombosis, and accelerated atherosclerosis and may result in lethal intestinal infarction. Other diverse causes of sudden death include myocarditis, epilepsy, pulmonary hypertension, pulmonary thromboembolism, and sepsis. The autopsy evaluation of such cases requires careful examination of all organs with extensive histological sampling to include blood vessels, and microbiological sampling for bacteria, viruses, and fungi.
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PMID:Lethal manifestations of systemic lupus erythematosus in a forensic context. 2130 76

The discovery and characterization of the TLR (Toll-like receptor) family has led to a better understanding of the innate immune system. The strategy of innate immune recognition is based on the detection of constitutive and conserved products of micro-organisms. However, host molecules that are released during injury can also activate TLRs. Engagement of TLRs by microbial or host-derived molecules induces the expression of pro-inflammatory cytokines, which may have both beneficial and detrimental effects on the host. In addition to being expressed in immune cells, TLRs are expressed in other tissues such as those of the cardiovascular system. In the present review, the role of TLRs in septic cardiomyopathy, viral myocarditis, atherosclerosis, ischaemia/reperfusion injury and cardiac remodelling after myocardial infarction are outlined, with attention paid to genetically modified murine models. Although much has been learned about stress-induced TLR activation in the tissues of the cardiovascular system, the role of individual TLRs in initiating and integrating homoeostatic responses within the heart remains to be defined. Accumulating evidence indicates that TLRs may play an important role in the pathogenesis of atherosclerosis, viral myocarditis, dilated cardiomyopathy, cardiac allograft rejection and sepsis-induced left ventricular dysfunction. Moreover, heart failure of diverse aetiology is also now recognized to have an important immune component, with TLR signalling influencing the process of cardiac remodelling and prognosis. In the present review, we outline the biology of TLRs as well as the current experimental and clinical evidence for the role of TLRs in cardiovascular diseases.
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PMID:Role of toll-like receptors in cardiovascular diseases. 2141 30

The worldwide outbreak of pandemic influenza A (H1N1 influenza) infection in 2009 caused numerous hospitalizations and deaths resulting from severe complications such as pneumonia, sepsis, and acute respiratory distress syndrome. Fulminant myocarditis caused by H1N1 infection has been reported in children but rarely in adults. We present an adult who contracted H1N1 infection followed by fulminant myocarditis. Early implementation of extra-corporeal membrane oxygenation support in conjunction with a specific anti-influenza viral medication (Oseltamivir) led to the patient's complete recovery from cardiogenic shock in 2 weeks.
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PMID:Fulminant myocarditis in an adult with 2009 pandemic influenza A (H1N1 influenza) infection. 2142 Dec 8


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