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)

CK-isoenzymes were measured in 31 patients hospitalised for suspected myocardial infarctions who had an increase in serum creatine kinase (CK) above 50 U/l. Of 26 patients with definite evidence of myocardial infarction, MB-isoenzyme--specific for myocardial necrosis--was demonstrated in 24. MB-isoenzyme was no longer detectable in two patients hospitalised 48 hours after the onset of symptoms. In the remaining five patients only MM-isoenzyme was found, the elevated CK activity in three patients having been due to an intramuscular injection, and in two others due to pulmonary embolism. Measurement of CK isoenzymes proved of great diagnostic value in three patients with sudden circulatory arrest of, at first, unknown cause after successful resuscitation. Acute myocardial infarction was proven by the presence of MB-isoenzyme. In one of these patients an additional BB-isoenzyme was seen, possibly due to concomitant cerebral ischaemia. In all other patients (with angina, after cardioversion, or after major surgical operations) only MM-isoenzyme was detected. MB-CK-isoenzyme was found to be a highly specific, as well as sensitive, indicator of myocardial necrosis. This being a rather difficult method, its use is not justified in the routine diagnosis, but in doubtful instances its value can hardly be overestimated.
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PMID:[The diagnostic value of CK-isoenzymes in suspected acute myocardial infarction (author's transl)]. 124 17

A 24-year-old man was sent to the emergency unit and evaluated with the symptom of acute right-sided chest pain. Myocardial infarction and pulmonary embolism were excluded. A creatine kinase (CK) serum concentration of 17,034 U/l (normally up to 270) was found. The patient gave a history of excessive body-building exercises on the previous day. During the follow-up period symptoms resolved within several days, and CK values gradually diminished. A review of current literature on rhabdomyolysis in patients with body-building is presented.
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PMID:[Rhabdomyolysis in body building. Report of a case and literature review]. 141 Sep 85

Diagnosis of injury to the myocardium is facilitated by information on the activities of creatine kinase (EC 2.7.3.2) MB isoenzyme (CK-MB) and lactate dehydrogenase (EC 1.1.1.27) isoenzyme 1 in serum, thee isoenzymes being present in higher activities in the myocardium than in other tissues or in normal serum. The temporal relationships of these isoenzymes, total creatine kinase, total lactate dehydrogenase, and aspartate aminotransferase (EC 2.6.1.1) are highly sensitive and specific for acute injury to the heart, particularly acute myocardial infarction. Chronic heart diseases, electric cardioversion for heart rhythm disturbances, coronary catheterization, and exercise usually do not produce increases of CK-MB, although abnormal aspartate aminotransferase, creatine kinase, lactate dehydrogenase, and lactate dehydrogenase isoenzyme 1 activities are seen in some individuals. Many other causes of increased activities of these enzymes and isoenzymes in serum are unrelated to injury to the heart. Because CK-MB is present in the skeletal muscle in low activities, substantial injury to skeletal muscle can increase CK-MB activities in the blood to abnormal values. Pulmonary embolism can mimic myocardial infarction in its clinical presentation. In patients with an accurately known time of onset of symptoms and serial enzyme analysis every 12 h during the first 48 h, acute myocardial infarction can be distinguished from pulmonary embolism by determinations of creatine kinase, CK-MB, aspartate aminotransferase, and lactate dehydrogenase isoenzyme 1 in serum.
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PMID:Serum enzymes and isoenzymes in the diagnosis and differential diagnosis of myocardial ischemia and necrosis. 699 25

The subject of this report is a 57-year-old obese, hypertensive woman who had been well until the onset of severe chest pain and hypotension. She had to be defibrillated four times on her way to the hospital. The diagnosis of acute inferior-posterior infarction was made by electrocardiogram (ECG) and there was a markedly elevated serum creatine kinase (CK) (including the MB fraction). The patient had a very low cardiac output and ejection fraction. A lung scan revealed possible pulmonary embolism for which she was anticoagulated. She remained hypotensive and hypoxemic and, on Day 17 of her hospital stay, she had a bout of severe dyspnea. A new systolic murmur was heard and the clinical diagnosis of ruptured papillary muscle was made and confirmed by echocardiography, and later at autopsy. All three coronary arteries were severely atherosclerotic and, in addition, the right coronary artery was completely closed by a thrombus. This case clearly illustrates the major pathological changes in the heart that correlate with the clinical findings in patients with a myocardial infarct that is complicated by left ventricular papillary muscle rupture. The pathophysiological effects of this condition, as illustrated in this case report, include the following:1. The posterior papillary muscle wa s almost completely separated from its base, with only a thin strip of muscle intact. The mistral valve thus was insufficient (a "flail valve''); this markedly reduced the ejection fraction of the left ventricle, increased its end-diastolic volume and pressure, produced a damming of blood in the pulmonary circulation, and this resulted in the pulmonary edema seen on the chest x-ray.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute myocardial infarction with papillary muscle rupture. 841 63

Although rare, exertional collapse and sudden death are the most serious potential complications of sickle cell trait. Studies suggest that this condition may occur in susceptible persons when poor physical conditioning, dehydration, heat stress or hypoxic states precipitate sickling of the abnormal erythrocytes. Sickling leads to endothelial damage, which can cause vasoconstriction, disseminated intravascular coagulation and local tissue damage. Cardiac effects include acute ischemia and arrhythmias. Muscle damage results in acute compartment syndromes and release of myoglobin into the circulation. Acute renal failure is possible. Diagnosis is based on a high index of suspicion, and characteristic presentation and laboratory findings, including myoglobinuria, hyperkalemia, hypocalcemia, hyperphosphatemia and elevated creatine kinase levels. The differential diagnosis includes pulmonary embolism, acute cardiac events, anaphylaxis and heat stroke. Management is based on stabilization, rehydration, and the treatment and prevention of complications.
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PMID:Exertional collapse and sudden death associated with sickle cell trait. 904 99

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

The group of idiopathic inflammatory myopathies encompasses polymyositis, dermatomyositis and inclusion body myositis. These diseases share the following features: progressive muscle weakness, an increase in serum creatine kinase activity and the presence of mononuclear cell infiltrates in the muscle biopsy. Polymyositis, dermatomyositis and inclusion body myositis are differentiated on the basis of the distribution of muscle weakness, and specific histopathological features. Many specialties may see these patients as the clinical presentation can vary widely and may be atypical, requiring further diagnostic procedures. A 40-year-old man with a heliotrope rash and periorbital oedema, but no muscle involvement, was diagnosed with dermatomyositis sine myositis. He was successfully treated with corticosteroids but died later of cardiac failure. A 72-year-old man with a pulmonary malignancy subsequently developed the clinical features of dermatomyositis. Steroid therapy diminished the complaints but he died of pulmonary embolism. A 54-year-old woman with the clinical features of inclusion body myositis did not have rimmed vacuoles in her muscle biopsy specimen and was initially erroneously diagnosed with polymyositis, for which she was treated with corticosteroids, but without beneficial effect.
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PMID:[Three patients with divergent presentations of idiopathic inflammatory myopathy]. 1203 18

A male patient with advanced Duchenne muscular dystrophy (DMD) had tonic-clonic convulsion. He showed transient elevations of serum creatine kinase (CK) and plasma D-dimer. Serum CK, ordinarily 122-386 IU/l, was elevated to 9,262 IU/l, while plasma D-dimer, below 66 ng/ml in normal subjects, was at 543 ng/ml, and these levels were significantly correlated. Serum fibrin and fibrinogen degradation products levels were within a normal range. In the present case, acute muscle destruction due to tonic-clonic convulsion was considered to transiently activate a coagulation cascade. Plasma D-dimer elevation is the result of fibrin thrombus and can induce thrombosis, such as a pulmonary embolism. Thrombosis is a serious life-threatening complication of DMD, though the mechanism remains unclear. There were no thrombotic complications in the present patient, however, acute muscle destruction enhances the coagulation and fibrinolysis status in patients with advanced DMD and may be a candidate cause of thrombosis.
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PMID:[A case of Duchenne muscular dystrophy showing coagulation cascade activation induced by muscle destruction due to convulsion]. 1293 34

The etiology of dyspnea can often be difficult to rapidly and accurately determine and can delay timely and appropriate therapies. The current literature reveals important diagnostic, prognostic, and therapeutic implications of several currently used biomarkers: sensitive d -dimer, myoglobin, creatine kinase-MB, cardiac troponins, and b-type natriuretic peptide. These biomarkers were found to have a high sensitivity and negative predictive value for rapidly ruling out potential serious etiologies of dyspnea, namely, pulmonary embolism (PE), acute myocardial infarction (AMI), and congestive heart failure (CHF). In the setting of a low to moderate pretest probability of PE, a negative sensitive d -dimer can rule out a PE with 97% accuracy. After 10 hours from the onset of symptoms, normal levels of myoglobin, creatine kinase-MB, and cardiac troponin I can rule out an AMI with greater than 96% accuracy. A b-type natriuretic peptide level less than 80 pg/mL can confidently rule out decompensated CHF with greater than 99% accuracy. However, no literature was found analyzing the use of these biomarkers in combination. A dyspnea biomarker panel could rapidly and accurately assist a clinician to rule out PE, AMI, and CHF. If a PE, AMI, or CHF is determined to be the cause of dyspnea, a biomarker panel could help risk stratify and help determine initial therapies. Subsequent clinical research is needed to corroborate this postulation.
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PMID:Evaluation and management of the acutely dyspneic patient: the role of biomarkers. 1591 17

Measurement of cardiac troponin I or T in serum (highly specific for the myocardium) have replaced classical markers, such as creatine kinase MB. Cardiac troponins are preferred markers because of their high specificity and sensitivity. This had led to modifications of the original World Health Organization criteria for acute myocardial infarction. Furthermore, the place of the troponins as superior markers of subsequent cardiac risk in acute coronary syndrome has now become firmly established, for both diagnostic and risk stratification purposes. The use of C-reactive protein and/or other inflammatory biomarkers may add independent information in this context. After non cardiac surgery, the total cardiospecificity of cardiac troponins explains why other biomarkers of necrosis should no longer be used. Recent studies suggest that any elevation of troponin in the postoperative period is indicative of increased risk of long-term cardiac complications. This prognostic value has been previously demonstrated in other clinical settings such as invasive coronary intervention (surgical myocardial revascularization and percutaneous coronary intervention) and after heart valve surgery. Increases of troponin indicate cardiac damage, whatever the mechanism (ischemic or not). Other causes of cardiac injury include: pulmonary embolism, myocarditis, pericarditis, congestive heart failure, septic shock, myocardial contusion. In most cases, elevation of troponins has been shown to be associated with a bad outcome.
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PMID:[The use of cardiac troponins (T or I) measurement in cardiology and various clinical settings]. 1601 83


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