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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary embolism is a major cause of death in the United States. A high index of suspicion is required to achieve an accurate diagnosis. We report a case of a patient with syncope, ischemic electrocardiographic changes, and an elevated troponin I level, presenting just like acute myocardial infarction. The case highlights the value of an early use of 2-dimensional echocardiography in obtaining an accurate diagnosis, thus avoiding unnecessary and inappropriate treatment.
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PMID:Pulmonary embolism mimicking acute myocardial infarction. 1043 62

Pulmonary embolism (PE) is a common and potentially fatal disease. Death usually occurs before hospital admission or in the initial in-hospital phase. A number of clinical and instrumental findings have been associated with a high risk of adverse short-term clinical outcomes in patients with PE. Advanced age, concomitant cardiopulmonary disease, and haemodynamic instability, as well as large perfusion defects at lung scanning and acute right heart dysfunction as assessed by echocardiography, are associated with adverse in-hospital outcome. Elevated serum levels of troponin I have been recently demonstrated to be associated with severe right ventricular dysfunction and adverse in-hospital outcome in patients with PE. Early recurrence of PE is associated with a high mortality rate. Right heart dysfunction, as assessed by echocardiography and an acute fall in platelet count, have been suggested as risk factors for recurrence of PE. A reduction in mortality in the subgroup of patients with a poor prognosis might be achieved by using more aggressive treatments such as thrombolysis and surgical or interventional procedures. However, such treatments are invariably associated with bleeding and other procedural complications.
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PMID:Risk factors for adverse short-term outcome in patients with pulmonary embolism. 1156 61

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 ECG is abnormal in over 70% of patients with pulmonary embolism. Certain ECG abnormalities have been observed to return to normal after treatment. This case report describes an instructive ECG series in a patient with massive bilateral pulmonary embolism as shown by spiral computed tomography. The initial ECG showed sinus tachycardia with P pulmonale, although atrial tachycardia could not definitively be excluded. The patient had an increased troponin I concentration and echocardiographic evidence of right ventricular dysfunction and underwent thrombolysis with alteplase and anticoagulation with warfarin. P wave amplitude gradually decreased throughout admission and her tachycardia resolved. This may reflect a reduction in right atrial strain after treatment. This phenomenon has apparently not been described in this setting. The significance of ECG changes and the role of thrombolysis in pulmonary embolism are briefly discussed.
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PMID:Instructive ECG series in massive bilateral pulmonary embolism. 1595 44

Right ventricular strain is a source of troponin elevation in some patients with acute pulmonary embolism. Acute and/or severe obstructive airway disease could lead to a sudden increase in pulmonary arterial pressure and right ventricular afterload. We report a case of troponin I elevation in a 40-year-old woman who presented with acute severe bronchospasm and had a negative evaluation for coronary artery disease.
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PMID:Troponin I elevation in a patient with acute severe bronchospasm. 1595 75

The debate about thrombolysis in acute pulmonary embolism (PE) as an adjunctive therapy to heparin is ongoing for about 35 years. Thrombolysis dissolves thromboemboli faster than heparin in combination with spontaneous lysis. So, thrombolysis achieves a faster normalization of the pulmonary artery pressure. Thrombolysis may be life-saving in patients with cardiogenic shock and in patients with hemodynamic instability due to massive PE. It is still on discussion whether patients with right heart strain who are hemodynamically stable should be treated with thrombolysis. Inconsistent definitions of right heart strain may be responsible for the lack of evidence for reducing mortality by thrombolysis. The authors' right heart score (R-S(Wacker)) enables physicians to describe the right heart strain in patients with PE quantitatively. The R-S(Wacker) is of prognostic value with regard to in-hospital mortality and 6-month mortality. Patients with a normal to moderately elevated R-S(Wacker) have an excellent outcome (0% in-hospital mortality) and do not profit from thrombolysis. In patients with relevant right heart strain thrombolysis may be discussed, especially in combination with an elevation of the biomarkers troponin I or T and brain natriuretic peptide (BNP). Patients with intracardiac thromboemboli, especially in the presence of a patent foramen ovale, should receive thrombolysis, in selected cases surgery should be done. Therapy and therapy escalation are highly dependent on the time interval after diagnosis of PE: patients who survive the first 24 h and who are on heparin in therapeutic dosage without any interruption have a good prognosis. Therefore, therapy escalation after 24 h or even later should be an exception.
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PMID:[Thrombolytic therapy in acute pulmonary embolism]. 1596 1

The troponin I values and echocardiographic data of 141 patients with acute pulmonary embolism (PE) were correlated with 30-day mortality. Patients with elevated troponin and right ventricular enlargement are at significantly greater risk for death after PE than patients with only 1 or with neither adverse prognostic marker.
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PMID:Prognostic significance of troponin elevation and right ventricular enlargement in acute pulmonary embolism. 1601 61

Over the last four decades there have been remarkable advances in the diagnosis and treatment of venous thromboembolism (VTE)-pulmonary embolism (PE) and deep venous thrombosis (DVT). We have moved from no objective documentation to a plethora of ever improving imaging studies. Evolving treatment modalities have reduced the mortality due to PE to approximately 2%. Shorter hospitalizations followed by outpatient therapy are a growing reality. The use of primary prophylaxis is increasing, but more widespread use must be encouraged. Despite the many accomplishments, too many patients with VTE with its high mortality without treatment remain undiagnosed. There is a critical need to improve the role of the patient's history in identifying patients who warrant objective testing. The ideal would be the development of a biological marker of VTE, similar to the creatinine kinase-MB, creatinine kinase-MM, or troponin I in acute myocardial infarction.
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PMID:Venous thromboembolism: past, present and future. 1608 66

A 70-year old man presented with retrosternal chest pain. His electrocardiogram showed nonspecific T wave changes. Cardiac-specific troponin I (cTnI) was elevated. His condition was managed as acute coronary syndrome, following which he had two minor episodes of hemoptysis. A CT pulmonary angiogram showed no evidence of pulmonary embolism, but a large mass lesion was seen in the mediastinum. Echocardiography and cardiac MRI demonstrated a large solid mass, arising from the right ventricular outflow tract and causing compression of the main pulmonary artery (MPA). The differential diagnosis included pericardial and myocardial tumors and clotted aneurysm of the MPA. At surgery, a clotted aneurysmal sac was identified originating from the MPA and the defect was healed. Aneurysms of the MPA are rare. They most commonly present with dyspnea and chest pain. Compression of surrounding structures produces protean manifestations. A high index of suspicion coupled with imaging modalities establishes the diagnosis. Blunt trauma to the chest, at the time of an accident 4 years previously, may explain this aneurysm. The patient's presentation with chest pain was probably due to compression and/or stretching of surrounding structures. Coronary artery compression simulating acute coronary syndrome has been documented in the literature. The rise in cTnI may have been due to right ventricular strain, as a result of right ventricular outflow obstruction by the aneurysm. This has not been reported previously in the literature. The saccular morphology and narrow neck of the aneurysm predisposed to stagnation leading to clotting of the lumen and healing of the tear, which caused the diagnostic difficulty.
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PMID:An unusual aneurysm of the main pulmonary artery presenting as acute coronary syndrome. 1660 8

Acute pulmonary embolism continues to cause significant morbidity and mortality despite advances in diagnosis and treatment. This retrospective analysis aimed to determine whether the combination of elevated troponin I and right ventricular dilatation (RVD) could provide a more powerful predictor for risk evaluation. The study data comprised records of 110 patients with either high-probability ventilation/perfusion lung scan or positive spiral computed tomography. All cause 100-day mortality was 18.2%. The hypotension and RVD variables significantly influenced 100-day mortality. For the combination of RVD and raised troponin I, the 100-day mortality rate was 31%. Notably, the group with elevated troponin I and no RVD had a 100-day mortality rate of only 3.7%. The combination of RVD and elevated troponin had a positive predictive value of 31% and a negative predictive value of 88% for 100-day mortality. Compared with existing reports, conflicting conclusions for the individual prognostic role of elevated troponin I, cancer, and heart failure were obtained. These conflicting conclusions most likely resulted from inappropriate cut-off troponin I values and the modest sample size. In conclusion, the combination of elevated troponin and RVD was able to identify a subset of patients most likely to benefit from aggressive therapy.
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PMID:Prognostic role of right ventricular dilatation and troponin I elevation in acute pulmonary embolism. 1710 48


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