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)

Anthracyclines, found to be efficacious in the treatment of a broad spectrum of pediatric malignancies, are cardiotoxic and may lead to heart failure even a long time after successful treatment of cancer. It is thought that subtle abnormalities can progress to the more permanent myocardial disease, resulting in cardiomyopathy which may progress to congestive heart failure. There are some precipitating factors leading to the sudden onset of cardiac symptoms such as increase in afterload or preload. We describe a young patient with congestive heart failure treated with doxorubicin (cumulative mean dose 420 mg/m2) in infancy because of pelvic sarcoma in whom the appearance of symptoms was related to pulmonary embolism. Four years before hospital admission, the patient presented echocardiographic abnormalities such as left ventricular fractional shortening and thickness reduction and he was treated with ACE-inhibitors. The myocardial ischemia, which is present in pulmonary embolism, probably worsened the left ventricular systolic function and caused congestive heart failure.
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PMID:[Heart failure in a subject treated with anthracyclines in childhood: myocardial dysfunction is not always the only reason of it]. 1534 97

Aortic dissection is a relatively uncommon but catastrophic illness classically thought to present with acute, sharp, chest pain with radiation to the back. However, aortic dissection can manifest in a number of different ways that include congestive heart failure, inferior myocardial infarction, stroke, focal pulse and neurologic deficits, abdominal pain, or acute renal failure. According to some studies, only about 80% of patients with type A dissection present with severe anterior chest pain, and only about 60% describe their pain as being sharp. Another series reports that treating clinicians fail to initially entertain the diagnosis of aortic dissection in up to 35% of cases. Many patients later found to have aortic dissection are initially suspected to have other conditions such as acute coronary syndrome, pericarditis, pulmonary embolism, or even cholecystitis. In this article we present a case of an unusual presentation of aortic dissection and a review of this condition.
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PMID:Aortic dissection: a dreaded disease with many faces. 1537 42

Acute respiratory failure can be the result of a variety of clinical conditions, such as congestive heart failure, pneumonia, pulmonary embolism, exacerbation of obstructive lung diseases, and acute respiratory distress syndrome (ARDS). This article focuses on developments related to acute lung injury and ARDS and reviews epidemiology, pathogenesis and therapeutic advances with an emphasis on the obstetric population. A brief discussion of tocolytic-induced pulmonary edema, preeclampsia, venous air embolism, and aspiration-related ARDS is included. Management of pregnant women with ARDS is outlined.
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PMID:Acute lung injury and acute respiratory distress syndrome in pregnancy. 1538 90

COPD is often accompanied with acute symptoms exacerbations. Patients in Ist stage: slide grade of COPD and IInd stage: middle grade of COPD suffer exacerbations accompanied with increased dyspnoea often together with increased cough and increased production of sputum. Patients in IIIrd stage (serious) and IVth stage (very serious) experience during exacerbations development of respiration insufficiency or its worsening and thus are usually treated in hospital. The most frequent causes of exacerbations are tracheobronchial tree infections and air pollution. The cause of approximately one third of serious exacerbations is not disclosed. Conditions which can resemble acute exacerbation are pneumonia, congestive heart failure, pneumothorax, pleural exudation, pulmonary embolism, and arrhythmia. Exacerbation treatment is symptomatic. Obstruction symptoms are treated with bronchodilatants and corticosteroids administration, hypoxemia with oxygen administration and signs of bacterial infection with antibiotics.
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PMID:[Treatment principle of the chronic obstructive pulmonary disease (COPD) exacerbation]. 1558 Sep 1

Limited information is available from large clinical investigations about the agreement among sources of diagnoses for endpoints. The authors used data from the Women's Health Initiative clinical trials and observational study from January 1994 to November 2000 to evaluate the agreement among self-report, hospital discharge codes, and two different levels of physician review of medical records for cardiovascular endpoints. For myocardial infarction, stroke, pulmonary embolism, and venous thrombosis, the agreement of hospital discharge codes or self-report with review by study physicians at clinical centers was substantial (kappa = 0.64-0.84). For coronary revascularization, agreement among these sources of information was substantial to almost perfect (kappa = 0.79-0.92), but for angina, congestive heart failure, and peripheral vascular disease, concordance was only fair to moderate (kappa = 0.37-0.56), indicating that these endpoints remain difficult to classify reliably. Agreement between physician adjudicators at clinical centers and central physician adjudicators was substantial to almost perfect (kappa = 0.67-0.94). The findings also suggest that, for the endpoint of myocardial infarction, physician review of events with hospital discharge codes for angina and congestive heart failure is an important source of validated events, and for stroke, review of all events with cerebrovascular codes is important.
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PMID:Comparison of self-report, hospital discharge codes, and adjudication of cardiovascular events in the Women's Health Initiative. 1558 67

BNP and NT-proBNP are new markers with potential applications for the diagnosis and management of patients with cardiovascular diseases. In patients with acute dyspnea, these markers might strengthen the clinical suspicion of decompensated congestive heart failure. Vice versa, below-threshold marker concentrations allow to virtually exclude significant left ventricular dysfunction in symptomatic patients. Furthermore, BNP and NT-proBNP are predictors of morbidity and mortality in patients with heart failure, but also in acute coronary syndrome, myocardial infarction, pulmonary embolism and other cardiovascular diseases. The markers therefore appear suitable for additional risk stratification. Independently from the clinical application, however, it is important to note that extracardiac variables may affect marker concentrations and need to be considered when marker concentrations are interpreted. Due to their diagnostic and prognostic value, the cardiac markers BNP and NT-proBNP have a clear potential to further improve the care of patients with cardiovascular diseases.
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PMID:[Clinical utility of the cardiac markers BNP and NT-proBNP]. 1573 51

The acute coronary syndromes (ACS) represent a pathological, diagnostic and risk continuum from unstable angina (UA) through myocardial infarction (MI) with or without ST segment elevation. The past 12 years have seen extensive investigations into the use of various cardiac markers to establish the diagnosis and prognosis in ACS and to evaluate perfusion after thrombolysis. The Troponins comprise a group of three proteins (C, I and T) which interact with tropomyosin to form a troponin-tropomyosin complex. Troponin-T is a structural component of the troponin complex and is known to exist in three isoforms. Troponins have both diagnostic, post-event risk stratification and prognostic significance. Apart from myocardial infarction however they are raised in several conditions like Myocarditis, dilated Cardiomyopathy, Severe congestive cardiac failure, severe pulmonary embolism with right ventricular strain and Preterm infants with respiratory distress. False positives have been reported with Angioplasty, cardiac surgery, RF ablation, Allograft rejection following cardiac transplant and seropositive rheumatoid arthritis. False negatives have been reported with early sampling, early reading, use of wrong anticoagulant, clotted blood, careless storage of kits. Significantly, lower troponin values have been reported in heparinised plasma than in serum.
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PMID:Troponins: current status in coronary artery disease. 1584 29

Chronic dyspnea is defined as dyspnea lasting more than one month. In approximately two thirds of patients presenting with dyspnea, the underlying cause is cardiopulmonary disease. Establishing an accurate diagnosis is essential because treatment differs depending on the underlying condition. Asthma, congestive heart failure, chronic obstructive pulmonary disease, pneumonia, cardiac ischemia, interstitial lung disease, and psychogenic causes account for 85 percent of patients with this principal symptom. The history and physical examination should guide selection of initial diagnostic tests such as electrocardiogram, chest radiograph, pulse oximetry, spirometry, complete blood count, and metabolic panel. If these are inconclusive, additional testing is indicated. Formal pulmonary function testing may be needed to establish a diagnosis of asthma, chronic obstructive pulmonary disease, or interstitial lung disease. High-resolution computed tomography is particularly useful for diagnosing interstitial lung disease, idiopathic pulmonary fibrosis, bronchiectasis, or pulmonary embolism. Echocardiography and brain natriuretic peptide levels help establish a diagnosis of congestive heart failure. If the diagnosis remains unclear, additional tests may be required. These include ventilation perfusion scans, Holter monitoring, cardiac catheterization, esophageal pH monitoring, lung biopsy, and cardiopulmonary exercise testing.
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PMID:Evaluation of chronic dyspnea. 1586 93

Current guidelines for the diagnosis of non-ST-segment elevation myocardial infarction are largely based on an elevated troponin level. While this rapid and sensitive blood test is certainly valuable in the appropriate setting, its widespread use in a variety of clinical scenarios may lead to the detection of troponin elevation in the absence of thrombotic acute coronary syndromes. Many diseases, such as sepsis, hypovolemia, atrial fibrillation, congestive heart failure, pulmonary embolism, myocarditis, myocardial contusion, and renal failure, can be associated with an increase in troponin level. These elevations may arise from various causes other than thrombotic coronary artery occlusion. Given the lack of any supportive data at present, patients with nonthrombotic troponin elevation should not be treated with antithrombotic and antiplatelet agents. Rather, the underlying cause of the troponin elevation should be targeted. However, troponin elevation in the absence of thrombotic acute coronary syndromes still retains prognostic value. Thus, cardiac troponin elevations are common in numerous disease states and do not necessarily indicate the presence of a thrombotic acute coronary syndrome. While troponin is a sensitive biomarker to "rule out" non-ST-segment elevation myocardial infarction, it is less useful to "rule in" this event because it may lack specificity for acute coronary syndromes.
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PMID:Narrative review: alternative causes for elevated cardiac troponin levels when acute coronary syndromes are excluded. 1586 11

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


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