Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
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Liposomal encapsulation of anthracyclines is claimed to reduce toxicity and to improve pharmacokinetics. Therefore, 15 patients with locally advanced or metastatic transitional cell cancer (TCC) of the urinary tract were entered into a phase II study assessing the response rate (WHO criteria) and toxicity of DaunoXome 100 mg/m2 given as a 1 h infusion every third week. During treatment, 6 patients remained stable and 8 had progressive disease. 1 patient died of pulmonary embolism after the first cycle and was not evaluable for response. No patient developed grade 4 myelotoxicity. Grade 3 leucopenia was seen in 5 patients and grade 1 thrombocytopenia in 1 patient, with no treatment-related changes of biochemical liver and kidney function tests. 4 patients complained of angina pectoris-like chest pain during the initial phase of the first or second infusion. The event was associated with a decrease in systolic blood pressure by 20-30 mm in 1 patient leading to permanent treatment discontinuation. In the other 3 and all subsequent patients, intramuscular application of 100 mg hydrocortisone 1 h prior to DaunoXome infusion prevented similar hypotensive reactions. In this study, intravenous (i.v.) DaunoXome 100 mg/m2 every third week showed no anticancer activity in advanced TCC.
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PMID:A phase II study of DaunoXome in advanced urothelial transitional cell carcinoma. 984 67

Chest pain can arise from cardiovascular or noncardiovascular causes. Among the latter are the skin, the chest wall, intrathoracic structures, or subdiaphragmatic organs. The problem to attribute the chest discomfort to either the heart or extracardiac organs arises because the heart, pleura, aorta, and esophagus are all supplied by sensory fibers from the same spinal segments. In contrast to the diseases mentioned above, angina pectoris in sensu strictu is defined as chest pain or discomfort of cardiac origin that arises because of temporary imbalance between myocardial oxygen supply and demand. The metabolic oxygen requirements of the myocardium are essentially dictated by myocardial contraction since only a fraction of the consumed oxygen is needed by the quiescent heart. Therefore, the factors that primarily influence myocardial oxygen consumption include heart rate, the force of cardiac contraction, and myocardial wall tension, as determined by pressure (afterload), volume (preload), and wall thickness. Extracoronary diseases, e.g. hypertensive heart disease, aortic stenosis or cardiomyopathies, can influence these factors and induce angina pectoris (Figure 1). On the other hand, different diseases influencing the oxygen supply, e.g. anemia, can cause angina pectoris, too. In addition, the modulation of the coronary tone by mediators and cytokines can cause angina, coronary spasm being one example. The neurophysiological substrate of angina pectoris are ganglia which are present within the heart, particularly in epicardial fat. The sympathetic nervous system is the main conveyer of afferent pain fibers from the heart and pericardium, but many fibers may travel by the vagus and the phrenic nerves. Therefore, multiple thoracic structures may cause similar pain syndromes in the distressed patient. The blood supply of intrinsic cardiac ganglia arises primarily from branches of the proximal coronary arteries. Adenosine, among a number of substances, can modulate the activity generated by cardiac afferent nerve endings and intrinsic cardiac neurones. During myocardial ischemia adenosine is released in large quantities into the interstitial space. Given as an intravenous bolus to healthy volunteers or to patients with ischemic heart disease and angina pectoris, adenosine provokes angina pectoris-like pain, which is similar to habitual angina pectoris with regard to quality and location. But other mediators (e.g. bradykinin, histamine, prostaglandins, potassium, lactate) can be involved in the development of angina pectoris, too. As most emphasis should be given to the most serious causes first, the cardiologist has to consider ischemic cardiac disease in the differential diagnosis of nearly every case of acute chest pain. The differential diagnosis contains several causes of nonischemic cardiac chest pain. Dissecting aortic aneurysm may cause severe anterior chest pain that can be mistaken for myocardial infarction. Patients frequently will note the sudden onset of the pain rather than the relatively slower onset of ischemic pain. Furthermore, they feel as a tear and describe it as the most severe pain they have ever had. Pericarditis can be characterized as a sharp precordial knife-like pain that is often increased by lying down, breathing, swallowing, or any other thoracic motion. Radiation of pericardial pain is often relieved by sitting up or leaning forward. It may involve the shoulders, upper back, and neck because of the irritation of the diaphragmatic pleura. Acute pulmonary embolism is associated with severe chest pain. It may mimic acute myocardial infarction. Pulmonary embolism should be suspected when dyspnea or tachypnea seems to be disproportionate to the severity of the chest pain. Diffuse esophageal spasm is the extracardiac condition that is confused most often with ischemic cardiac chest pain. This pain presents as a deep thoracic pain that may be present over most of the thorax. It may extend down the anterome
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PMID:[Angina pectoris in extracoronary diseases]. 1037 99

Antiplatelet drugs have been demonstrated to reduce the incidence of myocardial infarction (MI), stroke or vascular death in patients with vascular disease. There are no data suggesting that antiplatelet therapy acts differently in older people than in younger people and recommendations based on randomised clinical trials are probably generalisable to older people. Aspirin (acetylsalicylic acid) has been shown to reduce the incidence of non-fatal MI, nonfatal stroke and vascular death in patients with acute MI, a previous MI, angina pectoris or peripheral occlusive arterial disease (POAD), and to reduce cardiovascular morbidity and mortality in patients with a prior ischaemic stroke or transient ischaemic attack (TIA). It has also been shown to reduce the incidence of thrombus formation after coronary artery bypass graft surgery and percutaneous transluminal angioplasty, and in patients with atrial fibrillation and heart valve replacements. Deep vein thrombosis and pulmonary embolism after surgery are also prevented by aspirin. The available data allows the following recommendations to be made. Aspirin 160 to 325 mg daily should be administered to older men and women without contraindications to aspirin who have acute MI, prior MI, unstable or stable angina pectoris, ischaemic stroke, TIA or POAD, and continued indefinitely to reduce the risk of MI, stroke or vascular death. Aspirin should be started in patients before or immediately after revascularisation, and after heart valve replacement. Older men and women with nonvalvular atrial fibrillation who have contraindications to oral anticoagulant therapy but no contraindications to aspirin should be treated with aspirin 325 mg daily. It is reasonable to treat older men and women without contraindications to aspirin with aspirin 160 to 325 mg daily if they are at high risk for developing new coronary events. The incidence of stroke, MI or vascular death in patients after a stroke or TIA is reduced by ticlopidine. Therefore, ticlopidine 250 mg twice daily may be used in older men and women with a history of stroke or TIA who do not respond to or who cannot tolerate aspirin. Patients at high risk for coronary artery stent thrombosis benefit from combined therapy with aspirin plus ticlopidine. The annual incidence of ischaemic stroke, MI or vascular death was significantly reduced by clopidogrel in the Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events (CAPRIE) trial. Therefore, clopidogrel 75 mg daily may be used in older men and women with symptomatic atherosclerosis who do not respond to or who cannot tolerate aspirin to reduce the incidence of ischaemic stroke, MI or vascular death. It should be noted that the acquisition cost for either ticlopidine or clopidogrel is considerably greater than that for aspirin. Most data indicate that the combination of aspirin and dipyridamole is not more effective than aspirin alone in preventing vascular events, and available data do not support the use of sulfinpyrazone in patients with vascular disease.
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PMID:Antiplatelet agents in the prevention of cardiovascular morbidity and mortality in older patients with vascular disease. 1049 69

1999 has been a good year in the field of innovation in thrombosis. In coronary syndrome without ST elevation: low molecular weight heparin has been confirmed to be more effective than non-fractionated heparin (enoxaparin) and to improve the prognosis of non-revascularised patients (dalteparin) after the hospital phase; hirudin has been shown to be more effective in terms of incidence of myocardial infarction and recurrence of angina than non-fractionated heparin without a higher incidence of bleeding complications; the anti-GP IIb-IIIa (abciximab) has confirmed all its advantages at 6 months and 1 year after a coronary event. The association of heparin and aspirin, which has been the mainstay of antithrombotic treatment of acute coronary syndromes without ST elevation, will soon be improved upon at the beginning of the third millennium. In myocardial infarction, medical thrombolysis has probably reached a turning point in its history. The association of half doses of rt-Pa and anti-GP IIb-IIIa has been shown to be more effective in obtaining good reflow than the thrombolytic agent alone at conventional doses. These results were obtained without any increase in bleeding complication. The same anti-GP IIb-IIIa also improve mechanical revascularisation by optimising reperfusion after the 24th hour. This benefit is rapidly transformed into reduced left ventricular dysfunction. Pulmonary embolism remains a critical illness as the ICOPER registry reports a 3 year mortality of nearly 16%. This emphasises the importance of early diagnosis which is usually possible without resorting to invasive procedures and by modulating all the results of paraclinical investigations with respect to the pretest clinical probability.
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PMID:[The best of thrombosis and thromboembolic disease in 1999]. 1072 51

An analytical and clinical evaluation of cardiac troponin I (cTnI) on the IMMULITE system is presented. The assay results were compared with those of the Stratus II and the Dimension RxL-HM. A between-run imprecision CV < 20% was found at a cTnI concentration of 0.23 microg/L (functional limit of detection). On the basis of a reference study including 215 patients without ischemic heart disease (97.5th percentile: 0.294 microg/L) and 36 patients clinically classified as having stable angina pectoris (<0.22 microg/L) a preliminary cutoff level of 0.3 microg/L was defined. Assay linearity, sample stability, influence of sample material and method comparison studies were performed. In patients with Duchenne's disease, chronic hemodialysis treatment, pulmonary embolism, coronary artery bypass surgery and minimally cardiac surgery the cTnI results of the IMMULITE agreed better with the Dimension RxL-HM than with the Stratus II data. Of 142 samples from patients with unstable angina 67 samples were classified as cTnI positive with the IMMULITE, 76 with the Dimension RxL-HM, and 62 with the Stratus II. In conclusion, the new assay is sensitive for the determination of cTnI and easy to perform within 45 min.
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PMID:Comparison of diagnostic performance of cardiac troponin I on the IMMULITE system with other automated troponin I assays in minor myocardial damage. 1138 9

Blood clots form under hemodynamic conditions and can obstruct flow during angina, acute myocardial infarction, stroke, deep vein thrombosis, pulmonary embolism, peripheral thrombosis, or dialysis access graft thrombosis. Therapies to remove these clots through enzymatic and/or mechanical approaches require consideration of the biochemistry and structure of blood clots in conjunction with local transport phenomena. Because blood clots are porous objects exposed to local hemodynamic forces, pressure-driven interstitial permeation often controls drug penetration and the overall lysis rate of an occlusive thrombus. Reaction engineering and transport phenomena provide a framework to relate dosage of a given agent to potential outcomes. The design and testing of thrombolytic agents and the design of therapies must account for (a) the binding, catalytic, and systemic clearance properties of the therapeutic enzyme; (b) the dose and delivery regimen; (c) the biochemical and structural aspects of the thrombotic occlusion; (d) the prevailing hemodynamics and anatomical location of the thrombus; and (e) therapeutic constraints and risks of side effects. These principles also impact the design and analysis of local delivery devices.
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PMID:Engineering design of optimal strategies for blood clot dissolution. 1170 96

Chest pain does not necessarily indicate cardiac disease. The most common causes of acute chest pain encountered in dental situations include hyperventilation, pulmonary embolism, angina pectoris and myocardial infarction. Stress and fear often cause rapid breathing or hyperventilation. This usually occurs in young adults and although the hyperventilating patient often complains of chest pain, this is rarely a manifestation of cardiac disease. Pulmonary embolism usually indicates the occlusion of a pulmonary artery causing severe chest pain. The primary clinical manifestation of angina pectoris is chest pain. Although most instances of anginal pain are easily terminated, the dentist must always consider the possibility that the supposed anginal attack is actually a sign of acute myocardial infarction (AMI). AMI is a clinical syndrome caused by a deficient coronary arterial blood supply to a region of myocardium that results in cellular death. There is a high incidence of mortality among AMI with death often occurring within 2 hours of the onset of signs and symptoms. The initial clinical manifestations of all types of chest pain can be similar. Therefore the dentist must develop proficiency in constituting a differential diagnosis and an efficient management protocol. As in most medical situations prevention is the most powerful tool. However, if chest pains do occur, measures such as airway management, oxygen supplementation, coronary artery dilation, analgesis and in extreme cases, cardiopulmonary resuscitation and evacuation to the emergency room, may be necessary.
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PMID:[Chest pains in the dental environment]. 1185 49

In order to verify the safety of an ideal length of hospital stay (5-6 days) after open colectomy, we reviewed complications after 371 consecutive, elective colorectal resections for cancer at our institution between April 1991 and December 1998. Specifically, age of the patient, length of hospital stay and when the complication was diagnosed were registered. The median postoperative hospital stay was 9 days (range, 4-34 days). No difference in length of hospital stay was detected in patients < or = 65 years old versus > 65 years old (P = NS). All major complications (anastomotic leak, intestinal bleeding, intestinal occlusion, pneumonia, pulmonary embolism, pulmonary edema, stroke, angina pectoris, and fascial dehiscence) were diagnosed before the fifth postoperative day (P < 0.05). Among the minor complications (vomiting, packed red blood cells transfusion, diarrhea, wound infection, urinary tract infection, and pleural effusion), none requiring hospitalization was detected later then 5 days after the operation. We conclude that postoperative length of stay after colorectal resection for cancer can be reduced safely to five to six days after the operation.
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PMID:[The ideal length of hospital stay in the surgical treatment of colorectal cancer]. 1214 16

We report a case of suspected fatal physical abuse in which the cause of death was proved to be pulmonary embolism. A patient with mental retardation presenting aggressive behavior was admitted to a psychiatric hospital and was treated with major tranquilizers. She suddenly died subsequent to an angina-like attack. For several days before her death, she had been confined to her bed because of very low physical and mental activity. Bruises and abrasions were observed on the extremities, suggesting the recent restraints. There was no positive evidence of physical abuse. At autopsy, the cause of death was elucidated to be pulmonary embolism originating from thrombi in the left popliteal vein. This case indicates the risk of pulmonary embolism in immobilized patients in psychiatric hospitals.
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PMID:Pulmonary embolism: a case of sudden unexpected death in a psychiatric hospital. 1293 91

Pneumomediastinum is the presence of air in the mediastinum. Spontaneous pneumomediastinum (SPM) is an infrequent, benign, and self-limiting condition that predominantly affects young males and pregnant females. It is important to distinguish pneumomediastinum symptoms from similar clinical findings that require immediate treatment, such as cardiac tamponade, angina pectoris, dissecting aortic aneurysm, mediastinitis, and pulmonary embolism. This report describes 2 cases of SPM managed at University Hospital Hamburg-Eppendorf during the period 2000 to 2001. Spontaneous pneumomediastinum should be considered whenever there are anamnestic data for retrosternal chest pain that radiates to the neck or back accompanied by dysphagia, dysphonia, dyspnea, and a positive Hamman's sign.
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PMID:Spontaneous pneumomediastinum. 1527 60


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