Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrocardiographic (ECG) findings of pulmonary embolism (PE) include S1Q3T3 pattern, right bundle-branch block, right-axis deviation, and T-wave inversion in medial precordial leads. We report other uncommon ECG changes associated with various symptoms during recurrent PE as documented by computed tomography (CT) scans in a single patients. An 83-year-old woman was admitted with PE secondary to deep venous thrombosis in the left leg. During episodes of chest pain, ECG showed QTc prolongation (480 ms) with new T-wave inversion in leads III, aVF, and V1-V3, and ST-segment depression in leads V5-V6. Despite adequate anticoagulant therapy, recurrent episodes of PE occurred in the hospital. When the patient experienced sudden chest tightness, ECG showed a new S-wave notch in lead V1 and clock-wise rotation with sinus tachycardia. She also experienced transient syncope with hypotension. At this time, ECG showed transient atrioventricular junctional rhythm followed by sinus arrest, and CT scan showed a new massive embolus in the main pulmonary trunk with right ventricular dilatation, as demonstrated by echocardiography. The mechanism responsible for QTc prolongation with ST-T changes, the S-wave notch in lead V1 with clockwise rotation, or atrioventricular junctional rhythm with sinus arrest during PE may be associated with myocardial ischemia, acute right ventricular overload, or vagal reflex, respectively.
 ...
PMID:Uncommon electrocardiographic changes corresponding to symptoms during recurrent pulmonary embolism as documented by computed tomography scans. 982 4

Two previously healthy patients were admitted for chest pain, haemoptysis and dyspnoea. Perfusion-ventilation lung scanning demonstrated pulmonary embolism. Lower extremity duplex imaging and contrast venography revealed a thrombosed popliteal vein aneurysm as the source of emboli. After immediate anticoagulant therapy, the thrombo-embolic source was excluded by aneurysmectomy with lateral venography in the first patient. The second patient was treated by anticoagulants and percutaneous vena cava inferior filter placement to prevent recurrent pulmonary embolism. Anatomopathological findings, possible origin, diagnostic modalities and medical and surgical treatment of popliteal vein aneurysm are discussed.
 ...
PMID:Popliteal venous aneurysm with pulmonary embolism. 983 13

We experienced 23 cases of venous thrombosis after gynecological surgery for the past 12 years at Tokyo Women's Medical University Hospital, representing 0.345 % of all patients. Eighteen of the 23 cases had deep venous thrombosis (DVT) including five cases followed by pulmonary embolism (PE), and five cases had PE without any symptoms of DVT. The main risk factors for thrombosis in these 23 patients were (1) obesity, DM, hyperlipidemia; (2) huge abdominal tumor, severe adhesion; and (3) hemoconcentration, post-treatment of severe anemia. The onset of PE varied from 1 to 3 postoperative days, when the patients started to walk. Five cases had dyspnea, chest pain, and decreased PaO2 levels without leg pain, while five cases showed only calf pain and tenderness with decreased PaO2 levels. PE was confirmed by immediate diagnostic images such as RI venography with ventilation and perfusion lung scan, pulmonary arterial CT, or pulmonary arteriography. Two patients died and eight patients recovered. The best way of managing venous thrombosis might be as follows: (1) identify the risk factors of thrombosis before surgery; (2) perform prophylactic leg exercises in bed and/or active anticoagulant therapy depending on the degree of risk factors; (3) rapid diagnosis with the images; and (4) proper treatment.
 ...
PMID:Management of venous thrombosis and pulmonary embolism after gynecological surgery. 983 10

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.
 ...
PMID:A phase II study of DaunoXome in advanced urothelial transitional cell carcinoma. 984 67

Pulmonary embolism is commonly misdiagnosed as lung cancer, since sputum cytological tests often show atypical or malignant cells. We report three operated cases of pulmonary embolism incorrectly diagnosed as lung cancer. The first patient is a 39-year-old male with chest pain an bloody sputum. Chest x-ray revealed abnormal shadows and subsequent sputum cytological tests identified malignant cells. The second patient is a 63-year-old male with the same diagnostic pattern as the first case. The third patient is a 72-year-old male whose routine chest x-ray showed an abnormal shadow; malignant cells were identified by cytological tests on transbronchial fiberscope brushings. These three patients were histopathologically diagnosed as suffering pulmonary embolism by wedge resection under thoracotomy. When a patient has chest pain or bloody sputum with showing temporarily malignant cells on cytology, the possibility of pulmonary embolism should be taken into consideration.
 ...
PMID:[Three cases of pulmonary embolism incorrectly diagnosed as lung cancer]. 988 65

To provide clinical diagnostic criteria for pulmonary embolism (PE), we evaluated 750 consecutive patients with suspected PE who were enrolled in the Prospective Investigative Study of Acute Pulmonary Embolism Diagnosis (PISA-PED). Prior to perfusion lung scanning, patients were examined independently by six pulmonologists according to a standardized diagnostic protocol. Study design required pulmonary angiography in all patients with abnormal scans. Patients are reported as two distinct groups: a first group of 500, whose data were analyzed to derive a clinical diagnostic algorithm for PE, and a second group of 250 in whom the diagnostic algorithm was validated. PE was diagnosed by angiography in 202 (40%) of the 500 patients in the first group. A diagnostic algorithm was developed that includes the identification of three symptoms (sudden onset dyspnea, chest pain, and fainting) and their association with one or more of the following abnormalities: electrocardiographic signs of right ventricular overload, radiographic signs of oligemia, amputation of hilar artery, and pulmonary consolidations compatible with infarction. The above three symptoms (singly or in some combination) were associated with at least one of the above electrocardiographic and radiographic abnormalities in 164 (81%) of 202 patients with confirmed PE and in only 22 (7%) of 298 patients without PE. The rate of correct clinical classification was 88% (440/500). In the validation group of 250 patients the prevalence of PE was 42% (104/250). In this group, the sensitivity and specificity of the clinical diagnostic algorithm for PE were 84% (95% CI: 77 to 91%) and 95% (95% CI: 91 to 99%), respectively. The rate of correct clinical classification was 90% (225/250). Combining clinical estimates of PE, derived from the diagnostic algorithm, with independent interpretation of perfusion lung scans helps restrict the need for angiography to a minority of patients with suspected PE.
 ...
PMID:Accuracy of clinical assessment in the diagnosis of pulmonary embolism. 1005 Dec 64

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
 ...
PMID:[Angina pectoris in extracoronary diseases]. 1037 99

A 45-year-old man was admitted complaining of chest pain and pain and edema in the left lower extremity. Ultrasonography and venography results yielded a diagnosis of left femoral vein thrombosis, and pulmonary embolism was diagnosed later. Intravenous heparin therapy (10,000 IU/day) improved the patient's clinical signs. During this therapy, however, pain and edema of the right lower extremity developed, leading to a diagnosis of right femoral vein thrombosis. The patient was admitted to our hospital. At that time, coagulation studies showed an FDP level of 44.7 micrograms/ml and an FDP-DD level of 24.5 micrograms/ml. We surmised that the bilateral deep vein thrombosis had been caused by hyperhomocysteinemia (17.8 mumol/l). Genetic and other acquired risk factors for thrombophilia were ruled out. The patient's clinical signs again improved as a result of intravenous heparin therapy (15,000 IU/day), and FDP and FDP-DD levels returned to normal. We concluded that hyperhomocysteinemia is a risk factor for thrombosis and that it can generate thrombosis in other locations even during heparin therapy.
 ...
PMID:[Hyperhomocysteinemia: development of deep vein thrombosis in another location during heparin anticoagulation therapy]. 1039 Aug 88

A case of acute pulmonary embolism following high ligation and compression sclerotherapy for varicose veins is reported. A 54-year-old women developed superficial varicosities and stasis pigmentation on her left leg 1 year prior to her first visit to hospital. No deep vein thrombosis was detected by ascending phlebography performed 3 months prior to operation. High ligation combined with compression sclerotherapy was performed for the varicose veins. One day after treatment, the patient complained of chest pain and discomfort, and then collapsed. Perfusion scintigraphy revealed multiple embolisms in the bilateral lungs. The patient recovered after aggressive anticoagulant and thrombolytic therapy. Although pulmonary embolism is a rare complication of sclerotherapy, it is potentially one of the most serious.
 ...
PMID:Acute massive pulmonary embolism following high ligation combined with compression sclerotherapy for varicose veins report of a case. 1041 91

Pulmonary embolus in children is rare. A case of massive pulmonary embolus, after surgery, in a child of 14 years is described. Accident and emergency doctors should be aware that pulmonary embolus can occur in children and exercise a high index of suspicion for the diagnosis in those patients with risk factors for the condition who present acutely with typical symptoms such as dyspnoea, chest pain, haemoptysis, or collapse.
 ...
PMID:Massive pulmonary embolus in a 14 year old boy. 1041 42


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>