Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 29-year-old man with congenital protein C deficiency and acute myocardial infarction is reported. Four hours after the onset of chest pain, he was treated intravenously with tissue-type plasminogen activator. Subsequent coronary angiography revealed only slight stenosis of the left anterior descending coronary artery without any atherosclerosis. The propositus, his brother, and his mother, showed low levels of both protein C activity and antigen, while plasma thrombomodulin levels were normal. His grandfather had died from acute myocardial infarction at 38 years of age. We investigated several other risk factors for arterial thrombosis, including factor VII, fibrinogen, heparin cofactor II, lipoprotein (a), and anticardiolipin antibodies. No other haemostatic abnormalities apart from factor VII hyperactivity were detected in this family. To study the effects of protein C and factor VII on procoagulant activity, prothrombin time was measured after the addition of activated protein C and factor VII to protein C-deficient plasma. The prothrombin time ratio decreased along with an increase in the factor VII level. It also decreased with a decrease in the activated protein C level. These findings indicated that the procoagulant activity of factor VII was enhanced by low protein C levels, suggesting that concomitant factor VII hyperactivity may cause acute myocardial infarction in patients with protein C deficiency.
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PMID:Congenital protein C deficiency and myocardial infarction:concomitant factor VII hyperactivity may play a role in the onset of arterial thrombosis. 144 May 17

A 45-year-old man was admitted with left chest pain and hemoptysis. Chest CT on admission showed multiple areas of wedge-shaped consolidation in both lung fields. A perfusion lung scintigram showed bilateral deficits in both lungs, whereas a ventilation scintigram was normal. The serum concentration and the functional activity of protein C were 41% and 42%, respectively. The same results were obtained from studies of the patient's mother and two sons, which indicated that this was a case of congenital protein C deficiency with pulmonary infarction.
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PMID:[Congenital protein C deficiency with pulmonary infarction]. 773 77

A 32-year-old woman was hospitalized with recurrent left-sided chest pain and dyspnea on exertion, which had progressed for approximately 10 years. Since age 18 she had been spending more than twelve hours per day in a predominantly seated position on a floor mat, engaged in Japanese dressmaking. A chest roentgenogram showed marked dilation of the main pulmonary arteries, bilateral oligemia in the upper lung fields and a peripheral infiltration in the middle field of the left lung. The (99m)Tc-MAA perfusion lung scan showed multiple defects in both lungs, but no abnormal findings were detected on a 133Xe ventilation scan. A pulmonary angiogram showed multiple occlusions of pulmonary arteries in both lungs. Because recurrent chest pain and dyspnea had been present for a long time, and because ultrasonic cardiography revealed pulmonary hypertension repeatedly for several years, pulmonary thromboembolism was considered to be chronic and recurrent. The patient had none of the following risk factors for pulmonary emboli: malignancy, neurological disease, heart disease, obesity, pregnancy, or a congenital coagulative abnormality such as deficiency of AT-III, protein C, protein S, or plasminogen. Because no other cause could be found, the chronic recurrent pulmonary thromboembolism most likely resulted from extensive sedentary work that caused stagnation of venous return and deep vein thrombosis.
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PMID:[Chronic recurrent pulmonary thromboembolism associated with sedentary work]. 862 76

Thrombolytic therapy in acute myocardial infarction fails to re-establish coronary blood flow in a significant number of patients. One reason for this may be haemostatic imbalance. We investigated whether coagulation factor VII antigen (FVIIag), fibrinogen and protein C were related to reperfusion. Plasma from 45 patients was drawn before treatment and reperfusion assessed by means of continuous, on-line, vector-ECG analysis. Among the 17 patients with no reperfusion, FVIIag levels were significantly higher than among the 28 with signs of reperfusion (560 vs. 410 microg/l median, p = 0.006). Protein C levels where higher in the group with successful reperfusion (1.10 vs. 1.01 U/ml median, p = 0.03), whereas no difference was seen in fibrinogen levels. The findings were not influenced by plasma-triglycerides, body-mass index, age or time between onset of chest pain and thrombolytic therapy. The results suggest that FVII is of importance for the formation as well as resolution of coronary clots.
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PMID:Failure of thrombolytic therapy in patients with myocardial infarction is associated with high plasma levels of factor VII antigen. 960 23

There have so far been few reports on esophageal diverticulum in children. We experienced two symptomatic pediatric cases with esophageal diverticulum. Our cases manifested high fever and dysphagia with chest pain during swallowing. The patients underwent endoscopic diverticulotomy. The septum between the diverticulum and the esophagus was cut using the argon plasma coagulation (APC 3000) system. We recommend an endoscopic diverticulotomy as an effective treatment modality for such symptomatic cases.
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PMID:Endoscopic diverticulotomy for symptomatic pediatric esophageal diverticula. 1536 42

Although patients undergoing cardiac surgery often present with diverse comorbidities, those with coagulation derangements are especially challenging. The present report describes the management of a patient who presented with a Factor V Leiden mutation, lupus anticoagulant, and acquired activated protein C resistance. A 42-year-old female presented with acute shortness of breath and chest pain. She was otherwise healthy 1 month prior to admission when she presented with dysfunctional uterine bleeding, resulting in the transfusion of three units of packed red blood cells. Coagulation evaluation revealed that the patient had lupus anticoagulant, factor V Leiden mutation and an activated protein C resistance. The patient presented with an acute myocardial infarction and was found to have 90% stenosis of her left main coronary artery, moderate mitral and tricuspid regurgitation, and a left ventricular ejection fraction of 25%. An emergent off-pump coronary artery bypass procedure with placement of a vein graft to the left anterior descending artery was completed. Intraoperative thrombophilia was encountered as evidenced by both an elevated thromboelastograph coagulation index (+3.6) and an acquired antithrombin-III deficiency. Postoperatively, the patient was placed on low molecular weight heparin, but developed heparin-induced thrombocytopenia and was switched to a direct thrombin inhibitor, argatroban. The following case report describes the coagulation management of this patient from the time of admission to discharge 43 days later, and the unique challenges this combination of hemostatic defects present to the clinicians.
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PMID:Coagulation management of a patient with factor V Leiden mutation, lupus anticoagulant, and activated protein C resistance: a case report. 1591 49

As the debate on packaging of observation charges nears a climax, understand your facility's patient mix and admission policies in order to predict the likely impact and prepare for the changes ahead. If your facility's policy is to admit elderly patients with chest pain, then the packaging of observation charges would have little impact on your department. If you normally send all chest pain patients for observation in a separate unit, increase your efforts to work cooperatively with other units to improve throughput. Inpatient admissions could increase significantly. If APC panel's recommendations are followed, it should be "business as usual" for your ED.
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PMID:APC panel: don't finalize plan for observation packaging. 1807 52

The superior vena cava (SVC) syndrome is due to obstruction of the SVC and may present by dyspnea, chest pain, cough, headache, dysphasia, and symptoms of increased intracranial pressure; however, the affected patients can be asymptomatic. Numerous collateral veins are often seen on the upper chest, arms and neck. The syndrome may be caused by prolonged use of indwelling catheters, but is an infrequently reported complication in the hemodialysis patients. We report two patients who developed SVC syndrome several months after removal of hemodialysis indwelling catheters. The causes of this syndrome in our patients were stenosis in one patient and thrombosis in the other; venous endothelial injury and subnormal levels of protein C and S were possible contributory factors. These cases illustrate that SVC syndrome is a possible late complication after removal of hemodialysis indwelling catheters.
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PMID:The superior vena cava syndrome: late presentation after hemodialysis catheter removal. 1820 44

A 81-year-old woman was referred to the emergency department after having syncopal episode two days earlier. A chest computed tomography demonstrated a right main pulmonary artery embolism. The only prominent risk factor for thromboembolism was her poor response to activated protein C. Seven days later she demonstrated acute-onset chest pain with elevated troponin. Cardiac angiography showed stenosis of left anterior descending coronary artery which was successfully treated with angioplasty and stent implantation. This case illustrates the coincidence and the importance of clinical suspicion for the early diagnosis and treatment of acute coronary syndrome during massive pulmonary embolism.
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PMID:[Acute coronary syndrome following massive pulmonary embolism in a 81-year-old woman with thrombophilia]. 1853 61

Bicuspid aortic valve is one of the most common congenital heart valve disorders. We present the development of acute myocardial infarction (AMI) in an 18-year-old male patient with unrecognized bicuspid aortic valve and moderate aortic regurgitation. He presented with chest pain. The electrocardiogram showed ST-segment elevation in leads V2 to V6. Creatine kinase-MB level was elevated to 97 U/l and troponin I was very high (45,000 ng/ml). The diagnosis was made as anterior wall AMI. Following treatment with intravenous rt-PA, ST-segment elevation completely returned to normal. Transthoracic echocardiography showed a bicuspid aortic valve, moderate aortic regurgitation, and apical wall hypokinesia; left ventricular global systolic function was normal. The patient had no risk factors for coronary atherosclerosis, nor a history of substance addiction or a family history of coronary artery disease. Protein C, protein S and homocysteine levels were normal. He refused any further intervention. Two weeks after discharge, he presented again with chest pain. Electrocardiography, cardiac markers, and coronary arteriography were normal. He was discharged on appropriate medical treatment. The presented case is the first report of AMI in a patient with bicuspid aortic valve.
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PMID:Acute myocardial infarction in a young patient with bicuspid aortic valve. 2120 14


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