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)

We describe an autopsy case of severe intracranial hemorrhage which occurred during the infusion of tissue plasminogen activator (t-PA) for acute myocardial infarction. A 75-year-old man was admitted with substernal chest pain of 3-h duration and electrocardiographic changes consistent with an acute inferior myocardial infarction. Physical examination was unremarkable, except for an initial blood pressure reading of 160/96 mmHg. The patient received 3,000 IU intravenous heparin followed by a 2.4 x 10(6) IU bolus dose of tissue plasminogen activator (t-PA) (Alteplase). This was followed by a drip infusion of 21.6 x 10(6) IU of t-PA over 1 h (total dose 41 mg). Thirty minutes after the infusion of t-PA was initiated, the patient suddenly lost consciousness and began to have violent convulsions, followed by cardiac arrest. Autopsy revealed massive hemorrhage in the bilateral cerebrum and brain stem. To our knowledge, this is the first case of sudden death during t-PA infusion therapy.
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PMID:An autopsy case of intracranial hemorrhage during tissue plasminogen activator infusion. 840 27

A 1 year (1995) retrospective audit of all patients who were discharged or died, with a primary diagnosis of acute myocardial infarction (AMI) was conducted at Auburn Hospital, a level 4 district hospital in Sydney's western suburbs. After their first echocardiogram (ECG), 21 patients of 129 patients who had a primary diagnosis of AMI in the Emergency Department at this time were given thrombolytic therapy. For eight patients there was a time delay of over 60 min to commencement of thrombolytic therapy. This time delay exceeded the Australian Council of Health-care Standards guidelines and was targeted as a quality improvement activity. The hospital cardiologist convened meetings of medical and nursing staff, to develop an action plan for reducing these delays. The strategies adopted, implemented between April and September 1996, involved (i) keeping the ECG machine in the emergency department at all times, (ii) installing a facsimile machine, (iii) keeping Alteplase (rt-PA) in the emergency department, (iv) staff education, (v) allowing senior medical staff to initiate treatment if the consultant was not readily contactable. Resulting from these initiatives time delays (after first ECG) were reduced from a median time of 55 min in 1995 to a median time delay of 43 min in 1997. This study highlights areas of unnecessary delay in patients receiving thrombolytic therapy and shows that these delays can be reduced by the implementation of relatively simple strategies by medical and nursing staff. Time delays from the development of symptoms (usually chest pain) to arrival at triage were recorded when such a time was specified in the clinical notes. The median delay from the development of chest pain to triage was 73 min.
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PMID:Reducing thrombolytic therapy time delays in the emergency department. 963 47

A 61-year-old male with a history of severe heparin-induced thrombocytopenia (HIT) type II after aorto-femoral bypass surgery presented to the emergency department within 8 hours of development of substernal chest pain radiating to the left arm. Electrocardiogram (ECG) on arrival and at 3 hours showed no acute changes; cardiac enzymes revealed minimal MB elevation. Echocardiogram showed normal left ventricular systolic function with mild mitral and tricuspid regurgitation and trace aortic insufficiency. Five hours after arrival, the patient reported a recurrence of severe chest pain. ECG showed marked ST elevations consistent with acute myocardial infarction. Reteplase was administered with concomitant lepirudin. Follow-up ECG showed improvement in ST-segment elevation and eventual resolution to pre-event tracing; cardiac enzymes showed slight elevations. Catheterization revealed 90% midstenosis of the left anterior descending artery, which was successfully treated with percutaneous transluminal coronary angioplasty (PTCA) and stent placement. Repeat PTCA was performed 10 days postdischarge due to intraluminal stent occlusion. The patient was doing well at 6 months follow-up.
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PMID:Concurrent use of reteplase and lepirudin in the treatment of acute anterior wall myocardial infarction. 1172 71

Intracranial haemorrhage is a known complication after fibrinolytic therapy and occurs usually in the first 24 h. We report a 35-year-old woman who presented with severe central chest pain and she was diagnosed as anterior ST elevation myocardial infarction. She was given fibrinolytic therapy with Tenecteplase. She responded well to the treatment with a decrease in the intensity of chest pain and resolution of the ST segment elevation. She was taken for coronary angiogram the next day, which revealed an occlusion of the left anterior descending (LAD) artery, and stenting of LAD was carried out. Four days later, she developed severe headache, confusion, slurring of speech and right haemiparesis. CT brain revealed intracerebral haemorrhage and she was referred to an neurosurgeon who advised for conservative management. Her condition gradually improved with physiotherapy and was discharged home with no marked functional impairment.
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PMID:Intracranial haemorrhage 4 days after receiving thrombolytic therapy in a young woman with myocardial infarction. 2370 57

A 24-year-old male was presented to us with sudden onset of chest pain and dyspnea for the past one hour. There was no history of calf pain, trauma, surgery, prolonged immobilization, long-haul air travel, bleeding diathesis or any other co-morbidity. The patient denied any addiction history. The Electrocardiogram showed tachycardia with S 1Q 3T 3 pattern. The left arterio-venous Doppler study was suggestive of a thrombus in popliteal vein and sapheno-popliteal junction. The CT-Pulmonary Angiogram scan was suggestive of a massive pulmonary thromboembolism. The patient was thrombolysed with Intravenous Alteplase immediately and was put on tab Rivaroxaban for maintenance. He was later discharged after being stable. Unprovoked venous thromboembolism (VTE) is very rare and has the potential to lead to pulmonary embolism which could be disastrous, especially in young adults. We present such a case where unprovoked VTE was diagnosed and treated. This case suggests that high clinical suspicion is the key for the diagnosis of acute pulmonary embolism, especially in the absence of history suggestive of deep vein thrombosis.
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PMID:Case Report: Unprovoked venous thromboembolism in a young adult. 3098 84

A 24-year-old male was presented to us with sudden onset of chest pain and dyspnea for the past one hour. There was no history of calf pain, trauma, surgery, prolonged immobilization, long-haul air travel, bleeding diathesis or any other co-morbidity. The patient denied any addiction history. The heart rate was 114 beats/min, and blood pressure was 106/90 mmHg. Electrocardiogram showed tachycardia with S 1Q 3T 3 pattern. The left arterio-venous Doppler study was suggestive of a thrombus in popliteal vein and sapheno-popliteal junction. The CT-Pulmonary Angiogram scan was suggestive of a massive pulmonary thromboembolism. The patient was thrombolysed with Intravenous Alteplase immediately and was put on tab Rivaroxaban for maintenance. He was later discharged after being stable. Unprovoked venous thromboembolism (VTE) is very rare and has the potential to lead to pulmonary embolism which could be disastrous, especially in young adults. We present such a case where unprovoked VTE was diagnosed and treated. This case suggests that high clinical suspicion is the key for the diagnosis of acute pulmonary embolism, especially in the absence of history suggestive of deep vein thrombosis.
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PMID:Case Report: Unprovoked venous thromboembolism in a young adult male. 0