Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among 392 consecutive patients admitted for acute myocardial infarction and treated with thrombolytic drugs, 4 patients (1%) developed an early hemorrhagic pericardial effusion (without ventricular wall rupture) evolving within 24 h to cardiogenic shock consequent to cardiac tamponade. They all suffered from a large anterior myocardial infarction treated within 4 h after onset of symptoms with intravenous anisoylated plasminogen streptokinase activator complex (one case), recombinant tissue-type plasminogen activator (rt-PA) (two cases) or streptokinase (one case), anticoagulation with heparin (all cases) and aspirin (three cases). As soon as pericardial effusion was established by echocardiography, emergency percutaneous pericardiocentesis was performed at the bedside 20 +/- 6 h after thrombolytic therapy was started. This corrected immediately the clinical and hemodynamic status of each patient and a catheter was left in the pericardial space for 34 +/- 18 h. Thus, in the presence of unexplained clinical and hemodynamic deterioration occurring during the first 24 h after thrombolytic treatment of a large myocardial infarction, cardiac tamponade should be suspected. Immediate percutaneous pericardiocentesis followed by continuous drainage is a simple and definitive treatment for this complication.
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PMID:Cardiac tamponade early after thrombolysis for acute myocardial infarction: a rare but not reported hemorrhagic complication. 189 52

The effect of thrombolytic therapy on the frequency, time course and sequelae of pericardial effusion after myocardial infarction are unknown. A prospective, serial, 2-dimensional echocardiographic study of patients with myocardial infarction who received recombinant tissue-type plasminogen activator (rt-PA) was undertaken to address this issue. The study population comprised 52 of the 112 patients enrolled in the first Thrombolysis and Angioplasty in Myocardial Infarction trial at Duke University Medical Center. Enrollment in the serial echocardiography protocol was determined by equipment and support staff availability. Complete echocardiographic studies were performed within 90 minutes after initiation of thrombolytic therapy (day 0), and on days 1, 3 and 6. Patients undergoing serial echocardiography did not differ in demographic or clinical characteristics from those who did not. Pericardial effusion was present in 3 of 38 patients (8%) at day 0, in 2 of 44 (5%) at day 1, in 8 of 43 (19%) at day 3, and in 10 of 42 (24%) at day 6. By day 6, 3 of 10 pericardial effusions were moderate in size, 1 of 10 was large and the remainder were small. No patients developed echocardiographic or hemodynamic signs of cardiac tamponade. The prevalence and time course of pericardial effusion among patients with acute myocardial infarction who received rt-PA in this study are similar to observations reported in earlier studies in which patients did not receive thrombolytic therapy. Adverse sequelae of pericardial effusion after thrombolytic therapy are rare.
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PMID:Pericardial effusion after intravenous recombinant tissue-type plasminogen activator for acute myocardial infarction. 190 Jan 39

We report a rare case of coronary artery perforation by a guide wire for percutaneous transluminal coronary angioplasty (PTCA) complicating with postinfarction cardiac rupture (oozing type). The patient had acute myocardial infarction on the extensive anterior wall and developed cardiac rupture followed by serious cardiac tamponade during the emergency PTCA several hours after tissue plasminogen activator (t-PA) given intravenously. The meandering left anterior descending artery (LAD) was found injured by a PTCA guide wire apart from a small oozing-type cardiac rupture near the apex. We repaired urgently the perforated LAD as well as the ruptured left ventricle. It is thus suggested that coronary artery perforation by a PTCA guide wire may occur on meandering coronary arteries and develop a serious hemorrhagic complication, particularly after thrombolytic therapy.
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PMID:[A rare case of coronary artery perforation by a PTCA guide wire complicating with postinfarction cardiac rupture after thrombolytic therapy]. 759 50

The case of a 62-year-old diabetic and smoker male who was under study in another hospital due to anemia, thrombopenia and hematuria of several months of evolution is presented. The patient was admitted to the coronary unit for an acute extensive transmural myocardial infarction and treated with t-PA. A few hours later the patient presented hematuric urine, a decrease in hemoglobin and platelets and acute renal insufficiency. Hematologic study confirmed the diagnosis of paroxystic nocturnal hemoglobinuria. The evolution of the patient was poor despite intensive medical treatment requiring hemodialysis. The patient presented cardiac tamponade and died. The role of hematologic disease in acute myocardial infarction and the treatment and evolution of the coronary syndrome in the context of the disease are discussed.
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PMID:[Acute myocardial infarction in nocturnal paroxysmal hemoglobinuria]. 1125 45

A 56-year-old female presented to the emergency department with evolving cardiac tamponade after receiving alteplase for acute ischemic stroke. This is the first case report of cardiac tamponade from thrombolytics in the setting of recent pacemaker placement. Point-of-care ultrasound was used to make the diagnosis quickly and expedite the patient to the operating room where a pericardial window was performed.
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PMID:Alteplase Causing Cardiac Tamponade after Recent Cardiac Pacemaker Placement. 3008 36

Alteplase, or tissue plasminogen activator (tPA), lyses clots by enhancing activation of plasminogen to plasmin. Conversely, tranexamic acid (TXA) functions by inhibiting the conversion of plasminogen to plasmin, which inhibits fibrinolysis. TXA has proven safe and effective in major bleeding with various etiologies. A 76-year-old male developed acute ischemic stroke symptoms. Systemic alteplase was administered and he showed clinical improvement. Shortly thereafter, the patient became hypotensive and lost pulses. Point-of-care ultrasound revealed cardiac tamponade. TXA was immediately given to inhibit fibrinolysis since cryoprecipitate and blood products were not immediately available. Pericardiocentesis was performed and successfully removed 200 milliliters of blood with return of pulses. Clinicians must consider TXA as a rapidly accessible antagonist of tPA's fibrinolytic effects.
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PMID:Pericardial Tamponade After Systemic Alteplase in Stroke and Emergent Reversal With Tranexamic Acid. 3206 26