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epinephrine/infartarse

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Aspirin treatment is essential in patients with acute myocardial infarction (AMI) to block platelet thromboxane (TXA)₂ synthesis. Epinephrine is known to enhance platelet reactivity induced by other agonists and to be elevated in patients with AMI due to stress. Our objective was to study the

Prognostic value of plasma atrial natriuretic factor, norepinephrine and epinephrine in acute myocardial infarction.

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Neurohumoral activation in acute myocardial infarction (AMI) may reflect the degree of hemodynamic compromise, contribute to the progression of heart failure and augment to the risk of serious ventricular arrhythmias. Consequently, assessment of neurohumoral variables may provide an index of

Effects of epinephrine on automaticity and the incidence of arrhythmias in Purkinje fibers surviving myocardial infarction.

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The role of the sympathetic nervous system in the development of late-phase ventricular arrhythmias occurring 24 hr after myocardial infarction was investigated using canine ventricular preparations in vitro. One day after two-stage ligation of the left anterior descending coronary artery,

Myocardial infarction induced by coronary vasospasm after self-administration of epinephrine.

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A case of a 30-year-old man who developed a myocardial infarction after self-administering an Epi-Pen for an episode of idiopathic anaphylaxis is reported. The patient had numerous risk factors for coronary artery disease, and it was suspected that epinephrine-induced coronary spasm caused the
This study investigated whether epinephrine treatment during late ischemia and early reperfusion improves systolic shortening after 45 minutes of reperfusion at the cost of increased infarct size. A model consisting of both stunned and dead myocytes was used. The left anterior descending coronary

Cardiac anaphylaxis: a case of acute ST-segment elevation myocardial infarction after IM epinephrine for anaphylactic shock.

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A 62-year-old male smoker with no other comorbidities presented to emergency department with systemic anaphylaxis, due to oral diclofenac for toothache. He developed acute anterior wall myocardial infarction following IM epinephrine 1 mg 1:1000. Primary percutaneous coronary intervention was done,

Acute renal failure, anterior myocardial infarction, and atrial fibrillation complicating epinephrine abuse.

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After injecting the solution extracted from a Primatene Mist inhaler, a patient experienced epinephrine overdose that resulted in an acute myocardial infarction and acute renal failure. The exact amount of epinephrine injected was unknown, but was thought to be between 82.5 and 124 mg, more than 25

Unresponsiveness to hypoglycemia of centers controlling epinephrine release in cerebral infarct patients.

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Urinary excretion of catecholamines under insulin hypoglycemia was studied in cerebral infarct patients as well as in patients with Parkinson's disease and subjects with lumbar discopathy (control group). While in the last two categories of subjects a normal response to hypoglycemia, i.e., an

Myocardial infarction thought to be provoked by local epinephrine injection during endoscopic submucosal dissection.

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Due to its hemostatic effect, local epinephrine has been used to minimize mucosal bleeding during endoscopic submucosal dissection (ESD), but its clinical benefit remains unclear. On the other hand, several adverse events deemed to be caused by epinephrine have been observed during ESD. A
Ventricular arrhythmia observed in the acute stage of myocardial infarction is profoundly related to the autonomic balance. To investigate prediction of ventricular arrhythmia, heart rate variability and plasma catecholamine concentration were simultaneously measured for a week in 17 consecutive

Effects of epinephrine on the electrophysiologic properties of Purkinje fibers surviving myocardial infarction.

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The electrophysiologic effects of epinephrine on canine subendocardial Purkinje fibers were examined 24 hours after two-stage ligation of the left anterior descending coronary artery. Transmembrane action potential were monitored simultaneously in noninfarcted (NZ) and infarcted (IZ) zones during

Sulfinpyrazone decreases epinephrine-induced platelet aggregation after myocardial infarction.

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Platelet studies were performed during a controlled double-blind randomized clinical trial of sulfinpyrazone (Anturane Reinfarction Trial) in 41 patients who had recent myocardial infarction. Aggregation of platelet-rich plasma by thrombin (0.185, 0.246 U/ml), collagen, adenosine diphosphate, and

Intramuscular Epinephrine-Induced Transient ST-Elevation Myocardial Infarction.

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Introduction. Myocardial infarction in the setting of anaphylaxis may result from the anaphylaxis itself or from the epinephrine used to treat the anaphylaxis. While cases of myocardial infarction due to large doses of intravenous epinephrine have previously been reported, myocardial infarction

Acute myocardial infarction after administration of low-dose intravenous epinephrine for anaphylaxis.

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This case describes a 29-year-old woman who presented with an acute severe anaphylactic reaction to penicillin. In addition to other medications administered in the emergency department, she received 0.1 mg intravenously of 1:10 000 epinephrine, after which she immediately developed severe chest

Epinephrine Versus Norepinephrine for Cardiogenic Shock After Acute Myocardial Infarction.

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BACKGROUND Vasopressor agents could have certain specific effects in patients with cardiogenic shock (CS) after myocardial infarction, which may influence outcome. Although norepinephrine and epinephrine are currently the most commonly used agents, no randomized trial has compared their effects, and
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