Myocardial infarction electrocardiogram

Acute coronary syndromes Ischemic chest discomfort at rest, most often accompanied by ST-segment elevation, ST-segment depression, or T-wave inversion on the 12-lead electrocardiogram. Furthermore, it is caused by plaque rupture and partial or complete occlusion of the coronary artery by thrombus. Acute coronary syndromes include myocardial infarction and unstable angina. Former terms used to describe types of acute coronary syndromes include Q-wave myocardial infarction, non-Q-wave myocardial infarction, and unstable angina. 

Non-ST-segment elevation A type of myocardial infarction (MI) that is limited to the subendocardial myocardium and is smaller and less extensive than an ST-segment MI. There is usually no pathologic Q-wave on the electrocardiogram in non-ST-segment elevation. 

Gomes JA, Winters SL, Stewart D, Horowitz S, Milner M, Barreca P. A new noninvasive index to predict sustained ventricular tachycardia and sudden death in the first year after myocardial infarction based on signal-averaged electrocardiogram, radionuclide ejection fraction and Holter monitoring. J. Am. Coll. Cardiol. 1987 10 349-57. 

There were two cases of hypertension from the United States, or possible serotonin syndrome reported with fluvoxamine while on St. John s wort concomitantly. A 44-year-old male with obsessive-compulsive disorder received fluvoxamine and experienced severe hypertensive crisis (160-170/ 120mmHg) after two tablets of St. John s wort. The physician stated that the reaction was probably due to the combination of fluvoxamine and St. John s wort, which has MAOI activity. A 38-year-old male was on fluvoxamine for approximately two months and hypericum 600 mg daily for approximately two weeks before reporting possible serotonin syndrome with severe bitemporal headache. He was hospitalized to rule out myocardial infarction. There were no electrocardiogram (EKG) changes or apparent causative pathology. Symptoms resolved on discontinuation of both drugs. 

A 35-year-old man presents with a blood pressure of 150/95 mm Hg. He has been generally healthy, is sedentary, drinks several cocktails per day, and does not smoke cigarettes. He has a family history of hypertension, and his father died of a myocardial infarction at age 55. Physical examination is remarkable only for moderate obesity. Total cholesterol is 220 and high-density lipoprotein (HDL) cholesterol level is 40 mg/dL. Fasting glucose is 105 mg/dL. Chest x-ray is normal. Electrocardiogram shows left ventricular enlargement. How would you treat this patient ... 

The effects of coenzyme Q10 on coronary artery disease and chronic stable angina are modest but appear promising. A theoretical basis for such benefit could be metabolic protection of the ischemic myocardium. Double-blind, placebo-controlled trials have demonstrated that coenzyme Q10 supplementation improved a number of clinical measures in patients with a history of acute myocardial infarction (AMI). Improvements have been observed in lipoprotein a, high-density lipoprotein cholesterol, exercise tolerance, and time to development of ischemic changes on the electrocardiogram during stress tests. In addition, very small reductions in cardiac deaths and rate of reinfarction in patients with previous AMI have been reported (absolute risk reduction 1.5%). 

A day after a dose of intravenous methylprednisolone 60 mg a 79-year-old woman developed acute thoracic pain and collapsed. An electrocardiogram showed signs of a myocardial infarction and her cardiac enzyme activities were raised. She died within several hours. Autopsy showed an anterior transmural myocardial infarction and mild atheromatous lesions in the coronary arteries. 

A 59-year-old man with mild hemophilia A was given a test dose of desmopressin 30 micrograms (0.19 micrograms/kg) in 100 ml of saline by intravenous infusion over 30 minutes (29). Shortly afterwards, having had a cigarette, he developed chest pain. An electrocardiogram showed ST elevation, and a myocardial infarction was confirmed. 

Abbreviations ACS. acute coronary syndrome AECG. ambulatory electrocardiogram FLORIDA, fluvastatin on risk diminishment after acute myocardial infarction Ml. myocardial infarction MIRACL, myocardial ischemia reduction with aggressive cholesterol lowering nfMI. nonfatal myocardial infarction PACT, pravastatin in acute coronary treatment PROVE-IT TIMI 22. pravastatin or atoivastatin evaluation and infection therapy—thrombolysis in myocardial infarction 22 UAP, unstable anginapectoris. 

A 13-year-old boy taking lithium developed a pseudo-myocardial infarct pattern on the electrocardiogram this may have been an overinterpretation of nonspecific T-wave changes (118). 

A 31-year-old woman suddenly developed central chest pain, with a normal electrocardiogram. Changes in troponin and creatine kinase MB were consistent with acute myocardial infarction. Drug screening was positive for amphetamines and barbiturates. Coronary angiography showed an aneurysm with 99% occlusion of the proximal left circumflex coronary artery and extravasation of contrast material. A stent was inserted percutaneously and antegrade flow was achieved without residual stenosis. 

The incidence of acute myocardial infarction in cocaine-associated chest pain is small but significant (60). The electrocardiogram has a higher false-positive rate in these patients. A normal electrocardiogram reduces the likelihood of myocardial injury but does not exclude it. 

Aortic arch dissection can cause profound hypotension, with global, and sometimes boundary zone, cerebral ischemia or focal cerebral ischemia if the dissection spreads up one of the neck arteries. Clues to this diagnosis are anterior chest or interscapular pain, along with diminished, unequal or absent arterial pulses in the arms or neck and a normal electrocardiogram, unlike acute myocardial infarction, acute aortic regurgitation and pericardial effusion. 

A 62-year-old woman developed chest pain and sinus bradycardia (41/minute). She had third-degree heart block and was given atropine 1 mg intravenously. Three minutes later, her chest pain increased and the electrocardiogram now showed an acute inferior myocardial infarction, confirmed by serum markers. Angioplasty recanalized the right coronary artery. 

A 22-year-old man snorted an 8 mg crushed tablet of buprenorphine and 2 hours later had crushing chest pain, which resolved within a few minutes (4). The symptom recurred 3 weeks later after another inhalation of buprenorphine. An electrocardiogram suggested an acute anterior myocardial infarction caused by buprenorphine-induced coronary artery spasm. 

A previously healthy 19-year-old man took tablets containing a total of 24 mg of Ephedra alkaloids and 100 mg of caffeine, and 15 minutes later developed severe chest pain radiating down the left arm. An electrocardiogram showed an inferolateral myocardial infarct, confirmed by creatine kinase and troponin I measurements. He made a full recovery, and coronary angiography showed only minimal atherosclerotic disease of the left anterior descending artery. 

A 41-year-old man employed in a munitions factory was admitted with crushing chest pain on a Sunday morning. There was evidence of an acute inferior myocardial infarction, and cardiac catheterization showed 80% narrowing of the proximal right coronary artery, which was reduced to 10% by intracoronary administration of glyceryl trinitrate. The electrocardiogram became normal. 

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