Myocardial infarction lateral

Alteplase has proven effective in the early treatment of patients with acute myocardial infarction (i.e. those treated within 12 h after the first symptoms occur). Significantly increased rates of patient survival (as measured 1 day and 30 days after the initial event) are noted when tPA is administered in favour of streptokinase, a standard therapy (see later). tPA has thus established itself as a first-line option in the management of acute myocardial infarction. A therapeutic dose of 90-100 mg (often administered by infusion over 90 min) results in a steady-state alteplase concentration of 3-4 mg l 1 during that period. However, the product is cleared rapidly by the liver, displaying a serum half-life of approximately 3 min. As is the case for most thrombolytic agents, the most significant risk associated with tPA administration is the possible induction of severe haemorrhage. 

The levels of G-6-PDH in serum have been investigated in many patients suffering from a multiplicity of disorders (K6), without finding a significant change except in myocardial infarction (K7). In these cases, G-6-PDH activities reach their maxima later than other enzymes reported to increase following this event. The highest values were found about the sixth day after infarction (K6, K7). 

Amiodarone (11), a benzofuran derivative, was initially developed as a coronary vasodilator in the early 1960 s [11,12]. Several years later, the efficacy of the compound as an antiarrhythmic agent began to be exploited. The first clinical trials with amiodarone were reported in 1974 [13]. Amiodarone was effective in controlling the tachyarrhythmias of eleven patients with Wolff-Parkinson-White syndrome. Since that time the compound has been studied extensively [14,15]. Recently, in the Canadian Amiodarone Myocardial Infarction Arrhythmia Trial (CAMIAT), amiodarone was shown to reduce mortality during a mean 18 month period following myocardial infarction (13.8% deaths in placebo group vs. 2.1 % deaths in the treatment group) [16]. 

Obstacles remained as PTCA was not universally available and often associated with considerable time delay, especially in off peak hours. In the National Registry of Myocardial Infarction-2 (NRMI-2 >27,000 patients), total ischemia time (symptom onset to balloon inflation) was 3.9 h with onset to hospital arrival 1.6 h [45]. Unadjusted in-hospital mortality was higher in patients treated later. Door to balloon time > 2 h was related to in-hospital death (41-62% adjusted odds increase) and centers who treat >3 STEMIs/month had improved in-hospital mortality compared to less experienced facilities (Figs. 5.4 and 5.5). Lastly, similar to trials of unstable angina, PTCA was plagued by high restenosis rates... 

The results of several large clinical trials using the statin drugs (discussed later) show that the tested drugs decreased the risk of both primary and secondary cardiovascular events. The incidence of myocardial infarction and death from cardiovascular disease was reduced in patients with hypercholesterolemia who never had a... 

The paradigm shift in 1980 on the causation of acute myocardial infarction to acute coronary occlusion by a thrombus created the rationale for thrombolytic therapy of this common lethal disease. At that time—and for the first time-intravenous thrombolytic therapy for acute myocardial infarction in the European Cooperative Study Group trial was found to reduce mortality significantly. Later studies, with thousands of patients in each trial, provided enough statistical power for the 20% reduction in mortality to be considered statistically significant. Although the standard of care in areas with adequate facilities and experience in percutaneous coronary intervention (PCI) now favors catheterization and placement of a stent, thrombolytic therapy is still very important where PCI is not readily available. 

A 58-year-old man with a previous smoking history and a history of hypertension was severely biochemically hypothyroid (serum TSH 221 mU/1) and was given thyroxine, initially in a low dose (25 micrograms/day), increasing to 100 micrograms/day after 2 weeks. A month later he sustained a subendocardial myocardial infarction associated with only minor abnormalities on coronary angiography. 

A 71-year-old woman who had undergone total thyroidectomy with subsequent irradiation because of follicular carcinoma 3 years before (22). Since then, she had taken oral levothyroxine 0.15 mg and 0.2 mg on alternate days. When latent hypothyroidism became evident despite replacement therapy, the dose of levothyroxine was increased to 0.3 mg/day. Three weeks later, she had formed an acute posterior myocardial infarction, although she had no previous history of coronary artery disease. Subsequent coronary arteriograms revealed no evidence of disease of the major vessels. Myocardial scintigraphy 3 weeks after infarction still showed a persistent perfusion defect. 

It is well known that the response to a drug can differ between diseased and nondiseased individuals. For example, the expression of both pro- and anti-inflammatory mediators changes in many diseases and conditions such as rheumatic diseases, myocardial infarction, angina, aging, and obesity [21]. This may have an impact on toxicity and pharmacokinetics, and in particular, when the drug interacts with these mediators. In addition the pharmacokinetics of a drug can be affected by disease in general, a topic that is discussed later in this chapter. 

A 68-year-old man with a 5-year history of Alzheimer s disease was treated with thioridazine 25 mg tds because of violent outbursts (12). His other drugs, temazepam 10-30 mg at night, carbamazepine 100 mg bd for neuropathic pain, and droperidol 5-10 mg as required, were unaltered. Five days later, he was found dead, having been in his usual condition 2 hours before. Post-mortem examination showed stenosis of the coronary arteries, but no coronary thrombosis, myocardial infarction, or other significant pathology. The certified cause of death was cardiac dysrhythmia due to ischemic heart disease. Thioridazine was considered as a possible contributing factor. 

A 34-year-old man who smoked a pack of cigarettes a day took amfetamine for mild obesity. He developed an acute myocardial infarction 1 week later. Echocardiography showed inferior left ventricular hypokinesia and a left ventricular ejection fraction of 50%. Coronary cineangiography showed normal coronary arteries but confirmed the inferior left ventricular hypokinesia. Blood and urine toxicology were positive only for amfetamine. 

A 73-year-old man with a history of breathlessness, cough, and weight loss had some ill-defined peripheral shadow in the upper zones of a chest X-ray. He had fiberoptic bronchoscopy with cocaine and lidocaine and 5 minutes later became distressed, with dyspnea, chest pain, and tachycardia. Electrocardiography showed an evolving anterior myocardial infarction. Coronary angiography showed a stenosis of less than 25% in the proximal left anterior descending artery with coronary artery spasm. He made an uneventful recovery. 

A healthy 33-year-old man with prior cocaine use had a small myocardial infarction and, 36 hours later, having inhaled cocaine, developed a dissection of the left main coronary artery, extending distally to the left anterior descending and circumflex arteries. There was marked anterolateral and apical hypokinesis. 

A 74-year-old woman with a history of stroke, myocardial infarction, hypothyroidism, and probable multiinfarct dementia took nine donepezil tablets (a total dose of 45 mg). She developed nausea and vomiting 2 hours later. She fell asleep for 4-5 hours but remained rousable. About 9 hours after ingestion, she became flushed and had a bout of diarrhea. Donepezil was withdrawn for 3 days, and there were no adverse effects when it was reintroduced. 

Fig. 4 Serial left lateral gamma images of two dogs with acute experimental myocardial infarction injected with negative charge-modified In-111 labeled antimyosin Fab (right panels) and conventionally In-111 labeled antimyosin Fab (left panels) A and B = 30 min images, C and D = 1 h, E and F = 2h, and G andH = 3h post intravenous...

Fig. 6 Left lateral gamma image of a rabbit with a 216 mg experimental myocardial infarct visualized with In-111 labeled negative charge-modified antimyosin Fab. Arrow points to the small infarct visualized in vivo. (From Ref...

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