Acute myocardial infarction AMI

It is important to obtain a baseline EKG and cardiac enzymes to evaluate the possibility of an acute myocardial infarction. The short-term (2-4 weeks) stroke risk after acute myocardial infarction (AMI) is 2.5%. Stroke is usually an early (within 14 days) complication of AMI and is more common in anterior wall (4—12%) than in inferior wall infarction (1%). Approximately 40% of patients with an anterior wall myocardial infarction develop left ventricular thrombus. 

Indications Management of acute myocardial infarction (AMI), acute ischemic stroke, and acute massive pulmonary embolism... 

Indications The management of acute myocardial infarction (AMI) in adults for the improvement of ventricular function following a heart attack, the reduction of the incidence of congestive heartfailure,andthe reduction of mortality associated with AMI... 

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%). 

Some patients with acute myocardial infarction (AMI) are found to have HIT antibodies career state of HIT antibodies regardless of previous heparin usage. In those patients, early-onset HIT has been observed, which occurs within a very short period after UFH administration during PCI even if it is the initial exposure to UFH (10). Once HIT antibodies are generated after the exposure to UFH, the antibodies do not disappear for approximately 100 days after the cessation of UFH. If UFH intervention is resumed while the antibodies remain, HIT may readily develop as rapid-onset type of HIT (II). Thrombotic complications are highly anticipated following the abrupt onset of HIT in patients who have been exposed recently to UFH. 

Gerhardt W, Nording G, Ljungdahl L. Can troponin T replace CK-MB mass as "goldstandard for acute myocardial infarction ( AMI ) Scand J Clin Lab Invest 1999 59(suppl 230) 83-89. 

Same beneficial results were obtained from SOPHOS and studies in lesions study population was followed-up for one year. The endpoint was death, acute myocardial infarction (AMI), or need for angioplasty and was observed in 13,4%. Two deaths, five AMIs, and 32 revascularizations were observed. Angiographical restenosis was 17.7% with a lumen loss of 0.8 mm. Recently, the results of the SV stent study showed in 150 patients with reference vessel diameter of 2 to 2.75 mm in 19 centers in... 

TNKase Tenecteplase Genentech 6/2000 Reduction of mortality associated with acute myocardial infarction (AMI) CHO... 

Two immunosensors developed by O Regan et al. [89,90] have demonstrated their usefulness for the early assessment of acute myocardial infarction (AMI). Human heart fatty-acid binding protein (H-FABP) is a biochemical marker for the early assessment of AMI. The authors constructed an amperometric immunosensor for the rapid detection of H-FABP in whole blood. The sensor is based on a one-step, direct sandwich assay in which the analyte and an alkaline phosphatase (AP) labelled antibody are simultaneously added to the immobilized primary antibody, using two distinct monoclonal mouse anti-human H-FABP antibodies. The substrate p-amino-phenyl phosphate is converted to p-aminophenol by AP, and the current generated by its subsequent oxidation at +300 mV vs. Ag/AgCl is measured. The total assay time is 50 min, and the standard curve was linear between 4 and 250 ng ml . The intra- and inter-assay coefficients of variation were below 9%. No cross-reactivity of the antibodies was found with other early cardiac markers, and endogenous substances in whole blood did not have an... 

In a worldwide study of 27,000 people in 52 countries, 12,400 patients who experienced acute myocardial infarctions (AMI) were compared with 14,000 who never had a heart attack or any other form of cardiovascular disease. I49l The study concluded the following ... 

Properties of Cardiac Markers Used in the Evaluation of Acute Myocardial Infarction (AMI)... 

For many years lidocaine has been used for the treatment of ventricular arrhythmias in the setting of acute myocardial infarction (AMI). The efficacy seen in cardiac arrest, however, has not mirrored that seen in AMI. In the only published case-control trial where patients were classified according to whether they received lidocaine, no significant... 

Cardiovascular diseases (CVD) claimed 949,619 lives, or 1 of every 2.5 deaths, in the United States in 1998. More than 2600 Americans die of CVD each day, or on average of 1 death every 33 seconds. In 1998, the death rates from CVD were 532.0 (per 100,000) for black males, 419.3 for white males, 400.7 for black females, and 294.9 for white females. CAD was responsible for 459,841 deaths (or 48%) from CVD. Men die earlier from IHD and acute myocardial infarction (AMI) than women, and aging of both sexes is associated with a higher incidence of these afflictions. The disparity in mortality from IHD between men and women decreases with aging, being about four to five times more common in men in their mid-30s to a preponderance of female deaths in the very elderly. 

Finally, high intraluminal shear forces develop in these thinning or eroded areas of the plaque s fibrous cap, inducing macrophages to secrete additional metalloproteinases that further degrade the arterial-fibrous cap matrix. This contributes further to plaque rupture and thrombus formation (see Fig. 34.22). The consequence is a macrovascular ischemic event such as an acute myocardial infarction (AMI) or an acnte cerebrovascular accident (CVA). 

Thrombolytics are dmgs that promote the fibronolytic mechanism if administered within 4 hours following an acute myocardial infarction (AMI). An acute myocardial infarction (heart attack) can be caused by a thromboembolism blocking a coronary artery. This results in decreased circulation to that part of the heart. The ischemic (without oxygen) tissue becomes necrotic (dies) if left without an oxygen supply. Thrombolytics prevent or minimize necrosis that results from the blocked artery and therefore decreases hospitalization time. After thrombolytic treatment, the patient is evaluated for cardiac bypass or coronary angioplasty procedures. 

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