Myocardial infarction diagnosis

Aslan, K. and Geddes, C. D. (2006). Microwave Accelerated and Metal Enhanced Fluorescence Myoglobin Detection on Silvered Sur ces Potential Application to Myocardial Infarction Diagnosis Plasmonics 1 53-59. 

Indications for treatment with streptokinase include acute occlusion of arteries, deep vein thrombosis, and pulmonary embolism. Streptokinase therapy in coronary thrombosis, which is the usual cause of myocardial infarction (54,71,72), has proved to be valuable. In this frequently fatal condition, the enzyme is adrninistered intravenously at a dose of 1.5 million units over 60 min, or given by intracoronary infusion at a 20,000- to 50,000-unit bolus dose followed by 2000 to 4000 units/min for 60 min therapy must be instituted as soon as practicable after the diagnosis of heart attack is made. For deep vein thrombosis, pulmonary embolism, or arterial occlusion, streptokinase is infused at a loading dose of 250,000 units given over 30 min, followed by a maintenance dose of 100,000 units over a 60-min period. 

Troponin is a regulator of striated muscle contraction. Measurements of troponin I levels are routinely used in the diagnosis of myocardial infarction. In addition, mutations in the troponin I subunit are associated with familial hypertrophic cardiomyopathy. 

Use of the plasma enzyme creatine kinase Mb (CK-MB) in the diagnosis of myocardial infarction. 

Assay of plasma enzymes aids diagnosis and prognosis. For example, a myocardial infarction elevates serum levels of lactate dehydrogenase isozyme I,. 

HBD is a biochemical rather than electrophoretic assessment of the LD isoenzyme which is associated with heart. All five isoenzymes of LD exhibit some activity toward cx-hydroxy-butyrate as substrate, but heart LD shows the greatest activity. Serum HBD measurement is not as valuable as the electrophoretic determination of heart LD isoenzyme. High HBD activity has also been found in diseases of the liver. Rises associated with the hepatic effects of congestive heart failure can be disconcerting in the differential diagnosis of myocardial infarction. Wilkinson has used the serum HBD/LD ratio for the differentiation of myocardial disease from other disorders in which HBD activity is elevated, whereas Rosalki has not found the ratio to be helpful (39). 

Wagner et. al (46) studied 376 patients to evaluate the importance of identification of the myocardial-specific MB isoenzyme in the diagnosis of acute myocardial infarction. An attempt was made to determine the incidence of falsely positive (mb). No acute infarction was diagnosed in all patients in whom neither total CK nor the isoenzymes of LD indicated myocardial necrosis. Incidence of falsely negative (MB) was zero in 33 patients. They concluded that determination of the isoenzymes of CK provides both a sensitive and specific indication of acute myocardial infarction. 

Ronttinen, A. and Somer, H. Specificity of seriim creatine kinse isoenzymes in diagnosis of acute myocardial infarction. Br. Med. J. (1973), 1, 386-389. 

Symptoms may be confused for a myocardial infarction and objective testing must be performed to establish the diagnosis. 

Troponins T or I Proteins found predominantly in cardiac muscle that regulate calcium-mediated interaction of actin and myosin troponins I and T are released into the blood from myocytes at the time of myocardial cell necrosis after infarction. These biochemical markers become elevated and are used in the diagnosis of myocardial infarction. 

The same reaction was recently proposed to detect creatine kinase (CK), an enzyme of high clinical significance in relation to the investigation of skeletal muscle disease and the diagnosis of myocardial infarct or cerebrovascular accidents. As ATP is a reaction product obtained from the reaction of ADP with creatine phosphate catalyzed by CK, this enzyme can be indirectly measured by the CL intensity read from the subsequent reaction of ATP with luciferin. Using the technique of electrophoretically mediated microanalysis (EMMA), it is possible to detect the enzyme using nanoliter volumes of biological sample with an improved speed and simplicity with respect to a conventional colorimetric method [100],... 

Suggested Alternatives for Differential Diagnosis Acute respiratory distress syndrome, plague, congestive heart failure and pulmonary edema, HIV infection and AIDS, pneumonia, shock, phosgene, influenza, tularemia, phosphine toxicity, anthrax, silent myocardial infarction, and salicylate toxicity with pulmonary edema. 

It seems to be important that in myocardial infarction no increase of GSSGR activity could be found (K6, LI), thus representing the possibility for differential diagnosis in connection with other enzyme tests. 

K7. Kerppola, W., Nikkila, E. A., and Pitkanen, E., Serum glucose-0-phosphate dehydrogenase in the diagnosis of myocardial infarction. Acta Med. Scand. 160, 17-24 (1960). 

Anxiety is common among the elderly but the literature regarding the assessment, diagnosis, and treatment of these illnesses in older individuals is sparse (Blazer 1997). Most often anxiety does not present for the first time in late life. If that is the case one should suspect an underlying condition or other external cause. These causes could be medications such as digitalis, antipsychotics but also conditions as anaemia, chronic obstructive lung disease with hypoxia or myocardial infarction. 

Atrial fibrillation is commonly associated with heart failure, and the prevalence of atrial fibrillation is related to the severity of heart failure, with less than 5% affected with very mild heart failure to nearly 50% affected with advanced heart failure [66]. Heart failure and atrial fibrillation are both common cardiovascular disorders and share the same demographic risk factors, including age, history of hypertension, prior myocardial infarction, and valvular heart disease [67, 68]. Further, the incidence of heart failure increases dramatically after the diagnosis of atrial fibrillation [69]. Progression of LV dysfunction can clearly be associated with rapid ventricular rates [70-76]. Conversely, conversion to normal sinus rhythm or control of ventricular response in atrial fibrillation can improve LV function [71-74, 77]. Accordingly, rate control becomes very important in patients with heart failure and dilated cardiomyopathy, and likely even more so when ischemia from rapid rates complicate the patient s course. 

The hrefly Inciferin system is very sensitive and can be conpled to any enzymatic reaction that prodnces or nses ATP. For example, creatine phosphokinase can be determined by this method and hence be nsed in the diagnosis of myocardial infarction and mnscle disorders. The creatine phosphokinase converts AMP into ATP which then nndergoes the reaction with Inciferin as shown in Fignre 3.25. ATP pro-dnction is essential for every known life form and the firefly Inciferin system can be nsed to check for microbial life. Hence systems have been developed that use a portable luminescence workstation to monitor sanitation in food manufacturing and to check for sterile environments in technological workplaces. The system can also be applied in checking cell viability, for instance in cell cultures and to measure the toxic effects of chemicals on cells. 

Atropine can be used in the differential diagnosis of S-A node dysfunction. If sinus bradycardia is due to extracardiac causes, atropine can generally elicit a tachy-cardic response, whereas it cannot elicit tachycardia if the bradycardia results from intrinsic causes. Under certain conditions, atropine may be useful in the treatment of acute myocardial infarction. Bradycardia frequently occurs after acute myocardial infarction, especially in the first few hours, and this probably results from excessive vagal tone. The increased tone and bradycardia... 

The proper selection of patients for thrombolytic therapy is critical. The diagnosis of acute myocardial infarction is made clinically and is confirmed by electrocardiography. Patients with ST-segment elevation and bundle branch block on electrocardiography have the best outcomes. All trials to date show the greatest benefit for thrombolytic therapy when it is given early, within 6 hours after symptomatic onset of acute myocardial infarction. 

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