Necrosis myocardial infarction

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. 

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. 

Ridker PM, Rifai N, Pfeffer M, Sacks F, Lepage S, Braunwald E (2000) Elevation of tumor necrosis factor-alpha and increased risk of recurrent coronary events after myocardial infarction. Circulation 101 2149-2153... 

In ischemic episodes such as occur in myocardial infarction, lack of oxygen forces cells to rely on anaerobic glycolysis, which increases production of lactic add The consequent intracellular acidosis can cause proteins to denature and precipitate, leading to coagulation necrosis. 

In a myocardial infarction (MI), myocytes swell as the membrane potential collapses and the I cell gets leaky. Enzymes are released from the damaged tissue, and lactic acidosis contributes to protein precipitation and coagulation necrosis. 

Myocardial infarction ischaemia in the cardiac muscle leading to necrosis occurring as a result of reduction in coronary blood flow... 

Orotic acid or 6-methyluracil vide infra), when administered to rabbits with myocardial infarction induced by ligation of the anterior descending branch of the left coronary artery, can decrease the incidence of necrosis and increase the rate of regeneration for healthy cellular and fibrous connective tissue in the infarct region [182]. Rats with induced aortal stenosis which are treated with... 

Fig. 2.9 Effect of revascularization on myocardial viability in post myocardial infarction (MI) patients. Almost half of all post MI patients will have completed necrosis without remaining areas of viable myocardium...

Myocardial infarction. An area of coagulation necrosis in a tissue resulting from local ischemia in the heart. 

To maintain hemostasis, blood must be retained in the vasculature as fluid. At the same time, blood components must be able to respond rapidly with a clot when a vascular injury occurs. To repair a vascular injury, platelets in blood first adhere as aggregates to the endothelial cells at the affected site and form an initial blood clot. Platelets then stimulate and activate coagulation factors found in plasma to form a more stable fibrin clot. As the injury is resolved and healed, the clot is degraded. Thrombosis is a pathological event wherein a blood clot occludes a blood vessel, resulting in ischemic necrosis of the tissue fed by the blood vessel. Ischemic necrosis involves local anemia and oxygen deprivation. Thrombosis of a coronary artery may lead to myocardial infarction or unstable angina [20]. 

The observation that the agent accumulated in necrotic tissue and not specifically or preferentially into viable tumors led to the investigation of the agent as a marker for necrosis [110]. Acute myocardial infarctions were induced in rats... 

Many mediators of inflammation have been identified— cytokines IL-6, tumor necrosis factor alpha cell adhesion molecules intracellular adhesion molecule-1 (ICAM-I), P-selectin and acute phase reactants CR.R fibrinogen, serum amyloid A, and soluble CD40 (Fig. I) (3). Myeloperoxidase is an enzyme secreted from monocytes, neutrophils, and macrophages. A single measurement taken from patient with chest pain in the emergency department predicted the early risk of myocardial infarction and the risk of major cardiac of ends in the next 30 days to six months (15). 

The vast majority of ventricular septal defects (VSD) are congenital. Acquired VSDs are almost always a consequence of septal rupture following myocardial infarction, traumatic VSDs as a consequence of sharp or blunt chest trauma are exceptionally rare. Typically the post myocardial infarction ventricular septal defect (PMIVSD) occurs within the first week after the event (41). In the current era of thrombolysis about 0.2% of patients develop a VSD as a result of septal necrosis. Medical management of these patients is limited and carries a 30-day mortality of 94% compared with 47% who were treated surgically (42). 

Several disease states can result from abnormal blood clots. For example, strokes were mentioned previously. However, the most common and deadliest thrombotic disease is myocardial infarction (MI). Atherosclerosis has long been associated with reduced cardiac function and elevated mortality due to rupture of atherosclerotic plaques. The rupture of an atherosclerotic plaque usually results not only in blockage due to the plaque itself but also in the immediate formation of an occlusive blood clot, which results in an MI. Immediately after the initiation of an MI, a zone of necrosis begins to develop around the area as ischemia proceeds. It is during this early phase of ischemia (several hours) that therapeutic intervention not only can be life-saving but also can minimize the amount of necrotic heart tissue formed. 

C-reactive protein (CRP) is a protein produced by the liver during episodes of acute inflammation. CRP is not a specific test, however, and a positive CRP may indicate a number of things including inflammatory disease, malignancy, muscle necrosis (e.g. myocardial infarction) and trauma, as well as infection. A normal CRP is unlikely in the presence of a bacterial infection and a very high CRP (>100 mg/L) is more likely to occur in bacterial than viral infection. In this case, the patient s high CRP is consistent with a bacterial infection. CRP may be used to monitor a patient s response to therapy. 

Cardiovascular effects include tachycardia, hypertension, and increased cardiac irritability large intravenous doses can cause cardiac failure. Cardiac dysrhythmias have been ascribed to a direct toxic effect of cocaine and a secondary sensitization of ventricular tissue to catecholamines (17), along with slowed cardiac conduction secondary to local anesthetic effects. Myocardial infarction has increased as a complication of cocaine abuse (7,8). Dilated cardiomyopathies, with subsequent recurrent myocardial infarction, have been associated with long-term use of cocaine, raising the possibility of chronic effects on the heart (18). Many victims have evidence of pre-existing fixed coronary artery disease precipitated by cocaine (SEDA-9, 35) (19-21). However, myocardial infarction has been noted even in young intranasal users with no evidence of coronary disease (22), defined by autopsy or angiography (23,24). If applied to mucous membranes, cocaine causes local vasoconstriction, and, with chronic use, necrosis. 

Based on a retrospective study of 344 patients with cocaine-associated chest pain, it has been suggested that patients who do not have evidence of ischemia or cardiovascular complications over 9-12 hours in a chest-pain observation unit have a very low risk of death or myocardial infarction during the 30 days after discharge (59). Nevertheless, patients with cocaine-associated chest pain should be evaluated for potential acute coronary syndromes those who do not have recurrent symptoms, increased concentrations of markers of myocardial necrosis, or dysrhythmias can be safely discharged after 9-12 hours of observation. A protocol of this sort should incorporate strategies for treating substance abuse, since there is an increased likelihood of non-fatal myocardial infarction in patients who continue to use cocaine. 

Protein kinase signal transduction pathways have been extensively studied and characterized in the myocardium. Ischemic preconditioning (IP) and the role of individual kinases involved is where much of the research efforts have been focused. IP is the reduction in susceptibility to myocardial infarction that follows brief periods of sublefhal ischemia (Murry et al, 1986). This reduction can manifest itself as a 4-fold reduction in infarct size, this being secondary to a delay in the onset and rate of cell necrosis during the subsequent lethal ischemia (Marber et al., 1994). 

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