Myocardial infarction coronary occlusion

The heart attack occurs when one or more of the coronary arteries, which are responsible for supplying blood to the heart muscle, becomes blocked. The part of the heart that is consequentially robbed of oxygen and nutrients and therefore damaged is called an infarct. From this, the terms of myocardial infarct, coronary occlusion and coronary thrombosis (blood clot) all refer, either more or less precisely, to what is called a heart attack . 

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. 

Acute coronary syndromes most often result from a physical disruption of the fibrous cap, either frank cap fracture or superficial endothelial erosion, allowing the blood to make contact with the thrombogenic material in the lipid core or the subendothelial region of the intima. This contact initiates the formation of a thrombus, which can lead to a sudden and dramatic blockade of blood flow through the affected artery. If the thrombus is nonocclusive or transient, it may either be clinically silent or manifest as symptoms characteristic of unstable angina. Importantly, if collateral vessels have previously formed, for example, due to chronic ischemia produced by multi vessel disease, even total occlusion of one coronary artery may not lead to an acute myocardial infarction. 

Maroko, P.R. and Braunwald, E. (1973). Modification of myocardial infarction size after coronary occlusion. Ann. Intern. Med. 79, 720-733. 

One eritical factor that has been neglected in considering mechanisms of cardiac fatalities is the timeframe for various types of toxicities. For example, a majority of cocaine-related fatalities and near fatalities reported from emergency rooms are attributed to one or more types of cardiac ischemic or hypertensive episodes (Isner et al. 1986). Thus, these studies may discount the cocaine-induced arrhythmias and conduction defects as important direct causes of fatalities. Yet, if coroner reports are used as data sources (Virmani et al. 1988 Wetli and Wright 1979 Mittleman and Wetli 1984), there are great numbers of deaths in which pulmonary effusion and lack of evidence for coronary occlusion, acute myocardial infarction, or... 

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. 

More recent studies continue to support the unique antifibrillatory activity of bretylium. Kowey et al. [38] have shown that bretylium prevented spontaneous VF and decreased the effects on VF threshold in a feline myocardial infarction model. They attributed this beneficial effect to a decrease in the dispersion of refractoriness between normal and ischaemic regions of the heart. In contrast, clofilium (14, see below), which had little effect on dispersion of refractoriness after coronary occlusion, was unable to prevent spontaneous VF. Similar results were seen in isolated tissue studies with canine subendocardial Purkinje fibres and ventricular muscle which contained both normal and ischaemic regions [39]. In these studies bretylium caused a smaller increase in dispersion of refractoriness in subendocardial Purkinje fibres than either sotalol or clofilium. In ventricular muscle tissue, bretylium decreased dispersion while sotalol and clofilium increased dispersion of refractoriness. 

Myocardial infarction is caused by acute thrombotic occlusion of a coronary artery (A). Therapeutic interventions aim to restore blood flow in the occluded vessel in order to reduce infarct size or to rescue ischemic myocardial tissue. 

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. 

DeWood MA, Spores J, Notske R, et al. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N EnglJ Med 1980 303 897-902. 

Abbreviations AMI, acute myocardial infarction Art, artery A-V, arteriovenous CL, caprolactone CTO, chronic total occlusion LA, D.L-lactide NA, not available FTCA, percutaneous transluminal coronary angioplasty FTFE. polytetrafluoroethylene P-S, Palmaz-Schatz PUR, polyurethane SPUU-PEO, segmented polyurethaneurea-polyethylene oxide. 

Abbreviations ACS, acute coronary syndrome ACT, activated clotting time BP, blood pressure CTO, chronic total occlusion i.v., intravenous MI, myocardial infarction NSTEMI, non-ST-segment elevation myocardial infarction PCI, percutaneous coronary intervention RCA, right coronaiy artery STEMI, ST-segment elevation myocardial ... 

Possible complications include massive myocardial infarction due to retrograde flow around the occlusion balloon, complete heart block, ventricular fibrillation, stroke, dissection of the left anterior descending artery, and right coronary artery thrombosis. Though high grade atrioventricular blockage occurs relatively frequently, procedural mortality rate is low (0-4%) and severe complications are rare and often avoidable (7-10). 

Fig. 13.1 Phosphorylated c-Ski expression in cytosolic fraction of cells in post-MI rat heart. In post-MI rat hearts with chronic large myocardial infarction, phosphorylated c-Ski expression was noted in the cytosol of cells populating the infarct scar (predominantly myofibroblasts) and the remnant heart (mixed cytosolic fraction from myocytes and nonmyocytes). Hearts were sampled at different times after surgical ligation of coronary artery occlusion and Western analysis was carried out to assess phosphorylated c-Ski expression. Trends in -fold protein expression (target band intensity corrected for loading) are shown in curves.

Integrilin) coronary thrombolysis improvement in lysis of occlusive thrombus et al. 1994 myocardial infarction -thrombolysis with tPA in incidence and speed of reperfusion et al. 1997... 

Myocardial infarction (also known as a heart attack) occurs when the blood supply to a part of the heart is interrupted. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of an atherosclerotic plaque in the wall of the artery. The resulting ischaemia and oxygen shortage if left untreated can cause damage and/or death (infarction) of the heart muscle (myocardium). 

Myocardial infarction (MI) is caused by the acute thrombotic occlusion of a coronary artery. The myocardial region that has been cut off from its blood supply dies within a short time owing to the lack of 02 and glucose. The loss in functional muscle tissue results in reduced cardiac performance. In the infarct border zone, spontaneous pacemaker potentials may develop, leading to fatal ventricular fibrillation. The patient experiences severe pain, a feeling of annihilation, and fear of dying. 

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. 

A 22-year-old man with a 6-year history of intravenous heroin use was maintained on methadone 60 mg/day and dihydrocodeine 0.5 g/day. He had an extensive anterior myocardial infarction as a result of occlusion of the left anterior descending coronary artery, which was reopened by percutaneous transluminal coronary angioplasty. 

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