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Pathophysiology of myocardial infarction Risk Factors of myocardial infarction Evolution of myocardial infarction The treatment of myocardial infarction
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Heart failure due to myocardial infraction (MI) is most frequently a manifestation of coronary artery disease. The rupture of an atherosclerotic plaque is the most common cause of myocardial infarction. -This rupture can lead to partly or total occlusion of the coronary artery ischemia irreversible damage of myocardium If impaired blood supply lasts too long - Due to Apoptosis - Later on there is necrosis collagen scar tissue
This collagen scar formation results in the loss of the contractile function of the affected part of the heart!
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Activated macrophages and T-lymphocytes localized at the site of plaque rupture, release MMPs and cytokines weakening the fibrous cap. Plaque rupture reveals subendothelial collagen, which serves as a site of platelet adhesion, activation and aggregation, resulting in:
-The release of Thromboxane A2 (TXA2) -Fibrinogen -5-hydroxytryptamine (5-HT) -ADP Activation of the clotting cascade leads to fibrin formation and stabilization of the occlusive thrombus
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Ischemia can precipitate abnormal cardiac rhythms and conduction blocks, that can further impair the cardiac function. Conduction problems in the heart after myocardial infarction can occur -Injured myocardium conducts electric pulses more slowly than healthy myocardium. The difference in conduction velocity between injured and uninjured myocardium can trigger re-entry or a feedback loop that may cause lethal arrhythmias like: -Ventricular Fibrillation -Ventricular Tachycardia These arrhythmias may cause an inefficient pumping of the heart -Cardiac output reduced -Blood pressure falls This can lead to further extension of the infarct
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DEATH
Ventricular Fibrillation
Ventricular Tachycardia
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Summary
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There are a multiple risk factors for developing Myocardial Infarction (MI). These risk factors can be genetic of non-genetic. Genetic Hypertension High LDL / Low HDL Diabetes I Family History of heart disease (onset <55) Non-Genetic Age Gender Smoking Hypertension High LDL / Low HDL Diabetes II High fat diet Lack of physical activity Severe stress Alcohol/drug abuse
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Ischaemia
Immediate loss of contractility in the affected myocardium, a condition termed hypokinesis In some areas the myocardium is stunned and will eventually recover if bloodflow is restored. Contractility in the remaining viable myocardium increases, a process termed hyperkinesis
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Necrosis
develop in the subendocardium, about 1530 min after coronary occlusion. The necrotic region grows outward towards the epicardium over the next 36 h, eventually spanning the entire ventricular wall. A progression of cellular, histological and gross changes develop within the infarct.
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Cell damage is progressive, becomingly increasingly irreversible over about 12 h. coagulation necrosis :cell swelling, organelle breakdown and protein denaturation. After about 18 h, neutrophils enter the infarct After 3 4 days, granulation tissue appears at the edges of the infarct zone
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Infarct expansion
- This is the stretching and thinning of the infarcted wall within the first day or so after a MI. - progressive dilatation, not only of the infarct zone, but also of healthy myocardium. - ventricular remodelling is caused by an increase in enddiastolic wall stress. - Infarct expansion puts patients at a sub-stantial risk for the development of congestive heart failure, ventricular arrhythmias, and free wall rupture.
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1. Anti-platelet Agents
Aspirin (ASA) - at least 160mg immediately - Interferes with function of cyclooxygenase and inhibits the formation of thromboxane - ASA alone has one of the greatest impact on the reduction of MI mortality
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2. Supplemental Oxygen
Because MI impairs the circulatory function of the heart, oxygen extraction by the heart and other tissues may be diminished
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3. Nitrates
IV nitrates to all patients with MI and congestive heart failure, persistent ischemia, hypertension, or large anterior wall MI vasodilator effect Metabolized to nitric oxide in the vascular endothelium, relaxes endothelium Vasodilatation reduces myocardial oxygen demand and preload and afterload.
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4. Beta-blockers
Recommended within 12 hours of MI symptoms and continued indefinitely Reduces Myocardial mortality by decreasing arrythmogenic death. Decrease the rate and force of myocardial contraction and decreases overall oxygen demand
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5. Unfractionated heparin
Forms a chemical complex with antithrombin III inactivates both free thrombin and factor Xa Recommended in patients with MI who undergo PTCA or fibrinolytic therapy with alteplase
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7. Thrombolytics
MI and ST segment elevation greater than 0.1mV The plasminogen activators have been shown to restore coronary blood flow in 50-80% of patients. Contraindication active intracranial bleeding
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References
http://www.spiritus-temporis.com/myocardialinfarction/pathophysiology.html http://www.cvpharmacology.com/clinical%20topics/myocardial %20infarction.htm http://emedicine.medscape.com/article/759321-overview http://en.wikipedia.org/wiki/Myocardial_infarction http://www.blackwellpublishing.com/content/BPL_Images/Con tent_store/Sample_chapter/1405113278/Sample%20of%20Aar onson.pdf http://www.medicinenet.com/heart_attack/article.htm http://imaginis.org/heart-disease/heartattack.asp http://www.healthsystem.virginia.edu/uvahealth/adult_cardiac/ attack.cfm
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