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Myocardial Infarction Pathogenesis and Treatment

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Topic includes classification, pathogenesis and management of MI

Publicada em: Ciências
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Myocardial Infarction Pathogenesis and Treatment

  1. 1. Myocardial Infarction By Chiranjeevi Pudi V Pharm D (2013-14)
  2. 2. CLASSIFICATION • Acute coronary syndromes include ST-elevation MI (STEMI) Non ST-elevation MI ( NSTEMI) Unstable Angina
  3. 3. PREVALENCE • In the US, 1.3 million cases of nonfatal MI were reported in 2006 • Incidence of 600 per 100,000 people • Increase in the proportion of NSTEMI compared to STEMI • Approximately 500,000 to 700,000 deaths are caused by heart disease
  4. 4. HISTORY The history is critical in making the diagnosis of MI and sometimes provide only the only clues that lead to the diagnosis in the initial phase of presentation Chest Pain- anterior precordium tightness • Pain may radiate to jaw, neck and epigastrium • Dyspnea- angina equivalent, poor LV function • Nausea/abdominal pain with posterior MI • Anxiety
  5. 5. HISTORY • Nausea with and without vomiting • Diaphoresis or sweating • Syncope • Elderly present with MS changes, fatigue, syncope or weakness • As many as half of MI are clinically silent
  6. 6. CAUSES • Most frequent cause is rupture of an atherosclerotic lesion within coronary wall with subsequent spasm and thrombus formation • Coronary artery vasospasm • Ventricular hypertrophy • Hypoxia • Coronary artery emboli
  7. 7. RISK FACTORS FOR ATHEROSCLEROSIS • Age • Smoking • Hypercholesterolemia and triglyceridemia • Diabetes Mellitus • Poorly controlled hypertension • Family History • Sedentary lifestyle
  9. 9. Mechanisms of Myocardial damage The severity of an MI is dependent of three factors • The level of the occlusion in the coronary • The length of time of the occlusion • The presence or absence of collateral circulation
  10. 10. CARDIAC BIOMARKERS • Cardiac biomarkers are protein molecules released into the blood stream from damaged heart muscle • Since ECG can be inconclusive , biomarkers are frequently used to evaluate for myocardial injury • These biomarkers have a characteristic rise and fall pattern
  11. 11. Troponin T and I • These isoforms are very specific for cardiac injury • Preferred markers for detecting myocardial cell injury • Rise 2-6 hours after injury Peak in 12-16 hours Stay elevated for 5-14 days
  12. 12. Creatinine Kinase ( CK-MB) • Creatinine Kinase is found in heart muscle (MB), skeletal muscle (MM), and brain (BB) • Increased in over 90% of myocardial infraction • However, it can be increased in muscle trauma, physical exertion, post-op, convulsions, and other conditions
  13. 13. CK-MB • Time sequence after myocardial infarction Begins to rise 4-6 hours Peaks 24 hours returns to normal in 2 days • MB2 released from heart muscle and converted to MB1. • A level of MB2 > or = 1 and a ratio of MB2/MB1 > 1.5 indicates myocardial injury
  14. 14. MYOGLOBIN • Damage to skeletal or cardiac muscle release myoglobin into circulation • Time sequence after infarction Rises fast 2hours Peaks at 6-8 hours Returns to normal in 20-36 hours • Have false positives with skeletal muscle injury and renal failure
  15. 15. CBC •CBC is indicated if anemia is suspected as precipitant •Leukocytosis may be observed within several hours after myocardial injury and returns to levels within the reference range within one week
  16. 16. C-reactive Protein (CRP) • C- reactive protein is a marker of acute inflammation • Patients without evidence of myocardial necrosis but with elevated CRP are at increased risk of an event
  17. 17. Release of cardiac markers after acute myocardial infarction (AMI)
  18. 18. CHEST X-RAY • Chest radiography may provide clues to an alternative diagnosis ( aortic dissection or pneumothorax) • Chest radiography also reveals complications of myocardial infarction such as heart failure
  19. 19. ECG • An ECG can be used to detect patterns of ischemia, injury, and infarction Ischemia • On the ECG, myocardial ischemia results in T- wave inversion or ST segment depression in the leads facing the ischemic area. • The inverted T wave representative of ischemia is symmetrical, relatively narrow, and somewhat pointed.
  20. 20. Injury • the injury process begins in the subendocardial layer and moves throughout the thickness of the wall of the heart like a wave. • If the process is not interrupted, it eventually results in a transmural MI. • On ECG, the hallmark of acute myocardial injury is the presence of ST segment elevations. • With an acute injury, the ST segments in the leads facing the injured area are elevated. • The elevated ST segments also have a downward concave or coved shape and merge unnoticed with the T wave
  21. 21. (A)ST segment elevation without T-wave inversion. (B) ST segment elevation with T-wave inversion. The elevated ST segments have a downward concave or coved shape and merge unnoticed with the T wave.
  22. 22. INFARCTION When myocardial injury persists, MI is the result. • During the earliest stage of MI, known as the hyperacute phase, the T waves become tall and narrow. This configuration is referred to as hyperacute or peaked T waves. • Within a few hours, these hyperacute T waves invert. • Next, the ST segments elevate, a pattern that usually lasts from several hours to several days. • In addition to the ST segment elevations in the leads of the ECG facing the injured heart, the leads facing away from the injured area may show ST segment depression. • This finding is known as reciprocal ST segment changes. • Reciprocal changes are most likely to be seen at the onset of infarction, but their presence on the ECG does not last long. • Reciprocal ST segment depressions may simply be a mirror image of the ST segment elevations.
  23. 23. Therapy The goals of therapy in AMI are the expedient restoration of normal coronary flow and the maximum salvage of functional myocardium
  24. 24. Antiplatelet Agents • Aspirin at least 160–162 mg on hospital day 1 Followed by 75–162 mg daily starting hospital day 2 and continued indefinitely. • Interferes with function of cyclooxygenase and inhibits the formation of thromboxane • Clopidogrel is also used which acts through a blockade of ADP receptors on platelets • 300–600 mg loading dose on hospital day 1 followed by a maintenance dose of 75 mg PO qd starting on hospital day 2 Administer indefinitely in patients with an aspirin allergy.
  25. 25. Nitrates • Nitrates promote the release of nitric oxide from the endothelium, which results in venous and arterial vasodilation • Vasodilatation reduces myocardial oxygen demand and preload and afterload • 0.4 mg , repeated every 5 min × 3 doses • 5 to 10 mcg/min by continuous infusion titrated up to 75 to 100 mcg/min until relief of symptoms or limiting side effects headache or hypotension • most significant adverse effects - tachycardia, flushing, headache, and hypotension. Nitrate • CI - sildenafil and vardenafil within the past 24 hours and tadalifil within the past 48 hours.
  26. 26. Supplemental Oxygen • Because MI impairs the circulatory function of the heart, oxygen extraction by the heart and other tissues may be diminished • Supplemental oxygen should be administered to patient with symptoms and or signs of pulmonary edema or pulse oximetry readings less than 90%.
  27. 27. 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 Low-molecular weight heparin • Direct activity against factors Xa and IIa • Proven to be effective in treating ACS that are characterized by unstable angina or non ST- elevation MI • Their fixed doses are easy to administer and laboratory testing to measure their therapeutic effect is not necessary makes them attractive alternative of un-fractionated heparin
  28. 28. 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
  29. 29. Thrombolytics • Thrombolytic drugs lyse coronary thrombi by converting plasminogen to plasmin. • Thrombolytic therapy provides maximal benefit if given within the first 3 hours after the onset of symptoms. • Significant benefit still occurs if therapy is given up to 12 hours after onset of symptoms.
  30. 30. Thrombolytics • As a class the plasminogen activators have been shown to restore coronary blood flow in 50-80% of patients • Contraindication active intracranial bleeding, CNS neoplasm, HTN, coagulopathy • Intracranial bleed risk major drawback
  31. 31. Glycoprotein IIb/IIIa Antagonists • Potent inhibitors of platelet aggregation • Use during PCI and in patients with high risk features ACS have been shown to reduce the composite end points of death, reinfraction and the need for target lesion
  32. 32. Revascularization:
  33. 33. Percutanous Coronary Intervention • Alternative if performed by skilled operator in an experienced center • Standard is a “ door to balloon” time of 90 minutes • PCI can successfully restore coronary blood flow in 90 to 95% of MI patients • PCI definitive survival advantage over fibrinolytics for MI patients who are in cardiogenic shock
  34. 34. Stenting •A stent is introduced into a blood vessel on a balloon catheter and advanced into the blocked area of the artery • the balloon is then inflated and causes the stent to expand until it fits the inner wall of the vessel, conforming to contours as needed • the balloon is then deflated and drawn back •The stent stays in place permanently, holding the vessel open and improving the flow of blood.
  35. 35. Angioplasty • a balloon catheter is passed through the guiding catheter to the area near the narrowing. A guide wire inside the balloon catheter is then advanced through the artery until the tip is beyond the narrowing. • the angioplasty catheter is moved over the guide wire until the balloon is within the narrowed segment. • balloon is inflated, compressing the plaque against the artery wall • once plaque has been compressed and the artery has been sufficiently opened, the balloon catheter will be deflated and removed.
  36. 36. Bypass surgery  healthy blood vessel is removed from leg, arm or chest  blood vessel is used to create new blood flow path in your heart  the “bypass graft” enables blood to reach your heart by flowing around (bypassing) the blocked portion of the diseased artery. The increased blood flow reduces angina and the risk of heart attack.
  37. 37. Lipid Management • All post MI patients should be on AMA step II diet ( < 7% of calories from saturated fats) • Post MI patients with LDL > 100 mg/dl are recommended to be on drug therapy to try to lower levels to <100 mg/dl • Recent data indicate that all MI patients should be on statin therapy, regardless of lipid levels or diet
  38. 38. Long term Medications • Most oral medications instituted in the hospital at the time of MI are continued long term • Aspirin, beta blockers and statin are continued indefinitely • ACEI indefinitely in patients with CHF, ejection fraction <.40, hypertension, or diabetes
  39. 39. Thank you!!