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Myocardial Infarction
KABEER S Govt ayurveda college, tripunithura

Background
Myocardial Infarction if the rapid development of myocardial necrosis by a critical imbalance between oxygen supply and demand to the myocardium

Classification
Acute coronary syndromes include ST-elevation MI (STEMI) Non ST-elevation MI ( NSTEMI) Unstable Angina Cardiac markers in circulation indicates myocardial infarction and help categorize MI and is a useful adjunct to diagnosis

Classification
Anatomic or morphologic Transmural= Full thickness Non-transmural= Partial thickness ECG Q wave MI Non Q wave MI Does not distinguish transmural from a nontransmural MI as determined by pathology

History
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

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

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

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

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

Renal Failure and Renal Transplantation


Diagnostic accuracy of serum markers of cardiac injury are altered in patients with renal failure Cardiac troponins decreased diagnostic sensitivity and specificity in patients receiving renal replacement therapy Current data show levels of troponin I are unaltered while levels of troponin T may be elevated

Chemistry Profile
Potassium and magnesium levels should be monitored and corrected
Creatinine levels must be considered before using contrast dye for coronary angiography and percutanous revascularization

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

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

Echocardiography
Use 2-dimentional and M mode echocardiography when evaluating overall ventricular function and wall motion abnormalities Echocardiography can also identify complications of MI ( eg. Valvular or pericardial effusion, VSD)

Electrocardiogram
A normal ECG does not exclude ACS High probability include ST segment elevation in two contiguous leads or presence of q waves Intermediate probability ST depression T wave inversions are less specific

Localization of MI
ST elevation only Inferior wall- II, III, aVF Lateral wall_ I, aVL, V4-V6 Anteroseptal- V1-V3 Anterolateral- V1-V6 Right ventricular- RV4, RV5 Posterior- R/S ratio >1 in V1 and T wave inversion

Therapy

The goals of therapy in AMI are the expedient restoration of normal coronary flow and the maximum salvage of functional myocardium

Antiplatelet Agents
Aspirin at lease 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. Clopidogrel, ticlopidine, have not been shown in any large scal trail to be superior to Aspirin in acute MI

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%.

Nitrates
IV nitrates to all patients with MI and congestive heart failure, persistent ischemia, hypertension, or large anterior wall MI Primary benefit vasodilator effect Metabolized to nitric oxide in the vascular endothelium, relaxes endothelium Vasodilatation reduces myocardial oxygen demand and preload and afterload

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

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 unfractionated heparin

Thrombolytics
Indicated with MI and ST segment elevation greater than 0.1mV in 2 contiguous ECG leads, or new onset LBBB, who present less than 12 hours but not more than 24 hours after symptom onset The most critical variable in achieving successful fibrinolysis is time form symptom onset to drug administration

Thrombolytics
As a class the plasminogen activators have been shown to restore coronary blood flow in 50-80% of patients Contraindication active intracranial bleeding, CVA 2months, CNS neoplasm, HTN, coagulopathy Retaplase slightly higher angiographic patency but did not translate into survival benefit Intracranial bleed risk major drawback

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

Surgical Revascularization
Emergent or surgical revascularization in setting of failed PTCA in patients with hemodynamic instability and coronary anatomy amendable to surgical grafting Also indicated of mechanical complications of MI including VSD, free wall rupture, or acute MR Carries a higher risk of perioperative mortality than elective CABG

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

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

Thank You!

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