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Acute Myocardial Infarction By Jonathan Phillips Definition MI is irreversible necrosis of heart muscle secondary to prolonged ischemia. Results in imbalance of oxygen supply and demand. Appearance of cardiac enzymes in the circulation generally indicates myocardial necrosis. MI is considered part of a spectrum referred to as ACS which includes unstable angina and non-Q wave MI. Majority of ST-segment elevation will develop Q waves. Those w/o ST elevation will be diagnosed with unstable angina or NQWMI on the basis of the presence of cardiac enzymes. Etiology Atherosclerosis is the disease primarily responsible for the majority of ACS cases. Approximately 90% of MI result from acute thrombus that obstructs an atherosclerotic coronary artery. Plaque rupture is considered to be the major trigger of coronary thrombosis. Signs and Symptoms Shortness of Breath – – Shortness of breath may be the patient’s anginal equivalent or symptom of heart failure Due to elevated end-diastolic pressures secondary to ischemia, which then lead to elevated pulmonary pressures Signs and Symptoms Chest Pain – – – – – – Usually described as a substernal pressure sensation that also may be described as squeezing, aching, burner or even sharp pain Prolonged chest discomfort lasting longer than 30 minutes is most compatible with infarction Radiation to the left arm or neck is common Sensation is precipitated by exertion and relieved by rest and nitroglycerin Chest pain may be associated with nausea, vomiting, diaphoresis, dyspnea, fatigue, or palpitation Atypical chest pain is common, especially in patient with diabetes and the elderly Signs and Symptoms Atypical Presentations – – – – Common and lead to frequently lead to misdiagnosis Example: elderly patient may present with altered mental status Example: patient may present with abdominal discomfort or jaw pain as his/her anginal equivalent Low threshold should be maintained when evaluateing high and moderate risk patients, as their anginal equivalents may mimic other presentations Risk Factors Nonmodifiable – – – Age Sex Family history of CAD Modifiable – – – – – Smoking and other tobacco use Diabetes mellitus HTN Dyslipidemia Obesity Risk Factors New and other risk factors – – – – – – Elevated homocysteine levels Male pattern baldness Sedentary lifestyle and/or lack of exercise Psychosocial stress Presence of PVD Poor oral hygiene Risk Factors Nonatherosclerotic causes – – – – – – – – Vasculitis Coronary emboli Congenital coronary anomalies Coronary trauma Coronary spasm Drug use (cocaine) Heavy exertion, fever, hyperthyroidism Hypoxemia of severe anemia Differentials Anxiety disorders Aortic dissection Aortic stenosis Cholectystitis Esophageal spasm Esophagitis Acute gastritis GERD Myocarditis Pneumothorax PE Criteria for MI Diagnosis EKG Changes – – – ST segment elevation > 1 mm in 2 or more contiguous precordial or or limb leads New (or presumed new) LBBB ST segment depression with prominent R waves in leads V1 and V2, if thought to represent a posterior wall infarction rather than unstable angina Criteria for MI Diagnosis Lab Studies – Troponins – Considered criterion standard for diagnosing MI Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours and return to to baseline over 5-14 days Creatine kinase CK-MB levels increase within 3-12 hours at onset of chest pain and return to baseline withing 48-72 hours Criteria for MI Diagnosis Labs Studies (cont.) – Myoglobin Highly sensitive but not very specific. May be useful along with other studies in early detection of MI Imaging Studies – CXR: chest film used to assess patient’s heart size, CHF and pulmonary edema Criteria for MI Diagnosis Imaging Studies (cont.) – – Echo: can define an extended infarction and assess overall LV and RV function. Can detect such complications as acute MR, LV rupture or pericardial effusion Myocardial perfusion: obtain prior to discharge to assess extent of ischemia if the patient has not undergone a cardiac cath Criteria for MI Diagnosis Imaging Studies – Cardiac angiography: cardiac cath defines patient’s coronary anatomy and the extend of vessel disease. Patient’s with cardiogenic shock, intractable angina despite medications or severe congestion should undergo cardiac cath immediately Treatment Goal: restoration of the balance between the O2 supply and demand to prevent further ischemia; pain relief; and prevention, treatment of other complications that arise Treatment Bedrest NPO until stable ASA IV Heparin Warfarin Beta blockade (avoid agents known to cause reflux tachycardia) Digoxin-maybe of value for tachycardia associated with hypotension or CHF Analgesics Treatment ACE inhibitor Supplemental O2 Relieve pulmonary vascular congestion – Acute revascularization – – Diuretics, IV NTG, MSO4 Thrombolytic- standard of care Mechanical revascularization- cath, CABG Intra-aortic balloon pump Treatment Medications to avoid: – – – CCB Lidocaine IV magnesium Treatment Thrombolytic therapy – Criteria for use: < 6 hours most beneficial 6 to 12 hours less beneficial but still worthwhile > 12 hours: little apparent benefit unless ongoing chest discomfort or a “stuttering” course Treatment Thrombolytic therapy agents: – SK (streptokinase) and APSAC (anistreplase) – t-PA (alteplase, tissue plasminogen activator – Double bolus, 30 minutes apart) TNK-tPA (tenecteplase) – IV bolus and double infusion (accelerated dose) r-PA (reteplase) – IV infusion (SK), Single bolus (APSAC) Singe bolus (over 5 to 10 seconds) n-PA (lanoteplase) Single bolus Treatment Thrombolytic therapy (t-PA) – – Tissue plasminogen activator is superior to streptokinase in achieving a higher rate of coronary artery patency Recent trials show an even greater patency rate if a llb/llla receptor antagonist (abciximab) is combined with a half dose of thrombolytic agent as initial reperfusion strategy Treatment Aspirin – – – – Shown to decrease mortality and re-infarction rates after MI Clopidogrel may be used as alternative in cases of aspirin resistance or allergy Platelet glycoprotein, ASA, UFH to patients with continuing ischemia and to whom PCI is planned Abciximab can be used 12-24 hours in patient with unstable angina or NSTMI in whom PCI planned within next 24 hours. Treatment Beta-blockers – – Reduce rates of reinfarction and recurrent ischemia if administered within 12 hours after MI Administer routinely to all patients with MI unless contraindication is present Treatment Heparin – – – Established as adjunctive agent in patients receiving t-PA but not with streptokinase Indicated in patients undergoing primary angioplasty LMWHs have been shown superior to UFHs in patients with unstable angina or NQWMI Treatment Nitrates – – – No apparent impact on mortality rate Provides symptomatic relief and reload reduction Administer within first 48 hours, unless contraindicated (ie. RV infarction) Treatment ACE Inhibitors – – – – Reduce mortality rates after MI Administer as soon as possible if patient has no contraindications Greatest benefit in patients with ventricular dysfuction Continue indefinately after MI Surgical Care PTCA – – – Provides greater coronary patency (>96% thrombolysis in MI (TIMI) 3 flow) and lower risk of bleeding Studies show that primary PTCA has a mortality benefit over thrombolytics Stenting and adjunctive llb/llla therapy are improving the results of primary PTCA Surgical Care Cardiac Cath and Angioplasty – – For patients who don’t fit criteria for thrombolytic therapy or have persistent ischemia Treatment of choice for patients with cardiogenic shock, patients whom thrombolysis failed and those with high rise of bleeding or contraindications to thrombolytic therapy Surgical Care CABG – – For patients where angioplasty fails For patients who develop mechanical complication such as a VSD, LV rupture or papillary muscle rupture Concerns Right Ventricular Infarction – – – – – – 1/3 of patients with inferior Mi develop RV infarction Right-sided ECG with greater than 1mm ST elevation in V3R or V4R leads describes an RV infarction ECHO may be helpful in diagnosis PE shows inc.in JVD, right-sided S3, Kussmaul sign or hypotension Avoid nitrates or any medications that lower the reload Pulmonary artery cath can be helpful in guiding therapy Questions What is the most common cause of MI? a. b. c. d. Hyperlipidemia Acute thrombus that obstructs an atherosclerotic coronary artery Hypertension Plaque rupture Answer What is the most common cause of MI? a. b. c. d. Hyperlipidemia Acute thrombus that obstructs an atherosclerotic coronary artery Hypertension Plaque rupture Question What is the proven therapy shown to reduce mortality in acute MI? a. b. c. d. Aspirin Beta-blockers ACE inhibitors Thrombolytics Answer What is the proven therapy shown to reduce mortality in acute MI? a. b. c. d. Aspirin Beta-blockers ACE inhibitors Thrombolytics Question What is the most specific marker for the heart which goes up in 6 hours and peaks at 24 hours. a. b. c. d. Myoglobin CPK LDH Troponin I Answer What is the most specific marker for the heart which goes up in 6 hours and peaks at 24 hours. a. b. c. d. Myoglobin CPK LDH Troponin I