WORKUP	Section 5 of 11
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Lab Studies:

• Cardiac enzymes: In patients with suspected MI, obtain cardiac enzymes at regular intervals, starting upon admission and serially for as long as 24 hours.

• Creatine kinase level

• Creatine kinase comprises 3 isoenzymes, including creatine kinase with muscle subunits (CK-MM), which is found mainly in skeletal muscle; creatine kinase with brain subunits (CK-BB), predominantly found in the brain; and myocardial muscle creatine kinase (CK-MB), which is found mainly in the heart.

• Serial measurements of CK-MB isoenzyme levels were previously the standard criterion for diagnosis of MI. CK-MB levels increase within 3-12 hours of onset of chest pain, reach peak values within 24 hours, and return to baseline after 48-72 hours. Levels peak earlier (wash out) if reperfusion occurs. Sensitivity is approximately 95%, with high specificity. However, sensitivity and specificity are not as high as for troponin levels, and the trend has favored using troponins for the diagnosis of MI.

• Troponin levels

• Troponin levels are now considered the criterion standard in defining and diagnosing MI, according to the American College of Cardiology (ACC)/American Heart Association (AHA) consensus statement on MI (Braunwald, 2000).

• Cardiac troponin levels (troponin-T and troponin-I) have a greater sensitivity and specificity than CK-MB levels in detecting MI. They have important diagnostic and prognostic roles. Positive troponin levels are considered virtually diagnostic of MI in the most recent ACC/AHA revisions, as they are without equal in combined specificity and sensitivity in this diagnosis.

• Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to baseline over 5-14 days.

• Myoglobin levels

• Urine myoglobin levels rise within 1-4 hours from the onset of chest pain.

• Myoglobin levels are highly sensitive but not specific, and they may be useful within the context of other studies and in early detection of MI in the ED.

• Complete blood cell count

• Obtain a CBC count if MI is suspected to rule out anemia as a cause of decreased oxygen supply and prior to giving thrombolytics.

• Leukocytosis is also common, but not universal, in the setting of acute MI.

• A platelet count is necessary if a IIb/IIIa agent is considered; furthermore, the patient's WBC count may be elevated modestly in the setting of MI, signifying an acute inflammatory state.

• Chemistry profile

• In the setting of MI, closely monitor potassium and magnesium levels.

• Creatinine level is also needed prior to initiating treatment with an angiotensin-converting enzyme (ACE) inhibitor.

• Lipid level profile: This may be helpful if obtained upon presentation because levels can change after 12-24 hours of an acute illness.

• C-reactive protein (CRP) levels: Consider measuring CRP levels and other markers of inflammation upon presentation if an ACS is suspected.

Imaging Studies:

• Chest radiography

• Upon presentation, obtain a chest radiograph to assess the patient's heart size and the presence or absence of decompensated CHF with or without pulmonary edema.

• A chest radiograph may also assist in diagnosing concomitant disease, such as pneumonia in an elderly patient, as a precipitating cause for MI.

• Echocardiography

• An echocardiogram may play an important role in the setting of MI.

• Regional wall motion abnormalities can be identified, which are especially helpful if the diagnosis is questionable.

• An echocardiogram can also define the extent of the infarction and assess overall left ventricle (LV) and right ventricle (RV) function. In addition, an echocardiogram can identify complications, such as acute MR, LV rupture, or pericardial effusion.

• Myocardial perfusion imaging

• Prior to discharge, obtain myocardial perfusion imaging to assess the extent of residual ischemia if the patient has not undergone cardiac catheterization. The extent of ischemia can guide further therapy as to whether to proceed with catheterization or to continue conservative therapy.

• Myocardial perfusion has been shown to be a valuable method for triage of patients with chest pain in the ED. Significant variability exists among centers, and the results of the trials can be applied only to those centers with proven reliability and experience.

• Cardiac angiography

• Cardiac catheterization defines the patient's coronary anatomy and the extent of the disease. Most investigators recommend that all patients with MI should undergo cardiac catheterization, if it is available.

• Patients with cardiogenic shock, intractable angina despite medications, or severe pulmonary congestion should undergo cardiac catheterization immediately.

Other Tests:

	TREATMENT	Section 6 of 11
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Medical Care: Initial therapy for acute MI is directed toward restoration of perfusion in order to salvage as much of the jeopardized myocardium as possible. This may be accomplished through medical or mechanical means, such as angioplasty or coronary artery bypass grafting.

Further treatment is based on (1) restoration of the balance between the oxygen supply and demand to prevent further ischemia, (2) pain relief, and (3) prevention and treatment of any complications that may arise.

• Thrombolytic therapy has been shown to improve survival rates in patients with acute MI if administered in a timely fashion in the appropriate group of patients. If PCI capability is not available or will cause a delay greater than 90 minutes, then the optimal approach is to administer thrombolytics within 12 hours of onset of symptoms in patients with ST-segment elevation greater than 0.1 mV in 2 or more contiguous ECG leads, new left bundle-branch block (LBBB), or anterior ST depression consistent with posterior infarction. Tissue plasminogen activator (t-PA) is superior to streptokinase in achieving a higher rate of coronary artery patency; however, the key to efficacy lies in the speed of the delivery of therapy. Recent trials show a high patency rate if a IIb/IIIa receptor antagonist is combined with a half dose of a thrombolytic agent as the initial reperfusion strategy. The reduced dose of a thrombolytic agent combined with a potent platelet inhibitor may prove to be the preferred method for medical
  reperfusion. Larger clinical trials are pending.

• Aspirin and/or antiplatelet therapy

• Aspirin has been shown to decrease mortality and re-infarction rates after MI. Administer aspirin immediately, which the patient should chew if possible upon presentation. Continue aspirin indefinitely unless an obvious contraindication, such as a bleeding tendency or an allergy, is present. Clopidogrel may be used as an alternative in cases of a resistance or allergy to aspirin. Recent data from the CLARITY trial (CLopidogrel as Adjunctive ReperfusIon Therapy Thrombolysis in Myocardial Infarction [TIMI] 28) suggest that adding clopidogrel to this regimen is safe and effective. The clopidogrel dose used was 300 mg.

• Administer a platelet glycoprotein (GP) IIb/IIIa-receptor antagonist, in addition to acetylsalicylic acid and unfractionated heparin (UFH), to patients with continuing ischemia or with other high-risk features and to patients in whom a percutaneous coronary intervention (PCI) is planned. Eptifibatide and tirofiban are approved for this use. Abciximab also can be used for 12-24 hours in patients with unstable angina or NSTEMI in whom a PCI is planned within the next 24 hours.

• Beta-blockers reduce the rates of reinfarction and recurrent ischemia and possibly reduce the mortality rate if administered within 12 hours after MI. Administer routinely to all patients with MI unless a contraindication is present.

• Heparin (and other anticoagulant agents) has an established role as an adjunctive agent in patients receiving t-PA but not with streptokinase. Heparin is also indicated in patients undergoing primary angioplasty. Little data exist with regard to efficacy in patients not receiving thrombolytic therapy in the setting of acute MI. Low–molecular-weight heparins (LMWHs) have been shown to be superior to UFHs in patients with unstable angina or NSTEMI.

• Nitrates have no apparent impact on mortality rate in patients with ischemic syndromes. Their utility is in symptomatic relief and preload reduction. Administer to all patients with acute MI within the first 48 hours of presentation, unless contraindicated (ie, in RV infarction).

• ACE inhibitors reduce mortality rates after MI. Administer ACE inhibitors as soon as possible as long as the patient has no contraindications and remains in stable condition. ACE inhibitors have the greatest benefit in patients with ventricular dysfunction. Continue ACE inhibitors indefinitely after MI. Angiotensin-receptor blockers may be used as an alternative in patients who develop adverse effects, such as a persistent cough, although initial trials need to be confirmed.

Surgical Care:

• Percutaneous coronary intervention

• PCI is the treatment of choice in most patients with STEMI, assuming a door to needle time of less than 90 minutes. PCI provides greater coronary patency (>96% thrombolysis in myocardial infarction [TIMI] 3 flow), lower risk of bleeding, and instant knowledge about the extent of the underlying disease. Studies have shown that primary PCI has a mortality benefit over thrombolytic therapy.

• The choice of primary PCI should be individualized to each institution and to the patient's presentation and timing.

• The widespread use of stenting and adjunctive IIb/IIIa therapy are improving the results of primary PCI. A recently published trial showed that, in patients with acute MI, coronary stenting and abciximab lead to a greater degree of myocardial salvage and a better clinical outcome than fibrinolysis with thrombolytic therapy. Improvement of long- and short-term outcomes, however, depends highly on the speed with which reperfusion is achieved.

• Primary PCI is also the treatment of choice in patients with cardiogenic shock, patients in whom thrombolysis failed, and those with high risk of bleeding or contraindications to thrombolytic therapy.

• Only an experienced operator should perform primary PTCA, and PTCA should be performed only where the appropriate facilities are available. Operators should have at least 75 cases per year, while the center should perform at least 200 cases per year as per the recommendations of the ACC.

• Emergent or urgent coronary artery graft bypass surgery is indicated in patients in whom angioplasty fails and in patients who develop mechanical complications such as a VSD, LV, or papillary muscle rupture.

Consultations:

• ED personnel should initiate evaluation and treatment, including administering a thrombolytic agent.

• Obtain cardiology consultation immediately if primary PCI is considered. Otherwise, cardiology consultation may be obtained as needed and upon admission. Consultation may be obtained sooner if the patient presents with significant heart failure, mechanical complications, arrhythmias, or other complicating factors.

Diet:

• Initially, keep the patient on nothing by mouth (NPO) until his or her condition has been stabilized and treated. Following initial therapy and admission, a dietitian should instruct the patient regarding appropriate diet, as recommended by the AHA.

• A low-salt, low-fat, and low-cholesterol diet is generally recommended.

Activity:

• Confine patients to bed rest to minimize oxygen consumption until reperfusion and initial therapy are complete. This usually lasts about 24-48 hours; after that, the patient's activity may be accelerated slowly as tolerated and as the clinical situation allows.

• Initiate cardiac rehabilitation prior to discharge.

	MEDICATION	Section 7 of 11
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The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

	MISCELLANEOUS	Section 9 of 11
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Medical/Legal Pitfalls:

• Failure to make the diagnosis of an MI is the leading cause of litigation against ED physicians and cardiologists.

• Consider atypical presentations in elderly patients, patients with diabetes, and women. Assess all patients carefully, especially if they have significant cardiac risk factors.

• Review all ECGs that are obtained in a prompt fashion because time is crucial.

• Obtain cardiology consultation whenever the diagnosis is questionable.

• Consider an echocardiogram to assess wall motion abnormalities in difficult cases with nondiagnostic ECGs, such as with an LBBB.

Special Concerns:

• Right ventricular infarction

• Approximately one third of patients with inferior MI develop RV infarction. RV infarction presents a special challenge because the adjunctive therapy, other than reperfusion, is somewhat different.

• A right-sided ECG with greater than 1 mm ST elevation in V3R or V4R leads describes an RV infarct. An echocardiogram may be helpful in confirming the diagnosis. On physical examination, signs of right heart failure, such as elevated jugular venous pulsation, right-sided S3, Kussmaul sign, or hypotension, may be present, and the patient may have clear lung fields.

• The patient becomes volume dependent to maintain adequate LV and RV filling. Occasionally, dobutamine may be needed, or even an intraaortic balloon pump for hemodynamic support.

• Avoid nitrates or any medications that lower preload in this setting. A pulmonary artery catheter can be helpful in guiding therapy.

• Elderly patients

• Elderly patients with acute MI are at increased risk of developing complications. Treat these patients aggressively.

• Elderly patients have an increased risk of bleeding with thrombolytic therapy, but they also have the most to gain from this therapy.

• Very elderly patients should undergo primary angioplasty if available, but they should receive thrombolytics if excessive delay is anticipated before angioplasty can be performed.