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eMedicine Specialties > Cardiology > Coronary Artery Disease

Myocardial Infarction

Samer Garas, MD, FACC, Chief of Cardiology, Department of Interventional Cardiology, St Vincent's Hospital
A Maziar Zafari, MD, PhD, FACC, Associate Professor, Department of Medicine, Emory University School of Medicine; Chief, Section of Cardiology, Atlanta Veterans Affairs Medical Center

Updated: Oct 5, 2009

Introduction

Background

Myocardial infarction (MI) is the irreversible necrosis of heart muscle secondary to prolonged ischemia. This usually results from an imbalance of oxygen supply and demand. The appearance of cardiac enzymes in the circulation generally indicates myocardial necrosis. Myocardial infarction is considered, more appropriately, part of a spectrum referred to as acute coronary syndromes (ACSs), which also includes unstable angina and non–ST-elevation MI (NSTEMI). Patients with ischemic discomfort may or may not have ST-segment elevation. Most of those with ST-segment elevation will develop Q waves. Those without ST elevations will ultimately be diagnosed with unstable angina or NSTEMI based on the presence of cardiac enzymes.

Myocardial infarction may lead to impairment of systolic function or diastolic function and to increased predisposition to arrhythmias and other long-term complications.

Pathophysiology

Atherosclerosis is the disease primarily responsible for most acute coronary syndrome cases. Approximately 90% of myocardial infarctions result from an acute thrombus that obstructs an atherosclerotic coronary artery. Plaque rupture is considered to be the major trigger of coronary thrombosis. Following plaque rupture, platelet activation and aggregation, coagulation pathway activation, and endothelial vasoconstriction occur and lead to coronary thrombosis and occlusion.

Consider nonatherosclerotic causes of acute myocardial infarctions in younger patients or if no evidence of atherosclerosis is noted. Such causes include coronary emboli from sources such as an infected cardiac valve through a patent foramen ovale (PFO), coronary occlusion secondary to vasculitis, primary coronary vasospasm (variant angina), cocaine use, or other factors leading to mismatch of oxygen supply and demand, as may occur with a significant gastrointestinal bleed.

Frequency

United States

Approximately 1.5 million cases of myocardial infarction occur each year.

International

Cardiovascular diseases cause 12 million deaths throughout the world each year, according to the third monitoring report of the World Health Organization, 1991-93. They cause half of all deaths in several developed countries and are one of the main causes of death in many developing countries; they are the major cause of death in adults everywhere.

Mortality/Morbidity

  • Cardiovascular disease is the leading cause of death in the United States; approximately 500,000-700,000 deaths related to the coronary artery occur each year.
  • Ischemic heart disease is the leading cause of death worldwide.
  • Approximately 6.3 million deaths due to heart disease occurred in 1990 worldwide, which represents 29% of all deaths. The prevalence of coronary artery disease (CAD) is increasing rapidly in nonindustrialized countries.

Race

Cardiovascular disease is the leading cause of morbidity and mortality among African American, Hispanic, and white populations in the United States.

Sex

  • A male predominance in incidence exists up to approximately age 70 years, when the sexes converge to equal incidence.
  • Premenopausal women appear to be somewhat protected from atherosclerosis, possibly owing to the effects of estrogen.

Age

  • Incidence increases with age.
  • Most patients who develop an acute myocardial infarction are older than 60 years. Elderly people also tend to have higher rates of morbidity and mortality from their infarcts.

Clinical

History

Symptoms of myocardial infarction include the following:

  • Chest pain
    • This is usually described as a substernal pressure sensation that also may be described as squeezing, aching, burning, 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.
    • The sensation is precipitated by exertion and relieved by rest and nitroglycerin.
    • Chest pain may be associated with nausea, vomiting, diaphoresis, dyspnea, fatigue, or palpitations.
    • Atypical chest pain is common, especially in patients with diabetes and in elderly patients. However, any patient may present with atypical symptoms. These symptoms are considered the anginal equivalent for that patient.
  • Shortness of breath
    • Shortness of breath may be the patient's anginal equivalent or a symptom of heart failure.
    • It is due to elevated end-diastolic pressures secondary to ischemia, which may then lead to elevated pulmonary pressures.
  • Atypical presentations
    • 20% of patients are asymptomatic or have atypical symptoms.
    • Atypical presentations are common and frequently lead to misdiagnoses.
    • A patient may, for example, present with abdominal discomfort or jaw pain as his or her anginal equivalent.
    • An elderly patient may present with altered mental status.
    • Low threshold should be maintained when evaluating high- and moderate-risk patients, as their anginal equivalents may mimic other presentations.
    • Women tend to present more commonly with atypical symptoms such as sharp pain, fatigue, weakness, and other nonspecific complaints.

Physical

Physical examination findings for myocardial infarction can vary; one patient may be comfortable in bed, with normal examination results, while another may be in severe pain with significant respiratory distress requiring ventilatory support.

  • Low-grade fever may be present.
  • Hypotension or hypertension can be observed depending on the extent of the myocardial infarction.
  • Fourth heart sound (S 4 ) may be heard in patients with ischemia. With ischemia, diastolic dysfunction is the first physiologically measurable effect and this can then cause a stiff ventricle and an audible S 4 .
  • Dyskinetic cardiac bulge (in anterior wall myocardial infarction) can occasionally be palpated.
  • Systolic murmur can be heard if mitral regurgitation (MR) or ventricular septal defect (VSD) develops.
  • Other findings include cool, clammy skin and diaphoresis.
  • Signs of congestive heart failure (CHF) may be found, including the following:
    • Third heart sound (S 3 ) gallop
    • Pulmonary rales
    • Lower extremity edema
    • Elevated jugular venous pressure

Causes

  • Atherosclerosis with occlusive or partially occlusive thrombus formation
  • Nonmodifiable risk factors for atherosclerosis
    • Age
    • Sex
    • Family history of premature coronary heart disease
  • Modifiable risk factors for atherosclerosis
    • Smoking or other tobacco use
    • Diabetes mellitus
    • Hypertension
    • Dyslipidemia
    • Obesity
  • New and other risk factors for atherosclerosis
    • Elevated homocysteine levels
    • Male pattern baldness
    • Sedentary lifestyle and/or lack of exercise
    • Psychosocial stress
    • Presence of peripheral vascular disease
    • Poor oral hygiene
  • Nonatherosclerotic causes
    • Vasculitis
    • Coronary emboli
    • Congenital coronary anomalies
    • Coronary trauma
    • Coronary spasm
    • Drug use (cocaine)
    • Factors that increase oxygen requirement, such as heavy exertion, fever, or hyperthyroidism
    • Factors that decrease oxygen delivery, such as hypoxemia of severe anemia

Differential Diagnoses

Anxiety Disorders
Gastritis, Acute
Aortic Dissection
Gastroesophageal Reflux Disease
Aortic Stenosis
Myocarditis
Cholecystitis
Pericarditis, Acute
Esophageal Spasm
Pneumothorax
Esophagitis
Pulmonary Embolism

Other Problems to Be Considered

Pneumonia
Pancreatitis

Workup

Laboratory Studies

Lab studies for patients with myocardial infarction include the following:

  • Cardiac enzymes: In patients with suspected myocardial infarction, obtain cardiac enzymes at regular intervals, starting upon admission and serially for as long as 24 hours.
  • Troponin levels
    • Troponin levels are now considered the criterion standard in defining and diagnosing myocardial infarction, according to the American College of Cardiology (ACC)/American Heart Association (AHA) consensus statement on myocardial infarction.1,2
    • Cardiac troponin levels (troponin-T and troponin-I) have a greater sensitivity and specificity than CK-MB levels in detecting myocardial infarction. They have important diagnostic and prognostic roles. Positive troponin levels are considered virtually diagnostic of myocardial infarction 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.
    • According to a 2009 study published in the New England Journal new sensitive cardiac troponin assays have greater diagnostic accuracy than the standard assays, especially for early diagnosis. These assays can substantially improve the early diagnosis of acute myocardial infarction, particularly in patients with a recent onset of chest pain.32  
  • 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 myocardial infarction. 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 myocardial infarction.
    • 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 myocardial infarction in the emergency department.
    • Complete blood cell count
      • Obtain a CBC count if myocardial infarction 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 myocardial infarction.
      • 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 myocardial infarction, signifying an acute inflammatory state.
    • Chemistry profile
      • In the setting of myocardial infarction, 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 acute coronary syndrome 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 congestive heart failure 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 myocardial infarction.
    • A chest radiograph may be helpful in evaluation for aortic dissection.
  • Echocardiography
    • An echocardiogram may play an important role in the setting of myocardial infarction.
    • 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 mitral regurgitation, 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 emergency department. 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 myocardial infarction 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

  • The electrocardiogram (ECG) is the most important tool in the initial evaluation and triage of patients in whom an ACS is suspected (see Media files 1-3). It is confirmatory of the diagnosis in approximately 80% of cases.
    • Obtain an ECG immediately if myocardial infarction is considered or suspected.
    • In patients with inferior myocardial infarction, record a right-sided ECG to rule out RV infarct.
    • Qualified personnel should review the ECG as soon as possible.
    • Perform ECGs serially upon presentation to evaluate progression and assess changes with and without pain.
    • Obtain daily serial ECGs for the first 2-3 days and additionally as needed.
    • Convex ST-segment elevation with upright or inverted T waves is generally indicative of myocardial infarction in the appropriate clinical setting.
    • ST depression and T-wave changes may also indicate evolution of NSTEMI.

 


Acute anterior myocardial infarction.

Acute anterior myocardial infarction.



Acute inferior myocardial infarction.

Acute inferior myocardial infarction.



Posterolateral myocardial infarction.

Posterolateral myocardial infarction.


Treatment

Medical Care

Initial therapy for acute myocardial infarction is directed toward restoration of perfusion as soon as possible to salvage as much of the jeopardized myocardium as possible. This may be accomplished through medical or mechanical means, such as percutaneous coronary intervention 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 myocardial infarction if administered in a timely fashion in the appropriate group of patients. If percutaneous coronary intervention (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.
  • Aspirin and/or antiplatelet therapy
    • Aspirin has been shown to decrease mortality and re-infarction rates after myocardial infarction. 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.3 The clopidogrel dose used was 300 mg. Further studies suggest that a higher dose of clopidogrel may have added benefit.4
    • 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. Abciximab5,6 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.
  • Heparin (and other anticoagulant agents) has an established role as an adjunctive agent in patients receiving t-PA, but not in patients receiving streptokinase. Heparin is also indicated in patients undergoing primary angioplasty. Few data exist with regard to efficacy in patients not receiving thrombolytic therapy in the setting of acute myocardial infarction. Low molecular-weight heparins (LMWHs) have been shown to be superior to UFHs in patients with unstable angina or NSTEMI. Bivalirudin (a direct thrombin inhibitor) has shown some promise in the setting of STEMI if combined with high-dose clopidogrel load and may be an appropriate alternative strategy.
  • 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 myocardial infarction within the first 48 hours of presentation, unless contraindicated (ie, in RV infarction).
  • ACE inhibitors reduce mortality rates after myocardial infarction. 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 myocardial infarction. 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.
  • Beta-blockers may reduce the rates of reinfarction and recurrent ischemia. Administer to patients with myocardial infarction unless a contraindication is present. However, a large chinese trial showed no benefit to beta-blockade. This has created some doubt as to the benefit and may lead to a change in the guidelines.7

Surgical Care

  • Percutaneous coronary intervention
    • PCI is the treatment of choice in most patients with STEMI, assuming a door to balloon time of less than 90 minutes in at least 75% of the patients presenting with STEMI. 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. Door to balloon times correlate closely with mortality rates, making this the key measurement for any successful interventional program.
    • The choice of primary PCI should be individualized to each institution and to the patient's presentation and timing. PCI in patients with occluded arteries for more than 24 hours appears to offer no added benefit over medical treatment.
    • The widespread use of stenting and adjunctive IIb/IIIa therapy are improving the results of primary PCI. One trial showed that, in patients with acute myocardial infarction, coronary stenting and abciximab lead to a greater degree of myocardial salvage and a better clinical outcome than fibrinolysis with thrombolytic therapy.8 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.
    • Cantor et al studied high-risk patients with ST-segment elevated myocardial infarction (STEMI) who received fibrinolytic therapy in hospitals that do not have percutaneous coronary intervention (PCI) capabilities. The patients (n=1059) were randomized to either standard treatment (ie, if needed, included rescue PCI, or delayed angiography) or immediate transfer to another hospital and PCI within 6 hours following fibrinolysis. All patients received aspirin, tenecteplase, and anticoagulation (heparin or enoxaparin), and clopidogrel was recommended.

      The study’s primary endpoint was a composite of death, reinfarction, recurrent ischemia, new or worsening congestive heart failure, or cardiogenic shock within 30 days. The primary end point occurred in 11% of patients in the group that was immediately transferred compared with 17.2% of patients randomized to the standard treatment (P=0.004). A significant decrease in ischemic complications was observed in high-risk patients with STEMI who were treated with fibrinolysis and transferred for PCI within 6 hours following fibrinolysis.9
  • 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

  • Emergency department 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

The goals of pharmacotherapy for myocardial infarction are to reduce morbidity and to prevent complications.

Salicylates

The antiplatelet effects of these agents may improve mortality rate.


Aspirin (Anacin, Ascriptin, Bayer Aspirin)

Early administration of aspirin in patients with acute MI has been shown to reduce cardiac mortality rate by 23% in first mo.

Dosing

Adult

160-325 mg PO or chewed

Pediatric

10-15 mg/kg/dose PO q4-6h

Interactions

Antacids and urinary alkalinizers can decrease pharmacologic effects; corticosteroids decrease serum levels by increasing salicylate clearance; other anticoagulants can have an additive hypoprothrombinemic effect and may increase bleeding time; may antagonize uricosuric effects of probenecid and increase free phenytoin and valproic acid levels, increasing their toxicity; in doses > 2 g/d, may alter pancreatic beta-cell function and potentiate glucose-lowering effect of sulfonylurea drugs

Contraindications

Documented hypersensitivity, liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma
Because of association with Reye syndrome, do not administer to children (<16 y) who have flu

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in patients with chronic renal insufficiency—may cause transient decrease in renal function and aggravate chronic kidney diseases; patients with severe anemia, history of blood coagulation defects, or taking anticoagulants should avoid

Antiplatelet agent

Strong mortality benefit. Increased risk of bleeding in case of emergent CABG.


Clopidogrel (Plavix)

Selectively inhibits adenosine diphosphate (ADP) binding to platelet receptor and subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.

May have a positive influence on several hemorrhagic parameters and may exert protection against atherosclerosis, not only through inhibition of platelet function but also through changes in the hemorrhagic profile.

Shown to decrease cardiovascular death, MI, and stroke in patients with acute coronary syndrome (ie, unstable angina, non-Q-wave MI).

Dosing

Adult

Loading dose: 300 mg PO once or 600 mg once
Maintenance: 75 mg PO qd administered with aspirin 75-325 mg/d PO

Pediatric

Not established

Interactions

Coadministration with naproxen associated with increased occult GI blood loss; clopidogrel prolongs bleeding time; safety of coadministration with warfarin not established

Contraindications

Documented hypersensitivity; active pathological bleeding, such as peptic ulcer or intracranial hemorrhage

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in patients at increased risk of bleeding from trauma, surgery, or other pathological conditions; caution in patients with lesions with propensity to bleed (such as ulcers)

Anticoagulants

Unfractionated intravenous heparin and fractionated low molecular weight subcutaneous heparins are the two choices for initial anticoagulation therapy.


Bivalirudin (Angiomax)

Synthetic analogue of recombinant hirudin. Inhibits thrombin. Used for anticoagulation in unstable angina undergoing PTCA. With provisional use of glycoprotein IIb/IIIa inhibitor (GP IIb/IIIa inhibitor) indicated for use as anticoagulant in patients undergoing PCI. Potential advantages over conventional heparin therapy include more predictable and precise levels of anticoagulation, activity against clot-bound thrombin, absence of natural inhibitors (eg, platelet factor 4, heparinase), and continued efficacy following clearance from plasma (because of binding to thrombin).

Dosing

Adult

0.75 mg/kg IV bolus initially; followed by 1.75 mg/kg/h IV for 4 h for duration of procedure

Pediatric

Not established

Interactions

Clinical trials have shown that patients undergoing PTCA/PCI, coadministration of bivalirudin with heparin, warfarin, or thrombolytics may increase risks of major bleeding events compared with patients not receiving these medications concomitantly

Contraindications

Documented hypersensitivity; cerebral aneurysm; intracranial hemorrhage, general uncontrollable hemorrhage, or active major bleeding

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal impairment (dose only needs adjustment in patients with severe renal impairment of CrCl<30 mL/min and patients who are dependent on hemodialysis), recent surgery or trauma, GI ulceration; risk of bleeding; may cause back pain, nausea, headache, hypotension


Heparin

Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombus formation. Prevents reaccumulation of clot after spontaneous fibrinolysis.

Dosing

Adult

70 IU/kg IV bolus, followed by 15 mcg/kg/h infusion, adjust to maintain aPTT 1.5-2 times control

Pediatric

Loading dose: 50 IU/kg/h IV
Maintenance infusion: 15-25 mcg/kg/h IV; increase dose by 2-4 IU/kg/h q6-8h prn using aPTT results

Interactions

Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase toxicity

Contraindications

Documented hypersensitivity, subacute bacterial endocarditis; active bleeding; history of heparin-induced thrombocytopenia

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus

Precautions

Observe for prolonged or excessive bleeding at venipuncture sites; some preparations contain benzyl alcohol as preservative, and benzyl alcohol used in large amounts has been associated with fetal toxicity (gasping syndrome); use of preservative-free heparin recommended in neonates; use with caution in patients with shock or severe hypotension


Enoxaparin (Lovenox)

Enhances inhibition of factor Xa and thrombin by increasing antithrombin III activity. In addition, preferentially increases inhibition of factor Xa.
Indicated for treatment of acute STEMI managed medically or with subsequent PCI. Also indicated as prophylaxis of ischemic complications caused by unstable angina and non-Q-wave MI.

Dosing

Adult

Treatment regimens include aspirin (75-325 mg/d) if not contraindicated
NSTEMI
1 mg/kg SC bid
CrCl <30 mL/min: 1 mg/kg SC qd
STEMI
<75 years: 30 mg IV single bolus plus 1 mg/kg SC, then 1 mg/kg SC q12h; not to exceed 100 mg/dose for first 2 SC doses
<75 years and CrCl <30 mL/min: 30 mg IV single bolus plus 1 mg/kg SC, then 1 mg/kg SC qd; not to exceed 100 mg/dose for first 2 SC doses
>75 years: 0.75 mg/kg SC q12h (no initial IV bolus administered), not to exceed 75 mg/dose for first 2 doses
>75 years and CrCl <30 mL/min: 1 mg/kg SC qd (no initial IV bolus administered)
With PCI: If last enoxaparin dose administered >8 h before balloon inflation, administer an additional IV bolus of 0.3 mg/kg
With thrombolytic agent: Give dose specified for age and renal function between 15 min before and 30 min after the start of fibrinolytic therapy

Pediatric

Not established

Interactions

Platelet inhibitors or oral anticoagulants, such as aspirin, NSAIDs, dipyridamole, salicylates, sulfinpyrazone, and ticlopidine, increase risk of bleeding and should be used with care in patients taking enoxaparin

Contraindications

Documented hypersensitivity; major bleeding; history of heparin-induced thrombocytopenia

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in recent surgery, GI lesions that may be prone to bleeding, hematologic conditions, uncontrolled hypertension, diabetic retinopathy, or vitreous hemorrhage; caution in patients with renal insufficiency because elimination delayed, increasing anticoagulant effect; if thromboembolic event occurs despite LMWH prophylaxis, discontinue drug and initiate appropriate therapy; reversible elevation of hepatic transaminases seen occasionally; heparin-induced thrombocytopenia has been seen with LMWH; for significant bleeding complications, 1 mg of protamine sulfate reverses effect of approximately 1 mg of enoxaparin; obtain hemostasis at puncture site before sheath removal after PCI

Platelet aggregation inhibitors

These agents prevent acute cardiac ischemic complications in unstable angina unresponsive to conventional therapy.


Abciximab (ReoPro)

Chimeric human-murine monoclonal antibody. Binds to receptor with high affinity and reduces platelet aggregation by 80%. Inhibition of platelet aggregation persists for as long as 48 h after infusion stopped.

Dosing

Adult

0.25 mcg/kg bolus IV, followed by 0.125 mcg/kg/min infusion for 12 h

Pediatric

Not established

Interactions

Anticoagulants, antiplatelets, and thrombolytics may increase toxicity

Contraindications

Documented hypersensitivity; bleeding diathesis; thrombocytopenia (<100,000 platelets/µL); recent trauma; intracranial tumor; severe uncontrolled hypertension; history of vasculitis; cerebrovascular accident within 2 y

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Bleeding complications are rare and usually related to use of standard-dose heparin instead of weight-based dosing; severe thrombocytopenia has been associated with abciximab within first 24 h of use


Tirofiban (Aggrastat)

Nonpeptide antagonist of glycoprotein IIb/IIIa receptor. Reversible antagonist of fibrinogen binding. When administered IV, >90% of platelet aggregation inhibited.

Dosing

Adult

0.4 mcg/kg/min IV for 30 min, then continue at 0.1 mcg/kg/min; administer half dose in patients with severe renal insufficiency (CrCl <30 mL/min)

Pediatric

Not established

Interactions

Heparin and aspirin increase risk of bleeding compared with heparin and aspirin alone; if using with other drugs that affect hemostasis (eg, warfarin), monitor patients closely

Contraindications

Documented hypersensitivity; severe hypertension (SBP >200 mm Hg); active internal bleeding; history of intracranial hemorrhage; intracranial neoplasm; AV malformation or aneurysm; acute pericarditis; bleeding diathesis; trauma or stroke within previous 30 d; platelet count <100,000/µL; history of thrombocytopenia following prior exposure to this product; serum creatinine >2 mg/dL (for 180-mcg/kg bolus and 2-mcg/kg/min infusion) or >4 mg/dL (for 135-mcg/kg bolus and 0.5-mcg/kg/min infusion)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Most common complications are bleeding events; caution in patients with platelet count <150,000/µL and in patients with hemorrhagic retinopathy; monitor platelet counts, serum creatinine, hemoglobin, hematocrit, and PT/aPTT before treatment, within 6 h after loading infusion, and at least daily thereafter (or more frequently if evidence of significant decline); because these agents inhibit platelet aggregation, exercise caution when using concurrently with drugs that affect hemostasis (eg, thrombolytics, ticlopidine, NSAIDs, warfarin, dipyridamole, clopidogrel)
Measure ACT and maintain aPTT at 50-70 s unless PCI necessary; maintain ACT at 250-300 s during PCI; if platelets decrease to <100,000/µL, perform additional platelet counts to exclude pseudothrombocytopenia; if thrombocytopenia confirmed, discontinue GP IIb/IIIa inhibitors and heparin and appropriately monitor and treat condition; to monitor UFH, monitor aPTT 6 h after start of heparin infusion and adjust to maintain aPTT at 1.5-2 times control


Eptifibatide (Integrilin)

Cyclic peptide that reversibly inhibits platelet aggregation by binding to IIb/IIIa receptor.

Dosing

Adult

Unstable angina:
180 mcg/kg IV bolus, followed by 2 mcg/kg/min continuous infusion until discharge or surgery

Patients undergoing PCI:
135 mcg/kg IV bolus before PCI, followed by 0.5 mcg/kg/min continuous infusion

Pediatric

Not established

Interactions

Heparin and aspirin increase risk of bleeding compared with heparin and aspirin alone; if using concurrently with other drugs that affect hemostasis (eg, warfarin), monitor patients closely

Contraindications

Documented hypersensitivity; severe hypertension (SBP >200 mm Hg); active internal bleeding; history of intracranial hemorrhage; intracranial neoplasm; AV malformation or aneurysm; acute pericarditis; bleeding diathesis; trauma or stroke within previous 30 d; platelet count <100,000/µL; history of thrombocytopenia following prior exposure to this product; serum creatinine >2 mg/dL (for 180-mcg/kg bolus and 2-mcg/kg/min infusion) or >4.0 mg/dL (for 135-mcg/kg bolus and 0.5-mcg/kg/min infusion)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Most common complications are bleeding events; exercise caution in patients with platelet count <150,000/µL and in patients with hemorrhagic retinopathy; because these agents inhibit platelet aggregation, exercise caution with concurrent use of drugs that affect hemostasis (eg, thrombolytic agents, ticlopidine, NSAIDs, warfarin, dipyridamole, clopidogrel)
Measure ACT and maintain aPTT at 50-70 s unless PCI necessary; maintain ACT at 250-300 s during PCI; if platelets decrease to <100,000/µL, perform additional platelet counts to exclude pseudothrombocytopenia; if thrombocytopenia confirmed, discontinue GP IIb/IIIa inhibitors and heparin and appropriately monitor and treat condition; to monitor UFH, monitor aPTT 6 h after start of heparin infusion and adjust to maintain aPTT to 1.5-2 times control

Vasodilators

These agents relieve chest discomfort by improving myocardial oxygen supply, which in turn dilates epicardial and collateral vessels, improving blood supply to the ischemic myocardium.


Nitroglycerin (Nitro-Bid)

Causes relaxation of vascular smooth muscle via stimulation of intracellular cyclic guanosine monophosphate production, causing decrease in BP.

Dosing

Adult

400 mcg SL or spray q5min, repeat up to 3 times; if symptoms persist, 5-10 mcg/min IV infusion; titrate to 10% reduction in MAP or symptom relief, limiting adverse effects of hypotension

Pediatric

Not established

Interactions

Aspirin may increase serum concentrations; calcium channel blockers may cause marked symptomatic orthostatic hypotension (dose adjustment of either agent may be necessary)

Contraindications

Documented hypersensitivity; severe anemia; shock; postural hypotension; head trauma; closed-angle glaucoma; cerebral hemorrhage; known history of RV MI

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Exercise caution in patients with CAD or low systolic BP

Beta-adrenergic blockers

This category of drugs has the potential to suppress ventricular ectopy due to ischemia or excess catecholamines. In the setting of myocardial ischemia, beta-blockers have antiarrhythmic properties and reduce myocardial oxygen demand secondary to elevations in heart rate and inotropy.


Metoprolol (Lopressor)

Selective beta1-adrenergic receptor blocker that decreases automaticity and contractions. Goals of treatment are reduction in heart rate to 60-80 bpm. During IV administration, carefully monitor BP, heart rate, and ECG.

Dosing

Adult

5 mg IV slow infusion q5min; not to exceed 15 mg or desired heart rate
25 mg PO bid usual initial dose, up to 100 mg bid; titrate to desired effect

Pediatric

Not established

Interactions

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; astemizole (recalled from US market), calcium channel blockers, quinidine, flecainide, and contraceptives may increase cardiotoxicity; digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents may increase toxicity

Contraindications

Documented hypersensitivity; decompensated CHF; bradycardia; bronchial asthma; cardiogenic shock; AV conduction abnormalities

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Do not use in cocaine-related ischemia; beta-adrenergic blockade may reduce signs and symptoms of acute hypoglycemia and may decrease clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm, monitor patient closely and withdraw drug slowly; during IV administration, carefully monitor BP, heart rate, and ECG


Esmolol (Brevibloc)

Useful drug for patients at risk of experiencing complications from beta-blockers, particularly reactive airway disease, mild-to-moderate LV dysfunction, and peripheral vascular disease. Its short half-life of 8 min allows for titration to desired effect with ability to stop quickly if necessary.

Dosing

Adult

0.1 mg/kg/min IV starting maintenance dose, titrate in increments of 0.05 mg/kg/min q10-15min to total dose of 0.2 mg/kg/min

Pediatric

Not established

Interactions

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; astemizole (recalled from US market), calcium channel blockers, quinidine, flecainide, and contraceptives may increase cardiotoxicity; digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents may increase toxicity

Contraindications

Documented hypersensitivity; decompensated CHF; bradycardia; cardiogenic shock; AV conduction abnormalities

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use in cocaine-related ischemia; beta-adrenergic blockade may decrease signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm, withdraw drug slowly and monitor patient closely

Angiotensin-converting enzyme (ACE) inhibitors

These agents may prevent conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.


Captopril (Capoten)

Has short half-life, which makes it important drug for initiation of ACE inhibitor therapy. Can be started at low dose and titrated upward as needed and as patient tolerates.

Dosing

Adult

6.25 mg PO tid initially; may titrate to total 450 mg/d

Pediatric

Not established

Interactions

Patients receiving diuretic therapy, other vasodilator agents, agents causing renin release, agents increasing potassium, or agents affecting sympathetic activity should be monitored carefully

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Administer with caution in patients with renal insufficiency and those with borderline low BP; may worsen renal function, especially in patients with bilateral renal artery stenosis; administer cautiously in patients with aortic stenosis because afterload reduction may worsen coronary perfusion

Thrombolytics

The main objective is to restore circulation through a previously occluded vessel by the rapid and complete removal of a pathologic intraluminal thrombus or embolus that has not been dissolved by the endogenous fibrinolytic system.


Alteplase, t-PA (Activase)

Fibrin-specific agent with brief half-life of 5 min. Adjunctive therapy with IV heparin necessary to maintain patency of arteries recanalized by t-PA, especially during first 24-48 h.

Dosing

Adult

15 mg IV initial bolus, followed by 50 mg IV over next 30 min, and then 35 mg IV over next h; total dose not to exceed 100 mg

Pediatric

Not established

Interactions

Heparin, which has been administered with and after alteplase infusions to reduce risk of reocclusion, may cause bleeding complications, monitor closely for bleeding, especially at arterial puncture sites; drugs that alter platelet function (eg, aspirin, abciximab, dipyridamole) may increase risk of bleeding if administered prior to, during, or after

Contraindications

Documented hypersensitivity; active internal bleeding; recent intracranial or intraspinal surgery or trauma; intracranial neoplasm; AV malformation or aneurysm; history of cerebrovascular accident within last 2 mo; seizure at onset of stroke; suspicion of subarachnoid hemorrhage; bleeding diathesis; serious head trauma; severe uncontrolled hypertension; do not administer to patients with history of intracranial hemorrhage

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adverse effects include hemorrhage, particularly intracranial; elderly patients are at greatest risk


Streptokinase (Kabikinase, Streptase)

Acts with plasminogen to convert plasminogen to plasmin. Plasmin degrades fibrin clots, fibrinogen, and other plasma proteins. Increase in fibrinolytic activity that degrades fibrinogen levels for 24-36 h occurs with IV infusion of streptokinase. Adjunctive therapy with heparin not needed.

Dosing

Adult

1.5 million IU in 50 cc D5W IV over 60 min

Pediatric

Administer as in adults

Interactions

Antifibrinolytic agents may decrease effects; antiplatelet agents and anticoagulants may increase risk of bleeding

Contraindications

Documented hypersensitivity; active internal bleeding; intracranial neoplasm; aneurysm; bleeding diathesis; severe uncontrolled arterial hypertension

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Use with caution in patients with severe hypertension, those receiving medication via IM administration, and those who had trauma or surgery in previous 10 d; measure hematocrit, platelet count, aPTT, TT, PT, or fibrinogen levels before therapy initiated; either TT or aPTT should be less than twice normal control value following infusion and before instituting heparin; do not take BP in lower extremities, it may dislodge possible deep vein thrombus; monitor PT, aPTT, TT, or fibrinogen 4 h after initiation of therapy


Reteplase (Retavase)

Recombinant plasminogen activator that forms plasmin after facilitating cleavage of endogenous plasminogen. In clinical trials, has been comparable to alteplase in achieving TIMI 2 or 3 patency at 90 min. Heparin and aspirin usually administered concomitantly and after reteplase.

Dosing

Adult

10 IU IV over 2 min, followed by second 10-IU IV dose after 30 min

Pediatric

Not recommended

Interactions

May increase effects of warfarin, heparin, and aspirin

Contraindications

Documented hypersensitivity; uncontrolled hypertension; recent intracranial surgery; malformation of aneurysm; bleeding diathesis

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in cardiovascular arrhythmias, hypotension, and perfusion arrhythmias


Anistreplase (Eminase)

Non–fibrin-specific agent that activates conversion of plasminogen to plasmin and has half-life of 90 min. However, does not have any benefit over streptokinase, although has higher rate of allergic and bleeding complications. Easier to administer than t-PA, has lower cost ($1500), and does not require heparinization.

Dosing

Adult

30 IU over 2-5 min

Pediatric

Not established

Interactions

Increases effects of anticoagulants and aspirin

Contraindications

Documented hypersensitivity; recent intracranial surgery; uncontrolled hypertension; vascular malformation; aneurysm

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiovascular arrhythmias, hypotension, and perfusion arrhythmias

Analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who experience pain.


Morphine sulfate (Duramorph, Astramorph, MS Contin)

DOC for narcotic analgesia due to its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Administered IV, may be dosed in a number of ways and commonly is titrated until desired effect.

Dosing

Adult

2 mg IV q5-15min, titrate to symptomatic relief or adverse effects (eg, lethargy, hypotension, respiratory depression)

Pediatric

0.1-0.2 mg/kg IV q2-4h prn

Interactions

Phenothiazines may antagonize analgesic effects; tricyclic antidepressants, MAOIs, and other CNS depressants may potentiate adverse effects

Contraindications

Documented hypersensitivity; hypotension; potentially compromised airway in which establishing rapid airway control would be difficult

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid using this drug in patients with hypotension, emesis, constipation, respiratory depression, nausea, or urinary retention; exercise caution in patients with atrial flutter and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate; mental status changes, respiratory depression, and shock are possible adverse effects

Follow-up

Further Inpatient Care

  • Admit patients with myocardial infarction to a coronary care unit. Monitor patients carefully for arrhythmia, recurrent ischemia, and other possible complications. The patient may be transferred to a telemetry unit 24-48 hours after admission if no complications occur. Hospitalize the patient for approximately 4-5 days after myocardial infarction. Patients who undergo primary PCI or have an immediate cardiac catheterization may be discharged sooner if their hospital course is without incident.
  • Perform a coronary angiography on high-risk patients prior to discharge to evaluate their need for revascularization.
  • In the case of patients who have not had a cardiac catheterization and have no complications, perform a submaximal stress test prior to discharge to assess their subsequent risk.
  • To stratify mortality risk after PCI for acute myocardial infarction, Negassa et al have developed a prognostic classification model. Patients can be readily stratified into risk categories using this tree-structured model.10

Further Outpatient Care

  • Arrange for follow-up within 2 weeks of discharge.
  • Arrange for cardiac rehabilitation.

Inpatient & Outpatient Medications

  • The long-term use of aspirin in patients who have had an myocardial infarction results in significant reduction in subsequent mortality rate.
  • Beta-blocker therapy has confirmed therapeutic benefit in survivors of acute myocardial infarction. This therapy is most beneficial in patients with the highest risk.
  • ACE inhibitor use in patients with known coronary artery disease has been shown to reduce mortality rate.
  • Many trials have shown a clear benefit of lipid-lowering therapy in the secondary and primary prevention of coronary artery disease. The National Cholesterol Education Panel has set guidelines for target cholesterol levels. In general, patients who have experienced myocardial infarction should achieve low-density lipoprotein (LDL) level less than 100 mg/dL, high-density lipoprotein (HDL) level greater than 40 mg/dL, and triglyceride level less than 200 mg/dL. High-risk patients should be treated to a target LDL level of less than 70 mg/dL.
  • Schwartz et al recently showed in the MIRACL trial that initiating atorvastatin during hospitalization for an acute coronary syndrome, irrespective of lipid levels, reduces the frequency of recurrent ischemic events. This treatment significantly reduced the frequency of the combined end point of death, recurrent death, myocardial infarction, or worsening unstable angina requiring hospitalization.11
  • Clopidogrel should be prescribed for a year following discharge if the patient has no contraindications and cost is not prohibitive. To reduce the risk of bleeding, the aspirin dose can be reduced to 81 mg.

Transfer

A patient in whom thrombolytic therapy fails should be transferred to a facility where cardiac catheterization and angioplasty facilities are available.

Deterrence/Prevention

  • Smoking cessation
    • Cigarette smoking is a major risk factor for coronary artery disease. Risk of recurrent coronary events decreases 50% at 1 year after smoking cessation.
    • Provide all patients who smoke with guidance, education, and the support needed to avoid smoking.
    • Bupropion has been shown to increase the chances of patients' success in achieving smoking cessation.
  • Alcohol consumption
    • Mild alcohol consumption has been associated with a decreased risk of stroke and myocardial infarction.
    • Cautiously consider recommending and discussing alcohol use on a case-by-case basis.
  • Antioxidant therapy, including vitamin E, has not shown clear benefit in the prevention of coronary events.
  • Do not use long-term anticoagulant (ie, warfarin) therapy routinely in post–myocardial infarction patients but as an alternative in patients who cannot take antiplatelet agents. Patients with known LV thrombus, atrial fibrillation, or severe wall motion abnormalities have shown benefit from long-term anticoagulation, maintaining the international normalized ratio (INR) between 2 and 3.
  • Low-dose aspirin has shown substantial benefit for primary prevention of myocardial infarction and stroke, but its use must be weighed against the risk for hemorrhagic stroke and gastrointestinal bleeding. The Antithrombotic Trialists’ (ATT) Collaboration conducted meta-analyses of serious vascular events, including myocardial infarction, stroke, and vascular death, and major bleeds in 6 primary prevention trials and in 16 secondary prevention trials that compared long-term aspirin versus control. The primary prevention trials included 95,000 individuals at low average risk, and the secondary prevention trials included 17,000 individuals at high average risk.

    Aspirin was associated with significant reduction (12% proportional reduction) for serious vascular events (0.51% aspirin vs 0.57% control annually, p = 0.0001), but the net effect on stroke was not significant. This reduction was largely due to a 20% reduction in nonfatal myocardial infarction (0.18% vs 0.23% annually, p <0.0001). Aspirin increased risk for major gastrointestinal and extracranial bleeding. The use of aspirin for primary prevention must be advised in context with the patient’s personal risks and history.12
  • Do not start post–myocardial infarction patients on postmenopausal hormone therapy (HT). Patients already taking HT for more than 1 year may be continued on this therapy without increased risk.

Complications

  • A number of arrhythmias occur after myocardial infarction, ranging from benign to fatal. Arrhythmias are common in the setting of myocardial infarction and are a major cause of morbidity and mortality. Close monitoring and immediate treatment of arrhythmias may be the most important part of the treatment of a post–myocardial infarction patient within the first 48 hours. Pay close attention to exacerbating factors, such as electrolyte disturbances (especially potassium and magnesium), hypoxemia, drugs, or acidosis, and correct them accordingly.
  • Ventricular fibrillation and/or ventricular tachycardia occurring within the first 48 hours may be due to ischemia; however, if ventricular arrhythmias occur later, then further workup is indicated. Immediate cardioversion is the treatment of choice. Accelerated idioventricular arrhythmia is a ventricular arrhythmia that may occur in response to reperfusion. This rhythm has a benign prognosis and usually does not require therapy.
  • Supraventricular arrhythmias are also common. Sinus bradycardia may be due to drugs, ischemia, or a vagal response. Sinus tachycardia may be due to pain, anxiety, drugs, or other causes. Atrial fibrillation and other atrial tachycardias may also occur. Treat any tachycardia by correcting the cause first or by pharmacotherapy, because persistent tachycardias may lead to further ischemia.
  • Conduction abnormalities may result from ischemia, necrosis, or chronotropic drugs, or as a vagal response. Recognition and treatment of these abnormalities are important in short- and long-term outcomes. Possible therapies include medications, such as atropine, or even placement of a transvenous pacemaker if indicated. Conduction disturbances are seen more commonly in the setting of inferior myocardial infarction but are more ominous when seen with an anterior infarct.
  • Recurrent ischemia may be due to incomplete reperfusion. Postinfarct angina occurs in 20-30% of patients. This is an indication to proceed to cardiac catheterization followed by mechanical revascularization as needed.
  • Congestive heart failure can be due to systolic dysfunction or diastolic dysfunction in the setting of myocardial infarction. The severity of the heart failure and systolic dysfunction depends on the extent of the infarct and the presence of any other complications, such as acute mitral regurgitation. Aggressive treatment is indicated to avoid worsening of the situation. Treatment may include any or all of the following: nitrates, morphine, diuretics, ACE inhibitors, and other vasodilators if needed. Digoxin has no role in the setting of acute congestive heart failure due to ischemia.
  • Cardiogenic shock is defined as a systolic BP less than 90 mm Hg in the presence of organ hypoperfusion. The mortality rate due to cardiogenic shock is as high as 70% in some series. Patients usually require inotropic agents, such as dopamine or dobutamine, and occasionally an intraaortic balloon pump is required. Patients presenting with cardiogenic shock should proceed directly to the catheterization lab, if available, for mechanical revascularization.
  • Acute mitral regurgitation is most common in the setting of an inferoposterior myocardial infarction. This is secondary to ischemia, necrosis, or rupture of the LV papillary muscle (especially the posteromedial papillary muscle). This can lead to mild-to-severe mitral regurgitation with congestive heart failure. Diagnosis can be made on physical examination, but an echocardiogram is necessary to confirm the diagnosis and assess the severity, which helps in the choice of therapy. Treatment consists of aggressive afterload reduction, intraaortic balloon pump insertion, and immediate surgical repair.
  • Ventricular rupture occurs in the interventricular septum or the LV free wall. Both are catastrophic events with mortality rates greater than 90%. Prompt recognition, stabilization, and surgical repair are crucial to any hope of survival. Ventricular rupture is more common in women, patients with hypertension, and those receiving NSAIDs or steroids. An echocardiogram can usually define the abnormality, and a right heart catheterization can show an oxygen saturation step-up in the case of a septal rupture.
  • Other complications include pericarditis, ventricular aneurysms, mural thrombi, and hypertension. Recognition and treatment can be life saving.

Prognosis

  • Acute myocardial infarction is associated with a 30% mortality rate; half of the deaths occur prior to arrival at the hospital.
  • An additional 5-10% of survivors die within the first year after their myocardial infarction.
  • Approximately half of all patients with an myocardial infarction are rehospitalized within 1 year of their index event.
  • Overall, prognosis is highly variable and depends largely on the extent of the infarct, the residual LV function, and whether the patient underwent revascularization.

Patient Education

  • Diet
    • Diet plays an important role in the development of coronary artery disease. Educate post – myocardial infarction patients about the role of a low-cholesterol and low-salt diet.
    • Educate patients about the AHA dietary guidelines regarding a low-fat, low-cholesterol diet.
    • A dietitian should see and evaluate all patients post myocardial infarction prior to their discharge.
  • Smoking cessation
    • Educate all patients post myocardial infarction regarding the critical role of smoking in the development of coronary artery disease.
    • Smoking cessation classes should be offered to help patients avoid smoking after their myocardial infarction.
  • For excellent patient education resources, visit eMedicine's Cholesterol Center. Also, see eMedicine's patient education articles High Cholesterol, Understanding Your Cholesterol level, Lifestyle Cholesterol Management, Understanding Cholesterol-Lowering Medications, Chest Pain, Coronary Heart Disease, and Heart Attack.

Miscellaneous

Medicolegal Pitfalls

  • Failure to diagnosis a myocardial infarction is the leading cause of litigation against emergency department clinicians 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 myocardial infarction 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 V 3 R or V 4 R 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 S 3 , 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 myocardial infarction 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.

Multimedia

Acute anterior myocardial infarction.

Media file 1: Acute anterior myocardial infarction.

Acute inferior myocardial infarction.

Media file 2: Acute inferior myocardial infarction.

Posterolateral myocardial infarction.

Media file 3: Posterolateral myocardial infarction.

References

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Keywords

myocardial infarction, heart attack, acute coronary syndromes, ACS, MI, unstable angina, non–ST-elevation MI, NSTEMI, coronary artery disease, CAD, ischemic heart disease, chest pain, impaired systolic function, impaired diastolic function, myocardial necrosis, atherosclerosis, coronary thrombus, plaque rupture, coronary emboli, infected cardiac valve, coronary occlusion secondary to vasculitis, primary coronary vasospasm, variant angina

cardiovascular disease, congestive heart failure, CHF, coronary heart disease, smoking, diabetes mellitus, hypertension, dyslipidemia, obesity, elevated homocysteine levels, male pattern baldness, sedentary lifestyle, psychosocial stress, peripheral vascular disease, poor oral hygiene

vasculitis, congenital coronary anomalies, coronary trauma, coronary spasm, necrosis of heart muscle, coronary thrombosis, pulmonary rales, lower extremity edema, elevated jugularvenous pressure, cocaine use, heavy exertion, hyperthyroidism, severe anemia

Contributor Information and Disclosures

Author

Samer Garas, MD, FACC, Chief of Cardiology, Department of Interventional Cardiology, St Vincent's Hospital
Samer Garas, MD, FACC is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

A Maziar Zafari, MD, PhD, FACC, Associate Professor, Department of Medicine, Emory University School of Medicine; Chief, Section of Cardiology, Atlanta Veterans Affairs Medical Center
A Maziar Zafari, MD, PhD, FACC is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American Heart Association, American Society of Echocardiography, and Association of Professors of Medicine
Disclosure: Nothing to disclose.

Medical Editor

Eric Vanderbush, MD, FACC, MD, Chief, Department of Internal Medicine, Division of Cardiology, Clinical Assistant Professor, Harlem Hospital Center and Columbia University
Eric Vanderbush, MD, FACC, MD is a member of the following medical societies: American College of Cardiology and American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Marschall S Runge, MD, PhD, Charles and Anne Sanders Distinguished Professor of Medicine, Chairman, Department of Medicine, Vice Dean for Clinical Affairs, University of North Carolina at Chapel Hill School of Medicine
Marschall S Runge, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Physiological Society, American Society for Clinical Investigation, American Society for Investigative Pathology, Association of American Physicians, Association of Professors of Cardiology, Association of Professors of Medicine, Southern Society for Clinical Investigation, and Texas Medical Association
Disclosure: Pfizer Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Orthoclinica Diagnostica Consulting fee Consulting

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD, Assistant Professor of Medicine, Director of Coronary Care Unit, University of North Carolina at Chapel Hill School of Medicine
Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha
Disclosure: Up to Date Royalty Review panel membership

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