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Myocardial Infarction

Each year 1.5 million people are diagnosed with an acute myocardial infarction. The early mortality has decreased from 12% to 6-7% because of aspirin therapy and early reperfusion with thrombolytics or angioplasty.

Clinical Evaluation of Acute Myocardial Infarction

Accurate diagnosis of acute myocardial infarction has three classic components--clinical symptoms, electrocardiographic abnormalities and changes in the levels of serum markers of cardiac injury.

Clinical symptoms of MI may be characterized by a constricting or squeezing sensation in the chest. Pain can radiate to the upper abdomen, back, either arm, either shoulder, neck, or jaw.

Nausea, vomiting, shortness of breath, diaphoresis, weakness, dizziness, palpitations, anxiety or a sense of impending doom are also common.

Twenty to 60 percent of cases of acute myocardial infarction are discovered retrospectively because the patients did not experience enough distress to seek medical attention.

The presence of risk factors for coronary heart disease (age >45 in males, >55 in females, family history of coronary heart disease, smoking, hypertension, low HDL-cholesterol, diabetes) and a history of myocardial infarction should be assessed.

Cardiac exam may reveal a third or fourth heart sound. A fourth heart sound may be more audible with the patient in the left lateral position.

Differential Diagnosis of Chest Pain

Acute pericarditis is characterized by pleuritic-type chest pain and diffuse ST segment elevation on ECG.

Aortic dissection is characterized by a "tearing" chest pain with uncontrolled hypertension, widened mediastinum and increased aortic prominence on chest x-ray.

Esophageal rupture usually occurs after forceful vomiting; x-ray may reveal air in mediastinum or a left side hydrothorax.

Acute peptic ulcer disease manifests as epigastric pain with melena, or hematemesis and anemia.

Electrocardiographic Findings in Acute Myocardial Infarction

ST-segment elevation in two adjacent leads is diagnostic of MI. The sensitivity and specificity are 49% and 92%, respectively.

ST-segment depression is a nonspecific finding. Thrombolytic therapy has not been shown to be effective in non-Q-wave infarction.

Forty to 60 percent of patients who ultimately prove to have acute myocardial infarction, have nondiagnostic ECGs.

Laboratory Testing

Creatine Kinase Isoenzymes and CK Isoforms

Increased creatinine kinase, especially the isoenzyme CK-MB, is a sensitive sign of myocardial damage. Pathologic levels may not be reached for 6 to 8 hours, and the peak occurs at 12 to 18 hours. Within the first four hours, the sensitivity of CK-MB for myocardial infarction is 25%.

CK-MB produced in tissue is converted in plasma to CK-MB¹. At two to four hours after symptom onset, the presence of a MB²:MB¹ ratio greater than 1.5 has a sensitivity of 59%; at 4 to 6 hours, the sensitivity for myocardial infarction is 92%.

Troponins

Troponins are structural proteins that regulate actin and myosin in striated muscle. The main troponins are the cardiac isoforms of troponin T (c-TnT) and troponin I (c-TnI). Levels rise 3 to 12 hours after cardiac injury, and the levels remain elevated for 5 to 14 days. A rapid assay is available for c-TnT.

C-TnT is more specific for myocardial tissue than CK-MB (89% versus 63%); however, c-TnT also rises in patients with angina and may also rise in patients with muscular injury.

Myoglobin

Myoglobin is a cytoplasmic protein, found in both cardiac and skeletal muscle. It is detectable 1 to 4 hours after coronary occlusion, peaking at 6 to 9 hours and returning to baseline within 18 to 24 hours.

It is positive earlier than CK-MB, with a sensitivity at two hours of 23%, rising to 82% at two to four hours, and to 92% after four hours.

If by five and one-half hours the myoglobin remains normal, acute myocardial infarction is unlikely, with a negative predictive value of 89%.

Lactic dehydrogenase is elevated at 25-48 hours, and it may be useful when interpreted with troponin-T in patients who present late after onset of symptoms.

A fasting lipid profile should be obtained. Lipid measurements are valid for up to 8 hours after admission for MI.

Emergent Therapy for Myocardial Infarction

Primary Percutaneous Transluminal Angioplasty. Primary angioplasty is the most efficient method of restoring blood flow and conserving heart muscle. Primary angioplasty in patients with anterior MI results in a higher survival rate, lower rates of stroke, reinfarction and recurrent ischemia than does thrombolysis. The American College of Cardiology recommends primary PTCA in the following situations:

If performed within a few hours of symptom onset by a physician who does more than 75 PTCAs yearly, and in a hospital performing more than 200 PTCAs yearly.

In patients with cardiogenic shock.

In patients at risk of bleeding or other contraindications for thrombolytic therapy.

Indications for Thrombolytic Therapy in Myocardial Infarction

All patients who have had more than 20 minutes of chest pain or an anginal equivalent refractory to sublingual nitroglycerin, associated with $0.1 mV of ST-segment elevation, in two or more contiguous leads, should be considered for thrombolytic therapy.

Patients with a new left bundle branch block and a history suggesting acute myocardial infarction should also receive thrombolytic therapy.

Contraindications

Active internal bleeding (not including menses).

History of cerebrovascular hemorrhage or emboli.

Recent intracranial or intraspinal surgery or trauma.

Intracranial neoplasm, arteriovenous malformation, or aneurysm.

Known bleeding diathesis.

Severe uncontrolled hypertension $180 mmHg ststolic and/or $110 mmHg diastolic.

Relative Contraindications

Severe, uncontrolled hypertension on presentation (blood pressure >180/110 mm Hg).

History of prior cerebrovascular accident or known intracerebral disease not covered in contraindications.

Current use of anticoagulants in therapeutic doses (INR $2.0-3.0); known bleeding diathesis

Recent (within 2-4 weeks) trauma, including head injury, traumatic or prolonged (>10 min) CPR, or major surgery (<3 wk).

Non-compressible vascular punctures.

Recent (within 2-4 weeks) internal bleeding.

For use of streptokinase: prior exposure (within 5 days to 1 yr) or prior allergic reaction.

Pregnancy

Active peptic ulcer disease

History of chronic severe hypertension.

Streptokinase ( Streptase)

Streptokinase is the most commonly used and least expensive thrombolytic; it offers about the same benefit as tPA, except in those who present with an anterior MI within 4 hours of chest pain.

Streptokinase IV infusion: 1.5 million IU in 100 mL NS IV over 60 min. Administer methylprednisolone (Solu-Medrol), 250 mg IVP, and diphenhydramine (Benadryl), 50 mg IVP, prior to streptokinase.

Reteplase ( Retavase) 10 U IV push over 2 min. Repeat second 10 U IV push in 30 minutes. The 90 min patency rate is greater with reteplase than with alteplase; however, the 30-day mortality is the same.

Alteplase ( tissue plasminogen activator, tPA, Activase)

The 90 min patency rate is greater with tPA than SK, but there is no difference at 24 hours.

IV bolus of 15 mg, then 0.75 mg/kg (up to 50 mg) over 30 min, followed by 0.5 mg/kg (up to 35 mg) infused over the next 60 min.

Drug Therapy for Acute Myocardial Infarction

Aspirin

Patients with any sign of an acute coronary syndrome should immediately chew and swallow 325 mg of aspirin, followed by 160 mg PO qd on subsequent days. During recovery, the dosage can be decreased to 80 mg per day.

In MI aspirin decreases risk for the mortality by 25%.

Heparin

Heparin has no influence on mortality; however, it reduces the frequency of ischemic events and reocclusion after thrombolysis. Heparin should be continued for 48 hours, or longer if ischemic pain persists.

Use of heparin after reteplase and alteplase (tPA) is mandatory; however, heparin is optional after streptokinase. All patients at risk for systemic emboli (previous embolus, atrial fibrillation, left ventricular thrombus, large anterior MI) should receive heparin.

Heparin 5000 U IVP before thrombolysis, followed by 15 units/kg/h after reteplase or alteplase (tPA), and 10 units/kg/h after streptokinase. Titrate heparin to aPTT of 50-70 seconds.

Nitrates

Intravenous nitroglycerin should be given to patients with suspected MI or unstable angina unless hypotension is present.

Initial administration consists of a 12.5-25 mcg bolus, followed by 10-20 mcg/min, titrated to chest pain. The dose can be increased as needed to 200 mcg/min, provided systolic blood pressure is maintained at $100 mmHg.

Nitroglycerin should be continue for 24-48 hours. Thereafter, if the patient is free of chest pain, it should be tapered and discontinued. Oral nitrates should be substituted for IV nitroglycerin after stabilization. Sublingual nitroglycerin may also be given initially (0.4 mg SL q5min prn chest pain).

Contraindications to nitroglycerin include a systolic blood pressure less than 90 mm Hg and a heart rate less than 50 beats per minute.

Beta Blockers

Patients should receive a beta blocker within 12 hours of onset of myocardial infarction, unless contraindicated.

Contraindications include bradycardia, second- or third-degree atrioventricular block, hypotension, evidence of congestive heart failure (ie, rales, audible S₃), cardiogenic shock, and active bronchospasm.

Atenolol ( Tenormin), 5 mg IV, repeated in 5 minutes, followed by 50-100 mg PO qd.

Metoprolol ( Lopressor), 5 mg IV push every 5 minutes for three doses; followed by 25 mg PO bid. Titrate up to 100 mg PO bid.

Morphine Sulfate. Analgesia with morphine (2-4 mg IVP prn chest pain) should also be provided.

Angiotensin Converting Enzyme Inhibitors

ACE-inhibitors improve survival and decrease morbidity in patients with left ventricular dysfunction (ejection fraction < 40%) after myocardial infarction.

An angiotensin-converting-enzyme (ACE) inhibitor should be initiated within 24 hours after the onset of myocardial infarction in patients with a large anterior myocardial infarction or with evidence of left ventricular dysfunction. An echocardiogram should be used to evaluate left ventricular function before discharge in all patients with a transmural Q wave infarction.

Captopril ( Capoten) is given as an initial dose of 6.25 mg PO, and 4-6 hours later the dosage should be increased to 12.5 mg q8h. Gradually increase to 25-50 mg PO q8h.

Enalapril (Vasotec) 2.5 mg PO qd; titrate to 10-20 mg PO qd.

ACE-inhibitor therapy should not begin until the patient’s condition has stabilized with adequate perfusion pressure.

Contraindications to ACE-inhibitors: Systolic blood pressure under 90 mm Hg, clinical renal failure, significant valvular stenosis, bilateral stenosis of the renal arteries, or known allergy to the drugs.

ACE-inhibitor treatment may be stopped at 4-6 weeks in patients with normal left ventricular systolic function. It should be continued indefinitely in patients with a low ejection fraction (ejection fraction <40%).

Calcium channel blockers have no role in the routine management of acute MI except in situations where beta blockers are ineffective or contraindicated, as in patients with bronchospasm.

Magnesium has not been shown to produce a benefit in MI, and it should not be used routinely for MI, except to correct hypomagnesemia. §