Conditions with Similar Symptoms
View Conditions
  Drug Monographs
Thrombolytic Agents
  Supplement Monographs
Carnitine (L-Carnitine)
Vitamin C (Ascorbic Acid)
Vitamin E
  Learn More About
Massage Therapy
Western Herbalism
Look Up > Conditions > Myocardial Infarction
Myocardial Infarction
Risk Factors
Signs and Symptoms
Differential Diagnosis
Physical Examination
Laboratory Tests
Other Diagnostic Procedures
Treatment Options
Treatment Strategy
Drug Therapies
Surgical Procedures
General Measures
Complementary and Alternative Therapies
Patient Monitoring
Other Considerations


Myocardial infarction (MI) is the result of continuous and/or complete reduction in blood flow to a portion of the myocardium, thus producing some degree of myocardial death and necrosis. Oxygen deprivation results from blockage of coronary arteries supplying blood to the myocardium typically brought on by atherosclerotic plaque. Total coronary artery occlusion results in acute MI with Q-wave formation (non–Q wave infarctions have greatly narrowed infarct-related artery without total obstruction). Introduction of coronary care units in the 1960s and recent practices of urgent reperfusion and advances in pharmacologic interventions have decreased mortality rates from 30% to 40%, to 15% to 20% of admissions.

  • Atherosclerosis, resulting in narrowed or occluded arteries
  • Thrombosis, the immediate cause, caught within atherosclerotic plaque
  • Coronary vasomotor spasm
  • Coronary artery embolism
  • Congenital anomalies
  • Arteritis
  • Trauma

Risk Factors
  • Smoking
  • High fat diet, excess body weight
  • Family history of early MI
  • Diabetes
  • Second generation oral contraceptives
  • Hostile, aggressive personality (Type A)
  • Hypertension
  • Hypercholesterolemia
  • Males and postmenopausal females
  • Cocaine or amphetamine abuse

Signs and Symptoms
  • Pain, heaviness, tightness, burning—in chest (substernal), back, left arm, jaw, neck
  • Dyspnea
  • Dizziness, weakness
  • Nausea, vomiting
  • Anxiety
  • Arrhythmia
  • Hypotension, hypertension

Differential Diagnosis
  • Pulmonary embolism
  • Unstable angina
  • Esophagitis, or esophageal spasm
  • Myocarditis
  • Cholecystitis
  • Pericarditis
  • Aortic dissection
  • Hiatal hernia
  • Chest wall pains
  • Pneumothorax
  • Gastroenteritis

Physical Examination
  • "Crushing" chest pain, S4 gallop, ectopic impulse, systolic murmurs
  • Crackles—indicate elevated left ventricle (LV) filling pressure
  • Hypotension, elevated jugular venous pulse, clear lung auscultation—indicate right ventricular infarction
  • S3 gallop—indicates systolic dysfunction

Laboratory Tests
  • Serum cardiac enzymes increase as myocardial necrosis evolves
  • MB fraction of creatine kinase (CK-MB)—rises within 6 hours, peaks within 24 hours, and declines within 72 hours of MI; gold standard for diagnosis
  • Lactate dehydrogenase (LDH)—rises after 24 hours, peaks three to six days and returns to normal in a week to 10 days; increases diagnostic specificity
  • Troponin T (cTnT) and cardiac-specific troponin I (cTnI)—better sensitivity and specificity than CK-MB. Serum levels increase 3 to 12 hours after MI, peak at 24 to 48 hours, and return to baseline in 5 to 14 days.

  • Atherosclerotic plaque leads to platelet–fibrin thrombosis, resulting in coronary artery occlusion
  • Myocardium becomes ischemic, resulting in transmural spread of necrosis
  • Depth of plaque fissure, extent of atherosclerotic stenosis, thrombogenic plaque constituents—determine magnitude of thrombosis

  • Chest X ray to differentiate pneumothorax
  • CT/MRI or aortography to differentiate aortic dissection
  • Noninvasive radionuclide imaging—shows perfusion; e.g., technetium 99m sestamibi; for nondiagnostic ECGs, persistent chest pain

Other Diagnostic Procedures
  • Electrocardiogram (ECG)—diagnoses ventricular dysrhythmias and monitors sinus tachycardia (ST)-segment changes
  • History of symptoms; physical examination
  • Test cardiac enzyme levels
  • ST elevation—at least 1 mm in two contiguous precordial leads or in inferior limb leads; appears early in MI
  • Hyperacute T waves invert as ST segments return to normal
  • Q waves often appear with ST elevation
  • Left bundle branch block (LBBB)—Q waves in V5 and V6 with 7 mm ST elevation
  • Echocardiagram
  • Two-dimensional—determines ventricular function, wall and valvular abnormalities
  • Doppler—diagnoses mitral regurgitation or ventricular septal rupture
  • Angiography—diagnoses coronary occlusion and wall abnormalities for chest pain or nondiagnostic ECG

Treatment Options
Treatment Strategy
  • Immediate management of the patient aims to identify need for reperfusion, relieve pain, provide oxygen, and prevent or treat complications of MI.
  • Rapid reperfusion can reduce infarct size, preserve ventricular function, stop transmural spread of necrosis, increase electrical stability, and reduce morbidity and mortality. There are three main methods of reperfusion: thrombolytic therapy, percutaneous transluminal coronary angioplasty (PTCA) and other mechanical reperfusion, and surgery.
  • Treatment for all patients includes analgesics, nitroglycerin, anticoagulants, antiplatelet therapy, beta-andrenergic antagonists, and oxygen supplementation.

Drug Therapies

Thrombolytic therapy. Ninety percent of patients with acute MI have complete occlusion of the infarct-related artery.

  • Perform within 60 to 90 minutes, little benefit after 12 hours
  • Restores artery patency

Thrombolytic drugs include:

  • Streptokinase—70 minutes to lysis; half-life 20 minutes; coronary patency: 55% at 90 minutes, 85% at 24 hours; antigenic; 1.5 million units intravenously in 30 to 60 minutes, slower if blood pressure falls
  • Tissue plasminogen activator (Alteplase, rt-PA)—45 minutes to lysis; half-life 6 minutes; coronary patency: 75% at 90 minutes, 85% at 24 hours; nonantigenic; 100 mg IV in 90 minutes; 15 mg bolus, then 0.75 mg/kg over 30 minutes, then 0.50 mg/kg over 60 minutes
  • Anisoylated plasminogens streptokinase activator complex (Anistreplase APSAC)—more expensive but longer fibrinolytic activity than streptokinase; 30 mg IV in 5 minutes
  • Reteplase (r-PA) is similar to alteplase, 10 units as a 2-minute bolus, repeated after 30 minutes
  • Aspirin—antiplatelet affect; 169 to 320 mg then 85 mg for maintenance, consider contraindications
  • Heparin—improves coronary patency, controversial; best results with t-PA; 1,000 units/hour for 8 to 72 hours
  • Contraindications for thrombolytic therapy—severe bleeding, hypertension, liver or renal disease, pregnancy, recent surgery, stroke

Surgical Procedures

PTCA—mechanical reperfusion

  • Percutaneous transluminal coronary angioplasty (PTCA)—Superior treatment; can reestablish arterial blood flow in 90% of patients without some of the risks associated with fibrinolytic agents. Few facilities can perform expeditiously.
  • Intra-aortic balloon counterpulsation—maintains perfusion; for hypotension, ventricular rupture, mitral regurgitation; PTCA adjunct, CABG adjunct; temporizing method prior to PTCA or CABG, or to allow heart to recover
  • Intracoronary stenting—stabilizes dissection during PTCA

Coronary-artery bypass surgery (CABG)—for free wall and acute septal rupture, mitral regurgitation, refractory cardiogenic shock. To be utilized when the disease is too extensive for mechanical repurfusion.

General Measures
  • Analgesia—morphine sulfate 4 to 8 mg doses; intravenous morphine 2 to 4 mg, can be repeated every 5 to 10 minutes
  • Nitroglycerin—for recurrent ischemia, congestive heart failure (CHF), hypertension: 0.4 mg sublingual, can be given every five minutes in the absence of hypotension. Good response should be followed by IV nitroglycerin at 10 mcg/minute.
  • Antiplatelet therapy with aspirin—325 mg chewed to enhance absorption
  • Anticoagulants—for thromboembolic complications. Heparin IV bolus of 80 units/kg followed by infusion of 18 units/kg/hour
  • Oxygen—2 to 4 L per minute by nasal cannula
  • Angiotensin-converting enzyme (ACE) inhibitors—reduce ventricular dilation and remodeling; monitor renal function and hypotension. Captopril 6.25 mg orally, titrate to 25 to 50 mg orally tid over 24 to 48 hours.
  • Beta-blockers—reduce cardiac rupture, reinfarction, ventricular fibrillation. Metoprolol 5 mg, repeated every five minutes to a total of 15 mg, then switch to oral metoprolol or atenolol

Complementary and Alternative Therapies

Alternative therapies are most appropriate to prevent the first MI, minimize damage from an MI, and reduce the risk of a future MI, once the patient has been properly diagnosed and stabilized. There are no substitutes for immediate and appropriate medical care with a presentation of chest pain and/or suspected MI. See related subjects under angina, hypertension, and atherosclerosis.

  • L-carnitine (9 g/day IV for five days, then 6 g/day orally for 12 months) was studied within 24 hours of onset of chest pain and was found to decrease left ventricular dilation.
  • Diet: In another study, a diet high in antioxidants (vitamin C, vitamin E, and beta-carotene), soluble dietary fiber, and one that replaces fat with oils showed reduced plasma lipid peroxide and lactate dehydrogenase cardiac enzyme levels. This may reduce myocardial necrosis and reperfusion injury.
  • Bromelain (400 to 800 mg/day) has been used for thrombolysis and may help dissolve plaque.


Herbs should not be used in lieu of immediate medical attention. Herbs can be used as general heart tonics and specifically applied to treating conditions associated with MI, such as atherosclerosis, congestive heart failure, hypercholesterolemia, hypertension, and hypertriglyceridemia.


Homeopathy should not be used in lieu of immediate medical attention. An experienced homeopath should assess individual constitutional types and severity of disease to select the correct remedy and potency of heart tonics.

Physical Medicine

Beneficial for rehabilitation.


Useful for pain and rehabilitation.


Beneficial for rehabilitation.

Patient Monitoring


  • Electrocardiogram—2- to 3-lead bedside
  • Cardiac rate and rhythm
  • Look for complications

Other Considerations

Regular exercise, stress reduction, weight management, and avoidance or management of risk factors



  • Sinus bradycardia
  • Ventricular or sinus tachycardia
  • Atrial fibrillation


  • Rupture of free wall, interventricular septum, or papillary muscle
  • Mitral regurgitation
  • Hypertension
  • LV failure/CHF
  • Acute pericarditis
  • Dressler's syndrome
  • Cardiac arrest/sudden death
  • Anxiety, depression


Killip subgroups:

  • Class I—no evidence of pulmonary congestion or shock (mortality <5%)
  • Class II—mild pulmonary congestion, isolated S3 gallop (mortality 10%)
  • Class III—pulmonary edema, LV dysfunction, mitral regurgitation, S3 gallop, severe CHF (mortality 30%)
  • Class IV—systemic hypoperfusion, hypotension, cardiogenic shock (80% mortality)


Iliceto S, Scrutinio D, Bruzzi P, et al. Effects of L-carnitine administration on left ventricular remodeling after acute anterior myocardial infarction: the L-Carnitine Ecocardiografia Digitalizzata Infarto Miocardico (CEDIM) Trial. J Am Coll Cardiol. August 1995;26:380.

Kruzel T. The Homeopathic Emergency Guide. Berkeley, Calif: North Atlantic Books; 1992:58-60.

Murray MT. The Healing Power of Herbs: The Enlightened Person's Guide to the Wonders of Medicinal Plants. 2nd ed. Rocklin, Calif: Prima Publishing; 1998:184.

Rakel RE, ed. Conn's Current Therapy. 50th ed. Philadelphia, Pa: WB Saunders Co; 1998.

Singh RB, Niaz MA, Agarwal P, Begom R, Rastogi SS. Effect of antioxidant-rich foods on plasma ascorbic acid, cardiac enzyme, and lipid peroxide levels in patients hospitalized with acute myocardial infarction. J Am Diet Assoc. July 1995;95:775-780.

Singh RB, Singh NK, Niaz MA, Sharma JP. Effect of treatment with magnesium and potassium on mortality and reinfarction rate of patients with suspected acute myocardial infarction. Int J Clin Pharmacol Thera. 1996;34:219-225.

Washington Manual of Medical Therapeautics. 29th ed. Philadelphia, Pa: Lippincott-Raven Publishers; 1998.

Copyright © 2000 Integrative Medicine Communications

This publication contains information relating to general principles of medical care that should not in any event be construed as specific instructions for individual patients. The publisher does not accept any responsibility for the accuracy of the information or the consequences arising from the application, use, or misuse of any of the information contained herein, including any injury and/or damage to any person or property as a matter of product liability, negligence, or otherwise. No warranty, expressed or implied, is made in regard to the contents of this material. No claims or endorsements are made for any drugs or compounds currently marketed or in investigative use. The reader is advised to check product information (including package inserts) for changes and new information regarding dosage, precautions, warnings, interactions, and contraindications before administering any drug, herb, or supplement discussed herein.