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Cardiovascular Disorders
Abdominal Aneurysm
Aortic Insufficiency
Aortic Stenosis
Arterial Occlusive
Atrial Septal Defect
Buerger's Disease
Cardiac Arrhythmias
Cardiac Tamponade
Cardiogenic Shock
Coarctation of the Aorta
Coronary Artery Disease
Dilated Cardiomyopathy
Femoral And Popliteal Aneurysms
Heart Failure
Hypertrophic Cardiomyopathy
Hypovolemic Shock
Mitral Insufficiency
Mitral Stenosis
Myocardial Infarction
Patent Ductus Arteriosus
Pulmonic Insufficiency
Pulmonic Stenosis
Raynaud's Disease
Rheumatic Heart Disease
Septic Shock
Tetralogy of Fallot
Thoracic Aortic Aneurysm
Transposition of The Great Arteries
Tricuspid Insufficiency
Tricuspid Stenosis
Varicose Veins
Ventricular Aneurysm
Ventricular Septal Defect (VSD)

Myocardial Infarction (Heart Attack)

What is Myocardial Infarction?

Myocardial infarction (MI) results from reduced blood Flow through one of the coronary arteries, which causes myocardial ischemia and necrosis. The infarction site depends on the vessels involved. For instance, occlusion of the circumflex coronary artery causes a lateral wall infarction; occlusion of the left anterior coronary artery causes an anterior wall infarction. True posterior and inferior wall infarctions result from occlusion of the right coronary artery or one of its branches. Right ventricular infarctions can also result from right coronary artery occlusion, can accompany inferior infarctions, and may cause right-sided heart failure. In transmural (Qwave) MI, tissue damage extends through all myocardial layers; in subendocardial (non-Q ntave) MI, usually only the innermost layer is damaged.

Men are more susceptible to MI than premenopausal women, although incidence is rising among women who smoke and take oral contraceptives. The incidence in postmenopausal women resembles that in men.

Causes of Myocardial Infarction

MI results from occlusion of one of the coronary arteries. The occlusion can stem from atherosclerosis,thrombosis, platelet aggregation, or coronary artery srenosis or spasm. Predisposing factors include:

  • aging.
  • diabetes mellitus.
  • elevated serum triglyceride, low-density lipoprorein. and cholesterol levels, and decreased serum high-density lipoprotein levels.
  • excessive intake of saturated fats, carbohydrates, or salt
  • hypertension
  • obesity
  • positive family history of coronary artery disease . sedentary lifestyle
  • smoking
  • stress or a type A personality (aggressive, competitive attitude,addiction to work, chronic impatience).

In addition, use of drugs, such as amphetamines or cocaine, can cause MI.

Signs & Symptoms of Myocardial Infarction

  • Chest pain that increases in intensity
  • Shortness of breath
  • Sweating, which may be profuse
  • Severe pressure, fullness, squeezing, pain and/or discomfort in the center of the chest that lasts for more than a few minutes
  • Collapse and sudden death may occur with a large or severe MI.

Diagnostic Tests

In MI, diagnostic tests may provide the following results:

  • Serial 12-lead electrocardiography (ECG) readings may be normal or inconclusive during the first few hours after an MI. Characteristic abnormalities include serial ST-segment depression in subendocardial MI and ST-segment elevation and Q waves, representing scarring and necrosis, in transmural MI.
  • Serum creatine kinase (CK) level is elevated, especially the CK-MB isoenzyme, the cardiac muscle fraction of CK.
  • Serum lactate dehydrogenase (LDH) level is elevated. LDHI isoenzyme (found in cardiac tissue) is higher than LDHz (found in serum). This measurement isn't as reliable as the CK level.
  • White blood cell count usually appears elevated on the second day and lasts one week.
  • Myoglobin (the hemoprotein found in cardiac and skeletal muscle) is released with muscle damage and may be detected as soon as 2 hours after MI.
  • Troponin I. a structural protein found in cardiac muscle, is elevated only in cardiac muscle damage. It's more specific than the CK-MB level. Troponin levels increase within 4 to 6 hours of myocardial injury and may remain elevated for 5 to II days.
  • Echocardiography shows ventricular wall dyskinesia with a transmural MI and helps evaluate the ejection fraction.
  • Scans using I.V. technetium-99m pertechnetate can identify acutely damaged muscle by picking up accumulations of radioactive nucleotide, which appears as a "hot spot" on the film. Myocardial perfusion imaging with thallium-201 reveals a "cold spot" in most patients during the first few hours after a transmural MI.


The goals of treatment are to relieve chest pain, to stabilize heart rhythm, and to reduce cardiac workload. Treatment includes revascularization to preserve myocardial tissue. Arrhythmias, the most common problem during the first 48 hours after MI, may require antiarrhythmics, possibly a pacemaker and, rarely, cardioversion.

To preserve myocardial tissue, I.V. thrombolytic therapy should be started within 3 hours of the onset of symptoms (unless contraindicated). Thrombolytic therapy includes either streptokinase, alteplase, recombinant tissue plasminogen activator (TPA) , reteplase, or urokinase.

Percutaneous trasluminal coronary angioplasty (PTCA) may be another option. If PTCA is performed soon after the onset of symptoms, the thrombolytic agent may be administered directly into the coronary artery.

Drug therapy usually includes:

  • aspirin (5 g) to inhibit platelet aggregation (should be initiated within 24 hours after onset of symptoms)
  • lidocaine for ventricular arrhythmias; if lidocaine is ineffective, procainamide, quinidine sulfate, bretylium, or disopyramide may be used
  • atropine I.V. or a temporary pacemaker for heart block or bradycardia
  • nitroglycerin (sublingual, topical, transdermal, or I.V.); calcium channel blockers, such as nifedipine, verapamil, and diltiazem (sublingual, by mouth (P.O.). or I.V.); or isosorbide dinitrate (sublingual, P.O., or I.V.) to relieve pain by redistributing blood to ischemic area of the myocardium, increasing cardiac output, and reducing myocardial workload
  • diltiazem and verapamil, which may prevent reinfarction and ischemia in a non-Q wave MI
  • heparin I.V. (usually follows thrombolytic therapy)
  • morphine l.V., the drug of choice for pain and sedation
  • drugs that increase contractility or blood pressure
  • inotropic drugs, such as dobutamine and amrinone, to treat reduced myocardial contractility
  • betaadrenergic blockers, such as propranolol and umolol, after acute MI to help prevent reinfarction
  • angiotensin-converting inhibitors to improve survival rate in a low ejection fraction (as in large anterior wall MI).

Other therapies may be used, as follows:

  • Oxygen is usually administered (by face mask or nasal cannula) at a modest flow rate for 3 to 6 hours; a lower concentration is necessary if the patient has chronic obstructive pulmonary disease.
  • Bed rest with bedside commode is enforced to decrease cardiac workload.
  • Pulmonary artery catheterization may be performed to detect left- or right-sided heart failure and to monitor response to treatment.
  • Intra-aortic balloon pump may be used for cardiogenic shock.
  • Cardiac catheterization and coronary artery bypass grafting may also be performed.
Prevention Tips

To prevent a heart attack:

  • Stop smoking.
  • Lose weight if you are overweight.
  • Control your blood pressure.
  • Do not drink alcohol.
  • Take good nutritional diet.
  • Exercise daily or several times a week by walking and other exercises to improve heart fitness.


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