Myocardial Infarction Disease

BASICS

DESCRIPTION

Acute myocardial infarction (AMI) is the rapid development of myocardial necrosis resulting from a sustained and complete reduction of blood flow to a portion of the myocardium, produced by a superimposed thrombosis, generated by a ruptured atherosclerotic plaque

Clinical consequences – dependent on the size and location of the infarction and the rapidity with which blood flow can be re-established by pharmacologic or mechanical modalities
After total occlusion, myocardial necrosis is complete in 4–6 hours. Flow to ischemic area must remain above 40% of pre-occlusion levels for that area to survive
Infarctions can be divided into Q-wave and non Q-wave, with the former being transmural and associated with totally obstructed infarct-related artery, and the latter being non-transmural and associated with patent but highly narrowed infarct-related artery
Total occlusion of the left main coronary artery, which usually supplies 70% of the LV mass, is catastrophic and results in death in minutes
System(s) affected: Cardiovascular
Genetics: N/A
Incidence/Prevalence in USA: 600/100,000
Predominant age: Over 40
Predominant sex:
- Age 40–70: Male > Female
- Over age 70: Male = Female

SIGNS AND SYMPTOMS

Pain – arm, back, jaw, epigastrium, neck, chest
Anxiety
Lightheadedness, pallor, weakness, syncope
Nausea, vomiting, diaphoresis
Chest heaviness, tightness
Cough, diaphoresis, dyspnea, rales, wheezing
S4 heart sound
Arrhythmias
Hypertension, hypotension
Jugular venous distention
Cannon jugular venous A waves (in presence of heart block or right ventricular failure)

CAUSES

Coronary thrombosis – most common cause due to ruptured plaque inducing platelet aggregation; thrombosis has been identified as the initiating factor in most cases
Coronary artery spasm
Arteritis
Embolic infarction
Congenital coronary anomalies
Oxygen supply–demand imbalance; carbon monoxide poisoning
In situ thrombosis – hematologic in origin (e.g., polycythemia rubra vera)
Cocaine-induced vasospasm

RISK FACTORS

Hypercholesterolemia (increased LDL; decreased HDL)
Premature (<55) familial onset of coronary disease
Smoking
Diabetes mellitus
Hypertension
Sedentary lifestyle
Aging
Hostile, frustrated personality
Hypertriglyceridemia

DIAGNOSIS

LABORATORY

Troponin I – specific indicator of myocardial infarction. Appears 3–6 hours after MI, peaks at 16 hours, and decreases in 9–10 days
Creatine kinase (CK) – rises following infarction; begins in 4–8 hours, peaks in 18–24 hours, and subsides over 3–4 days. Specific indicator for myocardial necrosis but has a 15% false positive rate
CK isoenzymes – MM, MB, and BB forms identified: MM in skeletal muscle, BB in brain and kidney, MB in cardiac. Elevation of CK-MB in serum is highly suggestive of myocardial infarction
LDH – rises above normal values within 24 hours of an acute MI, peaks within 3–6 days, and returns to baseline within 8–12 days. Can be used to date recent episodes of acute MI past the acute episode
ESR – rises above normal within 3 days and may remain elevated for several weeks
Leukocytes – rise within several hours after an MI, peak in 2–4 days, and return to normal within 1 week

Drugs that may alter lab results: Refer to standard cardiology texts
Disorders that may alter lab results: Refer to standard cardiology texts

PATHOLOGICAL FINDINGS

Myocardial necrosis
Atherosclerosis, if etiologic
Thrombosis – usually not seen because spontaneous thrombolysis occurs within 24 hours in most patients

SPECIAL TESTS

Electrocardiography
- ST segment elevation in a regional pattern – typical of acute transmural ischemia
- ST segment depression with T-wave inversions – typical of subendocardial ischemia
- ST segment elevation and depression are early findings of myocardial ischemia. A significant percent of patients will have non-specific findings on presentation, such as peaked T-waves and ST-segment elevation less than 0.1 mV. A small percentage of patients with transmural infarction present with normal ECG
- Q-waves representing transmural myocardial necrosis appear within 24–48 hours
Echocardiography
- 2D and M-mode echocardiography useful in evaluating wall motion abnormalities in MI and overall left ventricular function
- Useful in delineating and assessing mechanical complications

IMAGING

Chest x-ray
- Findings dependent on severity of MI
Radionuclide studies
- Thallium scanning – accumulates in viable myocardium
- Technetium-99 gated blood pool scanning – noninvasive means of measuring ventricular function; accumulates in recently infarcted myocardium

DIAGNOSTIC PROCEDURES

Angiography prior to procedures to re-establish coronary perfusion

TREATMENT

APPROPRIATE HEALTH CARE

Inpatient coronary care unit

GENERAL MEASURES

General
- Analgesia, prevention and treatment of electrical and mechanical complications, limitation of infarct size, and salvage of myocardium
Arrhythmias
- Ventricular tachycardia: DC countershock, lidocaine, procainamide (Pronestyl), or IV cordarone
- Ventricular fibrillation: DC countershock and CPR/IV cordarone
- Atrial flutter and fibrillation: digitalis or IV diltiazem (Cardizem) or verapamil. If hemodynamic compromise – DC countershock or rapid atrial pacing
- Sinus bradycardia: no treatment unless accompanied by hypotension or hemodynamic compromise; then treat with atropine and if ineffective, electrical pacing
- Atrioventricular block: in inferior infarction, requires transvenous pacing if patient hemodynamically compromised; in anterior infarction, pacing usually required as escape rhythm is unstable with ventricular asystole occurring quite suddenly

SURGICAL MEASURES

Coronary reperfusion
- Emergency percutaneous transluminal angioplasty (PTCA) or stenting – mechanical form of coronary reperfusion. Recent studies suggest this technique may be superior to intravenous thrombolysis if initiated within the first hour
- Emergency surgical reperfusion – can be accomplished with low mortality. Must be carried out within 4 hours of onset. Many consider this treatment rarely indicated
Pump failure
- Intra-aortic balloon counterpulsation
- PTCA/stenting

ACTIVITY

Bedrest for first 24 hours; bedside commode
Medically supervised rehabilitation plan

DIET

Nothing by mouth until stable; later, low fat, low salt diet

PATIENT EDUCATION

Printed patient information available from: American Heart Association, 7320 Greenville Avenue, Dallas, TX 75231, (214)373-6300

FOLLOW UP

PREVENTION/AVOIDANCE

Avoid risk factors
Aspirin 81 mg/day may be helpful

POSSIBLE COMPLICATIONS

Congestive heart failure
Cardiogenic shock
Myocardial rupture
Left ventricular aneurysm
Left ventricular thrombus and peripheral embolism
Deep venous thrombosis and pulmonary embolism
Pericarditis
Dysrhythmias
Mitral regurgitation
Ventricular septal defect
Dressler's syndrome
Cardiac arrest
Death

EXPECTED COURSE AND PROGNOSIS

Overall mortality rate is 10% during the hospital phase, with an additional 10% mortality rate during the year after. More than 60% of deaths occur within one hour of the onset of the event
Killip classification

I - No CHF; mortality rate <5%
II - Mild-Moderate CHF (bibasilar rales and/or S3 gallop); mortality rate 10%
III - Severe CHF (rales over greater than 50% lung fields, S3 gallop, pulmonary edema); mortality rate 30%
IV - Cardiogenic shock BP <90 mm Hg (<12 kPa) with hypoperfusion, e.g., oliguria, confusion, clammy skin; mortality rate >80%

MISCELLANEOUS

ASSOCIATED CONDITIONS

Abdominal aortic aneurysm
Extracranial cerebrovascular disease
Atherosclerotic peripheral vascular disease

AGE-RELATED FACTORS

Pediatric: N/A
Geriatric: All incidences of complications are higher
Others: N/A

PREGNANCY

N/A

OTHER NOTES

N/A

ABBREVIATIONS

CHF = congestive heart failure

Clinical Investigations

ROLE OF HOMOEOPATHY

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