Acute Myocardial

InfarctionWillis E. Godin D.O., FACC

Acute Myocardial Infarction

Definition: Decreased delivery of oxygen and nutrients to

the myocardium Myocardial tissue necrosis causing irreparable

tissue/cell death

Pathophysiology

The most frequent cause of an acute MI is a disruption in the vascular endothelium that is associated with myocardial plaque

Plaque occurs over a period of years to decades

This combination causes the development of an intra-coronary thrombus, which causes the coronary artery to occlude

Within 20-40 minutes of an occlusion, irreversible myocardial cell damage/death occurs

Pathophysiology

2 primary characteristics of plaque development are 1) a fibromuscular cap and 2) an underlying lipid rich core.

The overall loss of structural stability of the plaque usually occurs at the junction between the fibromuscular cap and the vessel wall (shoulder region)

Thrombus develops (due to the platelet-mediated activation of the coagulation cascade) and partial or complete occlusion occurs causing an acute myocardial infarction.

Pathophysiology

The severity of an MI depends on three factors 1) The level of the occlusion in the coronary

artery Generally, the more proximal the coronary

occlusion, the more extensive the amount of myocardium that will be at risk of necrosis

2) The length of time of the occlusion The longer the period of vessel occlusion, the

greater the chances of irreversible myocardial damage distal to the occlusion

3) The presence or absence of collateral circulation

Pathophysiology

STEMI “complete” blockage of a coronary artery

NSTEMI “near-complete” blockage of a coronary artery

Pathophysiology

Left Coronary Artery Left Anterior Descending Artery (LAD)

“widow maker” Anterior MI Lateral MI

Left Circumflex Artery (LCx) Lateral MI Posterior MI

Right Coronary Artery Inferior MI RV MI

Prevalence

Myocardial Infarction is the leading cause of death in the United States

Approximately 450,000 people in the US die from coronary disease per year

50% of all acute MI’s in the US occur in people under the age of 65

No longer considered a “disease of the elderly”

Risk Factors

Dyslipidemia

Diabetes Mellitus

Hypertension

Tobacco use

Family History

Male gender

Diagnosis

Symptoms (gained by an accurate history)

Electrocardiogram (ECG)

Laboratory Tests CK CK-MB Troponin

Echocardiogram

Symptoms

Chest pain described as a pressure sensation, fullness, or squeezing in the midportion of the thorax

Radiation of chest pain into the jaw or teeth, shoulder, arm, and/or back

Associated dyspnea or shortness of breath

Associated epigastric discomfort with or without nausea and vomiting

Associated diaphoresis or sweating

Syncope or near syncope without other cause

Impairment of cognitive function without other cause

Electrocardiogram

ST elevation myocardial infarction (STEMI) > 1mm ST elevations in contiguous leads

Non-ST elevation myocardial infarction (NSTEMI) ST depression T wave inversions No obvious ECG changes

ECG - STEMI

ECG - STEMI

ECG -NSTEMI

ECG - NSTEMI

ECG - NSTEMI

Cardiac Enzymes

Serial blood draws

Every 4 hours x 4 sets

Myoglobin peaks first (detectable in 1-4 hrs)

Troponin peaks last (detectable in 3-12 hrs) most specific remains detectable in serum the longest

Cardiac Enzymes

Cardiac Enzymes

Imaging (Echocardiography)

An echocardiogram can be performed to assess areas of the left ventricle that are not contracting normally as compared to areas that are contracting normally

After normal blood flow is interrupted, the area of the myocardium affected by the occluded artery will not function normally.

This abnormal wall motion can be detected by echocardiography

Treatment Antiplatelets

Supplemental oxygen

Nitrates

Pain control

Beta Blockers

Statin Therapy

Heparin (unfractionated / low-molecular-weight heparin)

Fibrinolytics

Angiotensin-Converting Enyme Inhibitors / Angiotensin Receptor Blockers

Glycoprotein Iib/IIIa Antagonists

Aldosterone Antagonists

Other Treatment Options

Percutaneous Coronary Intervention PCI / coronary stenting

Surgical Revascularization CABG

Implantable Cardiac Defibrillators AICD

Treatment Outcomes

Long-term medications

Smoking cessation

Cardiac Rehabilitation

Long-Term Medications

Most oral medications instituted in the hospital at the time of acute MI will be continued long term

Aspirin, beta blockade, and statin therapy is continued indefinitely in all patients

ACE inhibitors are continued indefinitely in patients with CHF, left ventricular dysfunction, hypertension, or diabetes

Diet modification, regular exercise

Smoking Cessation

Smoking is a major risk factor for coronary artery disease and MI

For patients who have undergone an MI, smoking cessation is essential to recovery, long-term health, and prevention of re-infarction

In one study, the risk of recurrent MI decreased by 50% after 1 year of smoking cessation

Smoking Cessation

All STEMI and NSTEMI patients with a history of smoking should be advised to quit and offered smoking cessation resources Nicotine replacement therapy Pharmacologic therapy Referral to behavioral counseling or support

groups

Smoking cessation counseling should begin in the hospital, at discharge, and during follow up

Cardiac Rehabilitation

Provides a venue for continued education, reinforcement of lifestyle modification, and adherence to a comprehensive prescription of therapies for recovery from MI including exercise training

Participation in cardiac rehabilitation programs after MI is associated with decreases in subsequent cardiac morbidity and mortality

Other benefits include improvements in quality of life, functional capacity, and social support

Summary

MI results from myocardial ischemia and cell death, most often because of an intra-arterial thrombus superimposed on an ulcerated or unstable atherosclerotic plaque

Despite advances in therapy, MI remains the leading cause of death in the United States.

MI risk factors include hyperlipidemia, diabetes, hypertension, male gender, and tobacco use.

Diagnosis is based on the clinical history, ECG, and blood test results, especially creatine phosphokinase (CK), CK-MB fraction, and troponin I and T levels.

Summary

Outcome following an MI is determined by the infarct size and location, and by timely medical intervention.

Aspirin, nitrates, and beta blockers are critically important early in the course of MI for all patients.

Post-discharge management requires ongoing pharmacotherapy and lifestyle modification.