Myocardial Infarction

Snapshot

A 55-year-old man presents to the emergency department due to substernal chest pain. His symptoms began a few hours ago. He describes the pain as “crushing” and it radiates down the left arm. Medical history is significant for type 2 diabetes and hypertension. On physical exam the patient is diaphoretic. An electrocardiogram demonstrates ST-segment elevations and cardiac troponins are significantly elevated.

Introduction

• Clinical definition
• death of myocardial tissue secondary to prolonged and severe ischemia  
• also known as a “heart attack”

Types

ST-segment elevation myocardial infarction (STEMI)

• an acute coronary syndrome (ACS) with ST-segment elevations found on electrocardiogram (ECG)
• biomarkers of myocardial necrosis are present

Non-STEMI (NSTEMI)

• an ACS without ST-segment elevations found on ECG
• biomarkers of myocardial necrosis are present

unstable angina

• an ACS    
• without ST-segment elevations found on ECG
• and no elevation biomarkers of myocardial necrosis

Epidemiology

incidence

• increases with age

risk factors

• hypertension
  • cigarette smoking
  • hyperlipidemia
  • hypercholesterolemia
  • male
  • postmenopause
  • genetic and behavioral predispositions to arteriosclerosis
    • e.g., high-fat diet

Etiology

occlusion of a coronary artery can be caused by

• atheromatous plaque rupture with subsequent thrombi expansion 
• vasospasm
• emboli, which can be secondary to
• atrial fibrillation, sending an embolus from the left atrium to the coronary arteries
• vegetations from infective endocarditis
• material from an intracardiac prosthetic
• paradoxical emboli

Pathophysiology

occlusion of a coronary artery disrupts the blood supply to a region in the myocardium

• ischemia ensues, the myocytes become rapidly dysfunctional
• when ischemia persists, this can result in myocyte death
• after 30 minutes of severe ischemia, the damage becomes irreversible 

infarction patterns

subendocardial

• myocyte necrosis involving the inner cardiac wall
  • this is normally the least perfused portion of the myocardium
  • may be referred to as an NSTEMI

transmural

• myocyte necrosis involving the full thickness of the cardiac wall
  • may be referred to as a STEMI

ECG Changes and STEMI

ECG Changes and STEMI
Infarction Location	Involved ECG Leads	Involved Coronary Artery
Inferior wall	II, III, and aVF	RCA
Antero-apical	V3 and V4	LAD (distal)
Antero-septal	V1 and V2	LAD
Antero-lateral	V5 and V6	LAD or LCX
Lateral	I and aVL	LCX
Posterior	ST depression and tall R waves in V1-3V7-V9	Posterior descending artery

Morphological Myocardial Changes in an MI

Morphological Myocardial Changes in an MI
Time	Gross Features	Light Microscopy	Complications
0-24 hours	Initially no gross findings; however, over the course of the first 24 hours, dark mottling ensues	Early coagulation necrosis Wavy fibers  Elongated myocytes Neutrophil infiltration	ArrhythmiaHeart failure
1-3 days	Mottling with a yellowish infarct center	Extensive coagulation necrosis   Brisk neutrophil infiltration	Fibrinous pericarditis
3-14 days	3-7 dayshyperemic with central yellowing7-10 daysyellow-tan with reddish tan margins10-14 daysreddish gray infarct borders	Macrophage infiltration and tissue granulation	Myocardial wall rupture may lead to cardiac tamponade Papillary muscle rupture   mitral regurgitation  posterolateral muscle rupture is more likely than anteromedial muscle rupture Pseudoaneurysm of a ventricular wallmay rupture
2 weeks – several months	2-8 weeks gray-white scar> 2 monthscomplete scar	Collagenous scar	Dressler syndromeHeart failure True ventricular aneurysm a thrombus may form

Presentation

Symptoms 

chest pain

• features
  • squeezing
  • crushing
  • substernal
  • radiation
    • jaw
    • neck
    • left shoulder or down the arm

• nausea and vomiting
• dyspnea
• asymptomatic

• typically seen in patients with diabetic neuropathy
• nerve fibers are damaged and impair their ability to sense pain

Physical exam

• diaphoresis
  • variable findings

e.g., S3 or S4, signs of heart failure, bradycardia (in cases of an inferior wall MI)

Imaging

• Coronary angiography
• indication
• diagnostic study to assess coronary anatomy and to determine where the occlusion is

Studies

• 12-lead ECG
  • perform as soon as possible
  • findings
    • STEMI  
      • hyperacute or peaked T-waves
        • earliest finding
      • ST elevation
      • Q waves
        • a late finding (~2 weeks post-MI)
      • new left bundle branch block (LBBB)
        • considered to be an equivalent to a STEMI
    • NSTEMI 
      • ST depression
      • T wave inversion
    • Late
      • pathologic Q waves 
        • Q wave in leads V2–V3 lasting longer than 0.02 seconds
        • Q wave anywhere lasting longer than 0.03 seconds with an amplitude greater than 0.1 mV
• Biomarkers
  • Troponin
    • preferred marker as it has a high sensitivity and specificity for myocardial necrosis
    • troponin I increases after 4 hours and peaks around 24 hours
      • remains elevated for 7-10 days
  • CK-MB
    • a sensitive but not specific biomarker since skeletal muscle can also release it
• useful for assessing reinfarction 

Differential

• Unstable angina
  • differentiating factor
    • no elevation in cardiac biomarkers
• Costochondritis
  • differentiating factor
• chest pain that is reproducible with palpation 

Treatment

• Conservative
  • lifestyle modification
    • e.g., smoking cessation
• Medical
  • initial medical treatments include
    • aspirin
    • oxygen
    • nitroglycerin  
      • hypotension in an inferior wall infarction secondary to reduced preload  
    • morphine
      • only give if there is unacceptable pain 
        • appears to be associated with a mortality increase
  • P2Y12 (ADP) receptors blockers
    • indication
      • given in addition to aspirin
  • heparin
    • indication
      • given in addition to antiplatelet therapy
  • β-blockers
    • indication
      • given to all patients if there are no contraindications
  • statin
    • indication
      • given to all patients
  • angiotensin-converting enzyme (ACE) inhibitor
    • indication
      • given to patients with a myocardial infarction
      • recommended when there is
        • anterior infarction
        • heart failure
        • left ventricular ejection fraction < 40%
      • reduces mortality
    • contraindication
      • shock
      • bilateral renal artery stenosis
      • allergy
• Reperfusion therapy
  • percutaneous coronary intervention (PCI)
    • indications
      • if STEMI symptoms developed in < 12 hours and the procedure can be performed within 90-120 minutes
      • if fibrinolytic therapy is contraindicated
  • coronary artery bypass graft (CABG)
    • indication
      • when coronary anatomy does not allow for PCI
      • 3 vessel occlusion or 2 vessel occlusion in a patient with diabetes
      • significant stenosis of the left main coronary artery
  • fibrinolytic therapy
    • indication
• for patients who cannot receive PCI within 120 minutes

·· Three coronary vessels with > 70 percent stenosis

·· Left main coronary artery stenosis > 50–70 percent

·· 2 vessels in a diabetic

·· 2 or 3 vessels with low ejection fraction

Complications

• Heart failure
• Sudden cardiac death
• Arrhythmia
• Myocardial stunning