• Ischemia
• Atherosclerosis
• Dynamics of Ischemia in Occlusion
• ST Segment and Acute Coronary Syndrome
• Troponin and Infarction
• Acute Coronary Syndrome (ACS)
• Nomenclature of Infarction

Ischemia

• The heart has, in proportion to its volume, the highest oxygen consumption of all organs
• Oxygen extraction from the coronary circulation is 70-80%
  • Other organs have an extraction rate of about 25%
• The only way the heart protects itself from ischemia is by increasing blood flow through the coronary arteries
• At rest, coronary blood flow is about 250 ml of blood per minute.
• During exertion, the flow can increase up to 5 times
• Ischemia is a reduction in blood flow in the tissue
• Secondary hypoxia (lack of oxygen) occurs
• The most common causes of ischemia are changes in the coronary arteries:
• Atherosclerosis
• Spasm
• Thrombosis

Dynamics of Ischemia in Occlusion

• After the occlusion of a branch of the coronary artery, a STEMI infarction begins to develop
• Infarction (necrosis) gradually develops in the myocardial wall
• Time intervals are individual for each patient
• Myocardial viability depends on the collateral circulation
• Ischemia (<20 min.)
• The myocardium is hypoxic (lacking oxygen)
• Hypoxia (occlusion) lasts less than 20 minutes
• It is reversible
• On the ECG, there are hyperacute T waves
• Ischemic injury (>20 min.)
• The myocardium is hypoxic (lacking oxygen)
• Hypoxia (occlusion) lasts more than 20 minutes
• It is reversible
• On the ECG, there are already ST elevations
• Infarction (>2 hours)
• The myocardium is hypoxic (lacking oxygen)
• Hypoxia (occlusion) lasts more than 2 hours
• It is irreversible damage
• On the ECG, a pathological Q wave begins to develop

ST Segment and Acute Coronary Syndrome

• The ST segment is the main ECG marker of Acute Coronary Syndrome
• Troponin is the main laboratory marker of infarction
• It is released from necrotic cardiomyocytes during an infarction
• It is not released from ischemic myocardium

ST Segment and Acute Coronary Syndrome

• Acute stenosis (narrowing)
• Arterial flow is reduced but preserved
• Results in subendocardial ischemia
• On the ECG, there are ST depressions
• Rarely, the ST segment may be normal
• Acute occlusion (closure)
• Arterial flow is stopped
• Results in subepicardial ischemia, later transmural ischemia
• On the ECG, there are ST elevations
• Infarction (necrosis) can occur within 20 minutes after occlusion
• Transmural necrosis can occur within 4-9 hours after occlusion
• During necrosis, cardiomyocytes break down and release troponin

Troponin and Infarction

• Troponin (TnT) is the main laboratory marker of infarction
• It is specific to the myocardium
• It is released into the blood during infarction (cardiomyocyte breakdown)
• It is not released during myocardial ischemia
• Other enzymes (CK, AST, LDH) are not as specific
• Because they are also found in other organs
• Troponin release:
• Begins to be released 2-4 hours after occlusion
• Peaks at about 12-24 hours
• Persists for about 7 days

Acute Coronary Syndrome (ACS)

• ACS is an acute ischemic damage to the myocardium due to:
• Acute stenosis
• Acute occlusion
• The most common cause of ACS is thrombosis from plaque rupture
• Symptoms of ACS:
• Angina (chest pain lasting more than 20 minutes)
• Often radiates to the neck, shoulder, arm, and scapula
• Shortness of breath, anxiety, fear, weakness
• Symptoms are individual
• Patients with diabetes mellitus may have
• polyneuropathy and reduced pain threshold
• Symptoms may be minimal, rarely none!
• ACS is classified by extent into:
• Unstable Angina Pectoris (no necrosis occurs)
• NSTEMI infarction (results in partial necrosis of the myocardial wall)
• Non-ST Elevation Myocardial Infarction (Infarction without ST elevation)
• STEMI infarction (results in transmural necrosis)
• ST Elevation Myocardial Infarction (Infarction with ST elevation)

Nomenclature of Infarction

• Infarction is myocardial necrosis
• Troponin is released
  
  
• According to ECG, we distinguish between 2 types of infarction:
• STEMI Infarction
• NSTEMI Infarction
  
  

STEMI Infarction

• Occurs due to occlusion
• Necrosis is:
• Subepicardial
• Later becomes transmural
• On ECG, ST elevations are observed

NSTEMI Infarction

• Occurs due to stenosis
• Necrosis is:
• Subendocardial
• Not transmural
• On ECG, ST depressions are observed

• The following nomenclature is obsolete
• It is no longer used because the extent of myocardial necrosis does not always correlate with the ECG findings:
• Transmural Infarction
• This term is obsolete for STEMI
• STEMI is usually transmural necrosis, but this is not a rule
• Q Infarction
• This term is obsolete for STEMI
• STEMI usually causes transmural necrosis and a pathological Q wave, but this is not a rule
• Non-Transmural Infarction
• This term is obsolete for NSTEMI
• NSTEMI is usually non-transmural necrosis, but this is not a rule
• Non-Q Infarction
• This term is obsolete for NSTEMI
• NSTEMI usually involves non-transmural necrosis and does not produce a pathological Q wave, but this is not a rule

Unstable Angina Pectoris

• Sinus Rhythm
• Inverted T waves (I, aVL, V2-V6)
• Patient experienced approximately 10 minutes of angina and troponin was later normal
• The inverted T waves were not present in older ECG recordings
• Symptoms occurred spontaneously without exertion
• Diagnosis is unstable angina pectoris
• This is considered an acute coronary syndrome
• If the patient had elevated troponin later without ST elevation
• It would be classified as NSTEMI