CORONARY HEART DISEASE, ANGINA PECTORIS, MI

• The heart has the highest oxygen consumption of all organs
• Other organs have an extraction of about 25%
• With increased oxygen demand, coronary artery flow increases
• Oxygen extraction from the coronary circulation is 70-80%
• At rest, the heart has a coronary flow of about 250 ml/min
• During exertion, the flow can increase up to 5 times
• Ischemia is the reduction in blood flow in a tissue as a result of:

  • Atherosclerosis
  • Thrombosis
  • Spasm
• Physical activity (emotional stress) leads to activation of the sympathicus, increasing heart rate and contraction, which increases demand after oxygen supply
• Coronary artery obstruction due to atherosclerosis leads to a lack of blood (oxygen) supply, causing pain and ischemic myocardial damage
• Acute stenosis of the coronary artery is often reversible, with reduced but maintained arterial flow, leading to subendocardial ischemia
• Acute occlusion of the coronary artery stops arterial flow, leading to subepicardial ischemia, later transmural ischemia, necrosis (heart attack) may occur
• Classification according to ischemia localization:

  1. Subendocardial ischemia (occurs mainly in stenosis)

  2. Subepicardial ischemia (occurs mainly during occlusion)

  3. Transmural ischemia (almost always begins as subepicardial)
• Acute coronary syndrome includes:

  • Unstable angina pectoris
  • Acute myocardial infarction
  • STEMI myocardial infarction
  • nonSTEMI (NSTEMI) myocardial infarction
• Chronic ischemic heart disease includes:

  • Asymptomatic form of ischemic heart disease (IHD)
  • Stable angina pectoris
  • Vasospastic angina
  • Postinfarction state
  • Dyssrhythmia IHD
  • Chronic IHD with heart failure
• Angina pectoris is severe chest pain due to ischemia of the heart muscle, caused by obstruction of the coronary artery
• Types of Angina Pectoris:

  • Stable AP
  • Unstable AP
  • Variant (Prinzmetal´s, vasospastic) AP
• Degree classification of angina pectoris severity:

  • Degree I: caused only by extremely intensive exertion
  • Degree II: caused by greater exertion in normal life
  • Degree III: caused by little effort in normal life
  • Degree IV: occurs with minimal stress or at rest
• Myocardial infarction is the necrosis of heart cells due to interruption of blood supply, caused by rupture of unstable atherosclerotic plaque leading to thrombosis or coronary artery obstruction by stable plaque
• Silent ischemia, hibernating myocardium, and stunned myocardium are other forms of ischemia
• ECG diagnosis of ischemia includes T wave inversion, ST segment elevation, and pathological Q wave
• STEMI myocardial infarction dynamics of ischemia after occlusion:

  1. Ischemia < 20min: reversible damage, hyperacute T waves on ECG

  2. Ischemia > 20min: reversible damage, ST elevations on ECG

  3. Ischemia > 2h: irreversible damage, pathological Q waves on ECG
• Complications of myocardial infarction include dysrhythmias, heart failure, shock, hypotension, myocardial rupture, valve defects, embolization, and pericarditis
• Cardiac markers for myocardial infarction include myoglobin, troponin I (TnI), T (TnT), creatine kinase (CK), heart MB subtype (CK-MB), lactate dehydrogenase (LD), and aspartate aminotransferase (AST)
• Other cardiac markers include lipids, lipoproteins, lipoprotein receptors, homocysteine for atherosclerotic plaques, CRP, TNF, IL-1, IL-6, ICAM, VCAM for inflammation and instability of atherosclerotic plaques, and ischemia-modified albumin (IMA) for ischemic damage of the myocardium
• Practice yourself