IHD

• Ischaemic Heart Disease (IHD)


  A group of pathophysiologically related syndromes caused by myocardial ischaemia
• Myocardial ischaemia is caused by an imbalance between supply and demand for oxygenated blood to the heart
• Lack of oxygen leads to reduced ATP production, reduced availability of nutrients, and reduced removal of metabolites
• Coronary arteries


  • Epicardial arteries (90% of myocardial ischemia)
  • Intramural arteries
  • Arterioles
  • Capillaries
• Blood supply to the heart occurs during diastole
• IHD - Risk factors


  • Smoking
  • Hypertension
  • High blood cholesterol levels
  • Diabetes mellitus
  • Obesity
• IHD - Pathogenesis


  Insufficient perfusion relative to myocardial demand
• Causes of reduced blood supply


  • Narrowing of vessels due to atherosclerosis (in >90% of cases)
  • Vasospasm
  • Embolism
• Causes of increased demand


  • Myocardial hypertrophy
  • Tachycardia
  • Shock - low systemic blood pressure
• Compensatory mechanisms


  • Coronary autoregulation-dilatation of microcirculation
  • Formation of collaterals
• Risk of developing clinically important IHD


  Depends on number and structure of atheromatous plaques, degree of vessel obstruction
• Vessel obstruction


  • Luminal narrowing >75% - symptoms occur during exercise
  • Luminal narrowing >95% - blood flow is inadequate even at rest
• Acute plaque changes


  Rupture, superficial erosions, ulceration, fissuring, deep haemorrhage, associated with inflammation within the plaque and triggers thrombosis
• Other causes of IHD


  • Vasospasm
  • Embolization
  • Vasculitis involving intramural coronary vessels
  • Haematological abnormalities - sickle cell disease
  • Amyloid deposition in vessel wall
  • Vascular dissection
  • Marked hypertrophy of the left ventricle - AS
  • Lowered systemic blood pressure - shock
• Angina


  Inability of stenosed coronary artery to meet the demand - transient reduction in blood flow
• Myocardial infarction


  Acute plaque changes induce total thromboembolic occlusion leading to death of heart muscle
• Sudden cardiac death


  Myocardial ischaemia induce fatal arrhythmias
• Chronic ischaemic heart disease


  Refers to the long-term consequences of IHD
• Stable angina


  Occurs in chronic stenosing coronary atherosclerosis, caused by an imbalance between coronary perfusion and myocardial demand produced by increased cardiac workload
• Unstable angina


  Caused by disruption of an atherosclerotic plaque with superimposed partial thrombosis and possibly embolization or vasospasm
• Prinzmetal variant angina


  Episodic myocardial ischaemia due to coronary artery spasm
• Diminished blood supply to the myocardium - ischaemia


  Leads to cessation of aerobic oxidation and ATP production, accumulation of toxic metabolites, lack of oxygen and nutrients, and cessation of myocardial contractility
• Reversible cell injury


  Includes myofibrillar relaxation, glycogen depletion, cellular and mitochondrial swelling
• Irreversible cellular damage/necrosis


  Includes disruption of the myocyte sarcolemmal membrane, release of intracellular contents, and injury to the microvasculature
• Progression of necrosis


  Irreversible cell injury occurs first in the sub-endocardium (intramural), then extends towards the pericardium, with some becoming transmural infarcts
• The outcome depends on the location, severity and rate of development of coronary obstruction, area supplied by the obstructed vessel, duration of occlusion, metabolic and oxygen demand of the myocardium at risk, presence of collateral blood vessels, vascular spasm, and other factors like heart rate, cardiac rhythm, blood oxygenation
• Evolution of morphological changes in MI

  1. ½ -4 hours: No macroscopic changes, variable waviness of fibers at border

  2. 4-12 hours: Occasional reddish-blue discolouration, oedema, haemorrhage, initial coagulative necrosis

  3. 12-24 hours: Dark mottling, coagulation necrosis with pyknotic nuclei, hypereosinophilia, marginal contraction band necrosis, early neutrophilic infiltrate

  4. 1-3 days: Tissue becomes soft, yellow-tan colour, coagulation necrosis with loss of nuclei and striations, prominent interstitial infiltrate of neutrophils

  5. 3-7 days: Central infarcted area becomes soft and yellow-tan, dead myofibers begin to disintegrate, surrounded by dying neutrophils, early phagocytosis by macrophages

  6. 7-10 days: Yellow-tan colour more prominent, red-tan depressed margins, well-developed phagocytosis, formation of granulation tissue

  7. 10-14 days: Red-gray depressed infarct borders, well-established granulation tissue with new blood vessels and collagen deposition

  8. 2-8 weeks: Gray-white scar, progressive from border toward core, decreased cellularity of granulation tissue with increased collagen deposition

  9. >8 weeks: Dense collagenous scar tissue
• Triphenyl tetrazolium chloride


  Viable myocytes have dehydrogenases and stain brick-red, no staining in areas of dead tissue
• Post MI complications


  • Contractile dysfunction
  • MI associated arrhythmias
  • Myocardial rupture
  • Ventricular aneurysm
  • Pericarditis - Dressler syndrome
  • Infarct expansion
  • Mural thrombus
  • Papillary muscle dysfunction
  • Progressive late heart failure/ chronic IHD
• Contractile dysfunction


  Depends on the size of the infarct, can lead to hypotension, pulmonary vascular congestion, pulmonary oedema, and cardiogenic shock
• Right ventricular infarcts


  Can cause right-sided heart failure associated with pooling of blood in the venous circulation and systemic hypotension
• MI associated arrhythmias


  • Sinus bradycardia, atrial fibrillation, tachycardia, ventricular premature contractions, ventricular tachycardia, and ventricular fibrillation
  • Heart block if the atrioventricular conduction system is involved
• Myocardial rupture

  Occurs with transmural necrosis, most common is rupture of the ventricular free wall leading to cardiac tamponade, less common is rupture of the ventricular septum leading to acute VSD and left-to-right shunting, and papillary muscle rupture leading to acute mitral regurgitation