12.3 MI

• What factors are used in QRISK 3 to assess for CVD risk?

  • age
  • sex
  • ethnicity
  • smoking
  • diabetes
  • family history
  • taking sildenafil
  • cholesterol levels
  • hypertension
  • obestity
• what are the cardiac mechanisms which can lead to angina?

  Coronary blood flows only during diastole

  • ↑ cardiac work → ↓ perfusion

  • ↑ sympathetic activity

  • ↑ heart rate → ↓ proportion of time in diastole • ↑ contraction force → ↑ vessel closure

  • → ↓ cardiac efficiency

  • Use of beta blockers in angina

  coronary arteries & arterioles compressedno/limited flow
• What factors shorten diastole? What dies this lead to?

  • shortening diastole, when HR increases
  • increased ventricular end-diastolic pressure
  • reduced diastolic pressure

  could lead to angina
• How does atherosclerosis lead to sudden occlusion of arteries?

  • atherosclerosis is characterised by intimal lesions called atheromas that impinge on the vascular lumen and can rupture to cause sudden occlusion
• what is the structure of an atheromatous plaque?

  • soft friable lipid cores covered by fibrous caps
  • necrotic centre containing cell debris, cholesterol crystals, foam cells, calcium
• what is the response to injury hypothesis in the pathogenesis of angina?

  1. Normal wall under chronic endothelial injury (smoking, HTN)

  2. Chronic injury leads to dysfunction -> inc permeability which leads to leukocytes adhesion.

  3. Monocyte and smooth muscle cell migration into the intima, with

  macrophage activation.

  4. Macrophage and smooth muscle cell uptake of modified lipids, with further activation.

  5. Intimal smooth muscle cell proliferation with extracellular matrix production, forming a well-developed plaque.
• what is the response to injury hypothesis model in relation to angina?

  • Response-to-injury hypothesis: This model views atherosclerosis as a chronic inflammatory response of the arterial wall to endothelial injury:
• What are the three main mechanisms underlying the development of thrombosis on plaques?

  1. Stable angina - atherosclerotic plaque with necrotic core. Narrowing of arteriole
  2. UA/NSTEMI - ruptured fibrous cap with thrombus on top narrowing lumen
  3. NSTEMI/STEMI - complete occlusion
• what are the risk factors for fatty strep formation?

  • endothelial dysfunction
  • monocyte adhesion
  • smooth muscle migration to intima
  • extracellular matrix elaboration
  • lipid accumulation
• why does intimal thickening occur in angina?

  expansion of outer wall to maintain internal diameter

  at 40% stenosis, inner diameter begins to narrow
• what are the causes of myocardial ischemia?

  • CA thrombosis
  • spasm
  • arteritis
• what is acute coronary syndrome?

  A group of conditions caused by a sudden reduction or blockage of blood flow to the heart, including unstable angina and myocardial infarction (heart attack).
• what is the Canadian Cardiovascular Society functional classification of Stable angina?

  Class I - only angina with strenuous activity

  Class II - angina during ordinary activities (e.g. walking up hill)

  Class III - angina with low levels of activity

  Class IV - angina at rest or with any level of exercise
• what are the surgical treatments available after an MI?

  • Coronary artery bypass graft - invasive
  • Percutaneous coronary intervention - use of stent and balloon
• what pharmacological therapies are available in stable angina?

  1. vasodilators
  2. beta blockers - reduces myocardial oxygen consumption
  3. calcium channel blockers - decreases cardiac connective tissue contraction
  4. ivabradine
  5. nicorandil
  6. ranolazine
  7. event reducing drugs : anti platelets, ACE inhibitor or ARB, statins
• what event-reducing drugs are used for stable angina?

  1. anti platelets: aspirin: reversbile inhibition of platelet COX-1 and thromboxane. Clopidogrel used in aspirin intolerance
  2. ACE inhibitor or ARB Indicated if treating other condition, e.g. HTN, HF, CKD
  3. • Statins: Use to reduce LDL cholesterol