Unit 12 Myocardial infarction

• what is the risk scoring system for the risk of MI or stroke over the next 10 years?

  QRISK3
• what are common criteria in QRISK3

  • age
  • sex
  • ED drugs -> sidenafil
  • ethnicity
  • smoking
  • diabetes
  • family history
  • cholesterol
  • hypertension
  • obesity
• cardiac anatomy

  A) right coronary artery

  B) right atrium

  C) right ventricle

  D) left coronary artery

  E) left auricle

  F) circumflex brach of the left coronary artery

  G) left marginal branch of the circumflex artery

  H) right marginal branch of the right coronary artery

  I) posterior interventricular branch of right coronary art

  J) left ventricle

  
• what is artherosclerosis?


  • the formation of an intimal artheroma
  • artheromas contain a lipid cores, fibrous cap and medium/large vessels
• outline the formation of a plaque:

  1. endothelial injury from prolonged insult (smoking/HTN)
  2. causes endothelial dysfunction -> increased permeability -> leukocyte adhesion
  3. migration of monocytes and smooth muscle cells to the intima -> activation of macrophages
  4. macrophages store/ uptake the modified lipids
  5. increased intimal smooth muscle proliferation and ECM deposition -> formation of a plaque
• outline the progression of a plaque:

  normal -> fatty streak -> pathological intimal thickening -> plaque expansion -> 1 of 3 (thin cap, thick cap or a fibrotic plaques)

  what can happen to these three types of plaques?

  plaque ruptures, erosion + thrombosis and finally just for fibrotic plaques there is the fibrocalcific plaque which can lead to critical stenosis
• what is ischaemic heart disease and what are common pathophysiological reasons for developing IHD?

  • when there is a mismatch between the oxygen supply and demand from the body
  • mainly due to a fixed obstructive cause like CAD
  • other causes - arteritis, vasospasm and thrombosis
  • commonly seen in thyrotoxicosis or myocardial hypertrophy which leads to an increased cardiac output and subsequently has a higher oxygen demand
• Angina in patients with stable CAD can cause myocardial ischaemia and present as ST-T changes on an ECG with cardiac ischaemic pain. What are the symptoms of classical angina?


  • central / gripping / tight chest pain, may extend reterosternally
  • may radiate to the face or the arms
  • triggered by emotion or exercise
  • can be relieved by GTN -> triglyceryl trinitrate
• what are the 3 features of 'classical angina' which is used to make a diagnosis according to NICE?

  Classical angina:

  •‘Heavy’, ‘tight’ or ‘gripping’ central or retrosternal pain which may radiate to the jaw and/or arms.

  •Pain which occurs with exercise or emotional stress.

  •Pain which eases rapidly with rest or with GTN (glyceryl trinitrate).
• apart from variable angina what are the other types?

  1.Atypical angina: NICE = two out of three features of classical angina.

  2.Non-angina chest pain: NICE as chest pain = one out of three of above

  3.Variant (Prinzmetal’s) angina: spasm results, occurs without provocation, usually at rest.

  Characteristically, there is ST segment elevation on the ECG during the pain.

  4.Unstable angina: rapidly in severity

  5.Refractory angina: severe coronary disease where revascularization is not possible and angina is not controlled by medical therapy.

  6.Microvascular angina: good prognosis
• aetiology - what is the most common cause of angina?

  The most common cause is coronary artery atheroma (coronary artery disease-CAD), which results in a fixed obstruction to coronary blood flow
• which investigations can be done for angina?

  • FBC, Thyroid function test, fasting glucose, HbA1c , fasting lipid, GFR,
  • troponin
  • 12-ECG
  • Echo
  • CXR
  • Ambulatory ECG
• how is angina classified according to the Canadian Cardiovascular Society functional classification of Stable angina?

  I - No angina with ordinary activity; angina with strenuous activity

  II - Angina during ordinary activity, e.g. walking up hills, walking rapidly upstairs, with mild limitation of activities

  III - Angina with low levels of activity, e.g. walking 50–100m on the flat, walking up one flight of stairs, with marked restriction of activities

  IV - Angina at rest or with any level of exercise
• what disease is the Canadian cardiovascular society functional classification used for?

  stable angina
• A patient comes in and has symptoms of angina at rest and at any level of exercise you make them do, what class of stable angina do they have?

  class IV
• A patient comes in complaining that they find it difficult to carry out less than ordinary physical activity, you see they have symptoms of angina - how do you class them?

  class III
• A patient has symptoms of angina and experiences angina when doing ordinary activity like walking a dog, what class angina do they have?

  class II
• A patient is well but experience symptoms of angina when they partake in strenuous activity, what class angina do they have?

  class !
• what is the pathway of treatment for angina?


  here

  
• what are short-acting nitrates like Glyceryl Trinitrate used for?

  short acting -> quick onset and clearance

  • acutely in angina attacks, perioperative hypertension, acute heart failure to decrease preload and afterload
• what are long-acting nitrates like Isosorbide Mononitrate / dinitrate used for?

  • angina prophylaxis
  • chronic angina management
  • (heart failure treatment)
• what are examples of anti-anginals which are not beta-blockers or CCB?

  • ivabradine
  • ranolazine
  • nicorandil
• what is the MOA of ivadbradine?


  •Inhibits pacemaker If current in SA node

  •Use in sinus rhythm ± beta-blocker

  •Side-effects – bradycardia, phosphenes

  •Contraindications – sick sinus syndrome, AV block
• what is the MOA of nicorandil?

  •Activates ATP-sensitive potassium channels and has nitrate properties – peripheral and coronary vasodilation

  •Side-effects – headache, flushing, oral ulceration
• what is the MOA of ranolazine

  •Inhibits late sodium channels into cardiac cellslengthened QT

  •Side-effects – constipation, dizziness,
• what are examples of event-reducing drugs in angina?

  •Anti-platelets-

  Aspirin: Reversible inhibition of platelet COX-1 and thromboxane production

  Clopidogrel: Use in aspirin intolerance

  •ACE inhibitor or ARB: Indicated if treating other condition, e.g. HTN, HF, CKD

  •Statins: Use to reduce LDL cholesterol
• describe the manifestation of an MI on an ECG (ECG changes)

  here

  
• what can be seen in leads V1-V3 in an acute anteroseptal MI?

  • ST elevation
  • Q wave presence
  • ST depression in II, III and AVF

  
• what would and acute inferior wall myocardial infarction (II, III and AVF Leads) present as on an ECG

  • ST elevation

  
• what are causes of ST elevation?

  • MI
  • pericardial effusion
  • pericarditis
  • myocarditis
  • Left ventricular hypertrophy
  • Right bundle branch block
• what is the difference between a PTCA and a PCI?

  • coronary angioplasty is a procedure used to widen blocked or narrowed coronary arteries, AKA PTCA ->percutaneous transluminal coronary angioplasty

  •The combination of coronary angioplasty with stenting is percutaneous coronary intervention (PCI).

  
• how is angiography performed?

  1. a long catheter is inserted via an artery (femoral/brachial/ radial) into the heart
  2. a contrast agent/dye is injected into the heart via the catheter
  3. imaging of the dye in the arteries using X-ray (or CT-scan).
  4. sedatives with analgesics used for conscious sedation
• what are other surgical interventions other than PCI?

  • CABG - coronary artery bypass graft
  • IMA - internal mammary artery implantation

  in both examples the graft bypasses the LCA obstruction

  
• what are Typical ECG changes in myocardial infarction (STEMI)?

  here

  
• how does the response-to-injury hypothesis relate to the formation of an artherosclerosis?

  Response-to-injury hypothesis: This model views atherosclerosis as a chronic inflammatory response of the arterial wall to endothelial injury ​
• outline 4 possible artherosclerotic plaque fates

  1. Rupture, ulceration or erosion -> thrombus formation​

  • Thrombi may partially or completely occlude the lumen, leading to tissue ischemia​

  1. Haemorrhage into a plaque -> intra-plaque haemorrhage​

  • The resulting haematoma may cause rapid plaque expansion or plaque rupture​

  1. Atheroembolism -> microemboli composed of plaque contents​
  2. Aneurysm formation​

  • Atherosclerosis-induced pressure or ischemic atrophy of the underlying media, with loss of elastic tissue, causes structural weakening that can lead to aneurysmal dilation and rupture​
• outcomes of plaques


   here

  
• how does the ischaemic nature of angina cause pain?

  The damaged muscle produces algesics (bradykinin, adenosine & potassium) -> activate sensory nerve endings in the myocardium -> send nociceptive signals to the brain
• what is the pathophysiology of angina and stable angina?


  here

  
• what is meant by:

  • the zone of infarction
  • region of ischaemic tissue
  • transmural infarct

  • Zone of infarction – the area of muscle that’s lost its direct blood supply – cardiomyocytes die ​
  • Surrounding the central area of dead muscle – region of ischaemic tissue​
  • Chances of survival increase the further away it is​
  • If the infarction affects the full thickness of the ventricle wall – transmural