• Ischaemic Heart Disease (IHD)

    by  • 18/09/2013 • Cardiology


    1. is a disease characterized by ischaemia (reduced blood supply) to the heart muscle, usually due to coronary artery disease (atherosclerosis of the coronary arteries). Can present as angina (stable & unstable), or as an MI (silent or symptomatic).


    1. Stable angina = chest pain at determined levels of exercise (SOBOE). Reproducable.
    2. Unstable angina = pain at rest (SOBAR) = ACS, tx like MI.




    Presenting complaint

    1. Angina pectoris (in cold weather or emotional situations)
    2. Acute chest pain: acute coronary syndrome, unstable angina or myocardial infarction
    3. Heart failure (difficulty in breathing or peripheral oedema due to weakness of the heart muscle)
    4. The medical history distinguishes between various alternative causes for chest pain (such as dyspepsia, musculoskeletal pain, pulmonary embolism)


    Diagnostic tools/investigations

    1. ECG: STe/STd on 24 holter/on admission.
    2. Blood tests (cardiac markers): Trop T/I, CK.
    3. Cardiac stress testing: ETT
    4. Coronary angiogram: invasive angioplasty.
    5. CXR
    6. Myeloperoxidase has been proposed as a biomarker
    7. USS/Echo (stress echo: myocardial perfusion imaging / dobutamine stress echo).
    8. CT



    Its risk increases with:

    1. Age
    2. Smoking
    3. Hypercholesterolaemia (and high LDL = main factor)
    4. Diabetes
    5. Hypertension
    6. Gender >men
    7. First degree family history



    1. Main cause: atherosclerosis of the coronary arteries (>10% in >65yo)
    2. Stable angina is due to inability to supply the myocardium (heart muscle) with sufficient blood in situations of increased demand for oxygen, such as exertion.
    3. Unstable angina, STEMI and Non-STEMI are attributed to “plaque rupture”, where one of the plaques gets weakened, develops a tear, and forms an adherent blood clot that either obstructs blood flow or floats further down the blood vessel, causing obstruction there.

    Hereditary? Infective? How does it spread?

    Treatment and management (conservative/medical/surgical)

    Depending on the symptoms and risk, treatment may be with medication (statins, ACEi, aspirin…), percutaneous coronary intervention (angioplasty) or coronary artery bypass surgery (CABG).


    Stable angina (review):

    1. Supply problem = coronary atheroma and reduced flow
    2. Demand problem = AS, HOCM, HTN…
    3. Once diagnosed with stable angina = 10% die due to MI in first year. After this, risk of dying reduces year-on-year.
    4. Grading of angina (New York Heart Association functional classification): class I = SOBOE, class IV – SOBAR.
    5. P/c: SOB, chest/neck/jaw/left arm pain, male gender, 50-60yo.
    6. Getting topoint of angina is important – produces VEGF etc to force neovascularistion and collateral supply.
    7. Tx: RF modification, medical therapy (b-blockers, nitrates, statins, aspirin), balloon angioplasty, surgery, cardiac rehab.
    8. Drugs: nitrates = increase flow, b-blockers = reduce demand, CCB/nicornadil/procorolan = stabalise plaques, aspirin/clopidogrel = reduce clotting risk.


    Myocardial Infarction (review):

    1. MI myocardial cell death (=necrosis due to perfusion imbalance of myocardial tissue)
    2. Unstable angina = acute ischaemia
    3. MI = acute ischaemia AND NECROSIS
    4. Types of MI (5 types): most common = plaque rupture. Also, reduced supply MI, increased demand MI, sudden cardiac death etc…
    5. Pathophysiology: ruptured atheromatous plaque, and subsequent thrombi formation, leading to occlusion of coronary arteries = ischaemia and myocardial cell necrosis.
    6. ST changes: STd = ischaemia, STe = MI, STd and raised Trop T/I = ischaemia AND necrosis (=MI), variable T-waves = partial occlusion.
    7. Transmural MI: full thickness infarct (linked to major coronary disease – position: anterior, posterior, inferior…)
    8. Subendocardial MI: partial thickness (linked to prolonged ischaemia)
    9. Complications of MI: QT dispersion, arrhthymias (VF/VT/AF), complete HB, septal rupture, MVR/MVP, cardiogenic shock, stunning of myocardium, dressler’s syndrome (post-MI endocarditis), anxiety, 50% have depression).
    10. Death usually caused by electrical disturbance during MI = HB/arrhthymia… rarely a mechanical failure will cause death (although can = papillary muscle rupture septal rupture…)
    11. After the MI:
      1. o 4-12h: eosinophilia, contraction bands, Trop T/I at 12hours (<0.02?)
      2. o 12-24h: neutrophillia
      3. o 1-3d: necrosis
      4. o 3-7d: macrophages
      5. o 7-10d: phagocytosis
    12. Primary Mx of MI:
      1. o Resus and stabalise
      2. o Clopidogrel 300mg, heparin 1mg/kg, aspirin 700mg, morphine prn, b-blockers and nitrates if necc.


      1. o Fibrinolytic therapy, percutaneous coronary intervention (PCI.
    1. Secondary management:
      1. o Smoking cessation, cardiac rehab, diet, aspirin, b-blockers, statins, ACEi.   
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