MRCP cardiology learning points

Ischemic Heart Disease

  • Non atherosclerotic angina
    – AS, AR, HOCM
    – Thyrotoxicosis
    – Anemia
  • Monckeberg calcified medial sclerosis: benign condition involving the tunica media of arteries (muscular layer) in older patients
  • Basic science: 3 types of troponin (C,I,T)
    – C: binds to calcium
    – I: inhibits interaction with actin and myosin
    – T: binds to tropomyosin
    – Troponin is specific (rules out MI)
  • Coronary circulation is
    – Dependent on oxygen demand. High demand –> adenosine is released –> vasodilation
    – Autoregulated within a range of BP
  • AV node is supplied by PDA
    SA node is supplied by a branch from RCA 60% of the time
    RBBB in anterior MI = occlusion prior to S1
  • If typical sxs but ECG and troponin normal, next step is to do exercise test after the patient stabilizes with medical treatment.
  • Most specific feature in MI? presence of Q waves
  • GISSI I: Streptokinase provides mortality benefit in acute MI.
  • GISSI II: No difference between SK and alteplase. Also no difference between heparin and no heparin. SK + heparin caused more bleeding.
  • ISIS II: Aspirin + SK > SK or aspirin alone > no treatment
  • Omega 3 FA *fish oil) reduces all cause mortality in CAD by 20%. Vitamin E has no benefit. Ezetimibe lowers LDL but no data regarding mortality.
  • DIGAMI: IV insulin followed by 3 months of sub/c insulin improves mortality in MI (aggressive glycaemic control)
    – probably in patients <70 yo with no previous MI and not on insulin
  • Post MI VT: Holter adds little to management
  • MADIT trial: propylactic ICD in ischemic cardiomyopathy EF <30% reduces SCD
    – But increased events of HF in ICD group due to unknown reason
    – AHA/ACC recommendations:  prophylactic ICD is indicated in
    i) Non ischemic cardiomyopathy, post MI ICM with EF <35%, NYHA class II/III with expected survival > 1 year (level I, class A)
    ii) Post MI ICM with EF <30%, NYHA class I with expecte survival > 1 year (level I, class B)
  • Driving post MI
    – 1 month with thrombolytics/CABG
    – 1 week with PTCA

Congestive HF

  • basic science: BNP is released from ventricular myocardium due to stretch; function is opposite to angiotensin (vasodilation, increased GFR and diuresis)
    – Synthesis is increased by presence of stress hormones (thyroid, glucocorticoid & AT II)
  • Treatment: start with ACEi first then slowly uptitrate Beta-blocker
  • Digoxin has no added benefit in NSR
  • Digoxin level can be measured by drawing blood 6 hours after the last dose (DigoX – SiX)
  • High output cardiac failure in megaloblastic anemia: rx with blood transfusion !
  • Drugs that cause water retention
    – NSAIDs/celecoxib
    – Glitazones
    – OCP


  • SVT in pregnancy: beta blocker is first line over calcium channel blocker, but avoid it in first trimester
  • Avoid verapamil in VF/VT
    Flecainide: used with care as can precipitate incessant VT
    Adenosine is okay
  • Cardiac resynchronization indications
    – Low EF <30%
    – Wide QRS (LBBB)
    – NYHA class III and above
    3L: low EF, LBBB, low functionality of heart
  • ICD implantation indications
    – Prophylactically in poor EF post MI (<35%)
    – History of cardiac arrest with VF/VT
    – Syndromes eg long QT, Brugada, ARVD
  • Thromboembolic risk in AF remains for 6 weeks, so the need for anticoagulation for at least 6 weeks.

Valvular diseases

  • Annulus calcification of mitral valve is incidental finding and cause no symptoms.
  • OS in MS will remain in AF if the valve can still open.
  • Bicuspid aortic valve: calcify with aging
    – Congenital, sporadic
    – Systolic click
  • Most important prognostic factor in AS is LV function
    – Other: severity of valvular calcification
  • Absolute indication for surgery in AS = symptomatology
    – others: AS + HF (poor EF), AS + surgery in heart
  • Dilated LV: think AR
    Other valvular diseases except MS have LV hypertrophy (small LV)
  • Austin flint murmur
    – Can be indistinguishable from MS diastolic murmur
    – Due to partial closure of mitral valve in AR
    – DOES NOT predict AR severity
  • A.myxoma
    – Mid-diastolic click (tumour plop)
    – 1/3 asymptomatic, 1/3 emboli, 1/3 inflammation
    – LA dilatation due to obstruction
    – Carney complex: A.myxoma + skin pigmentation + endocrine abns
  • Poor prognostic factors in HOCM
    – History of syncope
    – Family history of SCD
    – ECG non sustained VT
    – Echo LV thickness > 3cm (most important)
    – Exercise drop in BP

Physical examination

  • Reversed splitting of S2
    – A2 delayed: LBBB, severe AS
    – P2 earlier: PDA, WPW type B
  • Loud S1: MS, PAC, tachycardia

Congenital HD

  • Most common is VSD
  • Most of congenital HB have unknown causes (not due to the presence of anti Ro)
  • Turner’s syndrome
    – COA is classical cause of hypertension, but the MOST COMMON is still essential hypertension
  • Differential cyanosis
    – PDA + COA
    – PDA + Eisemenger (reversal diminishes the loudness of the machinery murmur)

Hypertension and dyslipidemia

  • Hypertension in young
    <90th percentile: normal BP
    90-95th: preHTN
    95-99th: HTN stage I
    >99th: HTN stage 2
  • Most common cause is renal parenchymal (glomerulonephritis)
  • Basic science:
    – HDL gets cholesterol from peripheral tissues via ABCA1
    – The cholesterol is esterified by LCAT
    – The cholesteryl-ester is transferred to VLDL in exchange of its TG by CETP (CETP also transfers cholesterol from LDL to VLDL in exchange of its TG) –> this causes VLDL to become small dense LDL.
    – TG is unstable, so is degrade by lipase, forming small dense HDL & LDL.
    – The HDL is free to collect cholesterol again.
    – The small dense LDL is what contributes to atherosclerosis.
  • Abetalipoproteinemia: 3A
    – Acanthocytes (spur cells)
    – Affects retina (retinitis pigmentosa)
    – Affects neurons (neurodegeneration BUT IQ is normal)
  • Dyslipidemia:
    – Type I: chylomicron (LPL defect)
    – Type II: LDL
    IIa: LDL (LDL receptor problem)
    IIb: LDL + VLDL (LDL receptor problem + increased apoB)
    – Type III: IDL (apoE2 defect)
    – Type IV and V: VLDL (TG) (increased production)
  • Target cholesterol level
    Total: <4 mmol/L
    LDL: <2 mmol/L
    TG: <2 mmol/L
    HDL: >1 mmol/L


  • Types of pericarditis: HPS FC
    Hemorrhagic, purulent, serous, fibrinous, constrictive
  • In venous ulcer, before applying compression stocking, check ABI first to rule out arterial insufficiency. Arterial insuf is c/i for compression stocking
  • Hemachromatosis genetic
    – Homozygous C282Y/C282Y
    – heterozygous C282Y/H63D
    – Homozygous H63D/H63D has lower risk than the heterozygote
  • Sub/c nodules in rheumatic fever is NON TENDER and soft



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