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Iraqi Board Cardiology study materials
Iraqi Board Cardiology study resources

Iraqi Board Cardiology: Basic sciences relevant to cardiology

Iraqi Board Cardiology · Work through your exam, one topic at a time.

All guide sections

Basic sciences relevant to cardiology

This domain tests whether you can move from mechanism to bedside decision: why a drug changes mortality, why a murmur appears, why a channelopathy causes syncope. Questions are usually applied, not recall-only.

Structure and physiology

  • Coronary supply: LAD supplies the anterior two-thirds of the septum, apex and anterior LV; LCx supplies the lateral wall and gives the PDA in left-dominant circulation; RCA supplies the RV, inferior wall and, in most hearts, the SA and AV nodes.
  • Excitation-contraction coupling: L-type Ca2+ influx triggers ryanodine-receptor Ca2+ release (calcium-induced calcium release). Relaxation depends on SERCA2a (inhibited by unphosphorylated phospholamban) and the Na+/Ca2+ exchanger. Digoxin inhibits Na+/K+-ATPase, raising intracellular Na+, reducing Ca2+ extrusion and increasing inotropy.
  • Frank-Starling and Laplace: stroke volume rises with preload; wall stress = pressure x radius / (2 x thickness). Dilation raises afterload and oxygen demand; hypertrophy normalises wall stress at the cost of diastolic stiffness.

Pharmacology anchors

  • Mortality-reducing therapy in HFrEF: ARNI/ACE inhibitor, evidence-based beta-blocker, MRA, SGLT2 inhibitor.
  • Amiodarone is a class III agent with class I, II and IV properties; monitor thyroid, lung, liver and eyes.
  • Statins inhibit HMG-CoA reductase, upregulating hepatic LDL receptors.

Pathology and genetics

  • Atherosclerosis: endothelial injury, LDL retention and oxidation, monocyte recruitment, foam cells, necrotic core, fibrous cap; thin-cap fibroatheroma ruptures.
  • Hypertrophic cardiomyopathy is sarcomeric (MYH7, MYBPC3), autosomal dominant. Marfan syndrome is FBN1 with aortic root disease. Familial hypercholesterolaemia involves LDLR, APOB or PCSK9. Long QT: KCNQ1 (LQT1), KCNH2 (LQT2), SCN5A (LQT3); Brugada syndrome is SCN5A loss of function.

Worked example

A man with severe aortic stenosis has typical angina but clean coronary arteries. Why? Concentric LV hypertrophy raises oxygen demand, while raised filling pressure and compression of subendocardial vessels reduce supply. The mechanism is demand-supply mismatch, not epicardial obstruction.

Traps

  • Confusing calcium-induced calcium release with calcium reuptake.
  • Assuming the RCA always supplies the AV node.
  • Using a class label as if all members share the same outcome data.