module 1 take home points

What is hypertension?

Chronically elevated blood pressure.

What are the main risks associated with hypertension?

Increased risk of myocardial infarction, stroke, heart failure, kidney disease and premature death.

How do ACE inhibitors work?

They reduce angiotensin II and aldosterone production and increase bradykinin-mediated vasodilation.

What is an example of an ACE inhibitor?

Enalapril.

What are the side effects of ACE inhibitors?

Cough, angioedema, hyperkalaemia and hypotension.

How do ARBs work?

They selectively block AT₁ receptors, reducing the effects of angiotensin II and lowering blood pressure.

How do ARBs compare with ACE inhibitors?

They have similar antihypertensive benefits but a lower risk of some side effects. However, they do not have the beneficial bradykinin-mediated vasodilation associated with ACE inhibitors.

What is an example of an ARB?

Candesartan.

How do dihydropyridine CCBs work?

They block L-type voltage-gated calcium channels in vascular smooth muscle, causing vasodilation with minimal effects on heart rate and cardiac contractility.

How do thiazide diuretics work in the early phase?

Increased fluid loss decreases venous return and cardiac output, causing a fall in blood pressure.

How do thiazide diuretics work in the chronic phase?

Decreased total body Na⁺ reduces Ca²⁺ exchange into vascular smooth muscle cells, decreasing contraction and causing vasodilation.

How do alpha-1 blockers work?

They block alpha-1 receptors, reducing vasoconstriction and causing vasodilation.

How do beta-blockers lower blood pressure?

They reduce cardiac output by decreasing heart rate and the force of cardiac contraction.

What are statins used for in hypertension?

They lower lipids and are commonly used alongside antihypertensive treatment to reduce cardiovascular risk.

What is an example of a statin?

Atorvastatin.

What is the order of antihypertensive treatment?

1. ACE inhibitor or ARB → 2. ACE inhibitor/ARB + CCB → 3. ACE inhibitor/ARB + CCB + thiazide diuretic → 4. Add alpha-1 blocker or beta-blocker.

What causes stable angina?

Myocardial ischaemia caused by an imbalance between oxygen supply and demand, usually due to coronary atherosclerosis, without structural damage.

What causes unstable angina?

Atherosclerosis with a thrombus, causing unpredictable pain but no structural myocardial damage.

What causes myocardial infarction?

Usually atherosclerosis with a thrombus, causing ischaemia and subsequent myocyte death.

How does stable angina present?

Predictable chest discomfort triggered by exertion or stress and relieved by rest or GTN.

What is the first-line treatment for an acute angina attack?

Sublingual glyceryl trinitrate (GTN).

How does GTN work?

It releases nitric oxide, causing vasodilation and reducing cardiac workload and myocardial oxygen demand.

What drugs are used for long-term symptom control of angina?

Beta-blockers and non-dihydropyridine calcium channel blockers.

How do beta-blockers and non-dihydropyridine CCBs help with angina?

They reduce heart rate and myocardial oxygen demand.

Why is early treatment of angina important?

It improves quality of life and reduces progression to acute coronary syndromes or myocardial infarction.

What cardiovascular conditions are associated with thrombosis?

Acute coronary syndromes, ischaemic stroke, DVT and pulmonary embolism.

What do antiplatelet drugs target?

Primary haemostasis.

What do anticoagulants target?

Secondary haemostasis.

How does low-dose aspirin work as an antiplatelet drug?

It inhibits platelet COX-1, reducing thromboxane A₂ production for the lifespan of the platelet.

Why is low-dose aspirin effective for long-term cardiovascular prevention?

Its inhibition of platelet COX-1 and thromboxane A₂ lasts for the lifespan of the platelet.

What is dual antiplatelet therapy?

The combination of aspirin and clopidogrel.

How does dual antiplatelet therapy work?

It provides synergistic inhibition of platelet aggregation.

Why is dual antiplatelet therapy important after STEMI?

It reduces platelet aggregation and helps reduce further infarction.

What are the advantages of newer anticoagulants such as dabigatran?

Similar efficacy to warfarin with fewer interactions, rapid onset, predictable dosing and easier management.

What determines the dose of newer anticoagulants?

Patient-specific factors.

What causes cardiac arrhythmias?

Disturbances in ion channel activity that alter action potential generation or propagation.

How do antiarrhythmic drugs work?

They modify sodium, potassium, calcium or sympathetic signalling pathways.

How do Class I antiarrhythmics work?

They block sodium channels and primarily slow ventricular conduction.

What is an example of a Class I antiarrhythmic?

Lidocaine.

What does lidocaine preferentially target?

Ischaemic ventricular tissue.

How do Class II antiarrhythmics work?

They block beta receptors and reduce sympathetic-driven automaticity.

What is an example of a Class II antiarrhythmic?

Sotalol.

What is a key feature of sotalol?

It combines beta-blockade with potassium channel inhibition but carries a risk of QT prolongation.

How do Class III antiarrhythmics work?

They block potassium channels and prolong repolarisation.

What is an example of a Class III antiarrhythmic?

Amiodarone.

What is a key feature of amiodarone?

It has broad multi-class actions but significant risks of long-term toxicity.

How do Class IV antiarrhythmics work?

They block calcium channels and slow SA and AV nodal conduction.

What is an example of a Class IV antiarrhythmic?

Verapamil.

What is verapamil used to treat?

Tachycardias and atrial fibrillation.

What is a major adverse effect of verapamil?

Cardiac depression.

What is heart failure?

A condition in which the heart cannot pump enough blood to meet the body's needs.

What happens with chronic SNS and RAAS activation in heart failure?

They initially compensate for reduced cardiac output but ultimately worsen heart failure and contribute to disease progression.

What are the four pillars of disease-modifying treatment for heart failure?

ARNI (preferred) or ACE inhibitor/ARB, beta-blocker, mineralocorticoid receptor antagonist (MRA), and SGLT2 inhibitor.

What drugs can be used as the ARNI/ACE inhibitor/ARB component of heart failure treatment?

ARNI is preferred, with enalapril or candesartan as examples of ACE inhibitor/ARB alternatives.

What is an example of a beta-blocker used in heart failure?

Carvedilol.

What is an example of an MRA used in heart failure?

Spironolactone.

What is an example of an SGLT2 inhibitor used in heart failure?

Empagliflozin.

What are the benefits of the four pillars of heart failure treatment?

They slow disease progression, improve symptoms, and reduce hospitalisation and mortality.

What is the role of loop diuretics and digoxin in heart failure?

They provide symptomatic relief but do not slow disease progression.