PharmacologyTier 1Medical Sciences concept

Anti-anginal drug classes and mechanisms

Core concept

Angina = myocardial oxygen SUPPLY < DEMAND. Every anti-anginal moves one of those two
- Demand: heart rate, contractility, wall stress (preload x afterload)
- Supply: coronary flow (diastolic time, coronary tone, collaterals)
*Separate the two goals and never conflate them*
- Symptom control (anti-anginal): beta blockers, CCBs, nitrates, nicorandil, ivabradine, ranolazine, perhexiline
- Prognosis (not anti-anginal): aspirin, statin, ACEi/ARB, smoking cessation - these do not relieve angina
Revascularisation improves symptoms; in stable disease it does not reduce death or MI over optimal medical therapy (COURAGE, ISCHEMIA) - reserve for refractory symptoms or high-risk anatomy such as left main or severe LV dysfunction

Key detail

Class	Mechanism	Caution
Beta blocker (metoprolol, atenolol, bisoprolol)	dec HR, dec contractility -> dec demand; longer diastole -> inc coronary perfusion	First-line, especially post-MI or LV dysfunction. Avoid in vasospastic angina - unopposed alpha -> worse spasm
Dihydropyridine CCB (amlodipine, felodipine)	Arterial vasodilatation -> dec afterload; coronary dilatation	Ankle oedema, flushing; reflex tachycardia with short-acting agents
Non-dihydropyridine CCB (verapamil, diltiazem)	dec HR + dec contractility + vasodilatation	*Never combine with a beta blocker - bradycardia, heart block, negative inotropy. Avoid in HFrEF*
Nitrates (GTN, isosorbide mononitrate)	NO -> cGMP -> venodilatation -> dec preload; epicardial and collateral dilatation	*Tolerance - requires a nitrate-free interval of 8-12 h. Absolute contraindication with PDE5 inhibitors (24 h sildenafil, 48 h tadalafil)* - profound hypotension
Nicorandil	Nitrate + K-ATP channel opener	Painful mucosal/GI/perianal ulceration - often mistaken for IBD or malignancy
Ivabradine	Selective If ("funny current") inhibition in the SA node -> pure heart rate reduction	Sinus rhythm only. Visual phosphenes; bradycardia
Ranolazine	Late inward Na current inhibition -> dec Ca overload -> dec diastolic wall tension	No effect on HR or BP - useful when the BP will not tolerate more. QT prolongation
Perhexiline	CPT-1 inhibition -> shifts myocardium from fatty acid to glucose metabolism	Australian agent; requires therapeutic drug monitoring - hepatotoxicity and peripheral neuropathy in CYP2D6 poor metabolisers
Trimetazidine	Metabolic modulator	Not available in Australia

Clinical relevance

Start: short-acting GTN for all + beta blocker or CCB as background therapy
- Add the other class if symptoms persist (a dihydropyridine, not verapamil/diltiazem, if already on a beta blocker)
- Then long-acting nitrate, ivabradine, nicorandil or ranolazine
Target resting HR ~55-60 bpm where symptoms persist
Choose by comorbidity
- Post-MI or LV dysfunction -> beta blocker
- Vasospastic (Prinzmetal) angina -> CCB +/- nitrate; beta blockers contraindicated
- Asthma -> CCB (or a cardioselective beta blocker cautiously)
- AF with rapid rate -> beta blocker or diltiazem/verapamil
- Low BP -> ranolazine or ivabradine
*Every patient also gets: aspirin, high-intensity statin, BP and glycaemic control, smoking cessation, cardiac rehabilitation*
GTN technique: sit down, one spray/tablet, repeat at 5 minutes; call an ambulance if pain persists 10-15 minutes after the first dose

Correlations

INOCA/ANOCA (ischaemia with non-obstructive coronary arteries) - microvascular dysfunction or vasospasm; increasingly recognised, especially in women. Coronary function testing; treat with CCB, nitrate, ranolazine, statin, ACEi
Aortic stenosis, HOCM, severe anaemia, thyrotoxicosis, tachyarrhythmia - angina without coronary disease. Nitrates are dangerous in severe AS and HOCM
Vasospastic angina - transient ST elevation, young, smoking, cocaine
PDE5 inhibitor + nitrate - the interaction to never miss
Beta blocker + verapamil - the combination to never prescribe
Refractory angina - enhanced external counterpulsation, spinal cord stimulation, stellate ganglion block

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