Ischaemic heart disease: oxygen balance, stable disease and acute syndromes
Why narrowed heart arteries cause chest pain or a heart attack, and how drugs, stents and clot treatment fit together.
Myocardial ischaemia happens when the heart muscle gets less oxygen than it needs, usually because atherosclerotic plaques narrow the coronary arteries. Drugs help by lowering the heart's oxygen demand, improving supply, stopping clots and slowing the plaque. The approach differs between stable coronary disease and acute coronary syndromes, and drug-eluting stents add a local drug to mechanical treatment.
Supply and demand
The heart extracts most of the oxygen from coronary blood even at rest, so more demand can only be met by more flow. Demand is driven by heart rate, contractility and wall tension (which rises with blood pressure and ventricular size). Supply depends on the open diameter of the coronary arteries and on diastolic time, because the contracting muscle squeezes its own vessels in systole; a fast heart rate therefore both raises demand and cuts supply. A fixed narrowing causes exertional (stable) angina; spasm causes vasospastic angina; dysfunction of the small vessels causes microvascular angina.
How each antianginal drug helps
- Beta blockers: slower rate and less contractility, so less demand and more diastolic time. First choice for exertional angina, especially after infarction.
- Calcium channel blockers: dilate arteries and coronary vessels; verapamil and diltiazem also slow the heart. Useful in vasospastic angina; non-dihydropyridines are avoided in HFrEF.
- Nitrates: release nitric oxide, mainly dilating veins (less preload and wall stress) and large coronary arteries. Sublingual glyceryl trinitrate relieves an attack; long-acting forms need a nitrate-free interval to avoid tolerance. Never combined with PDE5 inhibitors.
- Ranolazine: reduces the late sodium current and the calcium overload it causes in ischaemic cells.
- Ivabradine: slows the sinus node via HCN channels without lowering blood pressure or contractility.
Stable coronary disease
Two goals run in parallel. Symptom control uses a beta blocker or calcium channel blocker first, with nitrates for attacks and other agents added if needed. Event prevention applies to every patient: lifestyle measures, a statin at high intensity, an antiplatelet (aspirin, or clopidogrel if aspirin is not tolerated), blood pressure and diabetes control, and an ACE inhibitor or ARB when there is diabetes, hypertension, kidney disease or reduced ejection fraction. Low-dose colchicine is a newer option for residual inflammation. In stable disease, opening arteries with a stent or bypass relieves angina, but a large trial found no clear advantage over optimal drugs alone for preventing events in most patients.
Acute coronary syndromes
Unstable angina, non-ST-elevation and ST-elevation myocardial infarction share one mechanism: an unstable plaque cracks, platelets stick and a thrombus forms. Treatment therefore centres on clotting.
- Aspirin at once, then a P2Y12 inhibitor (ticagrelor, prasugrel or clopidogrel) as dual antiplatelet therapy
- A parenteral anticoagulant such as heparin, enoxaparin, fondaparinux or bivalirudin
- Reopening the artery: primary angioplasty is preferred in ST-elevation infarction; a fibrinolytic such as tenecteplase or alteplase is given when a catheter laboratory cannot be reached quickly enough
- Nitrates for pain and congestion if blood pressure allows; oxygen only if saturation is low
- Before discharge: high-intensity statin, beta blocker, ACE inhibitor or ARB, and a mineralocorticoid antagonist if ejection fraction is low with heart failure or diabetes
Drug-eluting stents
Plain metal stents keep an artery open, but the injured wall often grows back over them (restenosis) through smooth-muscle proliferation. Drug-eluting stents carry a polymer coating that releases an antiproliferative drug into the vessel wall over weeks to months: sirolimus and its relatives (everolimus, zotarolimus), which block mTOR, or paclitaxel, which stabilises microtubules. Local release gives high concentrations where they are needed with almost no systemic exposure, and restenosis falls sharply. The trade-off is slower healing of the lining over the metal, so the stent can clot (stent thrombosis). For this reason dual antiplatelet therapy follows stenting, often for a year or longer depending on the stent and the bleeding risk. Stopping it early without the cardiologist's advice is a classic cause of stent thrombosis.
Test yourself
Think of the answer, then tap the question to see it.
Why does a fast heart rate worsen ischaemia in two ways?
It raises oxygen demand and shortens diastole, when most coronary flow occurs, so supply falls at the same time.
How do nitrates mainly relieve exertional angina?
They dilate veins, lowering preload and ventricular wall stress, which reduces oxygen demand; they also dilate large coronary arteries.
What drugs do drug-eluting stents release, and why?
Antiproliferative drugs such as sirolimus analogues or paclitaxel, to stop smooth-muscle regrowth inside the stent (restenosis).
Why is dual antiplatelet therapy needed after a drug-eluting stent?
The drug slows healing of the lining over the metal, so the exposed stent can form a clot; two antiplatelet drugs cover that period.
When is a fibrinolytic chosen in ST-elevation myocardial infarction?
When primary angioplasty cannot be done quickly enough, for example far from a hospital with a catheter laboratory.
Example drugs
- Glyceryl trinitrate
- Isosorbide mononitrate
- Metoprolol
- Diltiazem
- Verapamil
- Amlodipine
- Ranolazine
- Ivabradine
- Acetylsalicylic acid
- Clopidogrel
- Ticagrelor
- Prasugrel
- Heparin
- Enoxaparin
- Tenecteplase
- Alteplase
- Atorvastatin
- Sirolimus
- Everolimus
- Paclitaxel
Connections
Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.
Sources: Coronary Heart Disease - Treatment | NHLBI, NIH (National Heart, Lung, and Blood Institute, 2026); Heart Attack - Treatment | NHLBI, NIH (National Heart, Lung, and Blood Institute, 2026); Stents - What Are Stents? | NHLBI, NIH (National Heart, Lung, and Blood Institute, 2026).
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Representative model, for educational purposes only.