Angina & Nitrates: Easing the Starving Heart
A tiny tablet placed under the tongue can stop a crushing chest pain in ninety seconds — the same nitroglycerin once used to make dynamite. Angina is a heart starved of oxygen, and every drug that treats it works on one simple sum: the balance between how much oxygen the heart DEMANDS and how much it's SUPPLIED. Tip that balance back and the pain melts away.
A man climbing stairs feels a heavy, squeezing pressure spread across his chest — it eases when he stops to rest. This is stable angina: his coronary arteries, narrowed by plaque, can supply enough oxygen at rest but not when the exertion makes his heart demand more. He slips a nitroglycerin tablet under his tongue, and within a minute the pressure lifts. That little tablet, and the daily drugs that prevent the attacks, all obey one rule — restore the balance between the heart's oxygen supply and its demand.
Supply versus demand
Angina is an oxygen supply–demand mismatch. The heart muscle needs a constant oxygen supply from the coronary arteries. When narrowed arteries can't deliver enough for the heart's workload, the muscle becomes ischaemic and hurts — that's angina. So there are only two ways to fix it: reduce the heart's oxygen DEMAND, or increase its SUPPLY. Demand rises with heart rate, contractility, and the tension in the heart wall (which depends on preload and afterload). Every antianginal drug lowers one of these or widens the coronary arteries to boost supply — the same demand/supply logic that runs the whole section.
Nitrates: the classic reliever
Nitrates — sublingual glyceryl trinitrate (GTN) for an acute attack, and longer-acting isosorbide mononitrate for prevention — are converted in the body to nitric oxide, which relaxes vascular smooth muscle. Their main effect is to dilate the VEINS, which reduces the blood returning to the heart (preload) and so lowers the wall tension and oxygen demand; they also dilate the coronary arteries to improve supply. Sublingual GTN is placed under the tongue precisely to bypass the liver's heavy first-pass metabolism (the very drug from the routes-of-administration article). Their side effects come from vasodilation — throbbing headache, flushing, and low blood pressure.
Two nitrate rules save lives. First, nitrate tolerance: taken around the clock, nitrates stop working within a day, so long-acting nitrates need a daily 'nitrate-free interval' (usually overnight) to keep their effect. Second, and critical: never give a nitrate to someone who has taken a PDE5 inhibitor (sildenafil/Viagra and friends) — both raise cGMP, and together they can cause catastrophic, even fatal, hypotension. Always ask about erectile-dysfunction drugs before giving nitrates for chest pain.
The prevention drugs
To PREVENT attacks (not just abort them), we lower the heart's oxygen demand day to day. Beta blockers are first-line: by slowing the heart rate and reducing contractility, they cut demand and let a narrowed artery keep up — and they also improve survival after a heart attack. Calcium channel blockers help too, either by dilating vessels (the dihydropyridines) or slowing the heart (verapamil, diltiazem), and they're especially useful in vasospastic (Prinzmetal) angina, where the artery goes into spasm. Newer options like ranolazine (which reduces wall tension without slowing the heart) and ivabradine (which slows the heart rate alone) help when the standard drugs aren't enough. And underneath it all, the disease itself is treated with an antiplatelet (aspirin) and a statin — the subjects of later articles.
- Angina = oxygen supply < demand in a narrowed coronary artery.
- Treat by lowering demand (HR, contractility, wall tension) or raising supply (dilate coronaries).
- Nitrates → nitric oxide → mainly venodilation (↓preload); sublingual GTN aborts an acute attack.
- Nitrate tolerance needs a nitrate-free interval; never combine nitrates with PDE5 inhibitors.
- Prevention: beta blockers (first-line), calcium channel blockers, ranolazine, ivabradine.
- Giving a nitrate to a patient who took sildenafil. Risk of severe, even fatal, hypotension.
- Using long-acting nitrates continuously. Tolerance develops — allow a nitrate-free interval.
- Forgetting to treat the underlying disease with aspirin and a statin, not just the pain.
- Ignoring vasospastic angina — calcium channel blockers, not beta blockers, are preferred there.
Nitrates relieve angina mainly by:
- Angina = oxygen supply < demand; treat by lowering demand or raising supply.
- Nitrates (→ nitric oxide) venodilate to cut preload; sublingual GTN aborts an attack.
- Beware nitrate tolerance and the deadly nitrate + PDE5-inhibitor combination.
- Prevention: beta blockers first-line, plus calcium channel blockers, ranolazine, ivabradine.
- Katzung BG. Basic & Clinical Pharmacology — Drugs Used in Angina Pectoris (nitrates & antianginals).
- Brunton LL, et al. Goodman & Gilman's The Pharmacological Basis of Therapeutics — Treatment of myocardial ischemia.
- Rang HP, Dale MM, et al. Rang & Dale's Pharmacology — Antianginal drugs.
- ACC/AHA & ESC guidelines — Chronic coronary syndromes & stable angina therapy.
- Whalen K. Lippincott Illustrated Reviews: Pharmacology — Antianginal drugs.
