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Anatomy · Thorax

The Coronary Arteries: The Heart Feeds Itself Last

Five litres a minute pass through the heart, and the heart is not allowed a single drop of it. The blood standing inside its chambers is separated from the muscle that moves it by a wall too thick to feed through, so the heart must push its whole output out into the aorta and then buy a small share back through two arteries no wider than a drinking straw. Worse, it may only collect while it is resting: squeeze the muscle and you squeeze shut the very vessels inside it. Every coronary disease in medicine — angina, infarction, sudden death — is a variation on that one arrangement. This article is about the two arteries, what each of them owns, and the veins that carry the blood back.

14 min read🎯 Linked lesson: Coronary arteries and cardiac veins· Updated 2026-07-19
THE SCENE

A man of fifty-eight is shovelling snow off his drive on a cold morning. Halfway through, something settles on his chest — not a stab, he says later, but a weight, as though someone had put a heavy hand in the middle of his breastbone and leaned. It spreads up into his throat and jaw and down the inside of his left arm to the little finger. He is grey, sweating, faintly sick. In the ambulance a technician sticks ten electrodes on him and a paper strip prints out a heart's own account of what has happened: in four leads that look at the front of the heart, the tracing has lifted off the baseline. Somewhere in the anterior interventricular groove — a shallow furrow you could cover with a finger — a plaque has cracked and a clot has closed an artery about three millimetres wide. Downstream of that clot, muscle that has beaten roughly two billion times without pause is now dying at a rate of about a gram a minute. Every decision made in the next ninety minutes is really a decision about anatomy: which artery, which territory, how much heart is at the end of it.

Two mouths just above the valve

The first two branches of the aorta come off before the aorta has travelled a centimetre. The very beginning of the aorta is not a smooth tube: the wall bulges outwards behind each cusp of the aortic valve into three small pockets, the aortic sinuses — the sinuses of Valsalva. From the right sinus arises the right coronary artery; from the left sinus arises the left coronary artery; the third, posterior sinus gives nothing at all and is called the non-coronary sinus for that reason. Of all the branches the aorta will ever give, these two come first, before the head, before the limbs, before anything — and they are among the smallest, only about three to five millimetres across. The position of the two orifices, sitting just above the free edges of the aortic valve cusps, is not decoration. It is the whole mechanism.

During systole two things happen at once, and both of them shut the coronaries down. The opening cusps swing back against the aortic wall and lie across the coronary openings like flaps over letterboxes, and the contracting myocardium squeezes the vessels running through it — most severely in the subendocardium of the thick-walled left ventricle, where the muscle is deepest. Then the ventricle relaxes, the aortic valve snaps shut, and the column of blood in the elastic aorta recoils backwards against the closed cusps. The cusps fall away from the orifices, the muscle lets go of the vessels inside it, and the coronaries fill. The heart is perfused in diastole. That single fact explains an entire clinic: a very fast heart rate shortens diastole far more than systole, so tachycardia can starve the muscle at the exact moment it is working hardest, which is why exertion, fever, fear or an arrhythmia can provoke angina in someone whose arteries are merely narrowed rather than blocked; and why a leaking aortic valve or a very low diastolic pressure — from shock, or from over-treated hypertension — can starve a heart whose coronaries are perfectly normal.

THE ANALOGY

Imagine a baker who is forbidden by law to eat from his own oven. Everything he bakes must go out of the door to the market, and if he wants bread he must buy two loaves back through a hatch in the side wall — and the hatch only opens between customers, when he stops working. Serve customers faster and the hatch opens less often. That is the coronary circulation exactly: the heart's own supply is a small purchase made from its own output, and payment is only collected in the pauses. Now compare it with a skeletal muscle, which is squeezed rhythmically too but rests between efforts and can borrow oxygen from myoglobin and run up an oxygen debt. The heart has no such option — it never rests, it extracts about three-quarters of the oxygen in coronary blood at rest (almost every other tissue takes a quarter), and so it cannot meet extra demand by extracting more. It can only meet demand by receiving more flow. That is why coronary anatomy is destiny.

The left coronary artery: a short stem and two great branches

One or two centimetres of artery decide the fate of most of the working heart. The left coronary artery begins in the left aortic sinus, passes behind the pulmonary trunk, and after only one to two centimetres divides. That short segment is the left main stem, and it is the most feared piece of vasculature in the body: everything downstream of it is the anterior wall, the septum, the apex and the lateral wall of the left ventricle — which is to say, most of the pump. Occlude it acutely and the patient rarely survives to hospital; the nickname "the widow-maker" belongs here (and, by extension, to the proximal branch that follows it). In roughly a third of hearts the stem trifurcates rather than bifurcates, and the extra vessel between the two is the ramus intermedius, supplying the anterolateral wall.

The larger of its two branches is the anterior interventricular artery, known in every catheter laboratory in the world as the LAD — the left anterior descending. It runs down the anterior interventricular groove towards the apex, and in most hearts curls round the apex to end a short way up the posterior interventricular groove. It gives two families of branches: diagonal branches, which run out laterally across the front of the left ventricle, and septal perforating branches, which dive straight backwards into the interventricular septum and supply its anterior two-thirds — including, importantly, the right bundle branch and the anterior fascicle of the left bundle. Between them the LAD's branches feed the anterior wall of the left ventricle, the anterior septum, the apex and a strip of the anterior right ventricle. No other single artery owns so much muscle. The second branch, the circumflex artery, turns the other way: it runs leftwards into the left part of the coronary sulcus (the atrioventricular groove), curves round the left border of the heart and continues onto its back. Its named branches are the obtuse marginal arteries, running down over the rounded left border, and a left atrial branch; together they supply the left atrium and the lateral and posterior walls of the left ventricle.

The right coronary artery, and the question of dominance

The right coronary artery leaves the right aortic sinus, passes between the right auricle and the pulmonary trunk, and descends in the right part of the coronary sulcus, round the right border of the heart and onto its diaphragmatic surface. Its branches are few and consequential. Within the first centimetre or two it usually gives the sinuatrial nodal artery, which runs backwards to the upper right atrium; in about sixty per cent of people this artery comes from the right coronary and in the remaining forty per cent from the circumflex. At the sharp right border it gives the right marginal artery, running along the acute margin towards the apex and supplying the right ventricle. And where the coronary sulcus meets the posterior interventricular groove — a point called the crux of the heart — it gives the atrioventricular nodal artery, which supplies the AV node and the proximal bundle of His in the great majority of hearts. Between them these vessels supply the right atrium, most of the right ventricle, the inferior (diaphragmatic) wall of the left ventricle, the posterior third of the interventricular septum, and — the detail that matters most at the bedside — both nodes of the conducting system.

"Dominance" is not about size or importance. It has one strict definition. A heart is called right-dominant or left-dominant according to one thing only: which artery gives the posterior interventricular artery — the posterior descending artery, or PDA — that runs down the posterior interventricular groove to supply the inferior wall and the posterior third of the septum. In about eighty to eighty-five per cent of people the right coronary reaches the crux and gives the PDA, and the heart is right-dominant. In about eight to ten per cent the circumflex carries on past the crux and gives it, and the heart is left-dominant — in which case a single left coronary system supplies almost the entire ventricular mass, and an occlusion there is correspondingly catastrophic. In the remainder the two arteries share the territory and the heart is called co-dominant. Nothing about the term implies that the dominant artery is bigger or busier: in a right-dominant heart the left coronary still supplies far more muscle. Dominance is a piece of plumbing vocabulary, and its clinical value is that it tells you whose problem the inferior wall is.

💡 CLINICAL PEARL

The right coronary artery supplies little muscle of consequence and yet causes some of the most dramatic bedside events in cardiology — because it supplies the electrics. It feeds the SA node in about sixty per cent of hearts and the AV node in the great majority. So an inferior myocardial infarction, the classic right coronary occlusion, arrives not merely as chest pain but as a slow pulse: sinus bradycardia, first-, second- or third-degree AV block, sometimes a heart rate in the thirties in a patient who is nauseated and vomiting (vagal afferents run with the inferior wall too). The same event in the LAD territory kills far more muscle and yet leaves the rhythm alone at first. One artery owns the pump; the other owns the timing.

One artery, one territory, one set of ECG leads

Because each artery owns a defined block of muscle, and because the electrodes of an ECG look at the heart from defined directions, the map of the coronary tree can be read backwards off a paper strip. Occlusion of the LAD kills the anterior wall and the anterior septum, and the changes appear in the chest leads that face the front of the heart: V1 to V4 — an anteroseptal or anterior infarct, and if the LAD is occluded proximally the changes extend across V1 to V6 with I and aVL. Occlusion of the circumflex kills the lateral and posterior walls, and the changes appear in the leads that look at the left side: I, aVL, V5 and V6 — a lateral infarct, and the one most easily missed, because a purely posterior infarct shows itself only indirectly, as tall R waves and ST depression in V1 and V2, the mirror image of an injury on the far side. Occlusion of the right coronary kills the inferior wall, and the changes appear in the leads looking up from the diaphragm: II, III and aVF — an inferior infarct, with the bradycardia and block already described. Three arteries, three territories, three groups of leads: it is the single most useful piece of applied anatomy in emergency medicine.

An anterior view of the heart showing the coronary circulation: the left coronary artery arising from the left aortic sinus just above the aortic valve and dividing into the left anterior descending artery, which runs in the anterior interventricular groove towards the apex giving diagonal and septal perforating branches, and the circumflex artery, which runs in the left part of the coronary sulcus giving obtuse marginal branches; the right coronary artery arising from the right aortic sinus and running in the right coronary sulcus, giving the sinuatrial nodal branch, the right marginal branch, the atrioventricular nodal branch at the crux and, in the right-dominant majority, the posterior descending artery in the posterior interventricular groove; each artery's myocardial territory shaded — anterior and septal for the LAD, lateral and posterior for the circumflex, inferior and right ventricular for the right coronary — and labelled with the matching ECG leads of infarction, V1 to V4, I with aVL and V5 to V6, and II with III and aVF; and behind the heart the coronary sinus lying in the posterior coronary sulcus, receiving the great cardiac vein alongside the anterior descending artery, the middle cardiac vein alongside the posterior descending artery, the small cardiac vein and the oblique vein of the left atrium, and emptying into the right atrium.
The coronary circulation from the front. Read it as a map of ownership: the left main stem divides into the LAD in the anterior interventricular groove (anterior wall, anterior two-thirds of the septum, apex → leads V1–V4) and the circumflex in the left coronary sulcus (lateral and posterior left ventricle → I, aVL, V5–V6), while the right coronary runs in the right coronary sulcus giving the nodal branches and, in eighty to eighty-five per cent of hearts, the posterior descending artery (inferior wall, posterior third of the septum → II, III, aVF). The veins shadow the arteries and gather into the coronary sinus, which delivers most of the heart's used blood straight into the right atrium.

Functional end arteries: help that arrives too late

Anatomically the coronary arteries are not true end arteries: fine anastomoses do exist between the terminal twigs of the LAD and the PDA around the apex, between the circumflex and the right coronary at the back, and through small channels in the atrial walls. But these connections are, in an ordinary adult heart, far too narrow to carry any useful volume. That is what the phrase functional end artery means — a vessel with theoretical neighbours and no practical help. Close a coronary suddenly and the muscle beyond it infarcts, anastomoses or not. Close it slowly, however, and the story changes: a stenosis that tightens over months or years exposes the anastomotic channels to a persistent pressure gradient, and they widen, lengthen and remodel into a genuine collateral circulation. This is why an elderly patient with severe three-vessel disease may survive an occlusion that would kill a fit forty-year-old whose arteries were normal until the morning the plaque ruptured. Time, in the coronary circulation, is the only thing that buys a second route.

The way back: the coronary sinus

The heart's veins solve the same problem in reverse — and mostly through one short, wide channel. About sixty per cent of the venous blood of the heart is collected into the coronary sinus, a short wide vein about two to three centimetres long lying in the posterior part of the coronary sulcus, between the left atrium and the left ventricle. It opens into the right atrium between the orifice of the inferior vena cava and the tricuspid valve, its mouth partly guarded by a thin fold, the valve of the coronary sinus (the Thebesian valve). Four tributaries matter. The great cardiac vein begins at the apex and ascends the anterior interventricular groove beside the LAD, then turns left into the coronary sulcus to become the sinus itself. The middle cardiac vein ascends the posterior interventricular groove beside the posterior descending artery. The small cardiac vein accompanies the right marginal artery along the acute margin and runs back in the right coronary sulcus. And the oblique vein of the left atrium — the vein of Marshall — descends over the back of the left atrium to mark the point where the sinus begins; it is the remnant of the embryonic left superior vena cava. The remaining venous blood takes two shortcuts: the anterior cardiac veins, several small vessels that cross the front of the right ventricle and drain directly into the right atrium without joining the sinus at all, and the venae cordis minimae — the Thebesian veins — microscopic channels that open straight from the myocardium into the chambers, most of them into the right atrium and right ventricle. It is these last, tiny vessels that represent the only drop the heart ever takes from the blood inside it, and they are far too small to feed anything.

Pain in the arm, and two borrowed vessels

Ischaemic cardiac pain is felt almost anywhere except the heart. The visceral afferent fibres that carry it travel with the sympathetic nerves — through the cardiac plexus, up the cardiopulmonary and cardiac branches, into the sympathetic trunk and back into the spinal cord through the white rami of the upper thoracic segments, T1 to T4 or T5. The brain has no map for the heart, so it assigns the signal to the somatic dermatomes that enter at those same levels: the centre of the chest, the medial arm and forearm along the T1 and T2 dermatomes, and, by way of the cervical segments the cardiac nerves also reach, the neck and jaw. This is referred pain, and its distribution is a direct read-out of segmental innervation rather than of anything happening in the arm. The description is typical too: patients almost never say "sharp", they say pressure, weight, crushing, a band — because visceral pain is dull, poorly localised and midline. And in an inferior infarction, where vagal afferents are also stimulated, the presentation may be nausea, vomiting and epigastric pain, which is exactly why some heart attacks are mistaken for indigestion.

Opening an artery, and going round it

Coronary angiography threads a fine catheter from the radial artery at the wrist, or the femoral artery in the groin, retrogradely up the aorta to the aortic sinuses, engages each coronary ostium in turn and injects contrast — so the tree in the figure above is drawn, in real time, on a screen. A narrowed segment can then be crossed with a wire, dilated with a balloon and held open with a stent, which in an acute infarction is done as fast as the hospital can manage, alongside the drugs of acute coronary syndrome. When the disease is too diffuse or the left main stem is involved, the alternative is to bypass it. Coronary artery bypass grafting borrows vessels from elsewhere in the body: the internal thoracic (internal mammary) artery, which runs down the inside of the anterior chest wall a centimetre from the sternal edge, is divided low down and swung across to the LAD while its origin from the subclavian artery is left untouched; and lengths of the great saphenous vein are harvested from the leg, reversed so their valves do not obstruct flow, and sewn from the ascending aorta to the vessels beyond each blockage. The internal thoracic graft outlives them all — more than ninety per cent are still open at ten years, against roughly half of the vein grafts — because it is an artery being used as an artery: a wall built for pulsatile pressure, an endothelium that keeps making nitric oxide, a remarkable resistance to atherosclerosis, and only one anastomosis to fail rather than two.

Key points
  • The right and left coronary arteries arise from the right and left aortic sinuses (of Valsalva), just above the aortic valve cusps; the posterior sinus is the non-coronary sinus.
  • The coronaries fill in DIASTOLE: in systole the open cusps cover the orifices and the contracting myocardium compresses the intramural vessels, worst in the left ventricular subendocardium.
  • Tachycardia shortens diastole and can provoke angina; aortic regurgitation or a very low diastolic pressure starves even normal coronaries.
  • Left coronary → short left main stem → LAD (anterior interventricular groove; diagonal + septal perforating branches; anterior wall, anterior two-thirds of the septum, apex) + circumflex (left coronary sulcus; obtuse marginal branches; left atrium, lateral and posterior left ventricle).
  • Right coronary → right coronary sulcus; SA nodal branch (~60%), right marginal branch, AV nodal branch at the crux; right atrium, right ventricle, inferior left ventricle, posterior third of the septum.
  • Dominance is defined ONLY by which artery gives the posterior descending (posterior interventricular) artery: right in ~80–85%, left in ~8–10%, co-dominant in the rest.
Key points
  • Territory → ECG: LAD = anterior/anteroseptal (V1–V4); circumflex = lateral (I, aVL, V5–V6); right coronary = inferior (II, III, aVF).
  • Because the right coronary usually feeds both nodes, an inferior MI often brings sinus bradycardia and AV block — and, via vagal afferents, nausea and vomiting.
  • Coronaries are FUNCTIONAL end arteries: anastomoses exist but are too small to rescue a sudden occlusion; slowly progressive stenosis lets them enlarge into a collateral circulation over months.
  • The coronary sinus lies in the posterior coronary sulcus and drains into the right atrium between the IVC orifice and the tricuspid valve, guarded by the Thebesian valve.
  • Its tributaries: the great cardiac vein (with the LAD), the middle cardiac vein (with the PDA), the small cardiac vein (with the right marginal) and the oblique vein of the left atrium (of Marshall).
  • Not all venous blood uses it: the anterior cardiac veins drain the right ventricle directly into the right atrium, and the venae cordis minimae (Thebesian veins) open straight into the chambers.
⚠️ Common mistakes
  • Assuming the coronaries fill during systole like every other artery in the body. They fill in diastole — the reason a racing heart can starve itself and a short diastole is dangerous.
  • Thinking "dominant" means the artery supplying more muscle. It means only the artery that gives the posterior descending branch; in a right-dominant heart the LEFT coronary still supplies far more myocardium.
  • Saying the LAD supplies "the septum". It supplies the anterior two-thirds through its septal perforators; the posterior third belongs to the posterior descending artery — usually a right coronary branch.
🎓 Questions students ask
Why can't the heart simply absorb oxygen from the blood in its own chambers?
Because diffusion works over microns, not millimetres. The wall of the left ventricle is more than a centimetre thick, and oxygen leaving the cavity could nourish only the innermost few cell layers before the gradient ran out. Nature did try the shortcut: the venae cordis minimae, the Thebesian veins, open directly between the myocardium and the chambers, and a thin layer immediately under the endocardium does take some oxygen that way. But it is a trivial fraction of the requirement of an organ that consumes oxygen more avidly, gram for gram, than almost any other tissue in the body. Any muscle thicker than a sheet needs its own delivery system, which is precisely what a coronary artery is.
Why is the pain of a heart attack felt in the left arm and the jaw rather than in the chest alone?
Because the brain has no dedicated map for the heart. Cardiac pain fibres are visceral afferents that travel with the sympathetic nerves and enter the spinal cord at T1–T4/T5, the same segments that receive somatic sensation from the central chest and the inner arm and forearm; the cardiac nerves also reach up to cervical levels that serve the neck and jaw. The cord's second-order neurons receive both streams and cannot distinguish them, so the pain is referred to the body wall of those segments. It also explains the quality — pressure and weight rather than a sharp point — because visceral pain is inherently dull and poorly localised. And it explains why the same infarct in a diabetic with autonomic neuropathy may be silent altogether.
If the arteries are only three to four millimetres wide, why does a small plaque matter so much?
Two reasons, one physical and one anatomical. Physically, flow through a tube falls with the fourth power of the radius, so a plaque that halves the lumen cuts the possible flow to about a sixteenth — a vessel that is comfortable at rest and hopeless during exertion, which is stable angina. Anatomically, the coronaries are functional end arteries: nothing downstream can be rescued from a neighbouring vessel quickly enough to matter. And the dangerous plaque is often not the tightest one — a lipid-rich plaque narrowing the lumen by only forty per cent can rupture, expose thrombogenic core to the blood and occlude the artery in minutes. Degree of stenosis predicts symptoms; plaque stability predicts infarction.
Test yourself

A patient arrives with crushing central chest pain and ST elevation in leads II, III and aVF. His pulse is 42 and the monitor shows second-degree atrioventricular block. Which artery is occluded, and which anatomical fact best explains the bradycardia?

🫁 In one breath
  • The heart cannot use the blood inside its chambers: the right and left coronary arteries arise from the right and left aortic sinuses just above the valve cusps, and they fill in diastole, because systole both covers their orifices and squeezes the intramural vessels shut.
  • The left main stem divides into the LAD (anterior interventricular groove; diagonals and septal perforators; anterior wall, anterior two-thirds of the septum and apex) and the circumflex (left coronary sulcus; obtuse marginals; left atrium and lateral/posterior left ventricle).
  • The right coronary runs in the right coronary sulcus giving the SA nodal (~60%), right marginal and AV nodal branches, and in 80–85% of hearts the posterior descending artery — the branch that defines dominance — supplying the right chambers, the inferior left ventricle and the posterior third of the septum.
  • Territory maps onto the ECG (LAD V1–V4; circumflex I, aVL, V5–V6; right coronary II, III, aVF, with bradycardia and block from the nodal branches); the coronaries are functional end arteries whose collaterals only develop with slow disease; and the venous blood returns through the coronary sinus — great, middle and small cardiac veins and the oblique vein of the left atrium — plus the anterior cardiac veins and the tiny venae cordis minimae.
📚 Sources
  • Drake RL, Vogl AW, Mitchell AWM. Gray's Anatomy for Students — Thorax: the heart, coronary arteries and cardiac veins.
  • Moore KL, Dalley AF, Agur AMR. Clinically Oriented Anatomy — Coronary circulation, arterial dominance and referred cardiac pain.
  • Netter FH. Atlas of Human Anatomy — Heart: coronary arteries and cardiac veins, anterior and posterior views.
  • Last RJ. Last's Anatomy: Regional and Applied — The heart and its blood supply.
  • Snell RS. Clinical Anatomy by Regions — Coronary artery disease, myocardial infarction and coronary bypass grafts.
  • TeachMeAnatomy — The Heart: Vasculature; The Coronary Sinus.

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