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7.7 — The Coronary Circulation
The heart pumps 7,500 litres of blood a day and cannot use any of it. Blood inside the chambers is separated from the muscle by the endocardium, and the wall is far too thick for anything to diffuse across. The heart needs its own dedicated supply, and it takes it from the very first branches of the aorta, immediately above the aortic valve.
Coronary artery disease is the leading cause of death worldwide. Everything about why it kills follows from three anatomical facts on this page.
The arteries
Two arteries leave the aorta, from small pouches just above the aortic valve cusps.
The left main coronary artery is short — 1 to 2 centimetres — and divides into two:
Left anterior descending (LAD) — runs down the front of the heart in the groove between the ventricles. Supplies the front of the left ventricle, the front two thirds of the septum, and the apex. It supplies the largest share of the left ventricle, and it is why it is known informally as "the widow-maker": occlusion of the proximal LAD damages so much muscle at once that it is frequently fatal before hospital.
Circumflex — curves around the left side to the back. Supplies the side and back walls of the left ventricle.
The right coronary artery (RCA) runs around the right side. Supplies the right atrium, the right ventricle, and usually the bottom wall of the left ventricle.
Critically, it also supplies the SA node in about 60 percent of people and the AV node in about 85 to 90 percent.
That single fact explains a clinical pattern. An inferior heart attack — from the right coronary artery — commonly causes bradycardia and heart block, because the nodes lose their supply. An anterior attack from the LAD does not typically do this. So the rhythm disturbance tells you which artery, and it is one of the reasons an ECG localisation is acted on immediately.
"Dominance" refers to which artery supplies the back of the heart: right-dominant in about 70 percent, left-dominant in about 10 percent, and co-dominant in the rest.
Coronary blood flow is about 250 ml/min at rest, roughly 5 percent of cardiac output, for an organ that is under 0.5 percent of body weight. In exercise it rises four to five fold.
The three facts that make the heart vulnerable
Fact 1: the left ventricle is perfused only during diastole.
This is the most important idea on the page.
When the left ventricle contracts, its wall squeezes so hard that it compresses the coronary arteries running through it. Intramuscular pressure during systole approaches or exceeds the pressure in those vessels, so flow to the left ventricular muscle essentially stops during systole and occurs almost entirely during diastole.
Three consequences follow immediately.
A fast heart rate reduces coronary supply. Diastole shortens far more than systole when rate rises (Chapter 7.4), so the faster the heart beats, the less time it has to feed itself — precisely when its demand is highest. This is the central reason exercise provokes angina in someone with a narrowed artery, and why beta-blockers, which slow the heart, are effective anti-anginal drugs: they simultaneously cut demand and increase supply.
Diastolic blood pressure matters for the heart's own supply. Coronary perfusion pressure is essentially aortic diastolic pressure minus the ventricular pressure. This is why very low diastolic pressure is dangerous in someone with coronary disease, and why blood pressure is not simply "lower is better" in that group.
And the right ventricle is different. It generates much lower pressure, so it is perfused throughout the cycle — which is one reason isolated right ventricular ischaemia is less common.
Fact 2: the subendocardium is the most vulnerable layer.
The innermost layer of the ventricular wall, nearest the chamber, is compressed hardest during systole and is furthest from the arteries running on the outer surface.
So it is the first tissue to become ischaemic and the last to be rescued. This is why the earliest ECG change in ischaemia is ST depression, reflecting subendocardial ischaemia, and why an incomplete blockage produces a subendocardial infarct while a complete one produces a full-thickness infarct with ST elevation. Chapter 18.3.
Fact 3: the coronary arteries are functional end arteries.
There are small connections — collaterals — between the territories, but in most people they are not sufficient to save muscle if a major artery blocks suddenly.
However, collaterals grow when they are needed slowly. A gradually narrowing artery over months or years stimulates collateral development, and by the time it occludes completely there may be enough alternative supply to prevent an infarct.
This produces a genuinely counter-intuitive clinical fact: a person with severe long-standing coronary disease may survive a total occlusion that would kill someone with a previously normal artery, because they have had time to build a bypass. A sudden occlusion in a mildly diseased artery is more dangerous than a sudden occlusion in a severely diseased one.
And this is one reason exercise protects the heart — repeated demand promotes collateral growth.
How the heart adjusts its own supply
The heart extracts an unusually high fraction of the oxygen delivered to it. Most tissues extract about 25 percent; the heart extracts 60 to 75 percent at rest.
That has a hard consequence: the heart cannot meet increased demand by extracting more. There is very little left to take. The only way to increase oxygen delivery to the heart is to increase blood flow, which is why coronary flow must rise four to five fold in exercise, and why any limitation of flow shows up immediately as symptoms.
Local control is metabolic and dominant. Adenosine, released when ATP is broken down faster than it is made, is a powerful coronary vasodilator. So the harder the heart works, the more adenosine it produces, and the more its own arteries dilate.
Adenosine is used clinically because of this. It is given during cardiac stress testing to dilate the coronary arteries maximally, revealing regions supplied by narrowed vessels that cannot increase flow — those areas show reduced uptake on imaging. It is also used intravenously to terminate certain fast rhythms, because it briefly blocks the AV node; the effect lasts seconds and patients report an alarming but very short-lived sensation of chest tightness and impending doom, which is why they are warned beforehand.
Angina
Angina is chest pain from myocardial ischaemia — demand exceeding supply — without cell death.
Stable angina. A fixed narrowing, usually a plaque reducing the lumen by more than about 70 percent. At rest, flow is adequate. On exertion, demand rises, flow cannot rise enough, and pain results. It is predictable: it comes on at a reproducible level of effort, and it goes away within minutes of stopping.
The typical description matters because it drives the assessment: central, heavy or crushing, sometimes radiating to the jaw, neck or left arm, brought on by exertion or emotion, relieved by rest or by glyceryl trinitrate.
Atypical presentations are common and dangerous, and they cluster in specific groups. Women, people with diabetes, and the elderly frequently present without classical chest pain — with breathlessness, fatigue, nausea, or simply feeling unwell. In diabetes, autonomic neuropathy can blunt the pain sensation entirely, producing silent ischaemia, and silent heart attacks are found on later ECGs in people who never knew they had one.
This under-recognition is a genuine source of harm. Women having heart attacks are diagnosed later and treated less aggressively than men on average, and outcomes are correspondingly worse.
Unstable angina. Pain at rest, or of new onset, or increasing in frequency and severity. The mechanism is different: a plaque has ruptured and a partially occluding clot has formed (Chapter 18.1). This is an acute coronary syndrome and requires emergency assessment, not an outpatient appointment.
The distinction between stable and unstable is the difference between a scheduled clinic and an ambulance, and it rests entirely on whether the pattern is predictable and effort-related or new and occurring at rest.
Prinzmetal's (variant) angina — coronary spasm rather than fixed narrowing. Pain at rest, often at night, in people who may have normal arteries. Treated with calcium channel blockers and nitrates, and beta-blockers can make it worse by leaving unopposed constricting activity.
Treatment, and how each drug maps onto the physiology
Glyceryl trinitrate (GTN) — releases nitric oxide, raising cGMP and dilating vessels (Chapter 1.8). Its main benefit in angina is not coronary dilation but venous dilation, which reduces preload and therefore the work the heart has to do. Given under the tongue for speed and to bypass the liver's first-pass metabolism (Chapter 7.5).
And the interaction with sildenafil is absolute, for the reason given in Chapter 1.8: both act on the same pathway, and together they can drop blood pressure catastrophically.
Beta-blockers — reduce heart rate and contractility, cutting demand and lengthening diastole. They both reduce demand and increase supply, which is why they are first-line.
Calcium channel blockers — dilate coronary and systemic arteries; some also slow the heart.
Aspirin and statins — do nothing for the symptom and a great deal for the outcome, by preventing plaque rupture and clot formation (Chapters 18.1, 22.7).
Revascularisation when medical treatment is insufficient:
Percutaneous coronary intervention (PCI) — a catheter is passed from an artery in the wrist or groin, a balloon dilates the narrowing, and a stent holds it open. Modern stents release a drug that prevents the artery re-narrowing, and patients take dual antiplatelet therapy afterwards to prevent the stent clotting.
Coronary artery bypass grafting (CABG) — vessels taken from elsewhere are used to carry blood past the blockages. The internal mammary artery from inside the chest wall is the preferred graft, with over 90 percent still open at ten years, against around 50 to 60 percent for a leg vein graft. The reason is that an artery is built to withstand arterial pressure and a vein is not — vein grafts gradually thicken and develop their own atherosclerosis.
Bypass generally outperforms stenting in diabetes, in left main disease and in three-vessel disease, which is why the choice is made by a team rather than by whoever the patient sees first.
What the next page fixes
Around three litres of fluid leave the capillaries every day and are not reabsorbed (Chapter 7.5). Something must return them, and the same system is the highway along which immune cells travel and along which cancer spreads. Chapter 7.8 covers the lymphatic system.