18.3 — Heart Attack

Heart muscle begins to die around 20 to 30 minutes after its blood supply is cut, and the damage spreads outward over the following hours (Chapter 1.6).

"Time is muscle" is the phrase, and it is literal. Every 30 minutes of delay in opening the artery increases one-year mortality by around 7.5 percent.

Which makes recognition — by the person having it, or by whoever is with them — the single largest determinant of outcome.

What happens

A coronary plaque ruptures, a clot forms, and the artery occludes (Chapter 18.1).

And the extent of damage depends on three things: which artery, how completely it is blocked, and how long it stays blocked.

Only the third is modifiable.

The muscle downstream dies from the inside out — the subendocardium first, because it is compressed hardest during systole and is furthest from the arteries on the surface (Chapter 7.7).

Which gives the two categories:

STEMI — ST-elevation myocardial infarction. Complete occlusion, full-thickness damage. The artery must be opened immediately.

NSTEMI — partial occlusion or complete occlusion with collateral supply. Damage confined to the inner layer. Treated urgently but not in the same minutes.

Recognising it

The classic presentation:

Central chest pain — heavy, crushing, tight, or like a band. People frequently describe it with a clenched fist rather than a pointing finger.

Radiating to the left arm, both arms, the jaw, the neck or the back.

Lasting more than 15 to 20 minutes and not relieved by rest.

With sweating, nausea, breathlessness, and a sense of impending doom — which is a genuine and frequently reported symptom rather than a literary flourish.

And the atypical presentations, which are the ones that get missed:

Women more often present without chest pain, with breathlessness, fatigue, nausea, or back and jaw pain. Women are diagnosed later and treated less aggressively on average, and their outcomes are correspondingly worse — a documented and correctable disparity.

People with diabetes may have no pain at all, because autonomic neuropathy blunts the sensation (Chapter 11.9). Silent heart attacks are found on later ECGs in people who never knew.

Older people frequently present with confusion, collapse, or simply feeling unwell.

And indigestion is the commonest misattribution. New severe indigestion with sweating, in someone over 40, gets an ECG (Chapter 9.7).

What to do

And this is the part worth memorising.

Call an ambulance immediately. Not a car, not a taxi, not a GP appointment.

Two reasons. The ambulance carries a defibrillator, and around a third of deaths occur in the first hour, usually from ventricular fibrillation. And the ambulance can record an ECG and transmit it, so the receiving hospital can be ready and the patient can bypass the emergency department entirely.

Chew 300 mg of aspirin while waiting, unless allergic. Chewing rather than swallowing whole, because absorption is faster.

Sit down and stay calm and still.

Unlock the door.

And if the person becomes unresponsive and is not breathing normally: start CPR (Chapter 23.2).

What not to do: do not drive yourself, and do not wait to see if it passes. The commonest cause of delay is the patient, not the system, and the average delay from symptom onset to calling for help is measured in hours.

In hospital

An ECG within 10 minutes — because it identifies STEMI, which changes everything (Chapter 7.3).

The territory is read from the leads, which identifies the artery before any imaging.

Troponin — released from damaged heart muscle. High-sensitivity assays detect it within 1 to 3 hours, and it is interpreted as a rising or falling pattern rather than a single value, because it rises in many conditions other than heart attack (Chapter 16.5).

Then:

For STEMI: open the artery.

Primary percutaneous coronary intervention — a catheter, a balloon, a stent (Chapter 7.7). The target is under 120 minutes from first medical contact, and under 90 where the patient presents directly to a capable centre.

Thrombolysis — clot-busting drugs — where PCI cannot be delivered in time. Less effective than PCI and far better than nothing, and the difference matters most in rural and low-resource settings.

And a critical safety point: aortic dissection must be excluded before thrombolysis (Chapter 7.5), because giving it in a dissection is catastrophic.

For NSTEMI: risk stratification, medication, and angiography within 24 to 72 hours depending on risk.

Drug treatment in both: dual antiplatelet therapy — aspirin plus a second agent — anticoagulation, a beta-blocker, an ACE inhibitor and a high-intensity statin.

The complications

Arrhythmia — the commonest cause of early death, and ventricular fibrillation in the first hours is why the ambulance matters (Chapter 7.3).

Heart failure — from the muscle lost (Chapter 18.4).

Cardiogenic shock — the pump failing, with a mortality around 40 to 50 percent.

Mechanical complications, days later: rupture of a papillary muscle causing sudden severe mitral regurgitation (Chapter 7.2); rupture of the ventricular septum; and rupture of the free wall, which is usually immediately fatal.

These have become much less common with prompt reperfusion, which is one of the quieter benefits of modern treatment.

Pericarditis — early, or as a delayed immune phenomenon weeks later.

Afterwards

And this section matters as much as the acute treatment, because it is where the long-term outcome is decided.

Cardiac rehabilitation — a supervised programme of exercise, education and risk factor management.

And it works. Around a 20 to 25 percent reduction in cardiovascular mortality, comparable to some drugs, and it is substantially under-attended — uptake is frequently under 50 percent.

Secondary prevention medication, and the components are consistent:

Aspirin, indefinitely.A second antiplatelet, usually for 12 months.A high-intensity statin, regardless of the starting cholesterol.An ACE inhibitor or ARB.A beta-blocker.

Adherence is the problem. A substantial proportion of patients have stopped one or more within a year, and stopping antiplatelets early after a stent carries a specific risk of stent thrombosis, which is frequently fatal.

Lifestyle — stopping smoking is the single largest intervention, and stopping after a heart attack roughly halves the risk of a further event.

Return to normal life: most people return to work, driving and sexual activity within weeks. Sexual activity is safe for anyone who can climb two flights of stairs without symptoms, and it is a question people are frequently too embarrassed to ask and clinicians too embarrassed to raise.

Driving rules vary by jurisdiction and typically involve a short period off driving for private licences and longer for vocational ones.

Depression after a heart attack affects around 20 percent, is associated with worse outcomes, and is treatable — and it is routinely missed.

What has improved

Substantially, and it is worth stating.

In-hospital mortality from STEMI has fallen from around 20 to 30 percent in the 1960s to around 5 to 7 percent today.

The changes responsible: coronary care units and defibrillation; aspirin; thrombolysis, then primary PCI; statins; and systems of care that get people to the right hospital quickly.

And age-standardised cardiovascular mortality has fallen by more than half in most high-income countries since the 1970s — roughly half from prevention and half from treatment.

Which means the largest gains came from smoking reduction, blood pressure control and cholesterol lowering rather than from anything done in the acute phase.

What the next page fixes

Chapter 18.4 covers what happens when enough muscle has been lost, or the heart has been damaged in other ways — heart failure, which is common, progressive, and has better treatment than its name suggests.