Acute Coronary Syndrome

Acute coronary syndrome (ACS) is the sudden phase of coronary artery disease: a cholesterol plaque inside a heart artery ruptures, platelets and fibrin build a clot on it, and blood flow to the heart muscle collapses. The result is chest pain at rest, and it spans three diagnoses: unstable angina, non-ST-elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI).

Dr. Vikas Thakran, Consultant, Interventional Cardiology, BLK-Max Super Speciality Hospital, New Delhi, India, at the time of the masterclass (he has since moved to Manipal Hospital, Dwarka), presented the subject to international doctors as a sequence of decisions rather than a catalogue of facts. How does the blockage form? What does the patient feel? What does the first ECG show? And, given that answer, how fast must the artery be opened? His reasoning for the last question was a single comparison: a patient with a heart attack who goes untreated has a 30 to 50% chance of dying, and prompt treatment, whether by a procedure or by thrombolysis, brings that chance down to around 5%.

This guide covers the anatomy, the mechanism, the symptoms and the risk factors of acute coronary syndrome, and summarises the diagnostic and treatment pathway. Two companion articles go deeper: one on reading the ECG to separate STEMI, NSTEMI and unstable angina and to localise the blocked artery, and one on STEMI and NSTEMI treatment protocols, angioplasty and recovery.

Coronary artery anatomy: the three arteries that supply the heart

Three main coronary arteries supply the heart muscle. They are the first branches of the aorta, so the heart, which pumps blood to every organ, is itself the first tissue to receive freshly pumped blood. Dr. Thakran framed it simply: the heart is the first organ that gets the blood, and that supply is what keeps it pumping.

The three arteries are:

• Left anterior descending (LAD) artery, arising from the left main trunk, which supplies the front (anterior) wall of the left ventricle.
• Left circumflex (LCx) artery, the second branch of the left main trunk, which wraps around to the side and back of the heart. Dr. Thakran identified it as the artery of the posterior wall; it also supplies much of the lateral wall.
• Right coronary artery (RCA), on the right side, which supplies the inferior wall, the underside of the heart that rests on the diaphragm.

This map matters clinically because each artery leaves its own signature on the ECG. A blocked LAD produces an anterior wall infarction, a blocked RCA an inferior one, and a blocked LCx a posterior or lateral one. The ECG patterns that reveal which artery is involved are covered in detail in the companion article on ECG localisation.

How atherosclerosis narrows a coronary artery

Atherosclerosis narrows a coronary artery slowly, as fatty deposits in the artery wall mature into plaque, and it begins long before any symptom. In Dr. Thakran's description, a normal artery carries no blockage, but with age its wall accumulates fatty streaks, which mature into plaques covered by a fibrous cap. The process is driven by the deposition of low-density lipoprotein ("bad") cholesterol and accelerated by hypertension, diabetes, smoking and a sedentary lifestyle.

While the plaque only narrows the artery, the heart muscle receives enough blood at rest but not when demand rises. The patient feels pain on walking, exertion or stress, and the pain settles with rest. This is chronic stable angina: a partial obstruction, a predictable trigger and a predictable relief.

Stable angina vs acute coronary syndrome: what plaque rupture changes

Stable angina turns into acute coronary syndrome suddenly, not gradually: the change happens when the fibrous cap of a plaque breaks and a clot forms on it. Dr. Thakran walked through the sequence step by step:

1. The fibrous cap ruptures and exposes the subendothelium, the tissue beneath the artery's inner lining.
2. Platelets are recruited to the exposed surface.
3. The activated platelets release adenosine diphosphate (ADP), which activates further platelets.
4. Together with fibrin, the platelets form a clot that blocks the artery, partly or completely.

The clinical consequence is pain at rest. A vessel that was sub-occluded, producing pain only on exertion, becomes totally or near-totally occluded, and the chronic stable picture turns unstable. That shift, from pain on effort to pain without effort, defines acute coronary syndrome.

The mechanism also explains the treatment. Because platelet activation drives the clot, antiplatelet drugs are given to every patient with ACS. Aspirin blocks platelet thromboxane production, and the P2Y12 inhibitors (clopidogrel, prasugrel and ticagrelor) block the very ADP receptor that Dr. Thakran's mechanism describes.

Symptoms of acute coronary syndrome

Chest pain is the defining symptom, but Dr. Thakran listed a wider set that referring doctors should recognise:

• Chest pain, typically at rest or with minimal exertion.
• Severe anxiety.
• Palpitations.
• Breathlessness, which develops if attention is delayed and the heart muscle weakens as it is damaged.
• Syncope (sudden loss of consciousness), when irregular heart rhythms cause the patient to collapse.

Breathlessness and syncope signal that the damage, or a rhythm disturbance, has progressed. The life-threatening rhythms behind syncope, ventricular tachycardia and ventricular fibrillation, are treated with external defibrillation, as the treatment article explains.

Risk factors: what causes acute coronary syndrome

Asked directly what causes acute coronary syndrome, Dr. Thakran named six major risk factors:

• Smoking, which he named first, with particular reference to young patients.
• Diabetes.
• Hypertension.
• A family history of cardiac disease.
• A sedentary lifestyle.
• Lack of sleep.

He added two environmental triggers: air pollution, which he described as a factor in his own region, and extremes of temperature, which can precipitate an acute event in a patient whose arteries are already diseased.

The distinction between a cause and a precipitant is useful in practice. Cholesterol, diabetes, hypertension, smoking and inactivity build the plaque over years. Pollution and extremes of heat or cold act on the day, as precipitants of an event in an artery that is already diseased. Prevention therefore has two horizons: long-term control of the metabolic risk factors, and avoidance of acute triggers in patients known to have coronary disease.

How acute coronary syndrome is diagnosed: the ECG decides

Dr. Thakran reduced the diagnostic pathway to one rule: look at the ECG first. Once ACS is suspected, the ECG takes one of two paths.

• ST elevation: the artery is 100% blocked and the full thickness of the heart wall is involved. This is STEMI, and the patient is treated at once. No further investigation is needed; a single ECG is enough.
• No ST elevation (a normal ECG or ST depression): the next step is the cardiac markers, the blood tests for heart muscle damage, of which troponin is the standard. If the markers are positive, the diagnosis is NSTEMI. If they are negative, it is unstable angina.

ST depression, in his explanation, reflects partial involvement of the heart wall, while ST elevation reflects involvement of the whole wall. The distinction is what separates a patient who goes straight to the catheterisation laboratory from one who is stabilised first. The ECG article sets out this flow chart in full, together with the lead patterns that localise the blocked artery and a warning pattern, Wellens syndrome, that Dr. Thakran said precedes a large anterior heart attack in up to 80% of patients within two weeks.

Acute coronary syndrome treatment: open the artery or stabilise first

Treatment for acute coronary syndrome follows directly from the ECG: STEMI needs the blocked artery opened at once, while NSTEMI and unstable angina are stabilised first.

The pathway in summary:

For STEMI, Dr. Thakran's instruction was not to wait: relieve pain with intravenous opioids and sublingual nitrate, give oxygen (guidelines reserve it for patients whose oxygen saturation is below 90%) and open the artery. Percutaneous coronary intervention (PCI), the placement of a stent through a catheter, is the gold standard, and he stressed the importance of treating within the first two hours. Where PCI is not possible, fibrinolytic therapy (thrombolysis, a clot-dissolving drug given intravenously) is the alternative. Emergency bypass surgery is needed only rarely.

For NSTEMI and unstable angina, the artery is not presumed to be completely occluded, and the strategy is the opposite of haste. Patients receive antiplatelets and are stabilised. Those with continuing pain or clinical deterioration go for angiography (an X-ray of the coronary arteries using contrast dye) early, within the first two days; lower-risk patients continue antiplatelets for two days before angiography. In his experience, these patients do well with this measured approach, and taking them directly to the laboratory is not as beneficial. Current ESC guidance stratifies by risk: immediate angiography for very high-risk patients, and angiography within 24 hours considered for those with confirmed NSTEMI or other high-risk features.

The full protocols, including the use of nitrates in inferior wall infarction, how PCI is performed, when bypass is preferred, complication rates and nutrition after the event, are in the STEMI and NSTEMI treatment article.

Heart attack survival: why speed of treatment matters

An untreated heart attack carries a 30 to 50% chance of death, according to Dr. Thakran; with treatment by procedure or thrombolysis, that chance falls to around 5%. He closed the session on this comparison when explaining what motivates interventional cardiology, and it doubles as the clinical case for speed. In his view, few areas of medicine save so many lives in so short a time.

For referring doctors, the practical lessons are three. Recognise the symptoms, including anxiety, breathlessness and syncope, not only chest pain. Record an ECG immediately, because ST elevation needs no further test before treatment. And where a catheterisation laboratory is not within reach, do not let its absence delay reperfusion: thrombolysis exists precisely for that situation.

Specialist care for complex coronary disease

At BLK-Max, where Dr. Thakran practised at the time of the session, cardiologists and cardiothoracic surgeons worked as a heart team: each patient's angiogram was discussed jointly to decide between stenting and bypass. The centre treated complex coronary disease, including left main and bifurcation angioplasty, with rotablation (a high-speed rotating burr) and intracoronary lithotripsy (sonic pressure waves delivered by a balloon) for calcified arteries, and support from the Impella (a small heart pump) and the intra-aortic balloon pump for patients with very low blood pressure. These capabilities, the hospital's heart transplant and left ventricular assist device programme, and the process for transferring critically ill international patients are described in the treatment article. Indicative costs are on the angioplasty with stent cost page.

The questions doctors asked during the session, on evacuation of a critical patient, how PCI is performed, transplant volumes, nitrates and nutrition, defibrillation and complications, are answered in the session's Live Discussion. Dr. Thakran's background is on his doctor profile. For a protocol-led view of the same emergency, including drug loading and cardiac rehabilitation, see Dr. Rohit Goel's guide to ischaemic heart disease management; for long-term coronary artery disease and the choice between stent and bypass in stable patients, see Dr. Biswarup Purkayastha's guide to coronary artery disease. More heart care content is on the cardiology specialty page.