Coronary artery disease: from narrowing to heart attack

From hidden narrowing of the vessels to myocardial infarction and modern treatment

Coronary artery disease is the leading cause of illness and death worldwide. Behind the medical name lies disease of the coronary arteries — the vessels that supply the heart muscle itself with blood and oxygen. According to the guidelines of the European Society of Cardiology (ESC), it is a dynamic and progressive process that calls for timely diagnosis and comprehensive treatment.

1. What is coronary artery disease?

Medical definition:

Coronary artery disease is a condition in which there is a mismatch between the oxygen needs of the heart muscle (myocardium) and the ability of the coronary arteries to deliver it.

In plain terms:

The heart is a muscular pump that works around the clock. To contract properly it needs a constant supply of oxygen and nutrients, delivered by the main coronary arteries.

When atherosclerotic plaques — deposits of cholesterol, calcium and inflammatory cells — build up in those arteries, the vessel narrows. During physical or emotional exertion the heart beats faster and needs more blood, but the narrowed artery cannot supply it. The heart muscle begins to “starve” of oxygen (ischaemia), and the body signals this as pain or tightness in the chest.

2. Causes and risk factors

Atherosclerosis in the coronary vessels develops over years of accumulated risk factors that damage the inner lining of the vessel wall (the endothelium).

Risk factors that cannot be changed:

• Age: risk rises considerably with age — over 45 in men, over 55 in women.
• Sex: men are affected more often at a younger age. In women the risk rises and matches that of men after the menopause, with the loss of the protective effect of oestrogen.
• Family history: close relatives — father or brother under 55, mother or sister under 65 — with early heart attack or coronary disease.

Harmful habits, and why they lead to complications:

• Smoking: nicotine and the toxic components of cigarette smoke directly damage the vascular endothelium, provoke spasm of the vessels, raise blood pressure and increase the tendency of blood to clot.
• A sedentary lifestyle and poor diet: these lead to excess weight, high cholesterol and a slower metabolism.
• Excessive alcohol and chronic stress: these disturb vascular tone and hormonal balance and cause chronic constriction of the vessels.

Why harmful habits and untreated coexisting conditions lead to complications

The inside of a healthy artery is smooth. Harmful habits and uncontrolled coexisting conditions make that surface rough and vulnerable. Cholesterol is deposited easily on the damaged areas, chronic inflammation develops and an atherosclerotic plaque forms. If the plaque ruptures, its interior is no longer covered by the layer of endothelial cells and comes into direct contact with the blood — as with any injury. Within seconds a thrombus (blood clot) forms on it and closes the vessel. This is the immediate mechanism of acute myocardial infarction, known in medicine as acute coronary syndrome.

The main coexisting conditions:

1. Untreated or poorly controlled diabetes

In diabetes, persistently high blood glucose is toxic to the vessel walls (diabetic angiopathy). Atherosclerosis in people with diabetes develops earlier, affects more vessels and runs a more severe course.

Very important: because of diabetic polyneuropathy — damage to the nerve endings — people with diabetes often do NOT feel the typical chest pain of ischaemia. A heart attack may be “silent”, showing itself only as sudden breathlessness, weakness or nausea.

2. Untreated high cholesterol (dyslipidaemia)

Excess LDL cholesterol — the “bad” cholesterol — passes directly beneath the endothelium of the arteries, where it is oxidised and forms the core of the atherosclerotic plaque. Without medical control, plaques grow and progressively narrow the vessel.

3. Untreated arterial hypertension

High blood pressure creates mechanical stress and micro-tears in the vessels, making it easier for cholesterol to enter. It also causes the heart muscle to thicken, which further increases its oxygen demand.

3. Chronic versus acute coronary artery disease — what is the difference?

Coronary artery disease presents in two main clinical forms:

• Chronic coronary syndromes (stable angina): here the atherosclerotic plaque is stable and narrows the vessel gradually. Symptoms — chest pain — appear predictably, only at a certain level of physical or emotional exertion, and settle with rest or after taking nitroglycerin.
• Acute coronary syndromes (acute myocardial infarction and unstable angina): these arise when a plaque ruptures or ulcerates suddenly, leading to clot formation. If the clot closes the artery completely, part of the heart muscle is left without blood supply and begins to die — this is an acute myocardial infarction. It is a life-threatening emergency.

4. Symptoms

Symptoms vary with the form of the disease:

• Typical chest pain (angina pectoris):
• Character: described as tightness, heaviness, pressure or burning behind the breastbone. Patients often indicate the pain by pressing a fist against the chest.
• Radiation: the pain may spread to the left arm, the shoulder, the neck, the lower jaw, the back or the upper abdomen.
• Duration: in the chronic form it lasts two to ten minutes and passes with rest. In a heart attack it lasts more than 20 minutes, is extremely intense and is not relieved by rest.
• Breathlessness: sudden shortness of breath on minimal exertion or at rest — often in people with diabetes and in older patients.
• Fatigue and weakness: an unusual fall in physical capacity.
• Palpitations or extra beats (arrhythmia): the result of ischaemia affecting the conduction system of the heart.
• Autonomic symptoms (VERY CHARACTERISTIC): profuse cold sweating, sudden pallor, nausea, vomiting, dizziness and a strong sense of fear.

5. Methods of diagnosis

The diagnostic process follows clearly defined steps:

A. Assessment by a cardiologist — essential

The cardiologist takes a detailed history, assessing the character of the pain and the risk factors, and performs a physical examination.

B. Electrocardiogram (ECG)

An essential first test. In acute infarction it shows specific changes — ST segment elevation or depression, and T wave changes.

Note: a normal resting ECG does not rule out chronic coronary artery disease.

C. Echocardiography (ultrasound of the heart)

Assesses the anatomy, the valves and the contractile function of the heart. It helps detect areas of reduced contraction (hypokinesia) corresponding to a narrowed or blocked artery.

D. Stress testing (functional assessment)

Used to detect ischaemia while the heart is working under load:

• Exercise ECG (treadmill or bicycle ergometer): follows the changes in the ECG during controlled physical exertion.
• Stress echocardiography / stress MRI: assessment of the pumping function of the heart by ultrasound or magnetic resonance during exertion, either physical or induced with dobutamine or adenosine.

E. Non-invasive imaging

• CT coronary angiography: an extremely valuable non-invasive method with high diagnostic yield. It allows 3D visualisation of the vessels and plaques without inserting catheters.

F. Invasive methods

• Invasive coronary angiography: the “gold standard”. Through a fine catheter passed via an artery in the arm or leg, contrast is injected directly into the coronary arteries under X-ray guidance. The method shows the exact degree and location of the narrowings and allows immediate treatment, such as stent placement.

G. Laboratory tests and biomarkers

• Specific markers of myocardial damage:
• High-sensitivity troponin (hs-cTnT / hs-cTnI): the principal and most sensitive biomarker under ESC guidance for rapidly diagnosing or excluding acute myocardial infarction.
• CK-MB: an additional enzyme marker of myocardial necrosis.
• Total CK.
• LDH.
• Tests for coexisting conditions (essential routine panel):
• Lipid profile: total cholesterol, LDL-C, HDL-C, triglycerides and lipoprotein(a).
• Glucose status: fasting blood glucose and glycated haemoglobin (HbA1c), to detect undiagnosed diabetes.
• Kidney function: creatinine, eGFR and uric acid.
• Thyroid hormones (TSH) and full blood count, to exclude anaemia, which can provoke ischaemia.

6. Treatment

Treatment may be medical, interventional or surgical.

A decision made together (Heart Team and informed consent):

Under ESC recommendations, the choice of treatment strategy in stable patients must go through thorough discussion between the cardiologist, the cardiac surgeon and the patient — what is known as informed choice. The only exception is an emergency, life-threatening situation — for example massive infarction or cardiogenic shock — where the patient is unconscious and an immediate life-saving procedure is carried out.

A. Medical treatment

Used in all patients, to slow the disease and relieve symptoms:

• Antiplatelet drugs (aspirin, clopidogrel, ticagrelor): prevent clot formation.
• Statins (for example atorvastatin, rosuvastatin): lower LDL cholesterol aggressively and stabilise atherosclerotic plaques.
• Beta blockers: slow the pulse and reduce the oxygen demand of the heart.
• ACE inhibitors / ARBs: control blood pressure and protect the heart wall.
• Anti-anginal treatment (nitrates, trimetazidine, ranolazine): relieves chest pain.

B. Interventional treatment (percutaneous coronary intervention — PCI / stenting)

Under local anaesthetic, a catheter is advanced to the narrowed segment and a balloon widens it, after which a drug-eluting stent (DES) is placed to keep the vessel open. In other cases the functional significance of the narrowing is assessed first, to judge whether a stent is needed at all or whether balloon dilatation alone will suffice.

C. Surgical treatment (coronary artery bypass grafting)

When coronary atherosclerosis is too widespread across all the coronary vessels, stenting is not the best or most durable solution for chronic symptoms. Cardiac surgery is then used to create a bypass — a vein taken from the leg, or an artery from the chest or arm, used to build a detour around the blocked segment.

Selecting patients for bypass surgery (ESC indications):

The choice between stenting and bypass surgery rests on established criteria. Only some are listed here.

NOTE: they may be present in combination or on their own.

• SYNTAX score: an angiographic scoring system for the severity and complexity of the narrowings. With a high SYNTAX score (above 23–32), bypass surgery is clearly superior to stenting.
• Left main disease: narrowing of the main stem, which supplies over 70% of the heart.
• Three-vessel disease affecting all three main vessels, particularly in patients with coexisting diabetes.
• Low ejection fraction — below 40%: weakened pumping function of the left ventricle.
• Previous myocardial infarction with an extensive area of damage.
• Age and coexisting conditions: surgical risk (EuroSCORE II) and general condition are taken into account.

Why bypass surgery saves lives

A bypass provides a completely new source of blood supply to the heart muscle, despite the narrowings. One particularly important point: bypass surgery gives patients the chance to survive a future heart attack in their own arteries that would have been fatal without the grafts. Because the new grafts feed the heart beyond the infarcted area, they protect the myocardium from complete necrosis.

In summary for the patient: Coronary artery disease is serious but entirely controllable. Early detection through routine review with a cardiologist, and modern treatment to ESC standards, allow patients to keep a high quality of life for years to come.