Heart Disease (Coronary Artery Disease)

What is heart disease?

Heart disease is an umbrella term for conditions affecting the heart and blood vessels. The most common form is coronary artery disease (CAD): where fatty deposits (plaques) build up inside the coronary arteries over decades, narrowing them and reducing blood flow to the heart muscle. This process, called atherosclerosis, begins as early as the teenage years and progresses silently for decades before causing symptoms. CAD can cause stable angina (chest pain on exertion), unstable angina (at rest), or complete artery blockage causing a heart attack (myocardial infarction).

Blood tests for cardiac risk assessment

Heart attack warning signs

Cardiac risk factors you can control

• High LDL cholesterol: target <100 mg/dL (<70 if very high risk)
• High blood pressure: target <130/80 mmHg
• Type 2 diabetes: HbA1c <7%
• Smoking: doubles heart attack risk; quitting reduces risk within 1 year
• Obesity, especially abdominal fat
• Physical inactivity: around 150 minutes of moderate exercise per week is associated with a substantially lower rate of cardiac events
• Chronic stress and poor sleep

Prevention: medications that protect the heart

Questions to ask your doctor

• What is my 10-year cardiovascular risk (ASCVD score)?
• Should I start a statin?
• Do I need a stress test or calcium scoring CT scan?
• What is my Lp(a) level?
• Should I take aspirin?

References

The clinical information on this page is drawn from peer-reviewed sources indexed by the US National Library of Medicine. Links go to the source so you can read it yourself.

1. Coronary Artery Disease. In: StatPearls. Treasure Island (FL): StatPearls Publishing. NCBI Bookshelf NBK564304

References

Sources cited on this page. PubMed links open the original abstract.

1. Roth GA, Johnson C, Abajobir A, et al. Global, regional, and national burden of cardiovascular diseases for 10 causes, 1990 to 2015. J Am Coll Cardiol. 2017;70(1):1–25. PMID 28527533 · doi:10.1016/j.jacc.2017.04.052

Coronary heart disease – the atherosclerotic process

Coronary heart disease (CHD), also called coronary artery disease (CAD) or ischaemic heart disease (IHD), is caused by atherosclerosis – the progressive buildup of lipid-rich plaques within the walls of coronary arteries. The process begins in early adulthood as endothelial dysfunction (damage to the inner lining of arteries) allows LDL cholesterol to enter and become trapped in the arterial wall. Macrophages engulf oxidised LDL and become foam cells, forming the fatty streak. Over decades, a fibrous cap develops over this lipid core, creating an atherosclerotic plaque.

Most heart attacks occur not from gradual narrowing to complete blockage, but from plaque rupture – when an inflamed, vulnerable plaque's fibrous cap tears. The exposed lipid core triggers immediate platelet aggregation and thrombus (clot) formation, occluding the artery. The portion of heart muscle supplied by that artery undergoes ischaemia and, if flow is not restored within minutes to hours, irreversible infarction (death).

Key blood tests in CHD diagnosis and monitoring

• High-sensitivity troponin: Released by dying heart muscle cells within 1–3 hours of MI. The serial rise and fall pattern (measured at 0, 1, and 3 hours) distinguishes type 1 MI (plaque rupture) from chronic cardiac injury. hs-cTnT or hs-cTnI above the 99th centile with a rising pattern (change greater than laboratory's delta threshold) confirms MI.
• Lipid panel: LDL is the primary modifiable risk factor for atherosclerosis. After MI, all patients should be on high-intensity statins (atorvastatin 80 mg) targeting LDL below 1.8 mmol/L (European guideline) or 50% LDL reduction (NICE guideline). Lipid panels are checked 4–8 weeks after starting or changing statin therapy.
• HbA1c and fasting glucose: Diabetes doubles the risk of cardiovascular events. The combination of insulin resistance, dyslipidaemia, and hypertension in metabolic syndrome is the most common cardiovascular risk cluster in UK adults. New-onset glucose intolerance is commonly found after MI – approximately 30–40% of MI patients have previously undiagnosed diabetes or pre-diabetes.
• NT-proBNP: Post-MI left ventricular dysfunction causes natriuretic peptide release. An elevated NT-proBNP after MI predicts adverse remodelling and heart failure development – high values trigger early echocardiography and optimisation of heart failure therapy (beta-blocker, ACE inhibitor, MRA).
• CRP and fibrinogen: High-sensitivity CRP (hsCRP) above 2 mg/L indicates vascular inflammation independent of standard lipid levels. The JUPITER trial showed statins reduced events in people with normal LDL but elevated hsCRP – informing the expanded use of statins in "inflammatory" atherosclerosis. The ACC/AHA guidelines incorporate hsCRP into cardiovascular risk decision-making when the 10-year risk is borderline (7.5–20%).