Coronary heart disease is usually caused by atherosclerosis affecting the coronary arteries. Atherosclerosis is a progressive process in which atheroma, commonly described as fatty plaque, accumulates within the arterial wall. Over time, these plaques can enlarge and change the structure of the artery, reducing the available space for blood flow. The coronary arteries normally deliver oxygen-rich blood to the heart muscle, particularly when myocardial oxygen requirements rise. If atherosclerotic narrowing becomes significant, blood flow may become insufficient during exertion and produce angina. If a plaque becomes unstable and ruptures, a blood clot can form and suddenly obstruct the artery, potentially producing a heart attack.
Atherosclerosis is a complex biological process rather than simply the physical accumulation of dietary fat inside a pipe. Damage or dysfunction of the arterial endothelium can promote inflammation and altered permeability, allowing lipoproteins and other substances to enter the arterial wall. Low-density lipoprotein cholesterol is particularly important in the development of atherosclerotic cardiovascular disease. Retained lipoproteins can undergo modification and contribute to inflammatory responses, with immune cells and smooth-muscle cells participating in plaque development. Over years, plaques can develop fibrous components and lipid-rich regions. Some plaques are relatively stable and mainly cause fixed narrowing, while others have characteristics that make them more susceptible to rupture or erosion and acute thrombosis.
Several established risk factors increase the likelihood of coronary heart disease. These include high blood pressure, high cholesterol, diabetes, smoking, excess weight or obesity, physical inactivity, increasing age and a family history of coronary disease. These factors do not operate independently in every person, and having one does not mean that coronary heart disease is inevitable. Conversely, the absence of obvious lifestyle risk factors does not completely eliminate risk because age, inherited predisposition and other biological factors also contribute. The British Heart Foundation identifies smoking, high blood pressure, high cholesterol, diabetes, excess weight, physical inactivity, family history and increasing age among important risk factors.
Smoking contributes to coronary risk through several mechanisms, including endothelial injury, adverse effects on blood vessels, promotion of thrombosis and changes in lipid and inflammatory processes. High blood pressure exposes arterial walls to increased mechanical stress and is associated with accelerated vascular damage. Persistently high concentrations of atherogenic cholesterol can increase the amount of cholesterol retained within arterial walls. Diabetes is associated with metabolic and vascular abnormalities that increase cardiovascular risk. These factors can interact, so the combined cardiovascular risk of several abnormalities may be considerably greater than the significance of any one factor considered in isolation. Effective management therefore involves overall cardiovascular risk assessment rather than focusing on a single number or behaviour.
Age and inherited susceptibility also have important roles. Atherosclerosis develops over time, so the probability of clinically significant coronary disease generally increases with age. A family history of premature coronary disease can indicate inherited susceptibility involving lipid metabolism, blood pressure, thrombosis or other biological pathways. Familial hypercholesterolaemia is one particularly important inherited condition because markedly elevated cholesterol from an early age can accelerate atherosclerosis. Sex and hormonal factors also influence population-level risk, with coronary disease tending to occur at younger ages in men and risk increasing in women during and after menopause. These are population-level patterns rather than individual predictions.
Lifestyle influences are relevant but should not be interpreted as the sole cause. A diet high in saturated fats and overall excess energy intake can contribute to adverse cholesterol profiles and excess weight, while physical inactivity is associated with cardiovascular risk. Excessive alcohol consumption can also contribute to cardiovascular risk through effects including blood pressure and other metabolic pathways. Conversely, regular physical activity, a balanced diet, smoking cessation and appropriate weight management can reduce risk. These measures do not remove established plaque immediately, and a person with diagnosed coronary heart disease may still require medicines or procedures even after making substantial lifestyle changes.
Coronary heart disease can sometimes occur without obvious symptoms because atherosclerotic disease may progress silently. Some people are first diagnosed after investigations performed because of risk factors, while others may first present with angina or a heart attack. This is important because symptoms do not provide a complete measure of the amount of coronary atherosclerosis present. Conversely, chest pain does not automatically prove that coronary heart disease is present, because gastrointestinal, musculoskeletal, pulmonary and other conditions can also produce chest discomfort. Clinical assessment and appropriate testing are needed to distinguish these possibilities.
The most important causal distinction is between the chronic development of coronary atherosclerosis and the acute event that can occur when a plaque becomes unstable. Coronary heart disease describes the underlying coronary arterial disease, while a heart attack generally occurs when a coronary artery becomes acutely obstructed, most often by a thrombus forming over disrupted atherosclerotic plaque. Less common causes of myocardial infarction include spontaneous coronary artery dissection, exposure to certain stimulant drugs and severe reductions in oxygen availability. Thus, atherosclerosis is the principal long-term mechanism underlying most coronary heart disease, but not every coronary event follows precisely the same pathway.
