Coronary Heart Disease and Angina: Reduced Blood Flow to Heart Muscle

Coronary heart disease usually develops when atherosclerosis narrows the arteries supplying the heart muscle. Stable angina causes a predictable pattern during physical activity, while new, worsening or resting symptoms may represent an acute coronary syndrome. Clinical assessment and coronary imaging are needed because symptoms and a resting ECG cannot confirm or exclude the diagnosis alone.

What coronary heart disease is Coronary heart disease, usually shortened to CHD, affects the arteries supplying blood to the heart muscle. These vessels are called the coronary arteries. CHD is usually caused by atherosclerosis, which develops gradually within an artery wall. The terms coronary artery disease and ischaemic heart disease are also commonly used. What the coronary arteries do The heart muscle needs a continuous supply of oxygen and nutrients. The right and left coronary arteries arise near the beginning of the aorta. They divide into branches that supply different regions of the heart muscle. Blood flow must increase when the heart works harder during exercise, stress or illness. A narrowed artery may provide enough flow at rest but fail to meet increased demand. Atherosclerosis Atherosclerosis is a long term disease affecting the inner walls of arteries. Cholesterol containing particles enter and remain within a damaged or dysfunctional artery wall. Immune cells, smooth muscle cells and fibrous tissue then contribute to an atherosclerotic plaque. The plaque can enlarge gradually and narrow the channel carrying blood. Atherosclerosis is more complex than fat simply sticking inside a passive pipe. Atherosclerotic plaque A plaque contains lipid, inflammatory cells, connective tissue and sometimes calcium. A fibrous cap separates its inner contents from circulating blood. Some plaques become heavily calcified and stable. Others remain vulnerable to surface disruption despite causing only moderate narrowing beforehand. The plaque's biology therefore matters alongside the percentage narrowing seen on a scan. How a narrowing causes angina A fixed narrowing increases resistance to blood flow through a coronary artery. At rest, blood supply may still meet the heart muscle's oxygen requirement. During physical activity, the heart beats faster and contracts more strongly. If coronary flow cannot increase enough, part of the muscle becomes temporarily ischaemic. Ischaemia means that oxygen supply is insufficient for the tissue's current demand. Angina is a symptom Angina is discomfort caused by temporary myocardial ischaemia. It is commonly felt as pressure, tightness, heaviness or squeezing rather than a sharp pinpoint pain. Discomfort may occur in the chest, arms, shoulders, neck, jaw, back or upper abdomen. Breathlessness can accompany the discomfort or occasionally be the main recognised symptom. Angina describes a clinical syndrome rather than one test result. Angina does not always mean obstructive atherosclerosis Most stable angina discussed in this lesson results from atherosclerotic coronary disease. However, ischaemic symptoms can also arise from coronary spasm or small vessel dysfunction. These conditions are called vasospastic angina and microvascular angina. Anaemia, severe aortic stenosis and hypertrophic cardiomyopathy can also create angina like symptoms. Persistent typical symptoms require further assessment when major coronary arteries appear unobstructed. Stable angina Stable angina follows a broadly predictable pattern over time. Symptoms are usually triggered by physical exertion, emotional stress, cold weather or a heavy meal. They generally settle within several minutes after stopping and resting. Prescribed short acting glyceryl trinitrate, called GTN, can also relieve an episode. The amount of activity provoking symptoms tends to remain reasonably consistent. Predictable does not mean harmless Stable angina reflects underlying cardiovascular disease and an increased risk of heart attack and stroke. Treatment aims both to relieve symptoms and reduce future cardiovascular events. A person should not repeatedly push through angina during activity. Newly suspected stable angina requires medical assessment even when every episode settles with rest. Unstable angina Unstable angina is part of the acute coronary syndrome spectrum. Symptoms may be new, occur at rest or arise with much less exertion than before. Episodes may become more frequent, severe or prolonged. The pattern often reflects sudden plaque disruption and clot formation reducing coronary blood flow. Unstable angina requires urgent hospital assessment because it can precede a heart attack. Acute coronary syndrome Acute coronary syndrome, usually shortened to ACS, includes unstable angina and myocardial infarction. A myocardial infarction is commonly called a heart attack. In myocardial infarction, prolonged ischaemia causes heart muscle injury and cell death. Unstable angina produces acute ischaemic symptoms without the biomarker evidence required to diagnose myocardial infarction. The distinction is made in hospital using the history, ECG and serial troponin tests. Plaque rupture and clot formation A vulnerable plaque can rupture or erode at its surface. Platelets recognise the damaged area and begin forming a clot. The clot may narrow the artery suddenly or block it completely. This process can turn previously stable coronary disease into an acute coronary syndrome. A heart attack is therefore not always caused by the artery with the greatest earlier narrowing. Typical anginal chest pain NICE describes three features used to assess whether stable symptoms are typical of angina. The first is constricting discomfort in the chest, neck, shoulders, jaw or arms. The second is precipitation by physical exertion. The third is relief by rest or GTN within about five minutes. All three features form typical angina within this clinical framework. Atypical anginal chest pain Two of the three anginal features are described as atypical angina. Atypical does not mean imaginary, mild or unimportant. It means that the presentation does not contain the complete classic three feature pattern. Both typical and atypical angina warrant diagnostic testing when stable angina cannot be excluded. One or no feature is described as non anginal unless other history or risk factors raise concern. The limits of symptom labels Typicality helps structure professional assessment but does not diagnose coronary disease. Reflux, oesophageal spasm and musculoskeletal pain can resemble angina. Coronary disease can also produce symptoms outside the classic pattern. Symptoms that occur only for seconds or change with touching one small chest area are less suggestive. Clinical judgement remains necessary, particularly when cardiovascular risk is high. Presentation in women Women and men can both experience central pressure and the full classic angina pattern. The diagnostic definitions should not be applied differently according to sex. Women may also report breathlessness, nausea, sweating, fatigue, jaw discomfort or back discomfort. Women are more likely to have microvascular or non obstructive coronary mechanisms in some clinical populations. Symptoms must not be dismissed as anxiety or indigestion without appropriate assessment. Presentation in diabetes People with diabetes can develop the same typical angina symptoms as anyone else. Diabetic nerve damage can sometimes reduce or alter pain perception. Ischaemia may then present through breathlessness, sweating, nausea, unusual fatigue or reduced exercise tolerance. Some episodes may be clinically silent and discovered through investigations or a later complication. Absence of chest pain does not make unexplained exertional symptoms safe to ignore. Older adults and atypical presentations Older adults may report breathlessness, weakness, nausea, dizziness or collapse rather than prominent chest pain. Frailty, cognitive impairment and communication difficulties can make symptom descriptions less clear. Multiple conditions may coexist, including heart failure, anaemia and lung disease. The urgency depends on the complete clinical pattern rather than age alone. Exertional breathlessness Breathlessness during activity has many possible causes. These include lung disease, anaemia, heart failure, poor fitness, obesity and anxiety. It may also represent an anginal equivalent when myocardial ischaemia limits cardiac function during physical activity. The term anginal equivalent means an ischaemic symptom occurring without recognised chest discomfort. Testing is required rather than assuming that breathlessness identifies coronary disease. Chest pain has many causes Chest discomfort can arise from the heart, lungs, oesophagus, chest wall, nerves or skin. Life threatening alternatives include pulmonary embolism, aortic dissection and pneumothorax. Common alternatives include reflux, muscle strain and costochondritis. The clinician first decides whether the pattern could represent an acute emergency. Only then is a stable outpatient pathway appropriate. What makes stable angina more likely Cardiovascular risk factors increase the probability that exertional symptoms result from coronary atherosclerosis. Relevant factors include smoking, diabetes, high blood pressure and abnormal blood lipids. Age, health problems in the family, chronic kidney disease and previous cardiovascular disease also matter. Risk factors support interpretation but cannot diagnose the cause of one episode. A person without recognised risk factors can still develop coronary disease. Smoking Smoking damages blood vessel function, promotes inflammation and increases clot formation. It accelerates atherosclerosis and raises the risk of heart attack, stroke and peripheral arterial disease. Stopping smoking reduces cardiovascular risk even after coronary disease is established. Evidence based support can include behavioural help and stop smoking medicines. Vaping should not be presented as harmless, although switching completely from smoking may reduce exposure to tobacco toxins. High blood pressure Persistently high blood pressure places mechanical stress on artery walls. It accelerates atherosclerosis and increases the heart muscle's workload. Hypertension also raises the risk of stroke, heart failure and kidney disease. Lifestyle measures and blood pressure medicines reduce these risks. One isolated high reading does not establish persistent hypertension. Diabetes High glucose levels contribute to blood vessel injury and accelerated atherosclerosis. Diabetes is also associated with inflammation, altered lipids and increased clotting tendency. Good cardiovascular care includes glucose management, blood pressure control and lipid lowering treatment. The safest treatment plan depends on diabetes type, kidney function and other conditions. Blood lipids Low density lipoprotein cholesterol, called LDL cholesterol, contributes to plaque formation. Statins reduce the liver's cholesterol production and lower circulating LDL cholesterol. They also reduce future cardiovascular events in people with established coronary disease. Additional lipid lowering medicines may be needed when targets are not achieved or statins are unsuitable. Family history and inherited cholesterol A close relative with premature coronary disease can indicate increased inherited risk. Familial hypercholesterolaemia causes very high LDL cholesterol from an early age. Untreated disease can produce coronary events much earlier than usual. Family history should be considered alongside measured cholesterol and other risk factors. Lifestyle and coronary risk Regular physical activity, a balanced diet and maintaining a healthy weight support cardiovascular health. Reducing excess salt helps blood pressure control. Replacing saturated fats with unsaturated fats can improve lipid patterns. Alcohol does not need to be started for heart protection. Lifestyle treatment supports medicines rather than replacing indicated secondary prevention. Exercise with stable angina Regular activity is usually beneficial once the diagnosis and treatment plan are established. Exercise improves fitness, blood pressure, glucose regulation and psychological wellbeing. The person may need to pace activity and use prescribed GTN before predictable exertion. New or escalating symptoms during exercise require review rather than simply reducing all activity indefinitely. Cardiac rehabilitation can support safe progression after a coronary event or procedure. Clinical assessment of stable chest pain The clinician asks where discomfort occurs, what it feels like and how long it lasts. They identify triggers, relieving factors and associated breathlessness, sweating, nausea or dizziness. They review previous coronary disease, diabetes, blood pressure, smoking and health problems in the family. The examination looks for cardiovascular risk factors and alternative causes. No ordinary physical examination finding confirms stable angina. Resting electrocardiogram A resting 12 lead electrocardiogram, called an ECG, records the heart's electrical activity. It can show previous infarction, conduction abnormalities or ST segment and T wave changes. It may also identify an arrhythmia contributing to symptoms. A normal resting ECG does not exclude stable angina. The ECG does not directly measure coronary blood flow or the heart's pumping strength. ECG during acute symptoms An ECG should be obtained quickly when acute coronary syndrome is suspected. It may show ST segment elevation, depression, T wave changes or another acute pattern. A normal initial ECG does not safely exclude an acute coronary syndrome. Serial ECGs and troponin testing may be required in hospital. Emergency transfer should not be delayed merely to obtain an ECG outside hospital. Troponin Troponin is a protein released into blood when heart muscle cells are injured. High sensitivity troponin testing is used when an acute coronary syndrome is suspected. It is not routinely used to diagnose ordinary stable angina without an acute presentation. A raised troponin has several possible causes and does not automatically prove a coronary heart attack. The result requires interpretation with symptoms, ECG changes and timing. Blood tests Blood tests can identify conditions that worsen angina or cardiovascular risk. A full blood count can identify anaemia. Kidney function affects investigation choices and medicine safety. Glucose or HbA1c testing assesses diabetes, while a lipid profile guides prevention treatment. Blood tests cannot show directly whether a coronary artery is narrowed. CT coronary angiography CT coronary angiography, usually shortened to CTCA, is the current NICE first line anatomical test for suspected stable angina. It uses a CT scanner, intravenous contrast and ECG timing to image the coronary arteries. The scan can show plaque, calcification and narrowing within major coronary vessels. It is offered when clinical assessment indicates typical or atypical angina. It is also used for selected non anginal symptoms with concerning resting ECG changes. Preparing for CTCA The heart rate may need to be slowed so that the coronary arteries remain clearer during imaging. A beta blocker is commonly used when clinically suitable. GTN may be given to widen coronary arteries during the scan. The team checks kidney function, contrast details of allergy problems and pregnancy possibility where relevant. CTCA uses ionising radiation, although modern protocols aim to minimise exposure. What CTCA can show CTCA is good at excluding significant obstructive coronary disease in many people. It can reveal both calcified and non calcified atherosclerotic plaque. The report describes the location and estimated severity of narrowing. An anatomical narrowing does not always show whether blood flow becomes inadequate during physical activity. Further functional assessment may therefore be necessary. Limitations of CTCA Heavy coronary calcification can make the artery channel difficult to assess accurately. A fast or irregular heart rhythm can reduce image quality. Movement, obesity and previous coronary stents may also complicate interpretation. Contrast can rarely cause an allergic reaction and can affect vulnerable kidneys. A non diagnostic scan requires another investigation rather than an assumed result. Functional testing Functional testing asks whether a coronary abnormality causes reversible myocardial ischaemia. Options include stress echocardiography, myocardial perfusion imaging and stress cardiac MRI. The heart is stressed through exercise or a medicine, depending on the test. Functional imaging is used when CTCA shows disease of uncertain significance or is non diagnostic. It can also help assess symptoms in someone with previously confirmed coronary disease. Exercise ECG limitations An exercise treadmill ECG was historically used widely for suspected angina. NICE does not recommend exercise ECG to diagnose or exclude stable angina in people without known coronary disease. Electrical changes during exercise are not accurate enough for this purpose in many people. Exercise ECG can still have selected roles when coronary disease is already established. Fractional flow assessment from CT Computer analysis can sometimes estimate pressure loss across a narrowing seen on CTCA. This is called CT derived fractional flow reserve or FFRCT. It may help identify which anatomical lesions are likely to restrict blood flow. Availability and suitability vary across services. It does not replace clinical interpretation of the entire case. Invasive coronary angiography Invasive coronary angiography passes a catheter through an artery towards the heart. Contrast is injected directly into the coronary arteries while X ray images are recorded. It provides detailed information about the vessel channel and is used when intervention is being considered. Within the stable diagnostic pathway, it may follow inconclusive non invasive assessment. It is also used earlier when clinical risk or known anatomy makes this appropriate. Risks of invasive angiography Common effects include bruising or bleeding at the wrist or groin access site. Less common complications include artery injury, contrast related kidney injury, allergic reaction, stroke or heart attack. The specialist discusses risks in relation to the expected diagnostic or treatment benefit. The procedure does not automatically mean that a stent will be inserted. Diagnosing stable angina Diagnosis combines the clinical pattern with evidence of significant coronary disease or reversible ischaemia. A scan showing mild plaque does not automatically explain every chest symptom. A severe anatomical narrowing can occasionally be clinically silent. When large vessel obstruction is excluded, clinicians consider non cardiac causes and other cardiac mechanisms. Symptom relief and risk reduction are different goals Stable angina treatment has two linked purposes. Antianginal medicines reduce episodes and improve activity or quality of life. Secondary prevention treatment reduces future heart attack, stroke and cardiovascular death. A medicine can achieve one purpose without directly achieving the other. For example, GTN relieves symptoms but does not remove atherosclerotic plaque. Short acting GTN Short acting GTN is used to treat and sometimes prevent predictable angina episodes. It relaxes blood vessels and reduces the heart's workload. The medicine is usually taken under the tongue as a spray or tablet. Headache, flushing and light headedness can occur. A person should sit down when using it if dizziness is possible. Using GTN during an established angina episode A person with diagnosed angina should follow their individual written instructions. NICE advises repeating the prescribed short acting nitrate after five minutes if pain remains. An emergency ambulance should be called if pain remains five minutes after the second dose. A new or different severe episode should not be repeatedly treated at home while delaying emergency help. GTN response cannot establish whether pain is cardiac. Antianginal medicines A beta blocker or calcium channel blocker is usually offered first for stable angina. The choice depends on heart rate, blood pressure, other illnesses, contraindications and preference. If one is unsuitable or ineffective, the other can be substituted or combined appropriately. Long acting nitrates, ranolazine, ivabradine or nicorandil have roles in selected people. Treatment is reviewed and adjusted according to symptoms and adverse effects. Beta blockers Beta blockers reduce the effects of adrenaline on the heart. They slow heart rate and reduce the force of contraction. This lowers myocardial oxygen demand during physical activity. They may be unsuitable with marked bradycardia, certain conduction problems or some forms of severe asthma. Beta blockers should not usually be stopped suddenly without clinical advice. Calcium channel blockers Calcium channel blockers affect blood vessels, heart rate or both, depending on the medicine. Dihydropyridine medicines mainly widen arteries and lower blood pressure. Verapamil and diltiazem also slow the heart rate. Combinations require care because excessive slowing or low blood pressure can occur. Ankle swelling, headache and constipation are possible medicine specific effects. Statins Statins are central secondary prevention medicines for atherosclerotic coronary disease. They lower LDL cholesterol and reduce future cardiovascular events. Treatment continues even when angina symptoms improve because its purpose is risk reduction. Liver tests and possible adverse effects are managed according to current lipid guidance. Stopping a statin without discussing alternatives can remove important cardiovascular protection. Antiplatelet treatment Platelets contribute to clot formation after atherosclerotic plaque disruption. Low dose aspirin may be considered for people with stable angina caused by atherosclerotic disease. Bleeding risk, allergy, anticoagulant treatment and other conditions affect this decision. Alternative antiplatelet treatment may be used when aspirin is unsuitable. Antiplatelets should not be started from an educational lesson without individual clinical assessment. Blood pressure and diabetes treatment Treating high blood pressure reduces cardiovascular and kidney risk. An ACE inhibitor may be considered in stable angina with diabetes and for other established indications. Diabetes treatment should address both glucose and cardiovascular protection. Some glucose lowering medicines have additional cardiovascular or kidney benefits in appropriate people. Treatment choices require consideration of kidney function, blood pressure and medicine interactions. Percutaneous coronary intervention Percutaneous coronary intervention is usually shortened to PCI. A catheter carries a small balloon to a coronary narrowing. The balloon expands the narrowed area, and a stent usually supports the artery afterwards. PCI can relieve angina when symptoms remain despite optimal medical treatment. It is also used urgently during some acute coronary syndromes. Coronary stents A stent is a small expandable mesh tube placed within an artery. Most coronary stents release medicine that reduces excessive tissue growth within the treated segment. Antiplatelet treatment is required afterwards to reduce stent clotting risk. The duration and combination depend on the clinical setting and bleeding risk. A stent treats a selected narrowing but does not remove atherosclerosis throughout the arterial system. Coronary artery bypass grafting Coronary artery bypass grafting is usually shortened to CABG. A surgeon connects graft vessels to route blood around narrowed coronary segments. Arteries from the chest and veins from the leg are commonly used as grafts. CABG is major surgery requiring general anaesthesia and hospital recovery. It can relieve symptoms and improve outcomes in selected complex coronary disease. Choosing PCI or CABG The best revascularisation method depends on coronary anatomy and clinical factors. PCI is less invasive and usually has a shorter initial recovery. CABG can provide more durable revascularisation for some extensive or complex disease. CABG may offer a survival advantage for selected multivessel disease, including some people with diabetes. A multidisciplinary heart team reviews difficult decisions involving surgeons and interventional cardiologists. When revascularisation is considered Revascularisation is considered when symptoms remain unacceptable despite optimal medicines. It can also be recommended for anatomical patterns associated with prognostic benefit. The main purpose in ordinary stable angina is often symptom improvement. Neither PCI nor CABG removes the need for risk factor treatment and preventive medicines. A person with controlled symptoms does not automatically require a procedure. Revascularisation does not cure atherosclerosis PCI and CABG improve blood flow through selected routes. Atherosclerosis can remain in untreated arteries and continue developing over time. Smoking cessation, lipid treatment, blood pressure control and diabetes care remain essential. Symptoms can recur because of new disease, graft disease, restenosis or another cause. Cardiac rehabilitation Cardiac rehabilitation provides supervised education, exercise and risk factor support. It is routinely offered after myocardial infarction, PCI or CABG and may support other coronary pathways. The programme can address medicines, smoking, diet, activity and psychological wellbeing. Fear of activity is common after chest pain and should be discussed rather than left untreated. Living with stable angina Many people control stable angina through medicines, activity planning and risk factor treatment. Keeping GTN available and knowing the emergency plan are important. Symptoms should be reviewed when they limit ordinary activity or change from the established pattern. The person should understand which medicines relieve symptoms and which reduce long term risk. Follow up Follow up reviews angina frequency, exercise tolerance and medicine adverse effects. Blood pressure, lipids, diabetes and smoking status are reassessed. A changing symptom pattern may require repeat diagnostic assessment or angiography. Persistent pain despite apparently successful treatment should prompt reconsideration of the diagnosis. Prognosis Prognosis varies according to the extent of coronary disease and heart muscle function. Diabetes, kidney disease, smoking and uncontrolled blood pressure increase future risk. Preventive medicines and lifestyle changes substantially reduce cardiovascular events. Stable symptoms do not guarantee that a plaque will never become unstable. Emergency action remains necessary when the symptom pattern changes. What this lesson should not be used for This lesson cannot determine whether one episode of chest pain is angina, reflux or another emergency. Do not use response to rest or GTN as proof that pain came from the heart. A normal ECG does not safely exclude stable angina or an acute coronary syndrome. Do not start aspirin, beta blockers or another heart medicine without individual clinical advice. Call 999 for persistent, severe or unstable chest symptoms rather than attempting home diagnosis.

Coronary heart disease usually results from atherosclerosis within the coronary arteries. Stable angina follows a predictable exertional pattern, while new, worsening or resting symptoms may represent an acute coronary syndrome. CT coronary angiography is the current first line NICE anatomical test, while treatment combines symptom relief, cardiovascular risk reduction and selective revascularisation.