Heart Attack: Sudden Injury to Heart Muscle

A heart attack happens when heart muscle is injured because its blood supply becomes critically reduced. Most result from sudden clot formation over a disrupted coronary plaque. Rapid recognition, a 999 call, ECG assessment and timely reperfusion can limit permanent damage and save life.

What a heart attack is A heart attack is the common name for myocardial infarction, usually shortened to MI. It occurs when part of the heart muscle is injured and begins to die because blood flow is insufficient. Most heart attacks arise within a coronary artery already affected by atherosclerosis. A heart attack is an acute emergency, not simply a severe episode of ordinary stable angina. Heart muscle needs continuous blood flow The myocardium is the muscular wall that pumps blood around the body. Coronary arteries deliver oxygen and nutrients to this muscle. Heart cells have limited ability to tolerate prolonged interruption of their blood supply. The longer severe ischaemia continues, the more muscle can become permanently injured. This is why emergency treatment is time critical. Stable coronary disease and heart attack are different states Stable coronary disease usually involves a fixed atherosclerotic narrowing. Blood flow may meet demand at rest but become inadequate during physical activity, causing stable angina. A heart attack usually begins when a plaque changes suddenly rather than simply narrowing gradually. Plaque disruption can trigger clot formation and sharply reduce coronary blood flow. Someone can have a heart attack without previously recognised angina. Plaque rupture and plaque erosion An atherosclerotic plaque has a surface separating its contents from circulating blood. That surface can rupture or become eroded. Platelets then recognise the damaged area and begin forming a thrombus, meaning a blood clot. The clot can partly obstruct, intermittently obstruct or completely block the artery. The resulting injury depends on the artery involved, the duration of obstruction and alternative blood supply. Type 1 myocardial infarction The classic plaque disruption heart attack is called type 1 myocardial infarction. It results from an acute coronary event such as plaque rupture or erosion with thrombosis. This is the main mechanism discussed in emergency STEMI and NSTEMI pathways. However, not every myocardial infarction follows this mechanism. Other mechanisms of myocardial infarction A type 2 myocardial infarction occurs when oxygen supply and demand become severely mismatched without acute plaque thrombosis being the primary cause. Possible triggers include profound anaemia, severe infection, very fast heart rhythms, severe hypertension or shock. Coronary spasm, spontaneous coronary artery dissection and coronary embolism can also cause infarction. These conditions require specialist assessment because their treatment may differ from ordinary atherosclerotic MI. Myocardial injury is not automatically myocardial infarction Troponin enters the blood when heart muscle cells are injured. A raised troponin therefore shows myocardial injury, not its cause. Heart failure, myocarditis, pulmonary embolism, kidney disease, sepsis and prolonged rapid rhythms can also raise troponin. Myocardial infarction requires a compatible rise or fall in troponin together with evidence of acute myocardial ischaemia. Acute coronary syndrome Acute coronary syndrome, usually shortened to ACS, describes sudden coronary ischaemic conditions. It includes STEMI, NSTEMI and unstable angina. STEMI and NSTEMI both involve myocardial infarction. Unstable angina causes acute ischaemic symptoms without the troponin evidence required to diagnose infarction. All three require urgent hospital assessment. What STEMI means STEMI means ST segment elevation myocardial infarction. The ECG shows a regional pattern indicating severe acute coronary occlusion or an equivalent emergency pattern. The ECG allows the emergency team to activate a reperfusion pathway before troponin results return. STEMI usually requires immediate coronary angiography with primary PCI when this can be delivered promptly. What NSTEMI means NSTEMI means non ST segment elevation myocardial infarction. The ECG does not show the persistent regional ST elevation pattern used to identify STEMI. There may be ST depression, T wave inversion, other changes or an initially normal ECG. Troponin evidence confirms acute myocardial injury within a compatible ischaemic presentation. Treatment urgency is then guided by clinical stability, ECG changes, troponin and formal risk assessment. STEMI is not simply complete blockage STEMI is often associated with sudden complete coronary occlusion. NSTEMI is often associated with subtotal or intermittent obstruction. These are useful broad tendencies but not absolute definitions. Some NSTEMIs involve a completely blocked artery, and some STEMI patterns arise despite incomplete obstruction. The emergency categories are defined through the ECG, biomarkers and clinical context rather than a simple blockage percentage. Why the emergency pathways differ STEMI identifies a group in whom immediate reperfusion usually offers major benefit. Treatment aims to reopen the artery before more heart muscle becomes irreversibly damaged. NSTEMI does not usually trigger automatic immediate primary PCI solely from the initial label. Clinicians first stabilise the person, give antithrombotic treatment and assess short term risk. Immediate angiography is still required when an NSTEMI presentation is clinically unstable. The classic presentation A heart attack can cause central chest pressure, heaviness, tightness, squeezing or burning. The discomfort may spread to one or both arms, shoulders, neck, jaw, back or upper abdomen. It commonly lasts longer than 15 minutes and may not settle with rest. Sweating, nausea, vomiting, breathlessness and light headedness can occur. Some people describe indigestion rather than using the word pain. Pain intensity is not a safety test A heart attack can cause severe distress, but the pain can also be moderate or vague. A person may remain able to speak and walk during the early phase. Symptoms can improve temporarily and then return. The absence of dramatic pain must not be used to delay emergency help. Symptoms without central chest pain Not every heart attack presents with central chest pain as the main feature. Possible presentations include sudden breathlessness, sweating, nausea, collapse or profound weakness. Jaw, arm, back or upper abdominal discomfort can predominate. An unexplained abrupt reduction in exercise tolerance can also be concerning. These symptoms have several possible causes but require urgent assessment when ACS is possible. Presentation in women Women commonly experience the same central pressure and radiating discomfort described in men. The diagnostic criteria should not be weakened or changed according to sex. Women may also report nausea, breathlessness, back or jaw discomfort, dizziness or unusual fatigue. Bias can lead clinicians or patients to attribute these symptoms to anxiety or indigestion. Prompt emergency assessment should depend on the clinical pattern, not a stereotype. Presentation in diabetes People with diabetes can experience typical crushing or constricting chest discomfort. Diabetic autonomic neuropathy can reduce or alter pain perception in some people. A heart attack may then present through sweating, nausea, breathlessness, weakness or collapse. Some infarctions are discovered later through ECG changes, imaging or complications. Diabetes also increases the underlying risk of coronary atherosclerosis. Presentation in older adults Older adults may present with breathlessness, confusion, weakness, dizziness or collapse. Frailty, cognitive impairment and communication difficulties can obscure what the person describes. Heart failure or an arrhythmia may be the first obvious complication. Older age should increase clinical vigilance rather than reduce access to emergency assessment or reperfusion. Silent myocardial infarction A silent MI causes little recognised discomfort or symptoms that are not identified as cardiac. It may be discovered through later ECG changes, cardiac imaging or an episode of heart failure. Silent does not mean harmless. The person can still have permanent myocardial damage and increased future cardiovascular risk. Other conditions can mimic a heart attack Pulmonary embolism, aortic dissection, myocarditis and pericarditis can cause severe chest symptoms. Pneumothorax, pneumonia, oesophageal rupture and upper gastrointestinal disease can also mimic ACS. Some alternatives are themselves life threatening. The 999 pathway is appropriate because home symptom analysis cannot safely separate them. Call 999 rather than arranging ordinary transport A suspected heart attack requires an emergency ambulance. Ambulance clinicians can monitor the heart rhythm, treat cardiac arrest and alert a specialist heart attack centre. They can record an ECG and route a STEMI patient directly to a catheter laboratory pathway. Driving yourself or being driven privately can delay appropriate treatment and leaves no resuscitation support if the condition deteriorates. What to do while waiting Stop activity and sit in a supported position. Follow the emergency call handler's instructions. A conscious adult with suspected heart attack may be advised to chew 300 mg aspirin if it is available and there is no known aspirin allergy. A person with prescribed GTN can use it according to their existing angina plan, but this must not delay the ambulance. If the person becomes unresponsive and is not breathing normally, begin CPR and use an available defibrillator. Aspirin is not suitable for everyone Aspirin reduces platelet activation and can limit further clot growth. It also increases bleeding risk. Do not give it when there is a known serious aspirin allergy or when the emergency call handler advises against it. The diagnosis could be another emergency, so additional medicines should not be improvised at home. The pre hospital ECG Ambulance clinicians obtain a 12 lead ECG as soon as possible when ACS is suspected. The tracing may be transmitted to or reviewed by a specialist heart attack centre. A STEMI pattern can activate the primary PCI pathway before hospital arrival. Recording or sending the ECG must not delay transport. A normal pre hospital ECG does not exclude NSTEMI or another ACS. What an ECG records An electrocardiogram records the heart's electrical activity from the body surface. It can show ST elevation, ST depression, T wave changes, Q waves or an arrhythmia. It does not directly record coronary blood flow, myocardial contraction or the amount of permanent damage. The ECG can also be normal early during an infarction. Serial tracings may reveal changes that were absent initially. STEMI activation does not wait for troponin A convincing STEMI ECG in the correct clinical setting identifies a reperfusion emergency. Waiting for a laboratory troponin result would delay artery opening treatment. Blood is still taken for troponin and other investigations, but the ECG drives the immediate pathway. High sensitivity troponin Troponin I and troponin T are proteins found within heart muscle cells. High sensitivity tests can detect very small blood concentrations. A sample is taken on arrival when ACS is suspected. The laboratory result is interpreted against the assay's reference threshold, the symptom timing and the overall clinical picture. Troponin changes over time Troponin may remain below a diagnostic threshold very early after symptoms begin. Hospitals use validated pathways involving one or more timed samples. Repeat samples may be taken from about 30 minutes to several hours after the first, depending on the assay and risk pathway. A significant rise or fall supports an acute process. A stable chronic elevation suggests a different pattern but still requires explanation. One detectable troponin does not diagnose MI A detectable or raised first result is not sufficient by itself. Kidney impairment, heart failure, sepsis, pulmonary embolism and myocarditis can raise troponin. Clinicians examine the change between samples and look for ischaemic symptoms, ECG findings, imaging evidence or an angiographic clot. Sex specific 99th percentile thresholds may be relevant for some troponin assays. A low initial troponin does not always end assessment A very low first result can help rule out NSTEMI in selected low risk people using a validated protocol. It is not a universal home or triage rule. Early presentation, ongoing pain, abnormal ECG findings or higher clinical risk can require repeated testing and observation. Troponin does not rule out unstable angina because that condition does not produce diagnostic myocardial injury. Hospital assessment The hospital team assesses blood pressure, heart rate, oxygen saturation and consciousness. They look for pulmonary oedema, shock, dangerous rhythms and alternative causes of chest pain. Blood tests include troponin, full blood count, kidney function, glucose and electrolytes. Continuous rhythm monitoring is used when the risk of deterioration is significant. Echocardiography An echocardiogram uses ultrasound to assess heart structure and movement. It can identify regions that contract poorly after infarction. It estimates left ventricular ejection fraction and can show heart failure or mechanical complications. A normal echocardiogram does not automatically exclude a small NSTEMI. Left ventricular function is assessed after STEMI and when clinically indicated after other infarctions. Coronary angiography Coronary angiography passes a catheter through an artery towards the heart. Contrast outlines the coronary arteries under X ray. The procedure identifies the culprit lesion and other important disease. PCI can usually be performed during the same procedure when appropriate. Immediate aspirin treatment NICE recommends a 300 mg loading dose of aspirin as soon as possible for STEMI, NSTEMI or unstable angina unless there is a clear contraindication. Aspirin reduces platelet activation at the disrupted plaque. It does not dissolve an established clot by itself. Long term low dose aspirin is commonly continued after MI unless anticoagulation, allergy or bleeding risk changes the plan. Further antiplatelet therapy Most people with MI receive a second antiplatelet medicine as part of dual antiplatelet therapy. Options include prasugrel, ticagrelor and clopidogrel. The choice depends on STEMI or NSTEMI pathway, PCI, age, bleeding risk and any separate anticoagulant requirement. These medicines reduce recurrent clotting but increase bleeding risk. They are selected and prescribed through hospital protocols rather than taken independently. Anticoagulant or antithrombin treatment Anticoagulant medicines reduce the activity of the clotting system. They complement antiplatelet treatment because platelets and clotting proteins both contribute to coronary thrombosis. NSTEMI pathways commonly use fondaparinux when bleeding risk is acceptable and immediate angiography is not planned. Unfractionated heparin is used during PCI and in selected other situations. Kidney function, body weight, bleeding risk and timing of angiography affect the choice. Oxygen is not routinely given to everyone Extra oxygen does not improve outcomes when blood oxygen saturation is already adequate. It can therefore be withheld while saturation is monitored. NICE recommends oxygen when saturation is below the appropriate target or respiratory failure is present. This differs from older portrayals in which every person with chest pain automatically received oxygen. Pain and symptom relief GTN may reduce ischaemic discomfort when blood pressure is adequate. Opioid pain relief may be used for severe continuing pain, particularly when MI is suspected. Anti sickness treatment can be given when needed. Pain relief is important but must not replace reperfusion or other definitive treatment. GTN is unsafe with marked hypotension and certain recent erectile dysfunction medicines. Reperfusion therapy Reperfusion means restoring blood flow through an acutely obstructed coronary artery. It limits infarct size when delivered quickly enough. Primary PCI is the preferred reperfusion treatment for most eligible STEMI patients. Fibrinolysis is used when timely primary PCI cannot be delivered within the recommended window. Primary PCI Primary percutaneous coronary intervention is an emergency catheter procedure for STEMI. A balloon opens the culprit artery, and a drug eluting stent is usually inserted. NICE prefers primary PCI when symptoms began within 12 hours and it can be delivered within 120 minutes of when fibrinolysis could have been given. People presenting later may still benefit when ischaemia continues or shock is present. Why speed matters Heart muscle injury progresses while severe coronary obstruction continues. Earlier reperfusion generally preserves more functioning myocardium. Delay can increase heart failure, shock, arrhythmia and mortality risk. People should therefore call 999 immediately rather than waiting to see whether symptoms pass. Fibrinolysis Fibrinolytic medicines activate the body's clot dissolving system. They are offered for eligible STEMI patients presenting within 12 hours when primary PCI cannot be delivered promptly enough. An anticoagulant is given at the same time. The treatment can cause serious bleeding, including intracranial haemorrhage, so contraindications are checked carefully. Assessing fibrinolysis success An ECG is repeated 60 to 90 minutes after fibrinolysis. Persistent ST elevation can indicate failed reperfusion. Immediate angiography with rescue PCI is then offered when appropriate. Fibrinolysis is not simply repeated after failed treatment. Stable patients usually undergo coronary angiography during the same hospital admission. NSTEMI immediate treatment NSTEMI receives aspirin, appropriate anticoagulant treatment and close clinical monitoring. A second antiplatelet is added after the diagnosis and treatment strategy are established. The team treats pain, arrhythmia, heart failure and other complications. Unlike STEMI, routine fibrinolysis is not used for NSTEMI. Risk assessment in NSTEMI NICE recommends formal assessment of future cardiovascular risk after NSTEMI or unstable angina is diagnosed. The GRACE score is one established example. It incorporates age, blood pressure, heart rate, kidney function, ECG findings, troponin and clinical features. The score informs the timing and expected benefit of invasive investigation. It supplements rather than replaces clinical judgement. Angiography for unstable NSTEMI Immediate coronary angiography is offered when the person's clinical condition is unstable. Examples include continuing or recurrent ischaemia, haemodynamic instability, serious arrhythmia or acute heart failure. The aim is to identify and treat a culprit lesion without avoidable delay. Angiography for stable NSTEMI For an intermediate or higher risk person without a contraindication, NICE advises considering angiography within 72 hours of first admission. Lower risk people may receive initial medical management and later angiography if ischaemia recurs or testing demonstrates it. NSTEMI is therefore not a minor heart attack. Its pathway is risk stratified rather than automatically less urgent. PCI after NSTEMI Angiography may identify a narrowing suitable for PCI. A stent treats the culprit artery and sometimes other important lesions. The decision considers coronary anatomy, symptoms, bleeding risk and overall clinical stability. Complex multivessel or left main disease may lead to CABG discussion instead. Coronary artery bypass grafting CABG uses graft vessels to route blood around severe coronary disease. It is not the immediate treatment for most acute STEMI presentations. It may be required when coronary anatomy is unsuitable for PCI or when mechanical complications need surgery. The heart team balances urgency, anatomy and operative risk. Arrhythmias after MI Injured or ischaemic myocardium can become electrically unstable. Ventricular tachycardia and ventricular fibrillation can cause cardiac arrest. Bradycardia and heart block can occur, particularly with some infarct locations. Continuous monitoring allows rapid defibrillation, pacing or medicine treatment when needed. Cardiac arrest A heart attack is a common cause of sudden cardiac arrest. The person becomes unresponsive and stops breathing normally because the heart no longer pumps effectively. Immediate CPR maintains limited blood flow to the brain and heart. An automated external defibrillator can terminate a shockable rhythm. Emergency services must be called immediately. Heart failure Infarcted heart muscle may contract poorly. The left ventricle can then fail to pump blood forward effectively. Fluid can accumulate in the lungs, causing breathlessness, low oxygen levels and pulmonary oedema. Treatment can include oxygen when needed, diuretics, vasodilators and evidence based heart failure medicines. Cardiogenic shock Cardiogenic shock occurs when heart damage prevents adequate circulation to vital organs. Possible features include very low blood pressure, cold clammy skin, confusion and reduced urine output. It is associated with a high risk of death. Urgent revascularisation and specialist critical care are required. Mechanical complications Infarction can rarely rupture the wall separating the ventricles or damage a papillary muscle supporting a heart valve. The free wall of the heart can also rupture. These complications may cause sudden heart failure, a new murmur, shock or collapse. Emergency echocardiography and cardiac surgery may be required. Pericarditis after MI Inflammation can develop in the sac surrounding the heart after infarction. Pain may become sharp, worsen with breathing and improve when sitting forwards. New pain after MI must still be assessed because recurrent ischaemia and other complications remain possible. Recurrent ischaemia and reinfarction A treated artery can re occlude, a stent can thrombose or another plaque can destabilise. Recurrent chest discomfort after MI requires urgent reassessment. Stopping dual antiplatelet treatment without specialist advice can increase stent thrombosis risk. Left ventricular assessment The amount of damaged myocardium influences future risk. Left ventricular ejection fraction estimates the proportion of blood pumped out with each contraction. A reduced ejection fraction increases the risk of heart failure and some dangerous rhythms. It guides medicines and, after an appropriate interval, consideration of an implantable defibrillator in selected people. Discharge planning Discharge information should confirm the diagnosis, investigations, treatment and follow up plan. It should explain medicine doses, intended duration and required blood monitoring. The person needs clear instructions about recurrent symptoms and emergency action. A copy should be available to the person and their GP. Secondary prevention Secondary prevention aims to reduce another MI, stroke, heart failure and cardiovascular death. It begins during the hospital admission and continues long term. Core treatment commonly includes antiplatelet therapy, a high intensity statin, an ACE inhibitor and a beta blocker when suitable. Lifestyle and risk factor treatment are equally important. Dual antiplatelet therapy after MI Aspirin is usually continued indefinitely. A second antiplatelet is commonly continued for up to 12 months after MI unless bleeding risk or another anticoagulation indication changes the plan. Some higher risk people receive a different duration after specialist assessment. Treatment must not be stopped for dental work or another procedure without checking with the prescribing team. Statin treatment High intensity lipid lowering treatment reduces future atherosclerotic events. Atorvastatin 80 mg is the usual NICE preferred statin for secondary prevention when suitable. Cholesterol is rechecked, and additional lipid lowering treatment can be added if the target is not achieved. The statin remains important even when the culprit artery has been stented. ACE inhibitors and ARBs An ACE inhibitor is offered after MI once the person is haemodynamically stable. It reduces adverse heart remodelling and future cardiovascular risk. Kidney function, potassium and blood pressure are monitored during dose increases. An angiotensin receptor blocker can be used when an ACE inhibitor is not tolerated. Beta blockers Beta blockers reduce heart rate and myocardial workload. They are particularly important when left ventricular systolic function is reduced. The duration of treatment depends on ventricular function, symptoms and other indications. They should not be stopped suddenly without medical advice. Aldosterone antagonists An aldosterone antagonist is considered after MI when there are signs of heart failure and reduced left ventricular ejection fraction. Treatment usually begins within days after the infarction once ACE inhibitor therapy is established. Potassium and kidney function require monitoring. Blood pressure and diabetes Blood pressure control reduces recurrent cardiovascular risk. Diabetes care includes glucose management and medicines with cardiovascular benefit when appropriate. Hyperglycaemia during an acute MI does not by itself establish a diabetes diagnosis. People without known diabetes may need later HbA1c or fasting glucose testing. Smoking cessation Stopping smoking is one of the most effective ways to reduce recurrent risk. Support can combine behavioural treatment with nicotine replacement, varenicline or another suitable medicine. The approach should be practical and non judgemental. Cardiac rehabilitation Everyone should be offered cardiac rehabilitation after MI regardless of age. The programme combines supervised or supported exercise, education and risk factor management. It can be delivered in hospital, community, home or digital formats. NICE advises beginning the process before discharge and offering an early session after discharge. Exercise after MI Exercise is reintroduced gradually according to clinical stability and ventricular function. Rehabilitation staff help identify a safe intensity and build confidence. People with stable reduced ejection fraction can still participate in adapted exercise. New chest pain, severe breathlessness, dizziness or palpitations during recovery require review. Diet and weight A heart healthy eating pattern emphasises vegetables, fruit, whole grains, pulses, nuts, fish and unsaturated fats. Salt, saturated fat and highly processed foods should be limited. Weight management should be supportive and realistic rather than crash dieting. Alcohol does not need to be started for cardiovascular protection. Psychological recovery Anxiety, low mood and fear of another event are common after MI. Some people become afraid to exercise, sleep alone or resume sexual activity. Cardiac rehabilitation includes education and stress management support. Persistent anxiety, depression or trauma symptoms deserve active clinical care. Returning to work and ordinary activity Recovery time depends on infarct size, treatment, complications and the physical demands of work. Advice should be individualised rather than based on one fixed timetable. Driving rules depend on licence type, treatment and complications and must follow current DVLA guidance. Travel and competitive sport can require specialist advice. Prognosis after MI Outcome depends on how quickly blood flow was restored and how much myocardium was injured. Left ventricular function, age, kidney disease, diabetes and recurrent ischaemia influence risk. Modern reperfusion, medicines and rehabilitation substantially improve survival. A successful stent does not remove the underlying tendency to atherosclerosis. What this lesson should not be used for This lesson cannot determine whether one episode is STEMI, NSTEMI, unstable angina or another emergency. Do not wait for pain to become severe or for every classic symptom to appear. A normal initial ECG or troponin result does not always exclude acute coronary syndrome. Do not start or stop antiplatelet, anticoagulant or heart medicines without clinical advice. Call 999 for suspected heart attack symptoms rather than attempting home diagnosis.

A heart attack is acute myocardial injury caused by severe ischaemia, most commonly after plaque rupture or erosion triggers coronary thrombosis. STEMI usually activates immediate reperfusion with primary PCI, while NSTEMI follows stabilisation, antithrombotic treatment and risk stratified angiography. Rapid 999 access, ECG assessment and secondary prevention reduce death and future events.