Cardiology

The assessment includes symptoms and well-being, body habitus, and indicators of tissue perfusion. →

The supplied captions illustrate findings associated with infective endocarditis, cyanotic congenital heart disease and congestive cardiac failure. →

Arterial pulse examination assesses pulse character and regularity to identify haemodynamic and rhythm abnormalities. →

Continuity between the internal jugular vein, superior vena cava and right atrium allows jugular venous pulsation to reflect right atrial pressure. →

Precordial palpation assesses the position and character of the apex beat, parasternal movement, palpable heart sounds and thrills. →

Cardiac auscultation uses different stethoscope components, pulse timing and patient positions to identify heart sounds and murmurs. →

Two features limit prompt recognition of developing heart disease: prolonged clinically silent disease and limited diversity of presenting symptoms. →

The heart consists of two pumps arranged in series, with chamber structure reflecting their roles in pulmonary and systemic circulation. →

The coronary arteries arise from the aortic root and supply different regions of the cardiac chambers and interventricular septum. →

The target identifies normal right ventricular pressures and describes the direction of oxygenated and deoxygenated blood flow through the heart. →

Coronary arterial territories explain the rhythm disturbances and myocardial injury associated with arterial occlusion. →

Normal cardiac activation begins in the sinoatrial node, spreads through the atria and reaches the ventricles through the atrioventricular node and His–Purkinje system. →

Sympathetic and parasympathetic nerves regulate cardiac activity, with changes during rest, stress and disease. →

Myocardial contraction depends on connections between myocytes, the organisation of sarcomeres and calcium-triggered interactions between actin and myosin. →

Cardiomyocytes secrete peptides with humoral effects on the vasculature and kidneys. Their release responds to stretch, and their breakdown involves neprilysin. →

Blood passes through the pulmonary and systemic circulations through coordinated cardiac filling and ejection. Elastic central arteries help sustain pressure and flow between contractions. →

Sarcomere shortening follows exposure of the actin-binding site and a change in the angle of attachment of the myosin head. →

Resistance vessels regulate systemic blood flow through changes in radius and smooth muscle tone. Coronary vessels also use autonomic and homeostatic mechanisms to regulate flow. →

The endothelium maintains vascular homeostasis by balancing vasoactive mediators and regulating inflammatory cell recruitment and thrombus turnover. →

Respiration changes blood flow through the right and left sides of the heart, producing normal variations in blood pressure, pulse rate and heart sounds. →

Cardiac investigations help establish the diagnosis and assess disease severity; the facilities required depend on the test. →

The electrocardiogram (ECG) assesses cardiac rhythm and conduction and assists in diagnosing myocardial ischaemia and infarction. →

A structured ECG examination reviews rhythm, axis, atrial activity, conduction, ventricular complexes and repolarisation, using standard recording conventions. →

The 12-lead electrocardiogram (ECG) uses 10 skin electrodes to generate recordings from pairs or sets of electrodes. →

ECG polarity depends on the direction of depolarisation relative to an electrode; the frontal cardiac axis describes the average ventricular depolarisation vector. →

The shape of the QRS complex across the chest leads reflects the sequence of ventricular depolarisation. The left ventricle (LV) has the greater muscle mass and contributes the major component. →

Exercise electrocardiography records cardiac electrical activity during exertion to assess symptoms and inform the diagnosis of angina due to coronary artery disease. →

Ambulatory ECG extends rhythm recording beyond a standard ECG snapshot. The target material also lists indications and high-risk findings for exercise testing. →

B-type natriuretic peptide and its N-terminal fragment are blood biomarkers used in assessing left ventricular dysfunction and heart failure. →

Troponin I and troponin T are structural cardiac muscle proteins whose release during myocyte necrosis underpins their diagnostic use. →

Chest radiography helps assess cardiac size and shape, pulmonary blood vessels and lung fields. Projection and chamber-specific silhouette changes affect interpretation. →

Additional chest radiographic projections can reveal obscured calcification, while lung-field findings can show the effects of heart failure or increased pulmonary blood flow. →

Transthoracic echocardiography provides rapid assessment of cardiac structure and function. →

Doppler echocardiography provides information about blood flow within the heart and great vessels. →

Doppler echocardiography detects the speed and direction of blood flow in cardiac chambers and great vessels, helping assess valvular regurgitation and stenosis. →

Transoesophageal echocardiography (TOE) provides high-resolution images of cardiac and adjacent structures that may be poorly seen by transthoracic echocardiography. →

Stress echocardiography assesses myocardial contraction during pharmacological stress and can also examine viability in patients with impaired left ventricular function. →

Computed tomography (CT) images cardiac and adjacent structures and can assess vascular disease, coronary calcification and myocardial perfusion. →

Magnetic resonance imaging (MRI) assesses cardiac anatomy, function, perfusion and myocardial tissue characteristics. →

Cardiac catheterisation passes a specialised catheter through a peripheral vein or artery into the heart under X-ray guidance to obtain haemodynamic measurements and angiographic images. →

The supplied cardiac magnetic resonance imaging examples contrast findings in recent inferior and old anterior myocardial infarction. →

The supplied figure captions describe a coronary artery stenosis and paired left ventriculograms showing normal contraction. →

Electrophysiology studies investigate patients with known or suspected arrhythmia. →

Radionuclide imaging is a technique for evaluating cardiac function. →

Blood pool imaging evaluates cardiac isotope distribution to measure ventricular function and assess chamber structure. →

Myocardial perfusion scanning uses an intravenously administered radioactive labelled agent that is rapidly taken up by the myocardium. →

Cardiovascular symptoms can overlap with symptoms caused by disease in other systems, so diagnosis requires careful clinical assessment. →

The New York Heart Association (NYHA) functional classification describes limitation of activity associated with cardiac symptoms. →

Chest pain or discomfort can have cardiac or non-cardiac causes. →

Detailed history-taking is crucial for identifying the likely cause of chest discomfort and assessing features suggesting angina. →

Investigation of suspected angina includes baseline testing, assessment for coronary artery disease and evaluation of a murmur when present. →

Acute coronary syndrome is a potential cause of severe, prolonged cardiac chest discomfort. →

Acute coronary syndrome may occur in someone with previous stable angina or present as the first manifestation of coronary artery disease. →

Initial and repeat electrocardiography and cardiac troponin measurements help assess suspected acute coronary syndrome and guide discharge decisions. →

Breathlessness has a wide differential diagnosis that includes both cardiac and non-cardiac causes. →

Syncope is defined by the mechanism responsible for loss of consciousness. →

Palpitation is a common, sometimes frightening symptom that usually reflects a disorder of cardiac rhythm. →

The initial assessment seeks to identify the likely mechanism of palpitation and determine whether significant underlying heart disease is present. →

When the initial assessment suggests an arrhythmia, investigation aims to document the rhythm during symptoms. →

Palpitation is usually benign, but associated symptoms and underlying heart disease determine the need for investigation and treatment. →

Cardiac arrest is a sudden, complete loss of cardiac output requiring prompt treatment. The target passage also describes normal and abnormal heart sounds. →

An opening snap is an added heart sound associated with opening of stenosed mitral valve leaflets. →

An abnormal sound detected on auscultation may be the first indication of heart disease. →

Clinical assessment establishes whether an abnormal sound is cardiac, whether it is pathological and what causes it. →

Murmur timing, intensity, location, radiation and quality help identify its nature and underlying cause. →

Cardiac murmurs are assessed by their timing, intensity, location, radiation and acoustic characteristics. Their relationship to the cardiac cycle helps identify associated valve lesions. →

The timing and acoustic character of these murmurs reflect the valves or flow pathways involved and guide auscultation. →

Clinical evaluation determines whether an additional sound is cardiac and likely to be pathological. →

Management of additional heart sounds or murmurs depends on the underlying cause. Murmur characteristics and associated signs help distinguish common conditions. →

Heart failure is a clinical syndrome involving inadequate cardiac output or adequate output maintained only through elevated ventricular filling pressure. →

Heart failure predominantly affects older people and can cause prolonged hospitalisation, chronic disability and poor survival when untreated. →

Heart failure occurs when cardiac output cannot meet circulatory demands. Ventricular dysfunction and changes in the relationship between filling and performance explain its development. →

Reduced ventricular output triggers compensatory systems that can worsen loading conditions when ventricular function is impaired. Different mechanical abnormalities also produce distinct patterns of failure. →

Heart failure can reflect impaired filling or abnormal heart rate. Neurohumoral responses initially support circulation but can subsequently worsen myocardial injury and fluid retention. →

Heart failure can occur with excessive cardiac output or through impaired ventricular filling, obstructed outflow and ventricular overload. →

Heart failure may develop suddenly after myocardial infarction or gradually in valvular disease. Acute deterioration can also occur in compensated or established chronic heart failure. →

Pre-existing heart disease can decompensate after an additional stress. Chronic heart failure commonly follows a relapsing and remitting course with stable periods and episodes that may require hospitalisation. →

Advanced heart failure can impair renal function. The accompanying figure identifies congestive findings associated with left and right heart failure. →

Peripheral oedema may arise from cardiac disease, venous or lymphatic disorders, hypoalbuminaemia, drugs or an idiopathic cause. →

Heart failure can cause electrolyte disturbances, impaired liver function, thromboembolism and arrhythmias. Several complications are compounded by treatment or low cardiac output. →

Investigation of heart failure assesses pulmonary congestion, rhythm, underlying cardiac disease, complications and prognosis. →

Acute heart failure with pulmonary oedema is a medical emergency requiring urgent treatment, monitoring and escalation if initial measures fail. →

Supportive management of heart failure includes education, dietary measures, lifestyle changes and consideration of vaccination. →

Treatment aims to improve cardiac performance, relieve congestion and manage cardiac rate and rhythm through drugs, devices and selected interventions. →

Persistent oedema despite oral loop diuretics may require intensified diuresis, particularly when renal impairment accompanies severe chronic heart failure. Older patients also have specific treatment and tolerability considerations. →

These drug groups act through different renal and neurohumoral mechanisms and provide clinical benefits in heart failure. →

ACE inhibitors require attention to blood pressure, renal function and potassium. Angiotensin receptor blockers offer an alternative when ACE inhibitors are not tolerated. →

Neprilysin inhibition augments endogenous peptide activity, while venous and arterial dilators reduce different components of cardiac loading. →

The passage provides starting and target doses for several heart failure drugs and describes the benefits, initiation precautions and clinical roles of beta-blockers, ivabradine and digoxin. →

Selected patients with heart failure may benefit from amiodarone, defibrillators, cardiac resynchronisation, coronary revascularisation or transplantation. →

Heart transplantation can markedly improve quality of life, but pulmonary vascular resistance and post-transplant complications affect its suitability and outcomes. →

Ventricular assist devices mechanically assist cardiac output, unload the ventricles and support the pulmonary and systemic circulations. →

The passage defines cardiac arrhythmias and describes lead placement and function in a biventricular pacemaker and defibrillator. →

Normal cardiac activation starts in the sinoatrial node. Abnormal rhythms usually arise from pathology affecting the cardiac conduction system. →

Bradycardia can result from impaired impulse generation or impaired conduction, and a distal pacemaker may take over when the sinus rate becomes unduly slow. →

Many arrhythmias are asymptomatic, but sustained or extreme disturbances of heart rate can cause symptoms and serious outcomes. →

Capturing the cardiac rhythm during symptoms is central to diagnosing suspected arrhythmias. →

The nature of the arrhythmia determines its management. →

Sinus arrhythmia is a normal cyclical variation in heart rate during respiration. →

Sinus bradycardia can occur in healthy people; treatment depends on whether symptoms are present and whether they recur or persist. →

Sinus tachycardia commonly reflects increased sympathetic activity. Re-entry is a separate mechanism by which an electrical impulse can circulate repeatedly and sustain tachycardia. →

Sinoatrial disease, also called sick sinus syndrome, results from degenerative changes in the sinoatrial node and is commonest in older people, although it can occur at any age. →

Sinus bradycardia and sinus tachycardia have distinct listed pathological causes. Sinoatrial disease can produce several bradyarrhythmias, tachyarrhythmias and conduction abnormalities. →

Atrioventricular (AV) block involves impaired conduction from the atria to the ventricles. Its electrocardiographic pattern helps distinguish delayed conduction from intermittently failed conduction. →

Atrioventricular (AV) block can cause intermittent failure of atrial impulses to reach the ventricles or complete independence of atrial and ventricular activity. →

Complete atrioventricular block typically presents with recurrent syncope termed Stokes–Adams attacks. →

Complete atrioventricular block may be congenital or acquired. →

Management of atrioventricular (AV) block depends on symptoms, the type of block and the clinical setting. Block accompanying inferior myocardial infarction (MI) differs from block accompanying acute anterior MI. →

Damage to ventricular conducting branches alters the route and timing of ventricular depolarisation. Complete bundle branch block and fascicular block produce different electrocardiographic changes. →

Atrial ectopic beats usually have little clinical consequence, but their ECG appearance, frequency and symptom burden guide assessment. →

Atrial tachycardia may arise from increased atrial automaticity, sinoatrial disease or digoxin toxicity. →

The passage completes the treatment discussion of atrial tachycardia and illustrates how atrioventricular (AV) block can make atrial flutter waves visible. →

Atrial flutter involves a large atrial re-entry circuit; atrioventricular conduction determines the resulting heart rate and can obscure its ECG appearance. →

Atrial flutter can be managed by controlling the ventricular rate or restoring rhythm. The target passage also describes mechanisms and electrocardiographic features of atrial fibrillation. →

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and is associated with significant morbidity and increased mortality. →

Atrial fibrillation (AF) involves abnormal automatic firing and interacting atrial re-entry circuits. Disorganised atrial activity produces an irregular ventricular response. →

Atrial fibrillation (AF) can accompany structural heart disease or occur in structurally normal hearts. Older age adds specific presentation and anticoagulation considerations. →

Atrial fibrillation (AF) may cause symptoms and haemodynamic deterioration or remain unrecognised until an incidental diagnosis or embolic event. →

Assessment of newly diagnosed atrial fibrillation includes clinical evaluation and investigations for cardiac structural disease and thyrotoxicosis. →

Management of atrial fibrillation (AF) depends on its persistence, precipitating factors and symptoms. Stroke risk stratification and prevention remain central. →

Catheter ablation offers an alternative to anti-arrhythmic drugs. Persistent atrial fibrillation (AF) can be managed with rate or rhythm control, with thromboembolism prophylaxis required for either approach. →

Restoring and maintaining sinus rhythm is most successful in younger patients with atrial fibrillation (AF) lasting less than 3 months and no important structural heart disease. →

Loss of atrial contraction and left atrial dilatation promote blood stasis and left atrial appendage thrombus, creating a risk of stroke and systemic embolism in atrial fibrillation (AF). →

In atrial fibrillation, stroke risk scoring guides anticoagulation. The passage also describes the benefit and bleeding risk of anticoagulation and reversal options for life-threatening bleeding. →

This scoring system assigns points to clinical stroke risk factors and links the total to annual stroke risk and oral anticoagulation decisions. →

HAS-BLED assesses bleeding risk in patients receiving oral anticoagulation. The passage also describes warfarin targets, reversal of anticoagulation and the limitations of aspirin for embolic stroke prevention. →

Supraventricular tachycardia (SVT) describes a group of regular tachycardias with a similar appearance on the electrocardiogram. →

Atrioventricular nodal re-entrant tachycardia (AVNRT) is a supraventricular tachycardia caused by re-entry involving the atrioventricular node and its right atrial input pathways. →

Management includes termination of acute episodes and prevention of recurrent supraventricular tachycardia (SVT). Treatment is not always necessary. →

An accessory band of conducting tissue connects the atria and ventricles. Its direction of conduction determines whether it alters the electrocardiogram (ECG) during sinus rhythm. →

In Wolff–Parkinson–White (WPW) syndrome, ventricular activation through the AV node and accessory pathway produces different ECG appearances during sinus rhythm, orthodromic tachycardia and atrial fibrillation. →

This passage explains how an accessory pathway permits re-entry tachycardia and describes the ECG appearance and pulse effect of ventricular ectopic beats. →

In Wolff–Parkinson–White syndrome, an accessory pathway supports tachycardia and can permit dangerously rapid ventricular activation during atrial fibrillation. →

Ventricular premature beats (VPBs) occur in healthy people and in patients with heart disease. Their significance depends on whether underlying heart disease is present. →

Treatment of ventricular premature beats (VPBs) depends on symptoms and associated heart disease. Suppression with anti-arrhythmic drugs has not been shown to improve prognosis. →

Ventricular tachycardia (VT) usually occurs with significant ventricular disease, although it can occasionally arise in an otherwise healthy heart. →

Clinical history, electrocardiographic findings and lack of response to certain interventions can favour ventricular tachycardia. →

Ventricular tachycardia (VT) requires prompt restoration of sinus rhythm, usually followed by preventive therapy. Acute treatment depends on haemodynamic tolerance. →

Torsades de pointes is a form of polymorphic ventricular tachycardia associated with prolonged ventricular repolarisation and a prolonged QT interval. →

Treatment of torsades de pointes includes immediate arrhythmia suppression, correction of its cause and prevention of recurrence. The passage also introduces the related genetic disorder Brugada syndrome. →

The supplied figure description illustrates the rhythm sequence leading to torsades de pointes. →

The listed causes include bradycardia, electrolyte disturbances, several drug groups and congenital long QT syndromes. →

Cardiac arrhythmias can be managed using three broad treatment approaches. →

Anti-arrhythmic drugs can be categorised by their effects on the action potential and further classified by their molecular targets. →

Class I anti-arrhythmic drugs affect excitability and conduction in atrial or ventricular muscle by blocking sodium channels. →

Anti-arrhythmic drugs are grouped by their principal channel or receptor effects and their effects on the intracellular action potential. Some drugs fall outside this classification or have properties spanning multiple classes. →

Class Ia drugs affect cardiac action potential duration and tissue refractoriness and are used for arrhythmia prevention. →

The table compares class I–IV anti-arrhythmic drugs by indication, route, adult dosage and important adverse effects. →

These drugs have distinct roles in vagal bradycardia, supraventricular tachycardia and atrial fibrillation, with specific adverse effects and precautions. →

Class Ib drugs act predominantly in ventricular myocardium and include lidocaine and mexiletine. →

Anti-arrhythmic drugs are potentially toxic, so treatment requires careful selection, assessment of effectiveness and regular review. →

Class Ic drugs include flecainide and propafenone and are used mainly for prevention of atrial fibrillation. →

Class II drugs are β-adrenoceptor antagonists with nodal effects that support rate control and arrhythmia prevention. →

Class III anti-arrhythmic drugs prolong the action potential plateau and refractory period, with therapeutic benefits and pro-arrhythmic risks. →

Class IV drugs block slow calcium channels and are used for supraventricular tachycardia prevention and ventricular rate control in atrial fibrillation. →

These anti-arrhythmic drugs differ in their effects on cardiac conduction, clinical uses and precautions. →

Digoxin is a glycoside purified from the European foxglove, Digitalis lanata. Its effects differ between the atrioventricular node and other cardiac tissues. →

Electrical cardioversion terminates arrhythmias by depolarising the myocardium. Defibrillation is primarily used for cardiac arrest due to ventricular fibrillation. →

Temporary pacing delivers an electrical impulse to initiate cardiac tissue depolarisation and trigger contraction. It can be delivered through an intracardiac electrode or through the skin. →

Permanent pacemakers are small, flat metal devices implanted beneath the skin, usually in the pectoral area. →

Pacemaker chamber selection depends on the underlying rhythm and conduction disorder. Dual-chamber and rate-responsive systems provide additional physiological benefits in selected patients. →

Implantable cardiac defibrillator indications are divided into primary and secondary prevention. The passage also lists early and late complications of permanent pacing. →

Implantable cardiac defibrillators (ICDs) provide permanent pacemaker functions and can detect and terminate life-threatening ventricular tachyarrhythmias. →

Cardiac resynchronisation therapy (CRT) treats selected patients with heart failure whose left ventricular contraction is poorly coordinated because of left bundle branch block. →

These implantable devices have alternative arrangements associated with a lower likelihood of infection. →

Catheter ablation identifies and destroys arrhythmia-producing tissue. It is the treatment of choice for SVT or atrial flutter and is useful in selected patients with AF or ventricular arrhythmias. →

Coronary artery disease (CAD) is the commonest cause of angina and acute coronary syndrome and the leading cause of death worldwide. It also substantially impairs quality of life. →

Most coronary artery disease (CAD) results from atherosclerosis, a progressive inflammatory disorder of the arterial wall. →

Atherosclerotic plaque evolution involves inflammatory-cell recruitment, lipid accumulation and a smooth muscle repair response. →

Coronary artery disease produces different clinical syndromes according to whether the dominant process is fixed stenosis, thrombosis, supply–demand imbalance or myocardial damage. →

Plaque composition and mechanical stress influence rupture, while arterial remodelling changes the effect of atheroma on the lumen. Age and sex also influence disease risk. →

Coronary artery disease risk reflects inherited susceptibility, smoking, blood pressure, lipid and glucose abnormalities, haemostatic factors and physical activity. →

The interpretable heading and accompanying feature list identify the defining pathology of a type VI lesion. →

Cardiovascular risk is influenced by diet, obesity, alcohol use and social circumstances. Overall assessment must distinguish proportional risk increases from the actual probability of an event. →

Population-based coronary prevention includes specific recommendations for smoking, exercise, body weight and diet. →

Prevention of coronary artery disease (CAD) includes interventions before a clinical event and treatment aimed at preventing further events. →

Cardiovascular prevention includes public health measures, treatment directed at high-risk individuals and interventions for people who have already had cardiovascular disease. →

Angina pectoris is a symptom complex arising from a mismatch between myocardial oxygen supply and demand. →

Angina most commonly arises from coronary atherosclerosis, but structural cardiac disease, inflammation and coronary vasospasm can also cause it. →

Myocardial oxygen balance depends on cardiac work, coronary blood flow and oxygenation. Angina with normal coronary angiography may still have objective evidence of myocardial ischaemia. →

The clinical history is central to diagnosing angina, while symptom patterns and severity grading aid its assessment. →

Chest pain is classified by the number of characteristic anginal features. The NICE classification also incorporates the resting electrocardiogram. →

The Canadian Cardiovascular Society (CCS) angina score grades activity limitation. Assessment also includes examination for associated disease and selection of investigations according to whether coronary artery disease is already known. →

Exercise testing and non-invasive imaging help confirm suspected angina and stratify risk, but an exercise electrocardiogram (ECG) alone cannot reliably diagnose coronary artery disease (CAD). →

An illustrated exercise test demonstrates marked ECG changes despite a nearly normal resting ECG. →

Risk assessment in stable angina combines symptoms, associated illness, coronary anatomy and ventricular function. Imaging establishes coronary disease and helps guide further treatment. →

Management of angina aims to relieve symptoms and improve prognosis through education, lifestyle measures, risk-factor treatment and medication. →

Anti-anginal therapy seeks symptom control with a simple regimen that avoids side-effects. Nitrates reduce oxygen demand and increase oxygen supply through vasodilatation. →

Beta-blockers reduce myocardial oxygen demand, while activity advice and preventive nitrate use help patients manage stable angina. →

Nitrate preparations differ in peak action and duration. Other anti-anginal vasodilators include calcium channel antagonists and the potassium channel activator nicorandil. →

Calcium channel antagonists used for angina have different dosing schedules and distinguishing effects. Ivabradine and ranolazine act through different ion-channel mechanisms. →

Percutaneous coronary intervention (PCI) is a non-pharmacological treatment that dilates a coronary stenosis using a balloon, with possible stent deployment. →

Percutaneous coronary intervention (PCI) relieves symptoms of chronic stable angina. Its acute and long-term complications and the complexity of the target lesion influence outcomes. →

Coronary stenoses can be treated by catheter-based dilatation and stenting or by surgical bypass using the patient's own vessels. →

Coronary artery bypass grafting (CABG) provides substantial initial relief of angina and improves survival in specified patterns of coronary disease. Long-term outcomes depend on graft patency, disease progression and preventive treatment. →

Coronary artery bypass graft surgery bypasses narrowed or stenosed coronary arteries using saphenous vein grafts or the internal mammary artery. The passage describes an example reconstructed using multidetector CT. →

The comparison describes procedural risks, recovery and subsequent events after percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG). →

The burden of coronary artery disease (CAD) and the degree of left ventricular dysfunction determine prognosis. →

Acute coronary syndrome includes unstable angina and myocardial infarction. Recognition of myocardial injury, adverse risk markers and age-related presentations guides assessment. →

Acute coronary syndrome almost always occurs in patients with coronary atherosclerosis, with dynamic changes in the culprit lesion. →

Acute myocardial infarction (MI) requires acute myocardial injury with evidence of acute ischaemia. The classification distinguishes atherothrombotic, supply–demand, fatal and procedure-related events. →

Myocardial infarction can be recognised retrospectively from electrical, imaging or anatomical evidence. Acute MI subtypes differ in their mechanism and clinical setting. →

Acute coronary syndrome may present with central chest pain, breathlessness, vomiting or collapse; myocardial infarction may also be painless. →

Arrhythmias are common during acute coronary syndrome. Their significance and treatment depend on timing, rhythm and haemodynamic effects. →

The GRACE score is used for risk stratification in acute coronary syndrome. The passage illustrates estimated in-hospital mortality and describes Killip classes and the evolution of myocardial infarction. →

Acute coronary syndromes can produce prolonged cardiac pain, autonomic features and signs of impaired myocardial function. →

Acute coronary syndrome may be complicated by rhythm disturbances, recurrent ischaemia, acute heart failure and post-infarction pericarditis. →

After myocardial infarction, delayed inflammation, structural rupture, ventricular remodelling and thrombus formation produce distinct clinical complications. →

Structural changes after myocardial infarction can progressively impair ventricular efficiency or produce an aneurysm with mechanical, electrical and embolic complications. →

The 12-lead electrocardiogram is central to confirming myocardial infarction and deciding immediate management. Serial changes help estimate the approximate age of an infarct. →

ECG lead distribution helps localise myocardial infarction, while serial troponin measurements and other laboratory tests support assessment. →

Chest radiography can reveal pulmonary oedema that is not apparent on clinical examination. →

Electrocardiography, cardiac biomarkers, echocardiography and coronary angiography help identify myocardial infarction, assess complications and guide revascularisation. →

Early acute coronary syndrome carries a risk of death and recurrent myocardial ischaemia, requiring urgent admission, risk assessment and adequate analgesia. →

The passage describes ECG criteria, timing and outcomes of reperfusion, and distinguishes immediate treatment from inpatient intervention in non-ST elevation presentations. →

Continuing the discussion of thrombolysis for ST elevation myocardial infarction, this passage describes treatment timing, practical agents, bleeding hazards and circumstances for emergency PCI. →

The target contains fragments of an acute coronary syndrome treatment flowchart. The mortality categories and several treatment elements are readable, but the decision branches are incomplete. →

The passage outlines acute coronary syndrome treatment, intervention after thrombolysis and the use of aspirin with a P2Y12 receptor antagonist. →

This passage describes platelet inhibition and anticoagulation in acute coronary syndromes, followed by the main components of longer-term care after myocardial infarction. →

The target lists relative contraindications to thrombolytic therapy and describes nitrate, β-blocker and calcium-channel blocker use in unstable angina and myocardial infarction. →

This passage covers renin–angiotensin blockade, mineralocorticoid receptor antagonists, lipid lowering and lifestyle measures after acute coronary syndrome. →

Recovery involves graded return to activity and psychological support. Older patients may present atypically and have greater mortality and treatment hazards. →

The opening statement continues the discussion of implantable defibrillators. The target then distinguishes the management priorities of type 2 myocardial infarction. →

Prognosis depends on residual ischaemia, myocardial damage and ventricular arrhythmias, with different determinants of early death and later outcomes. →

Non-cardiac surgery can precipitate myocardial infarction and death in patients with coronary artery disease or other heart disease, particularly during major vascular, abdominal or thoracic operations. →

Certain pre-existing cardiac conditions increase the risk of cardiac complications during non-cardiac surgery. Atrial fibrillation is also a common postoperative complication in patients with heart disease. →

Peripheral arterial disease often has no presenting symptoms. Intermittent claudication is its commonest symptom and is associated with substantial cardiovascular mortality. →

In developed countries, almost all peripheral arterial disease is caused by atherosclerosis, with risk factors shared with coronary artery disease. →

Symptomatic peripheral arterial disease predominantly affects the lower limbs and can involve several arterial territories. →

Peripheral arterial disease may involve one or more arterial segments, with a variable and asymmetric distribution. →

The effects of peripheral arterial disease depend on the affected circulation, available collateral supply, speed of arterial occlusion and mechanism of injury. →

Lower-limb peripheral arterial disease (PAD) commonly presents with intermittent claudication. Critical limb ischaemia and diabetes-associated vascular and neurological abnormalities have additional clinical implications. →

The passage explains progressive night pain and tissue loss in limb ischaemia, alongside the effects of autonomic neuropathy on the diabetic foot. →

Acute limb ischaemia can rapidly threaten limb viability. Its cause influences treatment and prognosis, making immediate vascular surgical discussion essential. →

Assessment of acute limb ischaemia includes pain, pallor, pulselessness, coldness, paraesthesia and paralysis, but some findings have important limitations. →

Clinical patterns help distinguish peripheral arterial embolism from thrombosis. Upper-limb peripheral arterial disease may also present with digital atheroembolism or subclavian steal. →

Clinical examination and the ankle–brachial pressure index usually establish the presence and severity of limb ischaemia. Imaging defines arterial involvement, while blood tests identify treatable secondary causes. →

Medical management of peripheral arterial disease combines lifestyle measures, antiplatelet and statin therapy, and treatment of coexisting disease. →

Chronic lower limb ischaemia produces characteristic arterial, positional, venous and trophic findings. →

Medical management combines lifestyle measures, antithrombotic treatment, cholesterol reduction and treatment of associated conditions. →

The passage describes treatment for persistent disability in peripheral arterial disease and the usual intervention for subclavian artery disease. →

Age, established vascular disease, frailty and life expectancy influence the presentation and management described in this passage. →

Buerger disease, also called thromboangiitis obliterans, is an inflammatory arterial disease distinct from atherosclerosis. →

The passage contrasts the usual uncomplicated disorder in young women with more severe Raynaud syndrome associated with connective tissue disease. →

An aortic aneurysm is an abnormal dilatation of the aortic lumen, most commonly involving the infrarenal abdominal aorta. →

Aortic aneurysm development is associated with atherosclerosis, predominant vascular risk factors and inherited susceptibility. →

The clinical presentation of an aortic aneurysm depends on its site and effects on adjacent structures. →

Imaging has distinct roles in establishing the diagnosis, surveillance, screening and planning repair. →

Management of an abdominal aortic aneurysm (AAA) depends on diameter, symptoms, embolisation and rupture. The passage also describes repair techniques and treatment in Marfan syndrome. →

Aortic dissection creates a false channel within the aortic wall and can compromise the aortic valve, aortic branches or surrounding spaces. →

An abdominal aortic aneurysm (AAA) may be detected incidentally or present with pain, thromboembolism, compression or rupture. →

Aortic dissection may begin with an intimal tear or with bleeding within the aortic media. →

Aortic dissection is classified by involvement of the ascending aorta; the supplied continuation completes the distinction between type A and type B. →

Aortic dissection produces characteristic abrupt pain, vascular examination findings and complications from occluded aortic branches. →

Imaging establishes aortic dissection and may demonstrate associated aortic, pleural or cardiac findings. →

Acute aortic dissection requires urgent treatment because early mortality is approximately 1%–5% per hour. →

Aortitis may occur with syphilis or with the inflammatory conditions listed in the source. →

Marfan syndrome is a rare inherited connective tissue disorder associated with a high risk of aortic aneurysm and dissection. →

Marfan syndrome has cardiovascular, skeletal, skin, joint, ocular and pulmonary manifestations. →

Investigations confirm a clinically suspected diagnosis and assess aortic and valvular involvement. →

Management combines preventive drug treatment, activity advice and surgery for progressive aortic dilatation. →

Coarctation describes aortic narrowing at a specified location; similar narrowing can also occur in acquired conditions. →

Blood pressure is continuously distributed, so a diagnostic threshold must be interpreted alongside the individual's overall cardiovascular risk. →

Hypertension reflects multiple influences on blood pressure regulation. Most cases have no identifiable specific cause, and sustained hypertension produces structural changes in arteries. →

The target material lists blood-pressure categories and secondary causes of hypertension. It also describes a Doppler finding in chronic aortic dissection. →

Hypertension is usually detected incidentally or after a complication, while examination may identify an underlying cause or evidence of organ damage. →

Investigation confirms hypertension, evaluates cardiovascular risk and identifies causes, complications and comorbidities before treatment that generally entails a lifelong commitment. →

Accurate measurement includes appropriate technique and interpretation of ambulatory or home readings, alongside investigations for risk factors, causes and complications. →

All hypertensive patients require limited routine investigations, with additional testing appropriate for younger patients or resistant hypertension. →

Antihypertensive treatment aims to prevent adverse cardiovascular events, particularly coronary artery disease, stroke and heart failure. →

Antihypertensive treatment decisions incorporate blood pressure readings and cardiovascular risk, with ongoing monitoring and support. →

Hypertension management combines blood pressure targets, regular follow-up, lifestyle changes and adjustment of drug treatment when control is inadequate. →

The passage describes thiazides, ACE inhibitors, angiotensin receptor blockers, calcium channel antagonists and beta-blockers used for hypertension. →

Combined adrenergic blockers and other vasodilators provide additional antihypertensive options; antiplatelet therapy and statins address cardiovascular risk. →

Drug selection depends on patient characteristics and comorbidities, while inadequate control may require combination therapy and assessment of adherence or secondary causes. →

Accelerated hypertension is a rare complication of hypertension of any aetiology, characterised by rapidly progressive end-organ damage. →

Coexisting disease can favour a drug class or require caution, contraindication checks and specialist supervision. →

Management requires a controlled fall in blood pressure because altered autoregulation makes rapid reduction hazardous. →

Heart valves support forward blood flow and prevent backward flow; disease can impair either function. →

The passage describes the usual age range and geographical burden of acute rheumatic fever and the mortality associated with rheumatic heart disease. →

Acute rheumatic fever follows a delayed immune response to group A streptococcal infection. →

Acute rheumatic fever is a multisystem disorder that typically presents after streptococcal pharyngitis. Diagnosis combines clinical manifestations with evidence of preceding infection, with specified exceptions. →

The interpretable material explains drug classes and additional treatment options for resistant hypertension, followed by causes of acute valve failure and broader causes of valve disease. →

The supplied Jones criteria distinguish major and minor manifestations and require attention to evidence of preceding streptococcal infection. →

The passage continues the description of Sydenham chorea and outlines investigations for systemic illness, preceding streptococcal infection and carditis in acute rheumatic fever. →

Investigations monitor inflammation, seek evidence of preceding streptococcal infection and assess cardiac involvement. →

Management aims to limit cardiac damage and relieve symptoms, while antibiotic prophylaxis prevents further attacks. →

Glucocorticoids provide symptomatic treatment in rheumatic fever with carditis or severe arthritis. →

Chronic rheumatic heart disease produces lasting valvular disease after rheumatic fever, although the preceding illness may have gone unrecognised. →

Progressive fibrosis alters valve structure and function, while the resulting haemodynamic stresses can sustain further damage. →

Mitral stenosis is predominantly rheumatic, with calcific and congenital causes also described. →

Progressive narrowing of the mitral valve impedes left ventricular filling, raises left atrial pressure and produces pulmonary and right heart complications. →

Mitral stenosis commonly causes progressive limitation of exercise and characteristic heart sounds; physical signs may appear before symptoms. →

Investigations assess mitral valve narrowing, atrial enlargement and pulmonary pressure, while examination may identify accompanying mitral or tricuspid regurgitation. →

Evaluation of suspected mitral stenosis uses Doppler echocardiography, with additional investigations guided by rhythm findings and planned intervention. →

Management depends on symptoms, pulmonary hypertension and valve characteristics, with continued surveillance after valvuloplasty or valvotomy. →

Mitral regurgitation has several structural and functional causes and may also follow mitral valvotomy or valvuloplasty. Selection for balloon valvuloplasty requires suitable mitral stenosis anatomy and absence of important regurgitation. →

Mitral regurgitation can arise from the valve apparatus or from ventricular disease that prevents leaflet coaptation. Its haemodynamic effects differ between acute and chronic disease. →

Mitral regurgitation produces characteristic auscultatory findings and may arise from leaflet prolapse, altered ventricular geometry or endocarditis. →

The clinical presentation of mitral regurgitation depends on its cause and the speed at which it develops. →

Clinical findings in mitral regurgitation reflect abnormal flow, chamber enlargement, congestion and heart failure. →

The target contains a description of mitral regurgitation followed by an interpretable figure caption describing aortic stenosis. →

Investigation assesses regurgitation severity, valve and papillary muscle function, associated rhythm changes and suitability for surgery. →

Management depends on severity, symptoms and ventricular function, with regular clinical and echocardiographic reassessment. →

Management options include cardiac resynchronisation in eligible heart failure patients and percutaneous repair to improve leaflet coaptation. →

The target passage outlines medical treatment for mitral regurgitation and then groups causes of aortic stenosis by patient age. →

Age at presentation provides a clue to the cause of aortic stenosis, although obstruction generally develops slowly. →

Aortic valve obstruction initially permits maintained cardiac output but progressively increases the workload on the left ventricle. →

Aortic stenosis may be detected by its murmur before symptoms develop. Its three cardinal symptoms are angina, breathlessness and syncope. →

Clinical examination can suggest aortic stenosis, but its severity may be difficult to judge, especially in older patients. →

Investigations establish valve restriction and assess stenosis severity, while accounting for the effects of ventricular function and stroke volume. →

Aortic stenosis is evaluated using valve imaging, electrical findings and haemodynamic assessment. →

Management depends strongly on symptoms, with surveillance for asymptomatic disease and prompt valve replacement for symptomatic severe stenosis. →

Aortic regurgitation can arise from abnormalities affecting the valve cusps or the aortic root. →

Regurgitant blood increases the volume the left ventricle must handle, producing compensatory changes followed by ventricular failure as disease progresses. →

Aortic regurgitation may produce prominent heartbeat awareness and characteristic murmurs; acute severe disease can present predominantly with heart failure. →

This passage describes how aortic stenosis presents and is treated in older adults, followed by congenital and acquired causes of aortic regurgitation. →

Aortic regurgitation produces symptoms that vary with severity and characteristic pulse, murmur and cardiac findings. →

Investigations detect aortic regurgitation, quantify its degree, assess associated aortic dilatation and support assessment before cardiac surgery. →

Management includes treating underlying conditions, monitoring asymptomatic patients and identifying indications for aortic valve replacement. →

Assessment of aortic regurgitation includes auscultation and imaging of ventricular and aortic changes; aortic root dilatation can determine the required operation. →

Tricuspid stenosis is usually rheumatic and commonly accompanies other valve disease when it occurs in rheumatic heart disease. →

Tricuspid stenosis produces signs of impaired right ventricular filling and right heart failure, although associated mitral and aortic valve disease may dominate the symptoms. The passage also lists causes of tricuspid regurgitation. →

The described interventions depend on whether tricuspid stenosis is isolated or the patient already requires surgery to other valves. →

Tricuspid regurgitation is common, and its most frequent mechanism is functional. →

Tricuspid regurgitation may cause nonspecific symptoms, but characteristic jugular venous and hepatic findings help identify it. →

Management varies with the cause of regurgitation, pulmonary artery pressure, valve damage and whether mitral valve surgery is planned. →

Pulmonary stenosis is usually congenital, although it may also occur in carcinoid syndrome. →

Pulmonary stenosis produces characteristic auscultatory findings, with additional signs in severe disease. →

Investigation establishes pulmonary stenosis and may demonstrate associated ventricular and pulmonary artery changes. →

Treatment requirements depend on severity; mild to moderate isolated disease usually requires no intervention. →

Pulmonary regurgitation is rare in isolation and is usually associated with pulmonary artery dilatation caused by pulmonary hypertension. →

Diseased heart valves may be replaced with mechanical or biological prostheses, which differ in their usual heart sounds. →

Mechanical and biological heart valves differ in their anticoagulation requirements, durability and suitability for different patients. →

Transcatheter aortic valve implantation (TAVI) is an alternative to surgical aortic valve replacement, especially for aortic stenosis. →

Prosthetic valve dysfunction may present with unexplained heart failure and can arise through different mechanisms in mechanical and biological valves. →

Infective endocarditis is microbial infection involving cardiac or vascular structures and can affect native or prosthetic valves. →

The target material describes transcatheter aortic valve implantation and the distinctive presentation of endocarditis in old age. →

Infective endocarditis affects many older patients and can occur without a recognised pre-existing cardiac abnormality. →

Endothelial damage favours infection during bacteraemia, followed by vegetation formation, local destruction and systemic complications. →

The organisms causing endocarditis differ in their routes of bloodstream entry, clinical behaviour and associated conditions. →

Postoperative infections, animal exposure, fastidious organisms and fungal infections produce distinct associations and diagnostic challenges in infective endocarditis. →

The modified Duke criteria combine microbiological findings, evidence of endocardial involvement and minor clinical findings to classify endocarditis. →

Infective endocarditis may present acutely or develop insidiously. Subacute disease can initially go unrecognised and later cause sudden serious complications. →

Subacute endocarditis can produce cutaneous, digital, splenic and urinary findings that help prompt recognition of underlying heart disease. →

Endocarditis may produce peripheral clinical signs, a severe acute illness, or infection following heart valve surgery. →

Investigation identifies the organism, assesses vegetations and valve damage, detects complications, and monitors treatment progress. →

The supplied treatment material relates antimicrobial selection to organism susceptibility and valve type, and provides explicit instructions for alternatives and drug-level monitoring. →

Management combines multidisciplinary care, removal of infection sources, and antimicrobial selection based on presentation, suspected organism, prosthetic valves and penicillin allergy. →

Short-course treatment requires the listed microbiological, cardiac and clinical conditions to be satisfied. →

Surgery may be required to address valve damage, uncontrolled infection or embolic risk in infective endocarditis. →

The passage gives a limited statement on prevention of endocarditis during oro-dental procedures. →

The passage continues a list of patients considered susceptible to endocarditis. →

The table gives the percentage of all congenital heart defects represented by each lesion. →

Congenital heart disease may originate during cardiac formation or during the normal anatomical transition from fetal to newborn circulation. →

Normal fetal blood flow and cardiac development help explain the anatomical defects and maternal associations described in congenital heart disease. →

Congenital heart disease can present throughout life, with different manifestations and postoperative complications appearing at different ages. →

Clinical findings depend on the anatomical lesion, the direction of shunting, vascular resistance and associated congenital conditions. →

Persistent high pulmonary flow from a left-to-right shunt can cause irreversible pulmonary vascular disease. The target also describes the routes of blood flow in fetal circulation. →

The target passage describes the transition to pulmonary circulation at birth and the consequences of shunt reversal in prolonged pulmonary hypertension. →

Pregnancy increases circulatory demands, and its tolerance in congenital heart disease depends on the underlying condition. →

Persistent ductus arteriosus is an anomaly in which normal closure of the ductus after birth fails to occur. →

The ductus carries blood from the pulmonary artery to the aorta during fetal life, whereas its persistence produces an aorta-to-pulmonary artery shunt. →

Clinical manifestations vary with shunt size and may change when pulmonary vascular resistance increases. →

A persistent ductus arteriosus connects the aorta and pulmonary artery, with left-to-right shunting. →

Management depends on shunt significance, pulmonary resistance, ductal structure and whether ductal flow supports lung perfusion. →

Coarctation of the aorta is associated with other cardiovascular and cerebral vascular abnormalities; acquired disease is rare. →

Aortic narrowing near the ductal junction produces different circulatory effects proximal and distal to the obstruction. →

Aortic coarctation produces contrasting circulatory findings in the upper and lower body, with additional signs from associated valve disease and collateral vessels. →

Investigations identify the aortic narrowing, collateral-related radiographic changes and evidence of left ventricular hypertrophy. →

Coarctation involves narrowing of the aorta; the illustrated CT shows severe narrowing of the proximal descending aorta just beyond the arch. →

Atrial septal defect is a common congenital heart defect. Its anatomical types differ in location and associated valve abnormalities. →

Differences in ventricular compliance explain the atrial shunt and the resulting enlargement of right-sided cardiovascular structures. →

Atrial septal defect may remain asymptomatic for years. Its characteristic physical signs reflect right ventricular volume overload. →

Investigation of an atrial septal defect demonstrates the defect itself and the effects of left-to-right shunting on the right ventricle and pulmonary circulation. →

The target passage illustrates an atrial septal defect on transoesophageal echocardiography and explains how a percutaneous device seals it. →

Management depends on the magnitude of pulmonary flow and the presence of pulmonary hypertension or shunt reversal. →

The clinical findings of a ventricular septal defect vary with defect size, right ventricular pressure and the haemodynamic effect of the shunt. →

Treatment of ventricular septal defects depends on cardiac failure, development of pulmonary hypertension and the presence of Eisenmenger syndrome. →

Tetralogy of Fallot combines pulmonary stenosis, an overriding aorta, a ventricular septal defect and right ventricular hypertrophy. →

Tricuspid atresia, transposition of the great arteries, pulmonary atresia and Ebstein anomaly have distinct anatomical abnormalities, shunt pathways and treatment possibilities. →

Adults with surgically treated congenital heart disease may develop ventricular failure or arrhythmias and require continuing specialist follow-up. →

Myocarditis is often diagnosed after more common causes of cardiac dysfunction have been excluded. Imaging, blood markers and occasionally biopsy support assessment. →

Management of dilated cardiomyopathy focuses on heart failure control and reduction of sudden arrhythmic death risk. →

Obliterative cardiomyopathy is a rare form of restrictive cardiomyopathy affecting the endocardium of one or both ventricles. →

Systemic diseases and toxic exposures can cause heart muscle disease resembling different cardiomyopathy patterns. Treatment and prognosis depend on the underlying disorder. →

Primary cardiac tumours are rare, while the heart and mediastinum may also be sites of metastatic disease. →

Pericardial effusion may alter heart sounds and cause chest discomfort. Large or rapidly developing effusions can compress the heart and cause acute heart failure. →

The target passage lists clinical features of constrictive pericarditis, illustrates pericardial calcification and continues the discussion of diagnosing and treating tuberculous pericarditis. →

Cardiac tamponade can present with respiratory symptoms, circulatory compromise and characteristic findings on cardiovascular examination. →