Cardiology: Investigations

• Bedside: Key Bedside Signs
• The ECG: Reading an ECG | Cardiac Axis | Conduction Problems | Hypertrophy and Chamber Enlargement | Ischaemia and Infarction | Other Important ECG Patterns | Normal Variants and the Athlete's ECG
• Rhythm monitoring and testing: Ambulatory Rhythm Monitoring | Exercise Testing | Tilt Testing and EP Studies
• Imaging: Echocardiography | CT Coronary Angiography | Functional (Stress) Imaging | Cardiac MRI | Nuclear Cardiology and PET | Invasive Coronary Angiography | Right Heart Catheterisation
• Blood tests: Troponin | Natriuretic Peptides | Other Cardiac Blood Tests
• Revision: ECG Patterns at a Glance | Spot the Diagnosis | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🔬 Cardiac investigations answer three questions: what is the rhythm, how is the heart structured and working, and is the blood supply adequate? This chapter explains how to read an ECG systematically, which imaging test to choose (echo, CT, MRI, nuclear, angiography), and how to interpret troponin and natriuretic peptides.
Your four questions for every patient: What does the ECG show, and has it changed? What is the structure and function on echo? Is there coronary disease, and is it causing ischaemia? Do the blood tests fit the clinical picture?

Key Bedside Signs

Pulse character:

• Slow-rising, low-volume - aortic stenosis.
• Collapsing (water-hammer) - aortic regurgitation, PDA, high-output states.
• Bisferiens (double peak) - mixed aortic valve disease, HCM.
• Pulsus alternans (alternating strong and weak beats) - severe LV failure.
• Pulsus paradoxus (systolic fall of more than 10 mmHg on inspiration) - tamponade, severe asthma.
• Irregularly irregular - AF.
• Radio-femoral delay - coarctation.

Jugular venous pressure (JVP):

• Raised - right heart failure, fluid overload, tamponade, constriction, SVC obstruction (non-pulsatile).
• Large V waves - tricuspid regurgitation.
• Cannon A waves - complete heart block, VT (atria contract against closed valves).
• Absent A waves - AF.
• Kussmaul's sign (JVP rises on inspiration) - constrictive pericarditis, restrictive cardiomyopathy, RV infarction.

Heart sounds:

• Loud S1 - mitral stenosis.
• Soft S2 - severe aortic stenosis.
• Loud P2 - pulmonary hypertension.
• Fixed split S2 - ASD.
• S3 - heart failure (or normal in young people).
• S4 - stiff ventricle (LVH, HCM).
• Opening snap - mitral stenosis.
• Ejection click - bicuspid aortic valve.
• Mid-systolic click - mitral valve prolapse.
• Pericardial knock - constriction.

Murmurs are covered in detail in the Valvular Heart Disease chapter.

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Reading an ECG

Paper and timing (standard speed 25 mm/s):

• 1 small square = 0.04 s; 1 large square = 0.2 s.
• Heart rate = 300 ÷ number of large squares between R waves (regular rhythm), or the number of QRS complexes on a 10-second strip × 6.

A systematic approach - every time:

• 1. Patient details, date, calibration (10 mm = 1 mV).
• 2. Rate.
• 3. Rhythm - regular or irregular? P wave before every QRS? (sinus rhythm).
• 4. Axis.
• 5. P waves - shape (P mitrale, P pulmonale), absent (AF), flutter waves.
• 6. PR interval - normal 0.12–0.20 s:
  • Long - heart block.
  • Short - pre-excitation (WPW).
• 7. QRS - width (normal below 0.12 s), height (hypertrophy or low voltage), Q waves, delta waves.
• 8. ST segment - elevation or depression.
• 9. T waves - inversion, peaked, flattened.
• 10. QT interval - corrected for rate (QTc).
  • Normal below about 440 ms (men) and 460 ms (women).
  • Above 500 ms - high risk of torsades.
• 11. Compare with old ECGs - the most useful step of all.

💡 Clinical Pearl: Always compare with a previous ECG. A "new" LBBB, Q wave or T wave inversion is far more meaningful than one that has been there for years.

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Cardiac Axis

• What it shows: The overall direction of electrical activity through the ventricles. Normal is −30° to +90°.
• Quick method - look at the QRS in leads I and II (or aVF):
  • Both positive - normal axis.
  • Lead I positive, lead II negative - left axis deviation.
  • Lead I negative, aVF positive - right axis deviation.
• Causes of left axis deviation:
  • Left anterior fascicular block (the commonest).
  • Inferior MI.
  • LVH.
  • WPW.
  • Primum ASD.
  • Hyperkalaemia.
• Causes of right axis deviation:
  • RV hypertrophy or strain - pulmonary hypertension, PE, COPD.
  • Left posterior fascicular block.
  • Lateral MI.
  • Dextrocardia.
  • Secundum ASD.
  • Normal in tall, thin young people.

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Conduction Problems

• First-degree AV block: PR above 0.20 s; every P conducted. Usually benign.
• Second-degree AV block:
  • Mobitz I (Wenckebach) - PR lengthens until a beat is dropped. Usually AV node, often benign.
  • Mobitz II - sudden dropped beats with a constant PR. Below the AV node - risk of complete block, needs a pacemaker.
  • 2:1 block - cannot classify as type I or II.
• Third-degree (complete) heart block: P waves and QRS complexes are independent (AV dissociation). Slow escape rhythm; broad complexes mean a lower, less reliable escape.
• Right bundle branch block (RBBB):
  • QRS 0.12 s or more, RSR′ in V1 ("M"), wide slurred S in I and V6.
  • Can be normal, or seen with ASD, PE or RV strain.
• Left bundle branch block (LBBB):
  • QRS 0.12 s or more, broad notched R in I, aVL and V6 ("M" in V6), deep S in V1 ("W").
  • Always abnormal - IHD, hypertension, cardiomyopathy, aortic stenosis.
  • New LBBB with chest pain may be an MI.
• Fascicular blocks:
  • Left anterior fascicular block - left axis deviation.
  • Left posterior fascicular block - right axis deviation.
  • Bifascicular block - RBBB plus a fascicular block.
  • Trifascicular - bifascicular plus a long PR. With syncope, this suggests intermittent complete heart block.
• Pre-excitation (WPW): Short PR, delta wave (slurred QRS upstroke), broad QRS - an accessory pathway.

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Hypertrophy and Chamber Enlargement

• Left ventricular hypertrophy:
  • Sokolow–Lyon criterion: S wave in V1 plus R wave in V5 or V6 above 35 mm.
  • Often with a "strain" pattern - ST depression and T wave inversion in lateral leads.
  • Causes: Hypertension, aortic stenosis, HCM, coarctation.
  • Voltage criteria alone are common (and normal) in young, thin people and athletes.
• Right ventricular hypertrophy:
  • Dominant R wave in V1; right axis deviation; T wave inversion in V1–V3; deep S waves in V5–V6.
  • Causes: Pulmonary hypertension, pulmonary stenosis, COPD, congenital heart disease.
• Causes of a dominant R wave in V1:
  • RVH.
  • Posterior MI.
  • RBBB.
  • WPW (type A).
  • Dextrocardia.
  • HCM.
  • Normal in children.
• Atrial enlargement:
  • P mitrale - broad, notched P in II, suggesting left atrial enlargement (mitral stenosis).
  • P pulmonale - tall, peaked P in II, suggesting right atrial enlargement (pulmonary hypertension).
• Low-voltage QRS (small complexes in all leads):
  • Pericardial effusion.
  • Obesity; emphysema.
  • Hypothyroidism.
  • Cardiac amyloidosis - low voltages with a thick heart on echo is a classic clue.

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Ischaemia and Infarction

• ST elevation in 2 or more contiguous leads - acute coronary occlusion (STEMI). See the Cardiac Emergencies chapter for criteria and equivalents.
• ST depression and T wave inversion - ischaemia (NSTEMI, unstable angina), strain, digoxin, or reciprocal change.
• Pathological Q waves - previous transmural MI (wider than 0.04 s, or deeper than 25% of the R wave).
• Wellens' sign: Deep or biphasic T wave inversion in V2–V3 in a pain-free patient after chest pain - critical proximal LAD stenosis. Needs urgent angiography, and no exercise testing.
• Persistent ST elevation weeks after an MI - LV aneurysm.

Coronary territories:

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Other Important ECG Patterns

• Hyperkalaemia: Peaked T waves, then flat P waves, long PR, broad QRS, sine wave, VF.
• Hypokalaemia: Flat T waves, ST depression, U waves, apparent long QT.
• Hypocalcaemia: Long QT. Hypercalcaemia: Short QT.
• Hypomagnesaemia: Long QT, torsades.
• Digoxin effect: "Reverse tick" (sloping) ST depression - not by itself toxicity. Toxicity causes almost any arrhythmia.
• Hypothermia: Bradycardia, J (Osborn) waves, long intervals, shivering artefact.
• Pericarditis: Widespread saddle ST elevation with PR depression.
• Pulmonary embolism:
  • Sinus tachycardia - the commonest finding.
  • RV strain (T inversion V1–V4), RBBB, right axis deviation.
  • S1Q3T3 (uncommon).
• Long QT: Congenital, or acquired (drugs, low potassium, low magnesium, low calcium, bradycardia).
• Brugada pattern: Coved ST elevation in V1–V2 with RBBB-like appearance - risk of sudden death. Unmasked by fever and some drugs.
• ARVC: Epsilon waves and T wave inversion in V1–V3.
• HCM: Marked LVH, deep narrow Q waves, giant T wave inversion (apical HCM).
• Raised intracranial pressure or subarachnoid haemorrhage: Deep, wide T wave inversion ("cerebral T waves"), long QT.
• Dextrocardia: Inverted P and QRS in lead I; poor R wave progression; reversed limb leads look similar (check lead placement).

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Normal Variants and the Athlete's ECG

Common, normal findings - especially in trained athletes:

• Sinus bradycardia (even 30–40 at rest); sinus arrhythmia (rate varies with breathing).
• First-degree AV block and Mobitz I (Wenckebach) at night.
• Isolated voltage criteria for LVH.
• Early repolarisation - ST elevation with J point notching in the lateral and inferior leads.
• T wave inversion in V1–V4 preceded by J point elevation - normal in Black athletes.
• Incomplete RBBB.
• T wave inversion in V1–V3 in children and adolescents (under 16).

Abnormal findings that need investigation (international athlete ECG criteria):

• T wave inversion in the lateral or inferolateral leads (HCM, cardiomyopathy).
• ST depression.
• Pathological Q waves.
• LBBB.
• Pre-excitation.
• Long QT (QTc 470 ms or more in men, 480 ms or more in women).
• Brugada pattern; epsilon waves.
• Mobitz II or complete heart block.
• Frequent ventricular ectopics; atrial or ventricular arrhythmias.

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Ambulatory Rhythm Monitoring

Choose the monitor to match how often symptoms happen:

• Daily symptoms: 24–48-hour Holter monitor.
• Weekly symptoms: Patch monitors (up to 14 days) or 7-day recorders.
• Less frequent symptoms: Event recorders - patient-activated or looping, worn for weeks.
• Rare symptoms (e.g. unexplained syncope every few months): Implantable loop recorder - a small device under the skin that records for up to 3 years. Also used to look for AF after cryptogenic stroke.
• Consumer devices (smartwatches, handheld ECG devices): Can capture AF and other arrhythmias during symptoms. A clinician should confirm the diagnosis from a recorded ECG trace.

What counts: A symptom with a normal rhythm is as useful as one with an arrhythmia - it rules out an arrhythmic cause.

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Exercise Testing

• Exercise ECG (treadmill):
  • No longer recommended for diagnosing coronary disease (NICE CG95) - sensitivity and specificity are poor.
  • Still useful for:
    • Exercise-related symptoms and arrhythmias (e.g. CPVT, exercise-induced AF).
    • Heart rate response (chronotropic incompetence).
    • BP response.
    • Assessing exercise capacity and prognosis.
    • Asymptomatic severe aortic stenosis (specialist).
    • Testing an accessory pathway in WPW.
  • Contraindications:
    • Acute MI or ACS.
    • Symptomatic severe aortic stenosis.
    • Uncontrolled arrhythmia or heart failure.
    • Acute myocarditis or pericarditis.
    • Aortic dissection.
    • Wellens' pattern.
• Cardiopulmonary exercise testing (CPET): Measures oxygen uptake. Separates heart, lung and fitness causes of breathlessness; assesses heart failure severity (transplant assessment) and fitness for major surgery.

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Tilt Testing and EP Studies

• Head-up tilt table test:
  • The patient is tilted to about 70° for up to 45 minutes, with continuous BP and heart rate monitoring.
  • Reproduces vasovagal syncope, shows delayed orthostatic hypotension, and diagnoses postural orthostatic tachycardia syndrome (PoTS) - a heart rate rise of 30 or more without hypotension.
• Carotid sinus massage (with monitoring, in people over 40 with unexplained syncope; avoid with carotid disease or recent stroke): A pause of more than 3 seconds or a large BP fall suggests carotid sinus hypersensitivity.
• Electrophysiology (EP) study:
  • Catheters inside the heart record electrical activity and try to trigger arrhythmias.
  • Used to diagnose SVT mechanisms, assess conduction disease, and risk-stratify some patients.
  • Usually combined with catheter ablation.

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Echocardiography

• Transthoracic echo (TTE) - the workhorse of cardiology. It shows:
  • LV size and function (ejection fraction; regional wall motion).
  • Valves - stenosis, regurgitation, vegetations.
  • Wall thickness (hypertrophy, HCM, amyloid).
  • Diastolic function and filling pressures.
  • Atrial size.
  • RV function and estimated pulmonary artery pressure.
  • Pericardial effusion.
  • Congenital defects; intracardiac masses and thrombus.
• Transoesophageal echo (TOE) - a probe in the oesophagus, under sedation. Much clearer views of the back of the heart:
  • Endocarditis (prosthetic valves, abscesses).
  • Left atrial appendage thrombus before cardioversion.
  • Mitral valve assessment before repair.
  • ASD and PFO.
  • Aortic dissection.
  • Guiding structural procedures.
• Stress echo (exercise or dobutamine):
  • Shows ischaemia as walls that stop moving well under stress.
  • Assesses viability and low-flow aortic stenosis.
• Bubble contrast echo: Agitated saline injected into a vein to look for shunts - PFO (after cryptogenic stroke) and pulmonary AVMs.
• Contrast echo: Improves image quality when windows are poor; detects LV thrombus.
• Global longitudinal strain: Detects early heart muscle damage - e.g. during chemotherapy (cardio-oncology).

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CT Coronary Angiography

• NICE CG95: CT coronary angiography (CTCA) is the first-line test for people with stable chest pain that could be angina - typical or atypical angina, or non-anginal pain with an abnormal resting ECG. Clinical assessment alone can diagnose angina in some people.
• What it shows:
  • Coronary anatomy and plaques.
  • The degree of narrowing.
  • High-risk plaque features.
  • Coronary anomalies.
  • Bypass graft patency.
  A normal CTCA has a very high negative predictive value.
• Coronary artery calcium score: A quick non-contrast scan. A score of zero means a very low risk of events. It is used to refine cardiovascular risk and decide on preventive treatment.
• Requirements:
  • A slow, regular heart rate (beta-blockers or ivabradine beforehand).
  • Breath-holding.
  • IV contrast (check kidney function and allergy).
  Image quality is reduced in AF, heavy calcification and obesity.
• FFR-CT: Computer analysis of CTCA images that estimates whether a narrowing limits blood flow - this can reduce unnecessary invasive angiograms.
• Other cardiac CT uses: TAVI planning; left atrial anatomy before AF ablation; pericardial calcification; aortic disease.

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Functional (Stress) Imaging

Functional tests show whether a narrowing actually causes ischaemia. NICE recommends them when CTCA shows disease of uncertain significance, or for people with known coronary disease.

• Stress echocardiography - exercise or dobutamine. Wall motion abnormalities under stress. No radiation.
• Myocardial perfusion scintigraphy (SPECT) - a radioactive tracer (technetium) at rest and under stress (exercise, adenosine or regadenoson). Areas of poor uptake under stress mean ischaemia; fixed defects mean scar.
• Stress perfusion cardiac MRI (adenosine) - perfusion defects plus scar imaging in one test, without radiation. Very accurate.
• Vasodilator stress (adenosine, regadenoson):
  • Avoid in severe asthma and high-grade AV block.
  • Stop caffeine and theophyllines for 12–24 hours beforehand (they block the effect).
• Dobutamine stress: Avoid with severe hypertension or significant arrhythmias.

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Cardiac MRI

Why it is special: Cardiac MRI gives the most accurate measurement of chamber size and EF, and uniquely shows tissue character - scar, inflammation, fat, iron and infiltration.

• Late gadolinium enhancement (LGE) - the pattern of scar suggests the cause:
  • Subendocardial or transmural, in a coronary territory - infarction.
  • Mid-wall stripe - dilated cardiomyopathy.
  • Patchy - HCM (at RV insertion points).
  • Subepicardial or patchy - myocarditis; sarcoidosis.
  • Diffuse subendocardial, with abnormal gadolinium handling - amyloidosis.
• T2 imaging and mapping - oedema (acute myocarditis, acute MI, Takotsubo).
• T2* imaging - iron overload (thalassaemia, haemochromatosis).
• T1 mapping and extracellular volume - diffuse fibrosis, amyloid, Fabry disease (low T1).
• Other uses:
  • Viability - will a damaged area recover after revascularisation?
  • Congenital heart disease.
  • Pericardial disease.
  • Cardiac masses.
  • Aorta.
  • Stress perfusion.
• Limitations:
  • Long scan; claustrophobia.
  • Some devices are not MRI-conditional (check pacemakers and ICDs).
  • Gadolinium caution in severe CKD.
  • Arrhythmia degrades images.

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Nuclear Cardiology and PET

• Bone scintigraphy (DPD or PYP scan) - for ATTR cardiac amyloidosis:
  • Strong cardiac uptake (Perugini grade 2–3), together with no monoclonal protein in the blood and urine (serum free light chains, immunofixation), diagnoses ATTR without a biopsy.
  • A monoclonal protein must be excluded, because AL amyloid can also take up the tracer.
• MUGA scan (radionuclide ventriculography) - reproducible EF measurement. Historically used for chemotherapy monitoring; now often replaced by echo or MRI.
• FDG-PET:
  • Cardiac sarcoidosis (inflammation) - needs a special diet beforehand to suppress normal heart uptake.
  • Prosthetic valve and device infection.
  • Large-vessel vasculitis.
  • Viability.
• SPECT perfusion imaging - see Functional (Stress) Imaging.

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Invasive Coronary Angiography

• What it is: Catheters passed from the wrist (radial - preferred, fewer bleeding complications) or groin (femoral) into the coronary arteries. Contrast shows any narrowing, and angioplasty and stenting (PCI) can be done at the same time.
• Indications:
  • STEMI (primary PCI) and high-risk NSTEMI.
  • Angina not controlled by drugs.
  • Inconclusive non-invasive tests.
  • Before valve surgery.
  • Unexplained heart failure.
  • Survivors of cardiac arrest.
• Physiological assessment:
  • Fractional flow reserve (FFR) or iFR - a pressure wire measures whether a narrowing limits flow.
  • FFR of 0.80 or less means significant - PCI improves outcomes.
• Intracoronary imaging (IVUS, OCT) - plaque detail, sizing stents, SCAD.
• Microvascular and spasm testing (acetylcholine, adenosine) - for angina with normal coronaries (INOCA).
• Complications (about 1 in 1,000 serious):
  • Access-site bleeding, haematoma, pseudoaneurysm.
  • Contrast nephropathy (hydrate; check renal function).
  • Contrast allergy.
  • Stroke.
  • MI, coronary dissection.
  • Arrhythmias.
  • Death.
• Before the procedure:
  • Hold metformin around the procedure if kidney function is impaired.
  • Manage anticoagulants.
  • Check kidney function and allergies.

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Right Heart Catheterisation

• What it measures: Pressures in the right atrium, right ventricle and pulmonary artery, the pulmonary artery wedge pressure (an estimate of left atrial pressure), cardiac output, and oxygen saturations in each chamber.
• Uses:
  • Diagnosing pulmonary hypertension (mean PAP above 20 mmHg) and classifying it (pre- or post-capillary), plus vasoreactivity testing.
  • Shunt detection - a "step-up" in oxygen saturation (e.g. ASD, VSD).
  • Constriction versus restriction - simultaneous left and right heart pressures.
  • Heart transplant and LVAD assessment.
  • Guiding treatment in cardiogenic shock.

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Troponin

• What it shows: Troponin I and T are proteins released when heart muscle cells are damaged. High-sensitivity assays detect tiny amounts, allowing MI to be ruled in or out within hours.
• Rapid pathways (NICE DG40) - use the local assay protocol:
  • 0 and 1-hour or 0 and 3-hour testing.
  • A single very low result more than 3 hours after symptom onset can rule out MI in low-risk patients.
• Myocardial infarction requires a rise and/or fall of troponin, with at least one value above the 99th centile, plus clinical evidence of ischaemia (symptoms, ECG, imaging).
• Chronic (stable) raised troponin without a change - CKD, heart failure, LVH, older age.
• Other causes of raised troponin ("myocardial injury" without coronary occlusion):
  • Type 2 MI - supply–demand mismatch (anaemia, tachyarrhythmia, hypotension, sepsis, hypoxia).
  • PE.
  • Myocarditis, pericarditis.
  • Takotsubo syndrome.
  • Aortic dissection.
  • Heart failure.
  • Sepsis and critical illness.
  • Stroke and subarachnoid haemorrhage.
  • CKD.
  • Cardiac contusion, cardioversion, ablation.
  • Chemotherapy.
  • Extreme exercise.
  • Rhabdomyolysis (troponin T).

💡 Clinical Pearl: Troponin tells you the heart is damaged, not why. Interpret it with the history, ECG and the change between samples - and treat the cause rather than reflexively giving ACS treatment.

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Natriuretic Peptides

• What they are: BNP and NT-proBNP are released by stretched ventricular muscle.
• Heart failure diagnosis (NICE NG106) - NT-proBNP:
  • Above 2,000 ng/L - echo and specialist assessment within 2 weeks.
  • 400–2,000 ng/L - within 6 weeks.
  • Below 400 ng/L - heart failure unlikely (untreated).
• Raised by:
  • Age.
  • AF.
  • CKD.
  • PE and pulmonary hypertension.
  • Sepsis.
  • LVH, valve disease, ischaemia.
• Lowered by:
  • Obesity.
  • Heart failure drugs (diuretics, ACE inhibitors, ARBs, beta-blockers, MRAs).
  • Afro-Caribbean family origin (slightly).
• Prognosis: Higher levels mean a worse outlook. Falling levels on treatment are reassuring.
• Sacubitril/valsartan raises BNP (it blocks its breakdown) - use NT-proBNP to monitor.

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Other Cardiac Blood Tests

• Lipids - full profile; non-fasting is fine. Lipoprotein(a) once in people with premature CVD or a family history.
• HbA1c; U&E (potassium, kidney function for drug choice).
• TFTs - AF, heart failure, bradycardia.
• FBC and iron studies - anaemia, iron deficiency in heart failure.
• Magnesium and calcium - arrhythmias, long QT.
• Drug levels - digoxin (take at least 6 hours after the dose).
• Amyloid screen - serum free light chains, serum and urine immunofixation.
• Myocarditis and pericarditis - CRP, viral studies, autoimmune screen.
• Ferritin and transferrin saturation - haemochromatosis (cardiomyopathy).
• D-dimer - only to exclude PE or dissection in low-probability patients.
• Genetic testing - cardiomyopathies, channelopathies, aortopathies, familial hypercholesterolaemia (through specialist inherited cardiac conditions services).

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ECG Patterns at a Glance

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Spot the Diagnosis

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Exam-style Scenarios

1. A 60-year-old woman has exertional central chest tightness relieved by rest. ECG is normal.
Answer: Typical angina - CT coronary angiography (NICE CG95).

• Start antianginal and preventive treatment while awaiting the scan.
• If CTCA shows disease of uncertain significance: functional imaging.

2. A 45-year-old man with heart failure (EF 30%) has normal coronary arteries.
Answer: Non-ischaemic cardiomyopathy.

• Cardiac MRI for the LGE pattern (DCM, myocarditis, sarcoid, amyloid).
• Genetic testing and family screening if DCM.

3. An 80-year-old has a raised troponin after a fall with a hip fracture. He has no chest pain. ECG is unchanged; Hb 85 g/L; HR 115.
Answer: Probable type 2 MI or myocardial injury from anaemia and tachycardia.

• Treat the cause (transfusion, analgesia, fluids).
• Repeat troponin; echo if concerned.
• Do not give automatic ACS anticoagulation before surgery.

4. A 72-year-old man has HFpEF, bilateral carpal tunnel syndrome and a thick LV with low ECG voltages.
Answer: Suspected ATTR cardiac amyloidosis.

• Serum free light chains and serum and urine immunofixation (exclude AL).
• DPD bone scan.
• Cardiac MRI.
• Genetic testing for hereditary ATTR.

5. A 30-year-old woman has palpitations twice a week lasting 10 minutes. Resting ECG is normal.
Answer: A 7–14-day patch monitor or event recorder, to capture symptoms with an ECG.

• Also check TFTs and FBC.
• Echo if there is a murmur or abnormal ECG.

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Key Points

• Read every ECG systematically and compare with old ones.
• Normal values: PR 0.12–0.20 s; QRS below 0.12 s; QTc below about 440 ms (men) or 460 ms (women); above 500 ms is dangerous.
• LBBB is always abnormal; Mobitz II and complete heart block need pacing assessment.
• Know the coronary territories and the patterns for hyper- and hypokalaemia, digoxin, hypothermia, pericarditis, WPW and Brugada.
• Low voltages with a thick heart suggests amyloid.
• Choose the monitor by symptom frequency: Holter (daily), patch or event recorder (weekly), loop recorder (rare).
• CTCA is first-line for suspected stable angina; exercise ECG is no longer used for diagnosis.
• Functional imaging (stress echo, SPECT, stress MRI) or FFR shows whether a narrowing causes ischaemia.
• Cardiac MRI LGE patterns: infarct (subendocardial), DCM (mid-wall), myocarditis (subepicardial), amyloid (diffuse).
• DPD scan plus a negative paraprotein screen diagnoses ATTR amyloid without biopsy.
• Troponin rise and fall plus ischaemia means MI. Many conditions raise troponin.
• NT-proBNP is lowered by obesity and raised by AF, CKD and age.

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Guidelines and Further Reading

• NICE CG95: Recent-onset chest pain of suspected cardiac origin
• NICE DG40: High-sensitivity troponin tests for the early rule out of NSTEMI
• NICE NG106: Chronic heart failure in adults
• Fourth Universal Definition of Myocardial Infarction (2018)
• ESC Guidelines for chronic coronary syndromes (2024)
• International criteria for ECG interpretation in athletes
• British Society of Echocardiography and Society for Cardiovascular Magnetic Resonance guidance