Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Cardio-oncology and treatment-related cardiotoxicity
Cardiology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
!
Time-critical presentation
New chest pain, dyspnoea, arrhythmia, conduction disease or haemodynamic instability during immune-checkpoint-inhibitor treatment may be fulminant myocarditis: withhold further doses, obtain urgent ECG and cardiac biomarkers, admit for monitored specialist assessment and do not wait for a normal initial echocardiogram to exclude it.
Overview
Prevent, detect and manage cardiovascular toxicity from cancer therapy while preserving effective anticancer treatment through risk-adapted surveillance and multidisciplinary decisions.
Cardio-oncology spans baseline prevention, toxicity during treatment and late survivorship. Risk depends on the drug or radiation exposure, cumulative dose, combination therapy and pre-existing cardiovascular susceptibility.
Cancer-therapy-related cardiovascular toxicity includes ventricular dysfunction and heart failure, myocarditis, vascular and coronary syndromes, hypertension, arrhythmias, QT prolongation, thrombosis, valve disease and pericardial disease.
The objective is dual: avoid preventable cardiovascular harm without compromising oncological benefit. High-risk or complex decisions belong in a cardio-oncology multidisciplinary team with explicit communication to the patient.
Key points
Perform baseline cardiovascular risk assessment before a potentially cardiotoxic cancer therapy; the intensity of surveillance should match treatment and patient risk.
Record previous cardiovascular disease and cancer treatment, examination, blood pressure, ECG and relevant blood tests; use echocardiography with LVEF and GLS when the regimen or risk warrants it.
Practice
Two practice questions
Your practice draft is saved in this browser.
Question 1 of 2
0 correct
CardiologyOriginal SBA
Checkpoint-inhibitor red flag
A patient receiving an immune checkpoint inhibitor develops ptosis, chest discomfort, a rising troponin and new complete heart block. What is the best immediate approach?
Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Anthracycline toxicity is related to cumulative exposure; HER2-targeted treatment commonly causes left-ventricular dysfunction that may improve with interruption and cardiac therapy.
A relative fall in global longitudinal strain greater than 15% from baseline can identify subclinical cancer-therapy-related cardiac dysfunction before LVEF falls.
Immune-checkpoint-inhibitor myocarditis is uncommon but potentially rapidly fatal and can coexist with myositis or myasthenic features.
VEGF-pathway inhibitors often cause hypertension; BTK inhibitors can cause atrial fibrillation; fluoropyrimidines can provoke coronary vasospasm; several treatments prolong QT.
Do not stop effective cancer treatment reflexively for every abnormal test: grade severity and use cardio-oncology–oncology multidisciplinary decision-making.
Thoracic radiotherapy can cause coronary, valve, myocardial, pericardial and vascular disease years later, so survivorship history must include radiation field and dose.
Aetiology
01
Anthracycline-related myocardial injury
Anthracyclines can cause dose-related cumulative cardiomyocyte injury, with greater vulnerability in people with prior heart disease, cardiovascular risk, earlier cardiotoxic therapy or higher cumulative exposure.
02
HER2-pathway treatment
HER2-targeted therapy can impair cardiomyocyte survival signalling and cause LV dysfunction, particularly after anthracyclines. Dysfunction may improve with treatment interruption and cardiac therapy, but recovery is not guaranteed.
03
Immune-checkpoint inhibition
Loss of immune restraint can produce myocarditis, sometimes alongside myositis or myasthenia. Although uncommon, early conduction disease or ventricular arrhythmia makes this a high-consequence toxicity.
04
Vascular, electrical and radiation injury
VEGF-pathway inhibition can cause hypertension, fluoropyrimidines vasospasm, BTK inhibitors AF, and several drugs QT prolongation. Thoracic radiotherapy may cause coronary, valve, myocardial and pericardial disease years later.
Pathophysiology
1
Shared context: treatment and host susceptibility
Each therapy-specific exposure acts on a background of age, cardiovascular disease, risk factors and previous cancer treatment. Combination and cumulative exposure can reduce cardiovascular reserve further.
2
Myocardial branch: injury or signalling dysfunction
Anthracycline-related cellular injury or disruption of protective signalling during HER2-targeted therapy can reduce cardiomyocyte function. Subclinical change may first appear as a biomarker rise or relative GLS decline before LVEF falls.
3
Immune branch: potentially rapid myocarditis
Checkpoint inhibition may activate myocardial and conduction-system inflammation, causing troponin release, AV block, ventricular arrhythmia or pump failure despite an initially preserved LVEF.
4
Vascular and electrical branches
Depending on the treatment, hypertension can increase afterload, vasospasm or thrombosis can reduce coronary flow, and electrophysiological effects can contribute to QT prolongation, bradyarrhythmia or AF.
5
Outcome branch: remodelling or late radiation disease
Persistent myocardial injury can lead to fibrosis, dilatation and heart failure. Separately, radiation-related endothelial and tissue damage can evolve over years into premature coronary, valve, myocardial, vascular or pericardial disease.
Clinical features and red flags
Ventricular dysfunction or heart failure
New fatigue, breathlessness, orthopnoea, oedema, raised natriuretic peptide, reduced LVEF or a greater than 15% relative GLS decline during anthracycline, HER2 or other cardiotoxic treatment.
Immune-checkpoint-inhibitor myocarditisRed flag
Chest pain, dyspnoea, palpitations, syncope, troponin rise, new ECG change, AV block or ventricular arrhythmia; associated skeletal-muscle weakness, ptosis or dysphagia heightens concern.
Treatment-related ischaemia
Rest or treatment-linked chest pain with fluoropyrimidines may reflect coronary vasospasm; other therapies can accelerate thrombosis or atherosclerosis and require an ACS assessment.
Hypertension
A new or marked BP rise is particularly associated with VEGF-pathway inhibition and can precipitate heart failure, ischaemia or treatment interruption.
Arrhythmia or electrical toxicity
Atrial fibrillation, bradycardia, conduction block or QT prolongation may be therapy-related; check symptoms, interacting drugs and potassium, magnesium and calcium.
Late radiation injury
Years after mediastinal or left-sided chest radiotherapy, premature coronary disease, valve disease, pericardial constriction, cardiomyopathy or aortic disease may present earlier than expected.
Investigations
01Baseline cardiovascular assessmentFirst step
Why
Define pre-existing disease and therapy-specific risk before treatment.
Interpretation and limitations
Integrate cancer history and planned cumulative exposure with symptoms, examination, BP, ECG, lipids, glucose/HbA1c, renal function and prior cardiac/radiation records; do not use one test in isolation.
02Transthoracic echocardiography with 3D LVEF and GLS where feasible
Why
Establish baseline function and detect treatment-related change.
Interpretation and limitations
Use the same method and compare with baseline; a relative GLS reduction greater than 15% is significant even when LVEF remains preserved.
03Cardiac troponin and natriuretic peptide
Why
Detect myocardial injury or haemodynamic stress in selected regimens and risk groups.
Interpretation and limitations
Obtain a baseline if serial surveillance is planned; interpret trends with renal function, sepsis, pulmonary embolism and symptoms rather than labelling every rise as therapy toxicity.
04Resting 12-lead ECG
Why
Measure rhythm, conduction and QTc at baseline and during relevant therapies or symptoms.
Interpretation and limitations
A new conduction defect or ventricular arrhythmia during checkpoint inhibition is an emergency signal; correct electrolytes and review all QT-prolonging drugs.
Differential diagnosis
01
Cancer progression, anaemia or deconditioning
Breathlessness and fatigue may reflect tumour burden, anaemia or reduced conditioning rather than cardiac toxicity. Examination, blood count, imaging and objective ventricular or haemodynamic change help discriminate.
02
Acute coronary syndrome
New chest pain and troponin rise require standard ACS assessment even during potentially cardiotoxic therapy. Territorial ECG or wall-motion change and coronary imaging support an ischaemic mechanism.
03
Pulmonary embolism
Cancer and its treatment increase thrombosis risk. Abrupt dyspnoea, hypoxaemia, pleuritic pain, DVT features or RV strain should trigger probability-based pulmonary vascular assessment.
04
Sepsis or systemic inflammation
Infection can cause troponin elevation, tachycardia and potentially reversible ventricular dysfunction. Fever, cultures, inflammatory trajectory, exposure timing and the broader organ pattern help with attribution, although overlap with treatment toxicity is possible.
05
Non-treatment myocarditis or stress cardiomyopathy
Viral myocarditis and stress cardiomyopathy can mimic checkpoint-inhibitor or chemotherapy injury. Exposure timing, CMR pattern, coronary assessment and selected biopsy inform attribution, which may remain uncertain.
Management
01FirstBaseline risk before treatmentFirst stepA cancer therapy with recognised cardiovascular toxicity is planned.+
1Identify previous cardiovascular disease, risk factors, pregnancy potential, earlier anthracycline/HER2 therapy and thoracic radiotherapy; examine and record BP.
2Obtain ECG and relevant blood tests; arrange LVEF/GLS and baseline biomarkers according to the planned treatment and risk.
3Correct modifiable risk factors and optimise established cardiovascular disease without unnecessarily delaying time-sensitive cancer treatment.
4Refer high- or very-high-risk patients to cardio-oncology and agree a treatment-specific surveillance schedule.
02NextSurveillance during cancer therapyAnthracycline, HER2-targeted, VEGF-pathway, kinase-inhibitor or another cardiotoxic treatment is underway.+
1
Complications
01
LV dysfunction and heart failure
Myocardial injury or treatment-related signalling dysfunction can cause asymptomatic ventricular dysfunction, overt congestion or cardiogenic shock. It may also force interruption of effective cancer treatment and affect long-term survival.
02
Fulminant myocarditis
Checkpoint-inhibitor myocarditis can rapidly cause complete heart block, ventricular arrhythmia, biventricular failure and death, even when the first echocardiographic LVEF appears normal.
03
Ischaemia and infarction
Coronary vasospasm, thrombosis, accelerated atherosclerosis or radiation-related disease can produce ACS. Cancer-related bleeding and thrombocytopenia can complicate antithrombotic and invasive management.
04
Arrhythmia and sudden death
AF may worsen heart failure or embolic risk, while QT prolongation, conduction block and ventricular arrhythmia can cause syncope, torsades or cardiac arrest.
05
Late radiation cardiovascular disease
Years after thoracic radiotherapy, coronary stenosis, valve fibrosis, restrictive myocardial disease, pericardial constriction or aortic pathology may emerge, requiring durable survivorship records and surveillance.
Monitoring and follow-up
Keep a cumulative treatment record, including anthracycline-equivalent dose and thoracic radiation field/dose.
Measure blood pressure regularly during therapies associated with hypertension and treat sustained elevation promptly.
Use serial LVEF and GLS with the same imaging method and laboratory biomarkers from the same assay where practical.
For Herceptin-brand trastuzumab, repeat the baseline cardiac assessment every 3 months during treatment and every 6 months after stopping until 24 months from the last dose; after anthracycline-containing early-breast-cancer therapy, continue yearly up to 5 years, or longer if LVEF continues to fall. Check the actual product SmPC and oncology protocol.
Review QTc, potassium, magnesium, calcium and interacting medicines when using a QT-prolonging regimen.
At treatment completion, document risk-stratified follow-up and communicate it to primary care, oncology, cardiology and the patient.
Special situations
GLS can move first
A greater than 15% relative reduction from baseline may reveal subclinical dysfunction before a meaningful LVEF fall.
Normal LVEF does not exclude myocarditis
Checkpoint-inhibitor myocarditis can present with preserved systolic function but dangerous conduction disease or ventricular arrhythmia.
Biomarkers need a baseline
Serial troponin or natriuretic peptide is most useful when a pretreatment value and a predefined surveillance purpose exist.
Toxicity is treatment-specific
Anthracycline, HER2 therapy, fluoropyrimidine, VEGF inhibition, BTK inhibition, checkpoint inhibition and radiotherapy have different dominant phenotypes and timelines.
Stopping cancer therapy has a cost
Severity, reversibility, cancer prognosis and alternatives must be weighed jointly; a single mild abnormality should not trigger an unexamined permanent stop.
The history extends for decades
Late cardiovascular disease after chest radiation or anthracyclines remains relevant in adult survivors treated during childhood or young adulthood.
Common pitfalls
01
Starting cardiotoxic therapy without documenting baseline cardiovascular risk and measurements needed for comparison.
02
Excluding checkpoint-inhibitor myocarditis because the initial echocardiographic LVEF is normal.
03
Calling any troponin rise cardiotoxicity without assessing ACS, pulmonary embolism, sepsis, renal impairment and other causes.
04
Stopping effective cancer therapy reflexively without grading toxicity and multidisciplinary discussion.
05
Discharging a survivor without a cumulative exposure record or a long-term cardiovascular surveillance plan.
Clinical stateAwaiting review
JurisdictionUnited Kingdom
05Cardiac magnetic resonance
Why
Characterise suspected myocarditis, infiltrative disease or an unclear ventricular phenotype.
Interpretation and limitations
CMR can support myocarditis diagnosis but a non-diagnostic scan does not override strong clinical concern; endomyocardial biopsy may be needed in selected unstable or uncertain cases.
06Coronary and pulmonary vascular assessment
Why
Investigate chest pain, dyspnoea or thrombosis according to the suspected syndrome.
Interpretation and limitations
Use standard urgent pathways for ACS and pulmonary embolism while considering vasospasm, thrombosis, anaemia and cancer-related competing risks.
Ask about cardiovascular symptoms and measure BP at clinically appropriate treatment visits; review ECG/QTc for therapies with electrical risk.
2Repeat echocardiography and biomarkers at the regimen- and risk-specific intervals, using comparable technique and the baseline value.
3AlternativeIf a new abnormality appears, repeat/confirm as appropriate, grade the toxicity and exclude alternative causes such as sepsis, anaemia, PE or progression of prior disease.
4Use an oncology–cardio-oncology discussion to decide cardiac treatment, closer surveillance, cancer-therapy continuation, interruption or substitution.
03EscalationSuspected checkpoint-inhibitor myocarditisEscalationCompatible symptoms, troponin rise, new ECG change, conduction disease or ventricular arrhythmia during or soon after checkpoint inhibition.+
1Withhold checkpoint-inhibitor treatment and arrange urgent monitored admission with oncology and cardiology/cardio-oncology input.
2Obtain serial ECG, troponin, natriuretic peptide, FBC, renal/electrolyte tests, CK and echocardiography; assess for concurrent myositis or myasthenia.
3Use CMR and, in selected unstable or diagnostically uncertain cases, endomyocardial biopsy without delaying treatment when suspicion is high.
4ConfirmatoryOnce ICI myocarditis is considered likely, start methylprednisolone 500–1000 mg IV once daily for 3–5 days; do not delay the first dose in an unstable patient while confirmatory tests are pending. Monitor for block/ventricular arrhythmia and plan any future immunotherapy only through multidisciplinary review.
04Long termEnd-of-treatment and survivorship planCompletion of cardiotoxic therapy or a history of relevant cancer treatment.+
1Record cumulative drugs/doses, radiation field/dose, cardiovascular events and the end-of-treatment ECG, biomarkers and imaging where indicated.
2Re-stratify risk and give a written plan covering symptoms, risk-factor control and the timing of clinical review and repeat imaging.
3Continue cardiology follow-up for treatment-related dysfunction and structured long-term surveillance for high-risk anthracycline or chest-radiation exposure.
4Investigate new late symptoms on their merits; do not dismiss them because cancer treatment ended years earlier.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
Urgent first-line immunosuppression for both fulminant and non-fulminant immune-checkpoint-inhibitor myocarditis; give promptly in electrical or haemodynamic instability.
Methylprednisolone followed by prednisolone for ICI myocarditis
Methylprednisolone 500–1000 mg IV once daily for 3–5 days once ICI myocarditis is considered likely. If troponin falls by more than 50% from peak within 24–72 hours and LV dysfunction, AV block and arrhythmias resolve, switch to prednisolone 1 mg/kg orally once daily, maximum 80 mg/day, then taper under specialist surveillance.
Level 2/3 monitored care with oncology and cardio-oncology/cardiology input is required. Exclude ACS and infection in parallel without delaying lifesaving treatment; monitor glucose, BP, electrolytes, infection, GI and neuropsychiatric toxicity. Persistent troponin elevation, AV block, ventricular arrhythmia or LV dysfunction after 3 days indicates steroid-refractory disease needing urgent second-line multidisciplinary treatment.