Common Cardiovascular problems

CTR-CVT Definitions

Cancer-therapy related cardiac dysfunction

Encompasses cardiac injury, cardiomyopathy and heart failure[i].

Can be symptomatic of asymptomatic

1. Symptomatic CTRCD

HF syndrome with symptoms and clinical signs of volume overload and/or inadequate perfusion caused by structural and/or functional cardiac abnormalities

BNP <100pg/mL or NT-proBNP <300pg/mL excludes HF in acute setting;
BNP <35pg/mL or NT-proBNP <125pg/mL excludes HF in subacute setting

2. Asymptomatic HF

More frequent in cancer patients then symptomatic HF

Grading is based on the LVEF change; LV GLS and/or biomarkers help further determine severity

Symptomatic CTRCD	Very severe	HF requiring inotropic support, mechanical circulatory support or consideration of heart transplantation
	Severe	HF hospitalization
	Moderate	Need for outpatient intensification of diuretic and HF therapy
	Mild	Mild HF symptoms, no intensification of therapy neede
Asymptomatic CTRCD	Severe	New LVEF reduction to <40%
	Moderate	New LVEF reduction by ≥10 percent points to LVEF 40-49% OR New LVEF reduction by <10 percent points to LVEF 40-49% AND new decline LV GLS >15% from baseline OR new rise in cardiac biomarkers
	Mild	LVEF ≥50% AND new decline LV GLS >15% from baseline AND/OR new rise in cardiac biomarkers

Myocarditis

Myocarditis is an inflammatory disease of the heart; in the case of cancer patients mostly due to direct toxicity or to an immune-mediated event.

Pathohistological diagnosis (EMB)	Multifocal inflammatory cell infiltrates with overt cardiomyocyte loss by light microscopy.
Clinical diagnosis^#&	cTN elevation (new or significant change from baseline) with 1 major criterion or 2 minor criteria after excluding ACS and acute infectious myocarditis based on clinical suspicion. Major criterion: CMR diagnostic for acute myocarditis (modified Lake Louise criteria). Minor criteria: Clinical syndrome (including any of following: fatigue, myalgias, chest pain, diplopia, ptosis, shortness of breath, orthopnea, lower-extremity edema, palpitations, light-headedness/dizziness, syncope, muscle weakness, cardiogenic shock). Ventricular arrhythmias (incl. cardiac arrest) and/or new conduction disease Decline in LV systolic function with/without regional wall motion abnormalities in non-Tako-Tsubo pattern. Other immune-related adverse events, particularly myositis, myopathy, myasthenia gravis. Suggestive CMR findings.
Severity of myocarditis	*Fulminant:* haemodynamic instability, HF requiring non-invasive or invasive ventilation, complete or high-grade heart-block and/or significant ventricular arrhythmia. *Non-fulminant:* including significant but hemodynamically and electrically stable patients and incidental cases diagnosed at the same time as other immuno-related adverse events. Patients may have reduced LVEF but no features of severe disease *Smouldering (subclinical):* incidentally diagnosed myocarditis without clinical signs or symptoms *Steroid refractory:* non-resolving or worsening myocarditis (clinical worsening or persistent cTn elevation after exclusion of other aetiologies) despite high doses of methylprednisone
Recovery	*Complete recovery:* complete resolution of acute symptoms, normalization of biomarkers and recovery of LVEF after discontinuation of immunosuppression. CMR may still show LGE or elevated T1 due to fibrosis, but absence of any acute oedema *Recovering:* ongoing improvement in clinical symptoms, signs, biomarkers and imaging parameters, but not yet normalized, while on tapering doses of immunosppression

# Clinical diagnosis should be confirmed with CMR of endomyocardial biopsy if possible and wiothout causing delays of treatment

& In a patient that is unwell, treatment with immunosuppression should be initiated promptly while awaiting further confirmatory testing

Vascular toxicities

Vacular toxicity is the induction or aggravation of vascular disease due to cancer therapy

Can be symptomatic of asymptomatic.

A. Asymptomatic vascular toxicities

recognized by changes in diagnostic testing parameters beyond what can be expected based on analytical and biological variability and common thresholds for abnormality.

B. Symptomatic vascular toxicities

Defined by societal guidelines.

C. Hypertension

An increase in systolic and/or diastolic blood pressure (BP) after initiation of cancer therapy, without any other contributing changes.

Different agents may have variable hypertensive effects and there is remarkable inter-individual variation.

Confirm diagnosis with out-of-office BP measurements.

Category	Criteria
Normal	SBP ≤130 mmHg and DBP ≤80 mmHg
Threshold to initiate AH treatment before, during and after cancer therapy	CVD or ASCVD ≥10%: SBP ≥130 mmHg and/or DBP ≥80 mmHg Otherwise: SBP ≥140 mmHg and/or DBP ≥90 mmHg
Threshold to withhold cancer therapy	SBP ≥180 mmHg and/or DBP ≥110 mmHg
Exaggerated hypertensive response	Systolic BP increase >20 mmHg or mean BP increase >15 mmHg
Hypertensive emergency	(Very high) BP elevations associated with acute hypertension-mediated organ damage (heart, retina, brain, kidneys, large arteries), requiring immediate BP reduction to limit extension or promote regression of target organ damage

QTc prolongation

Fridericia formula (QTcF = QT/RR¹ᐟ³) is preferred for QT correction in cancer patients, as it reduces the overestimation of QT prolongation seen with Bazett’s formula — particularly at higher heart rates — and minimizes inappropriate management changes during QT-prolonging cancer therapy.

QTcF <480ms	Acceptable: continue current treatment
QTcF 480-500ms	Prolonging: proceed with caution; minimize other QT prolonging medications; replete electrolytes
QTcF >500ms	Prolonged: stop treatment and evaluate. May require dose reduction or alternative treatment

References

Lyon A et al (2022) 2022 ESCGuidelines on cardio-oncology developed in collaboration with the European HematologyAssociation(EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS)
Herrmann J et al. Defining cardiovascular toxicities of cancer: an International Society of Cardio-Oncology (IC-OS) consensus statement. Eur. Heart J. 2022; 43:280-299.
Richardson DR et al. Association of QTc Formula With the Clinical Management of Patients With Cancer. JAMA Oncol. 2022;8(11):1616–1623. doi:10.1001/jamaoncol.2022.4194

CTRCD & Heart failure in Anthracyclines

Incidence

Anthracycline administration can result in myocardial injury, LV dysfunction, and heart failure.
Incidence ranges from 3% to 48%, depending on anthracycline type, cumulative dose, concomitant cardiotoxic agents, and baseline cardiovascular risk.
Early detection increases the likelihood of reversibility with ACE-I and β-blocker therapy.

Types of Anthracycline Cardiotoxicity

Acute: during or immediately after treatment; usually reversible (<1%).
Early-onset: within 1 year post-treatment; most cases are asymptomatic LVEF decline (~98%).
Late-onset: >1 year after exposure; typically presents as hypokinetic and/or dilated cardiomyopathy.

Diagnosis
Diagnosis is based on:

New cardiovascular symptoms
New abnormalities on cardiac imaging
New elevation in cardiac biomarkers

Risk Assessment

The risk of anthracycline-related CTRCD depends on baseline cardiovascular factors, cancer type, and prior or planned therapies.
A comprehensive baseline CV risk assessment is recommended (https://www.heartscore.org/en_GB/ ), as well as cardiotoxicity risk assessment (https://www.cancercalc.com/hfa-icos_cardio_oncology_risk_assessment.php) .

Anthracycline equivalent dosis calculator: https://www.cancercalc.com/anthracycline.php

Prevention of Anthracycline-Related CTRCD

Beta-blockers and RAAS inhibitors (RAASi):
Early studies suggested benefit with combined therapy; however, subsequent trials have not consistently confirmed these findings.
ARNi:
No systematic clinical evidence currently supports ARNi for primary prevention of CTRCD. Randomized trials ongoing.
Mineralocorticoid receptor antagonists (MRAs):
Limited evidence suggests a potential protective effect on systolic and diastolic function; more robust data are required.
SGLT2 inhibitors:
Show promise based on preclinical and observational data, with meta-analyses suggesting reductions in HF hospitalizations and new HF diagnoses. Further prospective randomized studies are needed.
Statins:
May be considered in high-risk patients, although evidence remains mixed.
Ivabradine:
No clear benefit has been demonstrated for HF prevention in cancer patients.
Lifestyle and treatment-related strategies:
- Optimize pre-existing cardiovascular disease and risk factors
- Aerobic exercise before and during anthracycline therapy is recommended.
- Consider liposomal anthracyclines, dose reduction, or prolonged infusion time in patients at increased risk.
- Dexrazoxane may be used in high- or very high-risk patients, although availability varies by region.

Rechallenge with Anthracylines

Dose considerations	Consider dose reduction: Low cumulative dose (240–300 mg/m²): low cardiotoxicity risk High cumulative dose (>400 mg/m²): cardiotoxicity risk increases by >5%, even in absence of known heart disease
Schedule modification	Consider: Weekly vs 3-weekly dosing Prolonged infusion (72 h vs 48 h)
Formulation	Consider switching to liposomal anthracyclines
Cardioprotection	Consider dexrazoxane before each cycle (not reimbursed in Belgium)
Heart failure therapy	Aerobic exercise is recommended before and during anthracycline therapy
Cardiac monitoring	Close surveillance every 1–2 treatment cycles

Permissive cardiotoxicity

Continuation or initiation of cardiotoxic cancer therapy (e.g. anthracyclines, trastuzumab) may be feasible in selected patients with mild–moderate cardiotoxicity or pre-existing cardiac disease.

Key elements of perimissive cardiotoxicity:

MDT shared decision-making,
a predefined cardiac monitoring plan (every 1–2 cycles),
implementation of cardioprotective strategies

References

Lyon A et al (2022) 2022 ESCGuidelines on cardio-oncology developed in collaboration with the European HematologyAssociation(EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS). European Heart Journal (2022) 43, 4229–4361 https://doi.org/10.1093/eurheartj/ehac2447
Farmakis et al. Anthracycline-induced cardiomyopathy: secrets and lies European Journal of Heart Failure (2018) 20, 907–909
Camilli et al. Anthracycline Cardiotoxicity in Adult Cancer Patients: JACC: CardioOncologyState-of-the-Art Review. J Am Coll Cardiol CardioOnc. 2024 Oct, 6 (5) 655–677.
Bhasin V et al. Statins for the Primary Prevention of Anthracycline Cardiotoxicity: A Comprehensive Review. Curr Oncol Rep. 2024 Oct;26(10):1197-1204. doi: 10.1007/s11912-024-01579-6.
Porter et al. Permissive Cardiotoxicity The Clinical Crucible of Cardio-Oncology. J Am Coll Cardiol CardioOnc 2022;4:302–312
Omland T er al. Sacubitril/Valsartan and Prevention of Cardiac Dysfunction During Adjuvant Breast Cancer Therapy: The PRADA II Randomized Clinical Trial. Circulation. 2025 Oct 21;152(16):1136-1145.
Medina-Hernández, D, et al. SGLT2i Therapy Prevents Anthracycline-Induced Cardiotoxicity in a Large Animal Model by Preserving Myocardial Energetics. J Am Coll Cardiol CardioOnc. 2025 Feb, 7 (2) 171–184.
Neilan TG et al. Atorvastatin for Anthracycline-Associated Cardiac Dysfunction: The STOP-CA Randomized Clinical Trial. 2023;330(6):528–536.

CTRCD & Heart failure in Anti-her2 theraphy

Incidence

Asymptomatic LVEF decline occurs in 10–15% of patients treated with HER2-targeted therapies.
Incidence increases to 27% when combined with anthracyclines.
Symptomatic heart failure occurs in <1% with HER2 therapy alone and up to 4% with concomitant anthracyclines.
Risk is higher with:
- Concomitant or prior anthracyclines, cyclophosphamide or chest radiation
- Pre-existing cardiovascular disease
- Traditional cardiovascular risk factors

Diagnosis
Diagnosis is based on:

New cardiovascular symptoms
New abnormalities in cardiac imaging
New elevation in cardiac biomarkers

Pathogenesis

HER-2 targeted terapies inhibit HER2 signaling in cardiomyocytes, leading to cellular stress and increased reactive oxygen species, which can trigger apoptosis and reduce myocardial contractility.
Cardiotoxicity is not dose-dependent and is usually reversible.

Treatment of anti-HER2 therapy related CTRCD

Interruption of HER2-targeted therapy	Temporary interruption recommended for: Moderate or severe symptomatic CTRCD Severe asymptomatic CTRCD (LVEF <40%)
Continuation of HER2 therapy	Asymptomatic moderate CTRCD (LVEF 40–49%): Continue HER2-targeted therapy Start cardioprotective therapy (ACE-I/ARB + beta-blocker) Frequent cardiac monitoring required Asymptomatic mild CTRCD (LVEF ≥50% with significant GLS decline and/or biomarker rise): Continue HER2-targeted therapy Consider cardioprotective therapy (ACE-I/ARB and/or beta-blocker)
Heart failure therapy	Initiate and uptitrate guideline-directed HF therapy in: Symptomatic moderate or severe CTRCD Asymptomatic severe CTRCD
Rechallenge after CTRCD recovery	Possible in patients continuing or restarting HER2-targeted therapy after recovery (LVEF ≥40%, ideally ≥50%): Perform echocardiography and biomarkers every 2 cycles during the first 4 cycles Monitoring frequency may be reduced if cardiac function remains stable

Permissive cardiotoxicity

Continuation or initiation of cardiotoxic cancer therapy (e.g. anthracyclines, trastuzumab) may be feasible in selected patients with mild–moderate cardiotoxicity or pre-existing cardiac disease.

Key elements of perimissive cardiotoxicity:

MDT shared decision-making,
a predefined cardiac monitoring plan (every 1–2 cycles),

implementation of cardioprotective strategies

References

Lyon A et al (2022) 2022 ESCGuidelines on cardio-oncology developed in collaboration with the European HematologyAssociation(EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS). European Heart Journal (2022) 43, 4229–4361 https://doi.org/10.1093/eurheartj/ehac2447
Porter et al. Permissive Cardiotoxicity The Clinical Crucible of Cardio-Oncology. J Am Coll Cardiol CardioOnc 2022;4:302–312
Zhang, L et al. Cardiac safety analysis of anti-HER2-targeted therapy in early breast cancer. Sci Rep 12, 14312 (2022)

Arterial Hypertension

Hypertension is common in cancer patients (~40%) and contributes to their increased cardiovascular mortality. In cancer survivors, early-onset hypertension is an important clinical issue. Blood pressure should be measured both in the office and at home.
causes:
- pre-existing arterial hypertension : optimize BP control prior to cancer treatment initiation
- adjunctive medication
  - corticosteroids
  - NSAID
  - EPO
- stress, pain, excessive alcohol consumption, renal impairment, untreated sleep apnoea, obesity, and reduced exercise
- certain anticancer drugs

Anticancer Therapies Associated With Arterial Hypertension

Drug Class	Agents
VEGF pathway inhibitors (VEGFi)	Bevacizumab, aflibercept, ramucirumab
Multitargeted TKIs with VEGF inhibition	Sunitinib, sorafenib, pazopanib, axitinib, lenvatinib, cabozantinib
BCR-ABL tyrosine kinase inhibitors	Imatinib, dasatinib, nilotinib, ponatinib, bosutinib
BRAF inhibitors / MEK inhibitors	Vemurafenib, dabrafenib / trametinib, cobimetinib
ALK inhibitors	Crizotinib, alectinib, brigatinib, lorlatinib
Proteasome inhibitors	Carfilzomib, bortezomib
Bruton tyrosine kinase (BTK) inhibitors	Ibrutinib
Fluoropyrimidines	5-fluorouracil (5-FU), capecitabine
Platinum compounds	Cisplatin, carboplatin, oxaliplatin
Alkylating agents	Cyclophosphamide, ifosfamide
Aromatase inhibitors	Anastrozole, letrozole, exemestane
Androgen receptor pathway inhibitors (ARPI)	Abiraterone, bicalutamide, enzalutamide

Treament

no specific randomized controlled trials in patients with cancer
tailored to comorbidities
first line: ACE-I or angiotensin receptor blocker + dihydropyridine calcium channel blocker
thiazide-like diuretic: possible, but consider risk of volume depletion
second line: spironolactone; nitrates, betablocker (nebivolol, carvedilol)
defer causative cancer therapy if > 160/100mmHg

target: < 140/90mmHg (< 130/80mmHg if well tolerated)
- consider cancer prognosis
- Note: Cancer therapy–related arterial hypertension is usually reversible after treatment discontinuation; rebound hypotension may occur.

Important interaction between certain cancer therapies and antihypertensive drugs

Cancer Therapy	Avoid	Reason
ALL	verapamil, diltiazem	CYP3A4 inhibition
mTOR inhibotors	ACEi	angioedema
platinum-compounds	loop diuretics	oto- and nephrotoxicity
cyclophosphamide	thiazide	myelosuppression
abiraterone	spironolactone	paradoxical pro-androgenic (eplerenone is safe)

References

Lyon et al. ESC Guidelines on cardio-oncology. Eur Heart J 2022.
Cohen et al. Cancer Therapy–Related Hypertension: A Scientific Statement From the American Heart Association. Hypertension 2023
Pandey et al. Management of hypertension in patients with cancer. CKJ 2023

QTc Prolongation

Ventricular Arrhythmias (VA)

Overview
Ventricular arrhythmias are uncommon in cancer patients. The incidence increases with advanced disease and pre-existing cardiovascular comorbidities.

Proposed Mechanisms

Direct effects of anticancer drugs on cardiac ion channel activity, typically causing QTc prolongation
Development of a persistent arrhythmogenic substrate due to systemic inflammation, cancer-related factors, or therapy-induced cardiac injury

Management of Cancer Therapy–Related VA

Asymptomatic, self-terminating VA usually do not require drug discontinuation, unless additional cardiovascular risk factors or persistent ECG abnormalities are present
Symptomatic VA warrant cancer drug dose reduction or discontinuation
The use of antiarrhythmic drugs is limited by potential drug–drug interactions and QTc prolongation
Beta-blockers and class IB agents are preferred in most cases
The decision to initiate antiarrhythmic or device therapy should take into account life expectancy, quality of life, and complication risk

QTc Prolongation

Most cancer therapy–related VA are associated with QTc prolongation leading to torsade de pointes (TdP).
QTc prolonging cancer drugs and related risk factors are summarized in Tables 1 and 2

Normal QTc values

Men: ≤450 ms
Women: ≤460 ms
QTc ≥500 ms is associated with a 2–3× higher risk of TdP

Clinical guidance

A QTc increase >60 ms from baseline is acceptable if QTc remains <500 ms
Use Fridericia correction (QTcF = QT/³√RR) for cancer patients

Rechallenge with QTc prolonging therapies

A multidisciplinary approach is recommended: consider an alternative treatment if available; start with reduced dose; weekly ECG monitoring during the first 4-6 weeks, and monthly there after

Table 1. Cancer Drugs by QTc Prolongation Risk

Classification	Drugs
High risk (≥10 ms, TdP risk)	Aclarubicin, Arsenic trioxide, Glasdegib, Nilotinib, Oxaliplatin, Pazopanib, Ribociclib, Sunitinib, Toremifene, Vandetanib
Moderate risk (≥10 ms, low or uncertain TdP risk)	Abarelix, Belinostat, Brigatinib, Cabozantinib, Ceritinib, Crizotinib, Dovitinib, Entrectinib, Eribulin, Gilteritinib, Ivosidenib, Lapatinib, Lenvatinib, Osimertinib, Panobinostat, Rucaparib, Selpercatinib, Sorafenib, Tipiracil/Trifluridine, Vemurafenib
Low risk (<10 ms)	ADT, Afatinib, Axitinib, Binimetinib, Bortezomib, Bosutinib, Carfilzomib, Dabrafenib, Dasatinib, Encorafenib, Midostaurin, Pertuzumab, Ponatinib, Romidepsin, Quizartinib, Tamoxifen, Vorinostat

Table 2. Risk Factors for Drug-Induced QTc Prolongation and TdP

Correctable	Non-correctable
QT-prolonging drugs (antiarrhythmics, antibiotics, antidepressants, antifungals, antiemetics, antihistamines, antipsychotics, loop diuretics, methadone)	Acute myocardial ischaemia
Bradyarrhythmia	Age >65 years
Electrolyte abnormalities (↓K⁺ ≤3.5, ↓Mg²⁺ ≤1.6, ↓Ca²⁺ ≤8.5)	Baseline QTc prolongation
Inadequate dose adjustment for renal/hepatic clearance	Family history of sudden death (LQTS or genetic)
	Female sex
	Impaired renal or hepatic function
	History of syncope or drug-induced TdP
	Pre-existing CVD (CAD, HF, LVH)

References

Lyon A et al (2022) 2022 ESCGuidelines on cardio-oncology developed in collaboration with the European HematologyAssociation(EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS). European Heart Journal (2022) 43, 4229–4361 https://doi.org/10.1093/eurheartj/ehac2447

Bradyarrhythmias

Overview

Bradyarrhythmias may occur as a result of cancer therapy, most often with immune checkpoint inhibitors (ICI), immunomodulatory drugs (IMiD), and ALK inhibitors.

Mechanisms

AV conduction disease can be caused by ICI, with or without associated myocarditis
Sinus node dysfunction may occur with IMiD (thalidomide, pomalidomide) and ALK inhibitors (crizotinib, alectinib, brigatinib, ceritinib)

Management

ICI-associated AV conduction disease

New first-degree AV block (PR prolongation): serial ECG monitoring recommended
PR interval >300 ms: hospitalize for continuous ECG monitoring and initiate i.v. methylprednisolone
Evaluate for associated myocarditis
New 2^nd & 3^rd degree AV-block : treat as per current ESC guidelines on pacing + consider associated myocarditis

Drug-induced sinus bradycardia (IMiD, ALK inhibitors)

Perform holter monitoring in symptomatic patients to exclude significant sinus pauses
Asymptomatic patients: continue therapy with close observation
Symptomatic patients: temporary cancer drug withdrawal may confirm causality
Rechallenge can be considered after multidisciplinary team (MDT) discussion, balancing risks and benefits

References

Lyon A et al (2022) 2022 ESCGuidelines on cardio-oncology developed in collaboration with the European HematologyAssociation(EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS). European Heart Journal (2022) 43, 4229–4361 https://doi.org/10.1093/eurheartj/ehac2447

CAD: Acute Coronary Syndrome

Cancer increases the risk of PCI-related complications
- Higher rates of cardiac death and bleeding after PCI.
- Risk is particularly elevated in the first year after a cancer diagnosis.
Prevalence of cancer among ACS patients
- Current or recent cancer present in:
  - 3% of ACS cases (MINAP registry)
  - 4% of ACS cases (SWEDE registry)
- Patients with ACS and cancer are more often treated conservatively, which is associated with worse outcomes compared to non-cancer ACS patients.
Prognostic differences
- Similar prognosis to non-cancer patients:
  - Non-metastatic cancers such as breast, prostate, colon cancer.
- Worse prognosis:
  - ACS with metastatic cancer
  - Lung cancer
- Bleeding risk:
  - Highest in colon cancer patients (in-hospital bleeding).
Mortality patterns after ACS in cancer patients
- Cardiac death = most common cause of death in the first 30 days after ACS.
- Beyond 30 days up to 1 year → most deaths are non-cardiac and related to cancer or other causes.
Treatment implications
- ACS patients with cancer should receive the same urgent and guideline-based care as non-cancer patients.
- Exceptions only when:
  - life expectancy is limited,
  - invasive strategy no longer desired/appropriate,
  - patient or family preferences indicate otherwise.
DAPT considerations
- Keep dual antiplatelet therapy (aspirin and clopidogrel) duration as short as possible (≈ 1 month) due to high bleeding risk.
- Bleeding risk models are available (e.g., www.precisedaptscore.com).
- When cancer is included as a binary variable, 94% of cancer patients are classified as high bleeding risk.

References

Y. Ueki et al., “Ischemia and Bleeding in Cancer Patients Undergoing Percutaneous Coronary Intervention,” JACC CardioOncol, vol. 1, no. 2, pp. 145–155, Dec. 2019, doi: 10.1016/j.jaccao.2019.11.001.
A. Bharadwaj et al., “Acute myocardial infarction treatments and outcomes in 6.5 million patients with a current or historical diagnosis of cancer in the USA,” Eur Heart J, vol. 41, no. 23, pp. 2183–2193, Jun. 2020, doi: 10.1093/EURHEARTJ/EHZ851.
M. Dafaalla et al., “Outcomes of ST elevation myocardial infarction in patients with cancer: a nationwide study,” Eur Heart J Qual Care Clin Outcomes, vol. 9, no. 8, pp. 806–817, Dec. 2023, doi: 10.1093/EHJQCCO/QCAD012.
A. R. Lyon et al., “2022 ESC Guidelines on cardio-oncology developed in collaboration with the European Hematology Association (EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS)Developed by the task force on cardio-oncology of the European Society of Cardiology (ESC),” Eur Heart J, Aug. 2022, doi: 10.1093/EURHEARTJ/EHAC244.
M. Dafaalla et al., “Bleeding risk prediction after acute myocardial infarction-integrating cancer data: the updated PRECISE-DAPT cancer score,” Eur Heart J, vol. 45, no. 34, pp. 3138–3148, Sep. 2024, doi: 10.1093/EURHEARTJ/EHAE463.

CAD: Cronic Coronary Syndrom

The management of chronic coronary syndromes (CCS) is in similar in patients with and without cancer
Several cancer treatments are associated with an increased risk of stable angina, e.g. 5-FU and capecitabine
Patients receiving cancer therapy who present with new stable angina should have careful clinical evaluation, with aggressive modification of cardiovascular risk factors and an initial medical management of their symptoms

The decision to perform catheterization in this population should be made even more carefully than in non-cancer patients, since bleeding risk is almost always high [5]. Cancer therapy-related timing aspects should be taken into consideration, mainly potentially foreseeable surgical interventions.
DAPT duration should be kept as short as possible.

According to the Society for Cardiovascular Angiography & Interventions (SCAI) 2016 expert consensus document, the following rules of thumb apply:

There is no minimum platelet count to perform a diagnostic coronary angiogram
Prophylactic platelet transfusion is not recommended, unless decided by the oncologist/hematologist, e.g. for
- Platelet count < 20.000/ml and high fever, leukocytosis, rapid fall in platelet count or other coagulation abnormality
- Platelet count < 20.000/ml in solid tumor patients receiving treatment for bladder, gynecologic or colorectal turmors, melanoma or necrotic tumors
Aspirin may be used when platelet counts are >10.000/ml
For platelet counts <30.000/ml, revascularisation and DAPT should be decided after a multidisciplinary evaluation and risk/benefit analysis

As in non-cancer patients, radial approach is recommended
30-50 U/kg unfractionated heparin (3000-5000 U) is the initial recommended dose for thrombocytopenic patients undergoing PCI who have platelets <50.000/ml. ACT should be monitored.
DAPT with clopidogrel may be used when platelet counts are 30.000-50.000/ml. Prasugrel, ticagrelor, and IIB-IIIA-inhibitors should not be used in patients with platelets counts <50.000/ml.
If platelet counts are <50.000/ml, DAPT duration may be restricted to 2 weeks after plain old balloon angioplasty (POBA), and to 6 months after DES implantation with optimal stent expansion.
Consider POBA in case DAPT is not possible, i.e. for platelet counts <30.000/ml or when non-cardiac procedures or surgery is necessary as soon as possible

References

Vrints et al., “2024 ESC Guidelines for the management of chronic coronary syndromes,” Eur Heart J, vol. 45, no. 36, pp. 3415–3537, Sep. 2024, doi: 10.1093/EURHEARTJ/EHAE177.
U. Campia et al., “Cardio-Oncology: Vascular and Metabolic Perspectives: A Scientific Statement From the American Heart Association,” Circulation, vol. 139, no. 13, pp. E579–E602, Mar. 2019, doi: 10.1161/CIR.0000000000000641.
A. R. Lyon et al., “2022 ESC Guidelines on cardio-oncology developed in collaboration with the European Hematology Association (EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS)Developed by the task force on cardio-oncology of the European Society of Cardiology (ESC),” Eur Heart J, Aug. 2022, doi: 10.1093/EURHEARTJ/EHAC244.
C. A. Iliescu et al., “SCAI Expert consensus statement: Evaluation, management, and special considerations of cardio-oncology patients in the cardiac catheterization laboratory (endorsed by the cardiological society of india, and sociedad Latino Americana de Cardiologıa interv…,” Catheter Cardiovasc Interv, vol. 87, no. 5, pp. E202–E223, Apr. 2016, doi: 10.1002/CCD.26379.
M. Dafaalla et al., “Bleeding risk prediction after acute myocardial infarction-integrating cancer data: the updated PRECISE-DAPT cancer score,” Eur Heart J, vol. 45, no. 34, pp. 3138–3148, Sep. 2024, doi: 10.1093/EURHEARTJ/EHAE463.

ICI-related Myocarditis

Commonly / frequently implicated therapies

Anti-PD1 : nivolumab – pembrolizumab – cemiplimab
Anti-PDL1 : atezolizumab – avelumab – durvalumab
Anti-CTLA4 : ipilimumab
Anti-LAG3 : relatlimab
- Oncological (& hematological) treatment indications are rapidly expanding, currently commonly used in the following cancers (but not limited to) :
  – malignant melanoma
  – non small-cell lung cancer (NSCLC)
  – renal cell cancer
  – triple-negative breast cancer

Most commonly encountered toxicities :

Dyslipidemia* : 19.3/1000 patients
Ischaemic stroke* : 8.8/1000 patients
Heart failure* / NILVD (non-inflammatory LV dysfunction) : 8.7/1000 patients
Pericardial disease / pericarditis* : 8.3/1000 patients
Myocardial infarction / ACS* : 7.4/1000 patients
Myocarditis (ICI-M)^# : 3.2/1000 patients

* : diagnosis and treatment according to current ESC guidelines + see specific topic.
^# : most urgent diagnosis, specific therapeutic implications – see below.

ICI induced myocarditis:

A rare complication of ICI therapy with a high fatality rate
It develops most frequently develops during the first 12 weeks of treatment, although late cases (after week 20) may occur.
Risk is higher in patients receiving dual ICI therapy
Proposed risk score for the development of cardiomyotoxic events (including ICI related myocarditis) during ICI treatment

Diagnostic criteria for ICI-M : pathohistological diagnosis or clinical diagnosis :

Clinical diagnosis

Required	Cardiac troponin (cTn) elevation (new or significant change from baseline) AND ≥1 major criterion OR ≥2 minor criteria, after exclusion of acute coronary syndrome (ACS) and acute infectious myocarditis based on clinical assessment.
Major criterion	Cardiac magnetic resonance (CMR) diagnostic for acute myocarditis according to modified Lake Louise criteria
Minor criteria	Clinical syndrome suggestive of myocarditis (≥1): fatigue, myalgias, chest pain, diplopia, ptosis, dyspnoea, orthopnoea, peripheral oedema, palpitations, presyncope/syncope, muscle weakness, cardiogenic shock Ventricular arrhythmias (including cardiac arrest) and/or new conduction system disease New decline in left ventricular systolic function, with or without regional wall motion abnormalities (non-Takotsubo pattern) Concomitant immune-related adverse events, particularly myositis, myopathy, or myasthenia gravis CMR findings suggestive but not diagnostic for acute myocarditis

Pathohistological diagnosis (endomyocardial biopsy) : Multifocal inflammatory cell infiltrates with overt cardiomyocyte loss by light microscopy

In order to exclude alternative or co-existing cardiac disease a hierarchical diagnostic approach in ICI myocarditis has been proposed:

DIAGNOSTIC CAVEATS :

	Caveats
Symptoms	Often non-specific;dyspnoea is the most common presenting symptom; chest pain may be absent
ECG	Always exclude ACS; ventricular arrhythmias or high ectopic burden and/or new conduction abnormalities (including AV block or PR prolongation) may indicate fulminant disease; continuous telemetry is recommended.
Transthoracic echocardiography (TTE	LVEF may be normal in ~50% of cases; GLS abnormalities are prognostic for MACE; pericardial effusion may be present but is not required for diagnosis
Cardiac biomarkers	Troponin I or T may be used; Troponin T may be falsely elevated with concomitant myositis; magnitude of troponin rise has prognostic value; NT-proBNP has limited diagnostic utility
Cardiac magnetic resonance (CMR)	May be falsely negative if performed early (<72 h after symptom onset); Repeat CMR if negative but clinical suspicion remains high
Endomyocardial biopsy (EMB)	Low threshold recommended in haemodynamic instability (cardiogenic shock / fulminant myocarditis) or when coronary angiography is performed
FDG-PET/CT	Conflicting evidence regarding diagnostic accuracy Repeat CMR if negative but clinical suspicion remains high

Severity assessment in ICI-M :

Severity category	Definition / Clinical features
Severe	Haemodynamic instability; heart failure requiring non-invasive or invasive ventilation; complete or high-grade atrioventricular block; and/or significant ventricular arrhythmias
Non-severe (clinically significant)	Symptomatic myocarditis with haemodynamic and electrical stability; may have reduced LVEF; no features of severe disease
Smouldering (subclinical)	Incidentally diagnosed myocarditis without clinical signs or symptoms
Steroid-refractory	Non-resolving or worsening myocarditis (clinical deterioration or persistent troponin elevation after exclusion of other causes) despite high-dose methylprednisolone

Therapeutic approach

	Key points
Steroid initiation	Do not delay corticosteroid therapy in case of diagnostic uncertainty; delayed treatment is associated with significantly worse prognosis
Cardiac monitoring	Close in-hospital troponin surveillance (≥ once daily) Continuous ECG monitoring is mandatory due to risk of ventricular arrhythmias and high-grade atrioventricular block
Immunosuppression escalation and second-line therapy options	Low threshold for treatment intensification if insufficient response after ~72 h of high-dose steroids; Mandatory discussion with treating oncologist and/or BITOX; Potential second-line options include mycophenolate mofetil, IVIG, plasmapheresis, tocilizumab, abatacept ± ruxolitinib or belatacept (evidence limited; no formal recommendations)
Fulminant myocarditis / cardiogenic shock	Immunosuppression plus guideline-directed medical therapy (GDMT) ± decongestion remains the cornerstone of management In selected patients with favourable oncological prognosis consider mechanical circulatory support (MCS)as a bridge to recovery
Oncological considerations	Cancer prognosis ? Treatment intention and expectations ? ICI discontinuation : temporary vs. definite? Steroid tapering planning ? Alternative cancer treatment options in case of recovery ? Feasibility and risks of rechallenge?

Rechallenge : possibilities and caveats

ALWAYS discuss case with treating oncologist and/or BITOX :

Severe & fulminant ICI-M : AVOID rechallenge
Single-agent rechallenge / treatment continuation : possible in mild cases if close troponin surveillance.

In case of doubt :
Consider multidisciplinary discussion via BSMO BITOX Immunomanager submission

References

Lyon AR et al. 2022 ESC Guidelines on cardio-oncology developed in collaboration with the European Hematology Association (EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS). Eur Heart J (2022) : 00, 1-133.
Dolladille C et al. Cardiovascular immunotoxicities associated with immune checkpoint inhibitors : a safety meta-analysis. Eur Heart J (2021) : 42, 4964-77.
Bonaca MP et al. Myocarditis in the Setting of Cancer Therapeutics: Proposed Case Definitions for Emerging Clinical Syndromes in Cardio-Oncology. Circulation (2019): 140, 80-91.
Herrmann J et al. Defining cardiovascular toxicities of cancer therapies : an International Cardio-Oncology Society (IC-OS) consensus statement. Eur Heart J (2022) : 43, 280-99.
Power JR et al. Immune checkpoint inhibitor-associated myocarditis: a novel risk score. Eur Heart J (2025) : 00, 1-13.
BSMO BITOX Immunomanager : https://bsmo.be/multidiscplin-immunotox-meeting/

Pericardial Diseases

The pericardium is the protective membrane around the heart.
Pericarditis = inflammation of the pericardium (with or without effusion).
Pericardial effusion = accumulation of fluid in the pericardial space (with or without pericarditis).
Cancer patients are at increased risk because of:
- direct malignant involvement
- treatment effects
- immunosuppression
- stress or systemic inflammation

Causes

Category	Key causes
Cancer-related	Direct invasion; metastases (lung, breast, melanoma, lymphoma/leukaemia, neighbouring organs); mediastinal lymphatic obstruction
Treatment-related	Chemotherapy (anthracyclines, cyclophosphamide, bleomycin, cytarabine); thoracic radiotherapy; targeted therapies (ATRA, arsenic trioxide, TKIs—especially dasatinib); immune therapies (IL-2, IFN-α, ICI); combination therapy ↑ risk
Primary pericardial malignancy	Rare; pericardial mesothelioma
Infectious	Mainly in immunocompromised patients
Other causes	Trauma, cardiac disease, renal failure, thyroid dysfunction (esp. hypothyroidism), idiopathic

Symptoms

Symptoms are similar to the general population and range from typical pericarditic chest pain (worse when supine or with deep inspiration, relieved by sitting forward) to dyspnoea and fatigue with pericardial effusion, which may be asymptomatic. Cardiac tamponade is a medical emergency, presenting with severe dyspnoea, hypotension, tachycardia, syncope, and signs of poor peripheral perfusion

Diagnosis

Domain	Key points
ECG	ECG may show diffuse ST elevation and PR depression (pericarditis); low QRS voltages and electrical alternans (large effusion/tamponade); reactive atrial fibrillation may occur
Laboratory tests	CRP; high-sensitivity troponin I or T to exclude myocardial involvement; additional tests guided by differential diagnosis
Initial imaging	Chest X-ray may show enlarged cardiac silhouette
Cardiac imaging	Transthoracic echocardiography (gold standard) to assess effusion size and haemodynamic impact
Advanced imaging (CT / CMR)	Detailed assessment of pericardial inflammation; identification of local tumour invasion or masses
Diagnostic confirmation in effusion	Pericardial fluid cytology and/or pericardial biopsy required to confirm or exclude malignant involvement
Tumour markers	CEA, CYFRA 21-1, NSE, CA 19-9 may support diagnosis but lack diagnostic accuracy
Important note	~Two-thirds of pericardial effusions in cancer patients are non-malignant → cytology remains essential

Treatment

A multidisciplinary approach (cardio-oncology, oncology, radiotherapy, surgery) is recommended.

Acute pericarditis

Chemotherapy-related acute pericarditis often resolves with standard therapy or treatment interruption.
NSAID + colchicine is recommended in most of cases (reduces recurrence).
Steroids only for resistant cases except in ICI-related pericarditis.
Treatment of underlying cause

ICI-related pericarditis

Median onset ~30 days; associated with worse outcomes, especially with concomitant myocarditis.
In moderate/large effusion or severe pericarditis:
- Discontinue ICI
- High-dose steroids (methylprednisolone 1 mg/kg/day)
- ± colchicine
- Pericardiocentesis if tamponade
Refractory cases: consider additional immunosuppressive therapy.
Uncomplicated cases: ICI can sometimes continue with colchicine/NSAIDs.

Rechallenge after resolution → MDT decision with close monitoring

Pericardial Effusion

General

Treat underlying cause
Medical therapy as indicated (see acute pericarditis)
Pericardiocentesis (drainage ± intrapericardial therapy). In case cardiac tamponade – immediate drainage (medical emergency)
Surgical strategies (pericardial window, pericardiectomy) in:
- recurrent effusions, constrictive physiology, need for biopsy, inaccessible or unsafe percutaneous drainage, bacterial pericarditis (lavage)

Systemic antineoplastic therapy = foundation for malignant effusion treatment.
In some cases: local intrapericardial therapy:
- Eg. cisplatin (lung cancer), thiotepa (breast cancer)
- sclerosing agents to reduce recurrence
Extended drainage may be needed for repeated therapy and symptom relief.

Recurrence is common (>50%).

Additional options: pericardiotomy, pericardial window, balloon pericardiotomy.
Interventions are palliative in advanced disease and focus on symptom relief.
Radiotherapy can be effective in radiosensitive tumours (lymphoma, leukemia).

Short term prognosis

Strongly depends on the underlying cause.
Better prognosis if treatable cause (chemotherapy-induced pericarditis, infections).
Worse prognosis in malignant pericardial disease and presentation with heart failure

Long-term risks

Long-term risk after chemo-induced pericarditis generally low (anthracyclines, cyclophosphamide, cytarabine, bleomycin).
Dasatinib may cause chronic effusion/pericarditis.
Chronic complications from ICI appear uncommon.
RT-induced pericardial disease can appear months–decades later; constrictive pericarditis is the most serious.
- 5-yearly echocardiographic surveillance may be considered after RT-induced acute pericarditis.
Despite modern techniques, pericardial effusion remains frequent in:
- lung cancer (grade ≥2 ~40%)
- oesophageal cancer (~25%)

References

Lyon A et al (2022) 2022 ESCGuidelines on cardio-oncology developed in collaboration with the European HematologyAssociation(EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS). European Heart Journal (2022) 43, 4229–4361 https://doi.org/10.1093/eurheartj/ehac2447
Jeanette Schulz-Mengeret al. 2025 ESC Guidelines for the management of myocarditis and pericarditis: Developed by the task force for the management of myocarditis and pericarditis of the European Society of Cardiology (ESC) Endorsed by the Association for European Paediatric and Congenital Cardiology (AEPC) and the European Association for Cardio-Thoracic Surgery (EACTS), European Heart Journal, Volume 46, Issue 40, 21 October 2025, Pages 3952–4041,

Tako Tsubo Cardiomyopathy

Association with cancer

Malignant disease is frequent in patients with TTS and is associated with worse outcomes.
Recognised triggers/predisposing factors in oncology patients:
- The malignancy itself
- Certain cancer treatments:
  - 5-fluorouracil (5-FU) and other fluoropyrimidines
  - Immune checkpoint inhibitors (ICI)
  - VEGF inhibitors (VEGFi)
- Psychological and physical stress related to cancer diagnosis, investigations, and treatment

Diagnosis

General approach
- Diagnose using standard TTS criteria.
- Actively consider TTS in oncology patients with acute chest pain, dyspnoea, ECG changes or troponin rise.
Recommended initial work-up
- Clinical examination
- 12-lead ECG
- Transthoracic echocardiography (TTE)
  - Cardiac biomarkers: Cardiac troponin (cTn), Natriuretic peptides (BNP or NT-proBNP)
- Cardiac MRI (CMR), according to ESC 2022 Cardio-Oncology guideline algorithm
Coronary imaging
- In most patients, invasive coronary angiography is required to exclude acute myocardial infarction.
- In patients with advanced malignancy or significant thrombocytopaenia where invasive angiography is contraindicated, CT coronary angiography is recommended.
Timing and follow-up imaging
- Perform cardiac imaging as early as possible once TTS is suspected, as LV dysfunction can be transient.
- If significant LV dysfunction (LVD) is present:
  - Schedule repeat imaging to document recovery of LV function.

Therapy and oncology treatment

Cancer treatment
- Interrupt the culprit cancer drug in patients with TTS.
- Avoid QT-prolonging medications where possible.
ICI-associated TTS
- The role of immunosuppression is currently unclear.
- If CMR shows myocardial inflammation in a TTS pattern:
  - v. methylprednisolone is recommended, given the overlap between ICI-induced TTS and ICI-induced myocarditis.
- Data on ICI rechallenge after TTS and recovery of LV function are limited; decisions must be individualised.
Multidisciplinary management and monitoring
- A multidisciplinary discussion (cardio-oncology, treating oncologist, etc.) is recommended after recovery from the acute TTS episode.
- If restarting the culprit cancer drug is necessary from an oncology perspective:
  - Implement regular cardiac biomarker monitoring, e.g.:
    - cTn and NT-proBNP before every ICI cycle
    - Transthoracic echocardiography if a new rise in cardiac biomarkers occurs.

References

Lyon AR et al. 2022 ESC Guidelines on cardio-oncology developed in collaboration with the European Hematology Association (EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS). Eur Heart J (2022) : 00, 1-133.

Cancer associated thrombosis & VTE

Commonly / frequently implicated therapies associated with CAT

Chemotherapy	Carboplatin, cisplatin Asparaginase Cyclophosphamide Anthracyclines : epirubicin, doxorubicin, daunorubicin Antimetabolites : 5-fluorouracil, capecitabine, cytarabine, 6-mercaptopurine, fludarabine, methotrexate, gemcitabine, pemetrexed Irinotecan Taxanes : paclitaxel, docetaxel, cabazitaxel
Endocrine therapy	Tamoxifen
Targeted therapy	CDK-inhibitors : palbociclib, abemaciclib, ribociclib IMiDs : thalidomide, lenalidomide, pomalidomide Proteasome inhibitors : carfilzomib Angiogenesis-inhibitors : bevacizumab, axitinib, lenvatinib, pazopanib, sorafenib, sunitinib
Immune therapy	Immune checkpoint inhibitors CAR-T cell therapy
Other factors in cancer patients	Erythropoiesis-stimulating agents Central venous catheter <6mo after diagnosis

+ consider cancer type and stage

Diagnostic approach

The same diagnostic approach and monitoring of VTE (DVT & PE) as in non-cancer patients apply.

DIAGNOSTIC CAVEATS :

D-dimers are less reliable in cancer patients
Unprovoked VTE may be the first presentation of cancer (+/- 20% of unprovoked VTE)
Consider unusual site VTE in cancer patients : upper limb, portal vein, sinus venosus, PAC-thrombosis

Therapeutic approach : cardiovascular aspects

Aspect	Key points
Incidental VTE / PE	Treat identical to symptomatic VTE / PE
PAC-associated thrombosis	Catheter may remain if functional, non-infected, well-positioned, and still indicated; otherwise consider removal (discuss with oncologist). After removal: therapeutic anticoagulation for 3 months. If left in place: extended therapeutic anticoagulation
Choice of anticoagulant	DOACs (edoxaban, rivaroxaban, apixaban) are non-inferior to LMWH; avoid vitamin K antagonists (VKA)
Treatment duration	Minimum 6 months Consider sufficiently long anticoagulant therapy + imaging reassessment
Extended treatment – therapeutic dose	Continue therapeutic anticoagulation in active malignancy, ongoing cancer therapy, or metastatic disease
Extended treatment – secondary prevention	Consider reduced-dose apixaban for long-term prophylaxis in selected patients
IVC filter	Use in CAT remains controversial

Therapeutic approach : oncological aspects

Aspect	Key points
Very high bleeding risk	Active/recent (<1 month) major bleeding; recent/evolving intracranial lesions; platelets <25,000/mm³
Conditions favouring LMWH	Unoperated GI/GU cancer; GI comorbidities or toxicity; severe renal dysfunction (CrCl <15 mL/min); major drug–drug interactions with DOACs; platelets <50,000/mm³
Thrombocytopaenia (<50,000/mm³)	Multidisciplinary discussion required; consider dose-reduced LMWH
Primary VTE prophylaxis	Evidence strongest in post-operative setting: prophylactic LMWH up to 4 weeks postoperatively
Cancer therapy interruption	Generally not required in VTE unless in severe PE/VTE.
Severe VTE / ATE in IMID therapy / angiogenesis inhibition	Discuss alternatives with treating oncologist

References

Lyon AR et al. 2022 ESC Guidelines on cardio-oncology developed in collaboration with the European Hematology Association (EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS). Eur Heart J (2022) : 00, 1-133.
Gevaert SA et al. Evaluation and management of cancer patients presenting with acute cardiovascular disease: a Clinical Consensus Statement of the Acute CardioVascular Care Association (ACVC) and the ESC council of Cardio-Oncology—part 2: acute heart failure, acute myocardial diseases, acute venous thromboembolic diseases, and acute arrhythmias. Eur Heart J Acute Cardiovasc Care (2022) : 11, 865-74.
Mahé I, Carrier M, Didier M, et al. Extended reduced-dose apixaban for cancer-associated venous thromboembolism. NEJM. Published online March 29, 2025.
Bauersachs RM et al. Guidelines for the management of cancer and thrombosis – Special aspects in women, Thrombosis Research, Volume 135, Supplement 1, 2015,

Common Cardiovascular problems

Rechallenge with Anthracylines

Treatment of anti-HER2 therapy related CTRCD

Anticancer Therapies Associated With Arterial Hypertension

Important interaction between certain cancer therapies and antihypertensive drugs

Table 1. Cancer Drugs by QTc Prolongation Risk

Table 2. Risk Factors for Drug-Induced QTc Prolongation and TdP

Clinical diagnosis

DIAGNOSTIC CAVEATS :

Severity assessment in ICI-M :

Therapeutic approach

Causes

Diagnosis

Commonly / frequently implicated therapies associated with CAT

Therapeutic approach : cardiovascular aspects

Therapeutic approach : oncological aspects

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