Cancer - 2021 ESC Guidelines for the Diagnosis and Treatment of Acute and Chronic Heart Failure

HF occurs in patients with cancer as a result of the interaction among anticancer therapy, cancer itself, and patients’ CV background (risk factors and coexisting CV disease).

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Several anticancer thera- pies may cause HF directly, thorough their cardiotoxic effects (Table 23), or, indirectly, through other mechanisms, such as myocarditis, ischaemia, systemic or pulmonary hypertension, arrhythmias or valve disease.

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HF, in turn, may affect cancer outcomes by depriving patients of effective anticancer therapies.

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Some epide- miological and experimental evidence suggests a further reciprocal interaction between cancer and HF with some, though not all, studies showing a higher incidence rate of cancer in patients with HF.

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The prevention of HF in patients with cancer undergoing potential cardiotoxic therapies requires careful patient’s assessment and man- agement before, during, and after cancer therapy, preferably in the context of an integrated Cardio-Oncology service (Figure 18).

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A CV baseline risk assessment for all patients scheduled to receive potentially cardiotoxic cancer therapies using the HFA-ICOS risk assessment is advisable.

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Baseline CV risk assessment forms have been developed for different potentially car- diotoxic cancer therapies. History of HF or CMP characterizes patients as being at very high risk or at high risk for all cancer thera- pies, except anti-androgen treatments for prostate cancer. An LVEF

<50% is an additional factor for high-risk patients and elevated levels

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of NPs or troponin at baseline are additional criteria of medium risk for most of the cancer treatments.

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During cancer treatment with potential cardiotoxic therapies, LV systolic function can be monitored through echocardiography.

Chemotherapy should be reconsidered and treatment with an ACE-I and a beta-blocker (preferably carvedilol) should be started in patients who develop LV systolic dysfunction, defined as 10% or more absolute reduction in LVEF to a value below 50%.

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Global longitudinal strain can detect cardiac dysfunction at an earlier stage.

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A > _12% relative reduction in global longitudinal strain was compared with an LVEF decline in a prospective randomized trial in high-risk patients undergoing potentially cardiotoxic chemother- apy. Compared to treatment based on LVEF, treatment based on changes in global longitudinal strain led to the same decrease in LVEF (primary endpoint) but with fewer patients who developed cardiac dysfunction at the end of the study, thus suggesting usefulness of global longitudinal strain for the early detection of cardiotoxicity.

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Promising results for the early detection of cardiac dysfunction have also been obtained through monitoring of biomarkers, such as NPs and troponin.

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Patients on immunotherapy with immune check- point inhibitors are at increased risk of myocarditis and should be monitored for related symptoms and signs and by weekly assessment of cardiac troponin during at least the first 6 weeks of therapy and managed accordingly.

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Timing of the imaging procedures and biomarkers assessment depend on the anticancer treatment and patient’s risk profile (Figure 18).

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In general, all patients scheduled for potential cardi- otoxic therapies must undergo a baseline evaluation that would define the level of risk for cardiotoxicity (low, medium, or high) and the intensity of monitoring and follow-up during and after cancer treatment.

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Cancer survivors exposed to potentially cardiotoxic therapies should be periodically monitored in the long term as HF may develop several years after cancer therapy.

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Table 23 Cancer drugs causing heart failure

Cancer therapy Indication

Anthracycline chemotherapy

(doxorubicin, epirubicin, daunorubicin, idarubicin)

Breast cancer, lymphoma, acute leukaemia, sarcoma

HER2-targeted therapies

(trastuzumab, pertuzumab, trastuzumab emtansine T-DM1, lapatinib, neratinib, tucatinib)

HER2þbreast cancer HER2þgastric cancer

VEGF inhibitors

TKIs (sunitinib, pazopanib, sorafenib, axitinib, tivozanib, cabozantinib, regorafenib, lenvatinib, vandetinib) and antibodies (bevacizumab, ramucirumab)

VEGF TKIs: renal cancer, hepatocellular cancer, thyroid cancer, colon cancer, sarcoma, GIST

Antibodies: breast cancer, ovarian cancer, gastric cancer, gastro-oesopha- geal cancer, colon cancer

Multi-targeted kinase inhibitors:

second and third generation BCR-ABL TKIs (ponatinib, nilotinib, dasatinib, bosutinib)

Chronic myeloid leukaemia

Proteasome inhibitors (carfilzomib, bortezomib, ixazomib) Immunomodulatory drugs (lenalidomide, pomalidomide)

Multiple myeloma

Combination RAF and MEK inhibitors

(dabrafenibþtrametinib, vemurafenibþcobimetinib, encorafenibþ binimetinib)

RAF mutant melanoma

Androgen deprivation therapies GnRH agonists (goserelin, leuprorelin) Antiandrogrens (abiraterone)

Prostate cancer, breast cancer

Immune checkpoint inhibitors:

anti-programmed cell death 1 inhibitors (nivolumab, pembrolizumab)

anti-cytotoxic T-lymphocyte-associated protein 4 inhibitor (ipilimumab)

anti-programmed death-ligand 1 inhibitors (avelumab, atezolizumab, durvalumab)

Melanoma (metastatic and adjuvant)

Metastatic renal cancer, non-small cell lung cancer, small cell lung cancer, refractory Hodgkin’s lymphoma, metastatic triple negative breast cancer, metastatic urothelial cancer, liver cancer, MMR-deficient cancer

GIST = gastrointestinal stromal tumour; GnRH = gonadotropin-releasing hormone; HER2 = human epidermal growth factor receptor 2; MEK = mitogen-activated protein kinase;

MMR = mismatch repair; TKI = tyrosine kinase inhibitor; VEGF = vascular endothelial growth factor.

ESC 2021

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Management of patients receiving potential cardiotoxic treatments

Baseline risk assessment including clinical assessment, ECG, resting echocardiogram and

cardiac biomarkers (NP, troponin)

Pre-existing heart failure or high-risk cardiovascular disease

Medium- and high-risk patient^b

Increased^c surveillance with ECG and cardiac biomarkers

during treatment

Reassessment at 3 months and 12 months after completion of cancer therapy

Low-risk patient^b

Standard surveillance^d Before cardiotoxic

cancer treatment^a

After cardiotoxic cancer treatment^a During cardiotoxic cancer treatment^a

Reassessment at 12 months

after completion of cancer therapy

Surveillance every 5 years following therapies with established cardiotoxicity (e.g. high-dose anthracycline chemotherapy)^e

Follow-up by heart failure or cardio-oncology team for new heart failure or left ventricular systolic dysfunction

Figure 18 Management of patients with cancer and heart failure. ECG = electrocardiogram; HER2 = human epidermal growth factor receptor 2; HF = heart failure; HFA = Heart Failure Association; ICOS = International Cardio-Oncology Society; MEK = mitogen-activated protein kinase; NP = natriuretic peptide; VEGF = vascular endothelial growth factor.

Anthracycline chemotherapy, trastuzumab and HER2 targeted therapies, VEGF inhibitors, proteasome inhibitors, combination RAFþMEK inhibitors.

Low, medium and high risk may be calculated using the HFA-ICOS baseline cardiovascular risk proformas.

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Increased surveillance is intended between 1 and 4 weeks.

Standard surveillance is intended every 3 months.

5 yearly surveillance at follow-up = clinical review every 5 years with history, examination, NP and troponin levels, and echocardiogram.

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Dalam dokumen 2021 ESC Guidelines for the Diagnosis and Treatment of Acute and Chronic Heart Failure (Halaman 74-77)