Frequency of Left Ventricular End-Diastolic Volume–Mediated Declines in Ejection Fraction in Patients Receiving Potentially Cardiotoxic Cancer Treatment

Meléndez, Giselle C.; Sukpraphrute, Bunyapon; D’Agostino, Ralph B.; Jordan, Jennifer H.; Klepin, Heidi D.; Ellis, Leslie R.; Lamar, Zanetta S.; Vasu, Sujethra; Lesser, Glenn J.; Burke, Gregory L.; Weaver, Kathryn E.; Ntim, William O.; Hundley, W. Gregory

doi:10.1016/j.amjcard.2017.02.008

Cited by 37 publications

(20 citation statements)

References 19 publications

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“…Decline in ejection fraction after cardiotoxic therapy may occur through increased end-systolic volumes related to myocellular dysfunction, but may also be caused by decreased end-diastolic volumes from cancer therapy–related nausea and volume depletion. 19 , 20 At follow-up, patients treated with candesartan had a decline in end-diastolic volumes but no change in end-systolic volumes, whereas participants who did not receive candesartan experienced increasing end-systolic volumes, but no significant change in end-diastolic volumes. It seems unlikely that the decline in end-diastolic volume is caused by volume depletion >1 year after end of cancer therapy.…”

Section: Discussionmentioning

confidence: 99%

Prevention of Cardiac Dysfunction During Adjuvant Breast Cancer Therapy (PRADA): Extended Follow-Up of a 2×2 Factorial, Randomized, Placebo-Controlled, Double-Blind Clinical Trial of Candesartan and Metoprolol

et al. 2021

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Background: Adjuvant breast cancer therapy containing anthracyclines with or without anti–human epidermal growth factor receptor–2 antibodies and radiotherapy is associated with cancer treatment–related cardiac dysfunction. In the PRADA trial (Prevention of Cardiac Dysfunction During Adjuvant Breast Cancer Therapy), concomitant treatment with the angiotensin receptor blocker candesartan attenuated the reduction in left ventricular ejection fraction (LVEF) in women receiving treatment for breast cancer, whereas the β-blocker metoprolol attenuated the increase in cardiac troponins. This study aimed to assess the long-term effects of candesartan and metoprolol or their combination to prevent a reduction in cardiac function and myocardial injury. Methods: In this 2×2 factorial, randomized, placebo-controlled, double-blind, single-center trial, patients with early breast cancer were assigned to concomitant treatment with candesartan cilexetil, metoprolol succinate, or matching placebos. Target doses were 32 and 100 mg, respectively. Study drugs were discontinued after adjuvant therapy. All 120 validly randomized patients were included in the intention-to-treat analysis. The primary outcome measure was change in LVEF assessed by cardiovascular magnetic resonance imaging from baseline to extended follow-up. Secondary outcome measures included changes in left ventricular volumes, echocardiographic peak global longitudinal strain, and circulating cardiac troponin concentrations. Results: A small decline in LVEF but no significant between-group differences were observed from baseline to extended follow-up, at a median of 23 months (interquartile range, 21 to 28 months) after randomization (candesartan, 1.7% [95% CI, 0.5 to 2.8]; no candesartan, 1.8% [95% CI, 0.6 to 3.0]; metoprolol, 1.6% [95% CI, 0.4 to 2.7]; no metoprolol, 1.9% [95% CI, 0.7 to 3.0]). Candesartan treatment during adjuvant therapy was associated with a significant reduction in left ventricular end-diastolic volume compared with the noncandesartan group ( P =0.021) and attenuated decline in global longitudinal strain ( P =0.046) at 2 years. No between-group differences in change in cardiac troponin I and T concentrations were observed. Conclusions: Anthracycline-containing adjuvant therapy for early breast cancer was associated with a decline in LVEF during extended follow-up. Candesartan during adjuvant therapy did not prevent reduction in LVEF at 2 years, but was associated with modest reduction in left ventricular end-diastolic volume and preserved global longitudinal strain. These results suggest that a broadly administered cardioprotective approach may not be required in most patients with early breast cancer without preexisting cardiovascular disease. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01434134.

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Section: Discussionmentioning

confidence: 99%

Prevention of Cardiac Dysfunction During Adjuvant Breast Cancer Therapy (PRADA): Extended Follow-Up of a 2×2 Factorial, Randomized, Placebo-Controlled, Double-Blind Clinical Trial of Candesartan and Metoprolol

et al. 2021

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“…93,94 Strain measurement is more sensitive to subtle damage of the myocardial ultrastructure that would otherwise be undetectable by echocardiography. 47,95,96 Early indicators of LV systolic dysfunction (LVSD) such as GLS may be useful for identifying patients at risk of anthracycline-based cardiotoxicity before the development of HF. 97 Studies have consistently shown significant GLS reductions in patients at cumulative doses of doxorubicin as low as 100e200 mg/m 2 , despite normal LVEF at the time of GLS assessment.…”

Section: Annals Of Oncologymentioning

confidence: 99%

Management of cardiac disease in cancer patients throughout oncological treatment: ESMO consensus recommendations

et al. 2020

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Cancer and cardiovascular (CV) disease are the most prevalent diseases in the developed world. Evidence increasingly shows that these conditions are interlinked through common risk factors, coincident in an ageing population, and are connected biologically through some deleterious effects of anticancer treatment on CV health. Anticancer therapies can cause a wide spectrum of short-and long-term cardiotoxic effects. An explosion of novel cancer therapies has revolutionised this field and dramatically altered cancer prognosis. Nevertheless, these new therapies have introduced unexpected CV complications beyond heart failure. Common CV toxicities related to cancer therapy are defined, along with suggested strategies for prevention, detection and treatment. This ESMO consensus article proposes to define CV toxicities related to cancer or its therapies and provide guidance regarding prevention, screening, monitoring and treatment of CV toxicity. The majority of anticancer therapies are associated with some CV toxicity, ranging from asymptomatic and transient to more clinically significant and long-lasting cardiac events. It is critical however, that concerns about potential CV damage resulting from anticancer therapies should be weighed against the potential benefits of cancer therapy, including benefits in overall survival. CV disease in patients with cancer is complex and treatment needs to be individualised. The scope of cardio-oncology is wide and includes prevention, detection, monitoring and treatment of CV toxicity related to cancer therapy, and also ensuring the safe development of future novel cancer treatments that minimise the impact on CV health. It is anticipated that the management strategies discussed herein will be suitable for the majority of patients. Nonetheless, the clinical judgment of physicians remains extremely important; hence, when using these best clinical practices to inform treatment options and decisions, practitioners should also consider the individual circumstances of their patients on a case-by-case basis.

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“…Third, when assessing LVEF, one must consider whether a decline in LVEF occurs as a reduction in LVEDV or an increase in LVESV ( Figure 1 ). Meléndez et al ( 37 ) studied 120 patients with adult cancer 3 months after the administration of chemotherapy and observed that in those with LVEF declines >10%, nearly one-fifth experienced LVEF declines from isolated declines in LVEDV ( Figure 3 , Online Videos 1 , 2 , 3 , and 4 ). In a subsequent analysis on a subset of these same subjects, Jordan et al ( 38 ) observed that 16% of patients may experience deterioration in myocardial circumferential strain due to isolated declines in LVEDV ( 38 ).…”

Section: Dysfunctionmentioning

confidence: 99%

Cardiovascular Magnetic Resonance in the Oncology Patient

Jordan

Todd

Vasu

et al. 2018

JACC: Cardiovascular Imaging

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Patients with or receiving potentially cardiotoxic treatment for cancer are susceptible to developing decrements in left ventricular mass, diastolic function, or systolic function. They may also experience valvular heart disease, pericardial disease, or intracardiac masses. Cardiovascular magnetic resonance may be used to assess cardiac anatomy, structure, and function and to characterize myocardial tissue. This combination of features facilitates the diagnosis and management of disease processes in patients with or those who have survived cancer. This report outlines and describes prior research involving cardiovascular magnetic resonance for assessing cardiovascular disease in patients with or previously having received treatment for cancer.

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Frequency of Left Ventricular End-Diastolic Volume–Mediated Declines in Ejection Fraction in Patients Receiving Potentially Cardiotoxic Cancer Treatment

Cited by 37 publications

References 19 publications

Prevention of Cardiac Dysfunction During Adjuvant Breast Cancer Therapy (PRADA): Extended Follow-Up of a 2×2 Factorial, Randomized, Placebo-Controlled, Double-Blind Clinical Trial of Candesartan and Metoprolol

Prevention of Cardiac Dysfunction During Adjuvant Breast Cancer Therapy (PRADA): Extended Follow-Up of a 2×2 Factorial, Randomized, Placebo-Controlled, Double-Blind Clinical Trial of Candesartan and Metoprolol

Management of cardiac disease in cancer patients throughout oncological treatment: ESMO consensus recommendations

Cardiovascular Magnetic Resonance in the Oncology Patient

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