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Circulation. 2022;145:e895–e1032. DOI: 10.1161/CIR.0000000000001063 May 3, 2022 e977 CLINICAL STATEMENTS AND GUIDELINES

Patients with cancer and preexisting cardiovascular risk factors are at significantly higher risk of cancer therapy–related cardiomyopathy, representing a population in which pretherapy evaluation would have a significantly higher yield.2,5–10,42–47 4.	 The purpose of serial monitoring of LVEF in patients receiving potentially cardiotoxic anticancer agents is to identify subclinical cardiac injury, initiate cardioprotective agents, and consider temporary or permanent interruption of the offending agent.2,4,6,8,48 The practice of LVEF monitoring has mostly been implemented in patients receiving anthracyclines, trastuzumab, or both (Table 28). In a study of 2625 patients receiving anthracyclines for breast cancer or lymphoma who underwent serial LVEF monitoring, cancer therapy–related cardiomyopathy occurred in 9% of patients, of whom 81% had mild symptoms (NYHA class I to II).4 Beta blockers and ACEi-ARB were initiated in all patients, with 86% having at least partial recovery of LVEF.4 Patients with recovered LVEF had a lower incidence of cardiac events than those that did not.4 The clinical significance of an asymptomatic decrease in LVEF and the optimal frequency and duration of monitoring is less clear and likely depend on patient risk, the anticancer agent used, and its cumulative dose. Although a one-size-fits-all approach to monitoring for cancer therapy–related cardiomyopathy may be easier to implement systematically, it may not be the most cost-effective. Until additional data are available, limiting the monitoring to patients at higher risk of cancer therapy–related cardiomyopathy (Table 29) is a reasonable strategy. 5.	 Whether the preemptive use of ACEi-ARB, spironolactone, or selected beta blockers such as carvedilol and nebivolol is effective in reducing the risk of cancer therapy–related cardiomyopathy has been investigated in a number of small clinic trials, with conflicting findings.17–27,49 The most supportive of this practice is a study that randomized 114 patients receiving high-dose chemotherapy and having a posttreatment troponin rise >0.07 ng/mL to enalapril or placebo.20 None of the patients in the enalapril arm met the primary endpoint (>10% decrease in LVEF to below 50%), while 43% of patients in the standard of care group had a significant decrease in LVEF.20 Although other studies have shown similar findings, the magnitude of the difference in LVEF between arms was often small (<5%) and of questionable clinical significance.19,22 Not all studies have replicated these findings.18,21,24,26 Most importantly, none of the studies have assessed whether preemptive use of HF therapies in patients at risk for cancer therapy–related cardiomyopathy improves clinical outcomes, such as mortality or hospitalization for HF. Additional studies are needed to define the appropriate criteria and patient population in whom to initiate medical therapies for the primary prevention of cancer therapy–related cardiomyopathy. 6.	 Cardiovascular biomarkers, notably troponin, have been studied for cardiovascular risk stratification in patients undergoing potentially cardiotoxic therapies.29–32 A study of 452 patients with breast cancer showed that an elevated pretreatment level (>14 ng/L) was associated with a 4-fold increase in the risk of cancer therapy–related cardiomyopathy.32 Other smaller studies have found no advantage in measuring troponin or natriuretic peptides pretherapy.50–53 Overall, these biomarker studies were observational and small in sample size and number of events.54 Serial biomarkers may be more useful in risk stratification. For example, in a study of 703 patients receiving anthracyclines, an increase in troponin within 72 hours of chemotherapy and 1 month after the completion of treatment course were associated with a greater risk of cancer therapy–related cardiomyopathy.29 The clinical use of measuring biomarkers was assessed in 1 trial in which 114 patients with posttreatment increase in troponin to >0.07 ng/mL were randomized to enalapril or standard of care.20 None of the patients in the enalapril group had a decrease in LVEF, compared with 43% in the standard of care group.20 Data for the use of natriuretic peptides are limited. In practice, biomarkers could provide rapid risk stratification in patients for which echocardiographic findings are equivocal and help determine whether symptoms are cardiovascular in origin.

Table 29.  Risk Factors for Cancer Therapy–Related Cardiomyopathy Age ≥60 y Black race CAD Hypertension Diabetes Preexisting cardiomyopathy Previous exposure to anthracyclines Previous chest radiation Elevated troponin pretherapy CAD indicates coronary artery disease.

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