4.2 The electrifying performance of sacubitril/valsartan on
CTRCD
A retrospective case study described two anthracycline-related
cardiomyopathy survivors with HFrEF who were treated with
sacubitril/valsartan with success after poor responses to conventional
evidence-based drug treatment (37). Both subjects exhibited fair
recovery of NYHA functional class and normalization of NT-proBNP
concentration as well as no re-hospitalization for heart failure (37)
(Table 1 ). Canale et al. reported a case series of four
patients with CTRCD and severe HFrEF (38). All patients were managed
with sacubitril/valsartan with success while being combatting malignant
ventricular arrhythmias by wearing an automatic defibrillator until
heart function recovery (38) (Table 1 ).
In a pilot study, twenty-one patients with HFrEF and a history of
histologically confirmed cancer received sacubitril/valsartan (39).
Sacubitril/valsartan was well tolerated and effective over a median
duration of 12 months. Even patients with long-term
cardiotoxicity-related HFrEF could be titrated with ANRI to the target
dose, giving rise to significant improvement in NYHA cardiac function
grading and LVEF as assessed by echocardiography, as well as in their
NT-proBNP levels (39) (Table 1 ). A multicenter registry study
in six Spanish hospitals with cardio-oncology clinics followed up
sixty-seven cancer survivors managed with sacubitril/valsartan (40).
After a median duration of 4.6 [1; 11] months, sacubitril/valsartan
was well-tolerated and improved cardiac functional and structural
characteristics assessed by echocardiography, NT-proBNP concentration,
and NYHA functional class in patients with HFrEF regardless of the
achieved agent dose (40) (Table 1 ).
Renato et al. (41) reported two clinical cases of
cardiotoxicity-related HFrEF where therapeutic action of
sacubitril/valsartan against anthracycline cardiomyopathy was proven by
the improvement of symptoms and echocardiographic parameters
(Table 1 ). Ana et al. (42) evaluated the therapeutic
effect of sacubitril/valsartan on LVEF and LV remodelling assessed by
comprehensive multiparametric cardiac magnetic resonance (CMR) in ten
consecutive patients with cardiotoxicity-related HFrEF. LV volumes
decreased markedly and LVEF improved significantly after administration
of sacubitril/valsartan. A corresponding marked decrease in NT-proBNP
concentration and improvement in NYHA functional class were also
observed (42). LV dysfunction within CTRCD is partly restorable, but
this strongly dependeds on timely treatment with sacubitril/valsartan
(42) (Table 1 ). Twenty-eight patients with breast cancer and
refractory cardiotoxicity-related HFrEF were initiated with
sacubitril/valsartan after poor responses to conventional evidence-based
drug treatment (43). Twenty months after captopril or valsartan was
replaced with ARNI, there was a significant improvement in NYHA cardiac
function grade, six-minute walking distance, LVEF, LV diastolic
function, LV end-diastolic diameter and mitral regurgitation assessed by
echocardiography, as well as NT-proBNP levels, without drug reactions
(43) (Table 1 ). Although this research has some defects, such
as a limited sample and an inadequate description of past cancer
history, it provides new evidence for improving the clinical management
of patients with CTRCD.