Cardiotoxicity of Anthracyclines

Abstract

Cardiotoxicity is a feared side effect that may limit the clinical use of anthracyclines. It may indeed affect the quality of life and survival of patients with cancer, regardless of oncological prognosis. This paper provides an overview of anthracycline-induced cardiotoxicity in terms of definition, classification, incidence, risk factors, possible mechanisms, diagnosis, and treatment. We also report effective strategies for preventing cardiotoxicity. In addition, we discuss limiting current approaches, the need for a new classification, and early cardiotoxicity detection and treatment. Probably, anthracycline-induced cardiotoxicity is a continuous phenomenon that starts from myocardial cell injury; it is followed by left ventricular ejection fraction (LVEF) and, if not diagnosed and cured early, progressively leads to symptomatic heart failure. Anthracycline-induced cardiotoxicity can be detected at a preclinical phase. The role of biomarkers, in particular troponins, in identifying subclinical cardiotoxicity and its therapy with angiotensin-converting enzyme inhibitors (mainly enalapril) to prevent LVEF reduction is a recognized and effective strategy. If cardiac dysfunction has already occurred, partial or complete LVEF recovery may still be obtained in case of early detection of cardiotoxicity and prompt heart failure treatment.

Cardiotoxicity and Heart Failure: Lessons from Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes and Anticancer Drugs

“…Drug-induced cardiotoxicity is a major safety issue causing HF, which has to be considered during drug development and therapeutic applications. Among anticancer drugs, the anthracycline family members such as doxorubicin (DOX), daunorubicin, and mitoxantrone are known to induce cardiotoxicity and HF (reviewed in References [13][14][15]). DOX is a highly effective anticancer drug prescribed for the treatment of a variety of cancer types, including solid tumors and hematologic malignancies in both adults and children.…”

Cardiotoxic effects and myocardial injury: the search for a more precise definition of drug cardiotoxicity

“…Thanks to the results of these studies [31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46], some authors suggested that hs-cTn assay may be a reliable laboratory test for the early detection of asymptomatic or subclinical cardiotoxic damage even in patients undergoing cancer chemotherapy [15,17,18,47,48]. Indeed, several studies have demonstrated that hs-cTn assays enable the early detection of myocardial injury in cancer patients treated with chemotherapy agents [15,17,18,[47][48][49][50][51][52][53][54][55][56][57][58][59]. In particular, two recent studies using hs-Tn methods demonstrate that a progressive increase in biomarker concentration during chemotherapy allows the identification of patients more prone to developing myocardial dysfunction and MACE [52,53].…”

Sacubitril/valsartan versus candesartan in women with heart failure receiving adjuvant therapy for breast cancer - is there any antiarrhythmic effect?

“…Последний показатель позволяет точнее оценивать снижение функции ЛЖ [29], однако не всегда доступен при проведении химиотерапии у онкологических больных. В перечень методик обследования целесообразно включать не только визуализирующие исследования, но и определение уровней биохимических маркеров (вчТропонин I, NT-proBNP) [5,12]. Учет динамики комплекса показателей позволял нам сделать вывод о возможности проведения полихимиотерапии у наблюдавшихся пациенток в полном объеме, а также констатировать превосходство схемы лечения, включавшей сакубитрил/валсартан, по сравнению со схемой, в составе которой применялся кандесартан.…”

“…Типичным примером является кардиотоксичность антрациклинов, улучшающих прогноз при лечении рака молочной железы, но вызывающих дисфункцию левого желудочка (ЛЖ) [3,4]. Поэтому наиболее затруднительно применение антрациклинов у пациенток с исходно имеющейся сердечной недостаточностью (СН) [5].…”