Anticancer Therapy-Induced Atrial Fibrillation: Electrophysiology and Related Mechanisms

Abstract

Some well-established immunotherapy, radiotherapy, postoperation, anticancer drugs such as anthracyclines, antimetabolites, human epidermal growth factor receptor 2 blockers, tyrosine kinase inhibitors, alkylating agents, checkpoint inhibitors, and angiogenesis inhibitors, are significantly linked to cardiotoxicity. Cardiotoxicity is a common complication of several cancer treatments. Some studies observed complications of cardiac arrhythmia associated with the treatment of cancer, including atrial fibrillation (AF), supraventricular arrhythmias, and cardiac repolarization abnormalities. AF increases the risk of cardiovascular morbidity and mortality; it is associated with an almost doubled risk of mortality and a nearly 5-fold increase in the risk of stroke. The occurrence of AF is also usually researched in patients with advanced cancer and those undergoing active cancer treatments. During cancer treatments, the incidence rate of AF affects the prognosis of tumor treatment and challenges the treatment strategy. The present article is mainly focused on the cardiotoxicity of cancer treatments. In our review, we discuss these anticancer therapies and how they induce AF and consequently provide information on the precaution of AF during cancer treatment.

Regulatory Mechanisms of the NLRP3 Inflammasome, a Novel Immune-Inflammatory Marker in Cardiovascular Diseases

“…The levels of the NLRP3 inflammasome were notably increased in mice with TAC and were involved in the increase in inflammatory mediators and profibrotic factor production, leading to myocardial fibrosis, cardiomyocyte hypertrophy, and impaired cardiac function (93). When the oxidative stress system of myocardial cells is activated, accumulated ROS and Ca 2+ are released to the cytoplasm, resulting in changes in mitochondrial membrane potential, leading to apoptosis of myocardial cells (94). Pirfenidone improved TAC-induced left ventricular hypertrophy and myocardial fibrosis in a mouse model through inhibiting NLRP3 inflammasome assembly, and regulating the NLRP3-IL-1β signaling pathway in both the ROS-dependent and ROS-independent pathways (95).…”

Atrial Cardiomyopathy and Atrial Fibrillation in Cancer

“…Persistent AF induced by anthracyclines is common and the first episode of AF event often occurs between 8 and 36 months after starting therapy [ 19 ]. AF could also occur in patients treated with other anticancer drugs such as fluorouracil, methotrexate, alkylating agents, antimicrotubule agents (docetaxel, paclitaxel), tyrosine kinase inhibitors (imatinib, lapatinib, sunitinib), proteasoma inhibitor (bortezomib), bevacizumab (blocker of the vascular endothelial growth factor), trastuzumab (angiogenesis inhibitor), and immune-checkpoint inhibitors [ 10 , 20 – 22 ], and this cardiotoxicity complication has been shown related to poor prognosis. A prospective study investigated 249 lymphoma patients treated with anthracyclines showing that new-onset AF may predict unfavorable outcomes after chemotherapy [ 19 ].However, the lack of cardiac monitoring before chemotherapy makes it difficult to distinguish whether there was a preexisting undiagnosed arrhythmia or accompanying arrhythmia caused by chemotherapy.…”

The cancer patient and cardiology

“…Many authoritative reviews have illustrated how CV events (type and incidence rate) may vary according to cancer drugs, doses, use in combination with other agents or radiation therapy, and underlying patient risk factors. Table 1 shows examples of CV toxicities that have been associated with conventional chemotherapeutics, MTAs, radiation therapy and other oncologic therapies 3,5–19 . We will not discuss each cardiotoxic agent in detail, but emphasize that older drugs, newer drugs and radiation therapy, alone or in combination, may increase the risk for a number of diverse CV events.…”