Arrhythmia Challenges in Cardio-Oncology: High-Risk Therapies, Management, and Anticoagulation.

Cardiovascular disease and cancer are the leading cause of mortality in the United States. In 2021, there were 695,547 and 605,213 deaths due to heart disease and cancer, respectively. With novel oncologic and cardiac therapies, survival has improved leading to increased life-expectancy albeit with chronic illness burden.

Kinase Inhibitors and Atrial Fibrillation: Mechanisms of Action and Clinical Implications.

Recent advances have significantly expanded the options of available therapeutics for cancer treatment, including novel targeted cancer therapies. Within this broad category of targeted therapies is the class of kinase inhibitors (KIs), which target kinases that have undergone aberrant activation in cancerous cells. Although KIs have shown a benefit in treating various forms of malignancy, they have also been shown to cause a wide array of cardiovascular toxicities, with cardiac arrhythmias, in particular atrial fibrillation (AF), being 1 of the predominant side effects.

Outcomes by Class of Anticoagulant Use for Nonvalvular Atrial Fibrillation in Patients With Active Cancer.

Background: The choice of anticoagulant agent for patients with nonvalvular atrial fibrillation (NVAF) in the setting of active cancer has not been well studied.

Objectives: The aim of this study was to compare the rates of cerebrovascular accident (CVA), gastrointestinal bleeding (GIB), and intracranial hemorrhage (ICH) in patients treated with direct oral anticoagulant agents (DOACs) compared with warfarin for NVAF in patients with active cancer.

Methods: This was a retrospective electronic medical record review of eligible patients treated at a cancer hospital.

Can We Mitigate Coronary Heart Disease Risk in Patients with Cancer?

Purpose Of Review: The review focuses on the shared risk factors observed between coronary heart disease and cancer, cancer therapeutics causing coronary heart disease, and potential strategies to mitigate atherosclerosis in patients with cancer.

Recent Findings: The pathophysiology behind how traditional cardiovascular risk factors also contribute to cancer development and mortality is increasingly recognized. In addition, newer cancer therapies, such as immune checkpoint inhibitors, cause increased inflammation leading to increased cardiovascular events.

Radiation-Induced Cardiovascular Disease: Mechanisms, Prevention, and Treatment.

Purpose Of Review: Despite the advancements of modern radiotherapy, radiation-induced cardiovascular disease (RICVD) remains a common cause of morbidity and mortality among cancer survivors.

Recent Findings: Proposed pathogenetic mechanisms of RICVD include endothelial cell damage with accelerated atherosclerosis, pro-thrombotic alterations in the coagulation pathway as well as inflammation and fibrosis of the myocardial, pericardial, valvular, and conduction tissues. Prevention of RICVD can be achieved by minimizing the exposure of the cardiovascular system to radiation, by treatment of underlying cardiovascular risk factors and cardiovascular disease, and possibly by prophylactic pharmacotherapy post exposure.

Forkhead box A1 (FOXA1) is a key mediator of insulin-like growth factor I (IGF-I) activity.

The insulin-like growth factor receptor (IGF-IR) has been implicated in a number of human tumors, including breast cancer. Data from human breast tumors has demonstrated that IGF-IR is over-expressed and hyper-phosphorylated. Additionally, microarray analysis has shown that IGF-I treatment of MCF7 cells leads to a gene signature comprised of induced and repressed genes, which correlated with luminal B tumors.

Estrogen and insulin-like growth factor-I (IGF-I) independently down-regulate critical repressors of breast cancer growth.

Although estrogen receptor alpha (ERα) and insulin-like growth factor (IGF) signaling are important for normal mammary development and breast cancer, cross-talk between these pathways, particularly at the level of transcription, remains poorly understood. We performed microarray analysis on MCF-7 breast cancer cells treated with estradiol (E2) or IGF-I for 3 or 24 h. IGF-I regulated mRNA of five to tenfold more genes than E2, and many genes were co-regulated by both ligands.