Developing a Clinical Cardio-Oncology Program and the Building Blocks for Success: How To.

•Cardio-oncology programs are necessary to provide optimal cardiovascular care to cancer patients and survivors.•Focus on developing a clear vision and mission-successful programs must be tailored to an organization's unique landscape.•Fostering partnerships with cardiologists and oncologists to provide high-quality patient-centered care is crucial.

QTc prolongation risk among patients receiving oral targeted antineoplastic medications: A real-world community-based oncology analysis.

Introduction: Thirty oral targeted antineoplastic agents are associated with prolongation of the QT interval. However, limited data exists regarding QTc prolongation and associated risk factors in the ambulatory oncology setting.

Methods: This retrospective study was completed to describe QTc prolongation incidence among patients receiving oral targeted tyrosine kinase inhibitors (TKI) and identify potential risk factors in the ambulatory community-based oncology clinic.

Update on cancer therapy-induced atherosclerosis.

Purpose Of Review: Recent advances in oncologic therapies have significantly improved overall survival for patients with malignancy. However, cardiovascular complications have not only increased in this population due to shared risk factors and pathophysiology, but also due to the therapies themselves. One key mechanism that warrants further attention is accelerated atherosclerosis due to these agents.

A multidisciplinary approach to heart failure care in the hospital: improving the patient journey.

Background: Despite advancements in care for patients with heart failure (HF), morbidity and mortality remain high. Hospitalizations and readmissions for HF have been the focus of significant attention among health care providers and payers, with an eye toward reducing health care costs. However, considerable variability exists with regard to inpatient workflows and management for patients with HF, which represents a significant opportunity to improve care.

Clinical Approach to Cardiovascular Toxicity of Oral Antineoplastic Agents: JACC State-of-the-Art Review.

Precision medicine has ushered in a new era of targeted treatments for numerous malignancies, leading to improvements in overall survival. Unlike traditional chemotherapy, many molecular targeted antineoplastic agents are available in oral formulation, leading to enhanced patient convenience and a perception of reduced risk of adverse effects. Although oral antineoplastic agents are generally well-tolerated, cardiovascular toxicities are being reported with increasing frequency in part due to U.

Enhanced Response to Drug-Induced QT Interval Lengthening in Patients with Heart Failure with Preserved Ejection Fraction.

Background: Patients with heart failure (HF) with reduced ejection fraction demonstrate enhanced response to drug-induced QT interval lengthening and are at increased risk for torsades de pointes. The influence of HF with preserved ejection fraction (HFpEF) on response to drug-induced QT lengthening is unknown.

Methods And Results: We administered intravenous ibutilide 0.

An evaluation of risk factors for major adverse cardiovascular events during tocilizumab therapy.

Objective: To evaluate associations between lipid levels, inflammation, and rheumatoid arthritis (RA) disease activity, at baseline and during treatment, with the risk of major adverse cardiovascular events (MACE) in tocilizumab-treated patients with RA.

Methods: In retrospective post hoc analyses, data were pooled for 3,986 adult patients with moderate to severe RA who received ≥1 dose of tocilizumab (4 mg/kg or 8 mg/kg) intravenously every 4 weeks in randomized controlled trials and extension studies. Cox proportional hazards modeling was used to evaluate associations between baseline characteristics and posttreatment changes in laboratory and disease characteristics (week 24) and change in disease activity and laboratory values from baseline to week 24 with the risk of future MACE during extended followup.

Regulation of mTOR and S6K1 activation by the nPKC isoforms, PKCepsilon and PKCdelta, in adult cardiac muscle cells.

Activation of both mTOR and its downstream target, S6K1 (p70 S6 kinase) have been implicated to affect cardiac hypertrophy. Our earlier work, in a feline model of 1-48 h pressure overload, demonstrated that mTOR/S6K1 activation occurred primarily through a PKC/c-Raf pathway. To further delineate the role of specific PKC isoforms on mTOR/S6K1 activation, we utilized primary cultures of adult feline cardiomyocytes in vitro and stimulated with endothelin-1 (ET-1), phenylephrine (PE), TPA, or insulin.

PKC-epsilon regulation of extracellular signal-regulated kinase: a potential role in phenylephrine-induced cardiocyte growth.

Hypertrophic growth of cardiac muscle is dependent on activation of the PKC-epsilon isoform. To define the effectors of PKC-epsilon involved in growth regulation, recombinant adenoviruses were used to overexpress either wild-type PKC-epsilon (PKC-epsilon/WT) or dominant negative PKC-epsilon (PKC-epsilon/DN) in neonatal rat cardiocytes. PKC-epsilon/DN inhibited acute activation of PKC-epsilon produced in response to phorbol ester and reduced ERK1/2 activity as measured by the phosphorylation of p42 and p44 isoforms.

Tyrosine phosphorylation and dissociation of occludin-ZO-1 and E-cadherin-beta-catenin complexes from the cytoskeleton by oxidative stress.

The oxidative-stress-induced alteration in paracellular junctional complexes was analysed in Caco-2 cell monolayer. Oxidative stress induced a rapid increase in tyrosine phosphorylation of occludin, zonula occludens (ZO)-1, E-cadherin and beta-catenin. An oxidative-stress-induced decrease in transepithelial electrical resistance was associated with a redistribution of occludin-ZO-1 and E-cadherin-beta-catenin complexes from the intercellular junctions.