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Mechanistic and Clinical Overview Cardiovascular Toxicity of BRAF and MEK Inhibitors (JACC: CardioOncology State-of-the-Art Review March 2022-1)
Mechanistic and Clinical Overview Cardiovascular Toxicity of BRAF and MEK Inhibitors JACC: CardioOncology State-of-the-Art Review

Rapidly accelerated fibrosarcoma B-type (BRAF) and mitogen-activated extracellular signal-regulated kinase (MEK) inhibitors have revolutionized melanoma treatment. Approximately half of patients with melanoma harbor a BRAF gene mutation with subsequent dysregulation of the RAF-MEK-ERK signaling pathway. Targeting this pathway with BRAF and MEK blockade results in control of cell proliferation and, in most cases, disease control. These pathways also have cardioprotective effects and are necessary for normal vascular and cardiac physiology. BRAF and MEK inhibitors are associated with adverse cardiovascular effects including hypertension, left ventricular dysfunction, venous thromboembolism, atrial arrhythmia, and electrocardiographic QT interval prolongation. These effects may be underestimated in clinical trials. Baseline cardiovascular assessment and follow-up, including serial imaging and blood pressure assessment, are essential to balance optimal anti-cancer therapy while minimizing cardiovascular side effects. In this review, an overview of BRAF/MEK inhibitor–induced cardiovascular toxicity, the mechanisms underlying these, and strategies for surveillance, prevention, and treatment of these effects are provided.

JACC CardioOncology Editor-in-Chief and CME Editor
Bonnie Ky, MD, MSCE, FACC

Authors
Claire Glen, MBCHB
Ninian N. Lang, MBCHB, PHD

Important Dates

Date of Release: March 15, 2022    
Term of Approval/Date of CME/MOC/ECME Expiration: March 14, 2023 

Summary
Availability: On-Demand
Expires on Mar 14, 2023
Cost: FREE
Credit Offered:
1 CME Credit
1 ABIM-MOC Point
1 ECME Credit
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