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Review
. 2017 Nov 14;70(20):2536-2551.
doi: 10.1016/j.jacc.2017.09.1096.

Cardiovascular Complications of Cancer Therapy: Best Practices in Diagnosis, Prevention, and Management: Part 1

Hui-Ming Chang  1 , Rohit Moudgil  2 , Tiziano Scarabelli  3 , Tochukwu M Okwuosa  4 , Edward T H Yeh  5
Affiliations
Review

Cardiovascular Complications of Cancer Therapy: Best Practices in Diagnosis, Prevention, and Management: Part 1

Hui-Ming Chang et al. J Am Coll Cardiol. .

Erratum in

  • Correction.
    [No authors listed] [No authors listed] J Am Coll Cardiol. 2018 Feb 6;71(5):587. doi: 10.1016/j.jacc.2017.12.041. J Am Coll Cardiol. 2018. PMID: 29406874 No abstract available.

Abstract

Modern cancer therapy has successfully cured many cancers and converted a terminal illness into a chronic disease. Because cancer patients often have coexisting heart diseases, expert advice from cardiologists will improve clinical outcome. In addition, cancer therapy can also cause myocardial damage, induce endothelial dysfunction, and alter cardiac conduction. Thus, it is important for practicing cardiologists to be knowledgeable about the diagnosis, prevention, and management of the cardiovascular complications of cancer therapy. In this first part of a 2-part review, we will review cancer therapy-induced cardiomyopathy and ischemia. This review is based on a MEDLINE search of published data, published clinical guidelines, and best practices in major cancer centers. With the number of cancer survivors expanding quickly, the time has come for cardiologists to work closely with cancer specialists to prevent and treat cancer therapy-induced cardiovascular complications.

Keywords: cancer therapy; cardiomyopathy; cardiovascular complication; ischemia.

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Conflict of interest statement

Disclosures: No conflict of interest disclosures for all authors.

Figures

Figure 1
Figure 1. Mechanism of Doxorubicin-induced Cardiotoxicity
Doxorubicin inhibits topoisomerase 2β to induced DNA double strand break, leading to p53 activation and death of cardiomyocytes. Doxorubicin-bound topoisomerase 2β binds to promoters of anti-oxidative genes and PGC-1 that are required for expression of anti-oxidative enzymes and electron transport chains. Thus, topoisomerase 2β is able to account for the three hallmarks of doxorubicin-induced cardiotoxicity: cardiomyocyte death, generation of ROS, and mitochondriopathy (24,25).
Central Illustration
Central Illustration. Management of cancer therapy-induced cardiovascular complications
Best practices in the management of cancer therapy-induced cardiomyopathy and ischemia. EF=ejection fraction; GLS=global longitudinal strain; VSP=VEGF signaling pathway; BB=beta blocker; ACEI= angiotensin converting enzyme inhibitor; CAD=coronary artery disease; DAT=dual anti-platelet therapy; DES=drug-eluting stent.
See this image and copyright information in PMC

References

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