Abstract
Cardiac toxicity is one of the most important long-term toxicities experienced by cancer survivors so that survival rate due to anticancer therapy may be negatively affected due to cardiac complications. Thus, the search for novel methods to lower the incidence of treatment-related cardiotoxicity is a priority for all cancer-related disciplines. In this review, we provide an overview of the available preclinical and clinical data evaluating the role of angiotensin-converting enzyme inhibitors in the prophylaxis of cardiac dysfunction secondary to anthracyclines and trastuzumab use. The available clinical data suggest some degree of protective utility for the use of some angiotensin-converting enzyme inhibitors against anthracycline-related cardiotoxicity while the data are scarce with regard to a similar role for patients receiving trastuzumab.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending or royalties.
Cardiac toxicity is one of the most important long-term toxicities experienced by cancer survivors so that the survival benefit due to anticancer therapy might be affected by increased mortality due to cardiac complications.
The search for novel methods including angiotensin-converting enzyme inhibitors administration to cut down the treatment-related cardiotoxicity has been a priority for all cancer-related disciplines.
The available clinical data suggest some degree of protective utility for the use of some angiotensin-converting enzyme inhibitors against anthracycline-related cardiotoxicity while the data are scarce with regard to a similar role for patients receiving trastuzumab.
These findings need to be further validated in larger randomized controlled studies with more stress on the clinically relevant end points like death and development of clinical heart failure.