Extract

We thank Coughlin and Kapuku for their thoughtful commentary (1) on our study (2).

The authors highlight that high-sensitivity cardiac troponin T (hs-cTnT) is a sensitive marker of subclinical myocyte damage and that levels can be elevated in the setting of acute cardiotoxicity from cancer therapies and other conditions with cardiac involvement. While hs-cTnT is highly heart-specific, it is not disease-specific; there are many clinical conditions that can result in elevated hs-cTnT (3). This is an important point. Hs-cTnT is a global marker of cardiac damage and, as Coughlin and Kapuku rightly point out, it is highly prognostic for future cardiovascular events and death (4, 5).

Our results are highly consistent with prior studies that demonstrate elevated cardiovascular risk with time from cancer diagnosis (6). We agree with Coughlin and Kapuku that the high risk of cardiovascular disease in cancer survivors is an important and underrecognized issue. We also agree that additional studies are needed to further elucidate the determinants and mechanisms of troponin elevation in cancer survivors. Even in the absence of knowledge of the exact mechanisms, the prognostic implications of elevated hs-cTnT remain. Several studies have demonstrated that in the general population and among patients with cancer, elevated hs-cTnT in the absence of overt cardiac disease or administration of cardiotoxic therapies is associated with overall and cardiovascular disease mortality (4, 7).

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