Objective This study compared the clinical features, cardiac structure and function evaluated by echocardiography, cardiopulmonary response to exercise and long-term clinical outcomes between patients with heart failure (HF) induced by cancer therapy (CTHF) and heart failure not induced by cancer therapy (NCTHF).
Methods We evaluated 75 patients with CTHF and 894 with NCTHF who underwent clinically indicated cardiopulmonary exercise testing, and followed these individuals for a median of 4.5 (3.0–5.8) years, during which 187 deaths and 256 composite events (death, heart transplantation and left ventricular (LV) assistant device implantation) occurred.
Results Compared with NCTHF, patients with CTHF were younger, with lower prevalence of cardiovascular comorbidities, higher LV ejection fraction (LVEF), but similar global longitudinal strain. LV diastolic function (higher E/e′ ratio) and compliance (higher end-diastolic pressure/LV end-diastolic volume index ratio) were worse in CTHF and were both associated with adverse outcomes. Despite a favourable clinical profile, peak VO2 and VE/VCO2 slope were similarly impaired in CTHF and NCTHF. In multivariable Cox regression analysis including clinical characteristics, cardiopulmonary exercise testing variables and LVEF, CTHF was associated with a significantly higher risk of death (HR 2.64; 95% CI 1.53 to 4.55; p=0.001) and composite events (HR 1.79; 95% CI 1.10 to 2.91; p=0.019) compared with NCTHF.
Conclusions CTHF is characterised by a distinct clinical profile, better LVEF but worse LV diastolic properties, and similarly impaired global longitudinal strain, functional capacity and ventilatory efficiency. Accounting for differences in clinical characteristics, CTHF was associated with worse long-term prognosis than NCTHF.
- heart failure
- cardiopulmonary exercise testing
- diastolic function
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Contributors WNJ and AMS contributed to the design of the work, and to the analysis and interpretation of data. EW, MoS, GLG, MaS, JDG, DEF, BC, HS and AN contributed to the acquisition, analysis and/or interpretation of data. WNJ drafted the work, and EW, MoS, GLG, MaS, JDG, DEF, BC, HS, AN and AMS revised it critically for important intellectual content. All authors approved the version to be published and are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.
Funding This work was supported by NHLBI (K08HL116792 and R01HL135008 to AMS), AHA (14CRP20380422 to AMS), a Watkins Discovery Award from the Brigham and Women’s Heart and Vascular Center to AMS and the Brazilian National Council for Scientific and Technological Development (306154/2017-0 to WNJ).
Competing interests AMS reports receiving research support from Novartis and Bellerophron, and consulting fees from Philips Ultrasound. The other authors have nothing to disclose.
Patient consent Not required.
Ethics approval Partners Human Research Committee.
Provenance and peer review Not commissioned; externally peer reviewed.
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