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Right ventricular dysfunction in cancer patients

DISCOVERIES (ISSN 2359-7232), 2019, April-June issue

CITATION: 

Cherata DA, Donoiu I, Diaconu R, Glodeanu A, Cârstea D, Militaru C, Istrătoaie O. Longitudinal strain analysis allows the identification of subclinical deterioration of right ventricular function in patients with cancer therapy-related left ventricular dysfunction. Discoveries 2019, 7(2): e94. DOI: 10.15190/d.2019.7

Submitted: June 5th, 2019; Revised: June 24th, 2019; Accepted: June 25th, 2019; Published: June 27th, 2019; 

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Longitudinal strain analysis allows the identification of subclinical deterioration of right ventricular function in patients with cancer therapy-related left ventricular dysfunction

Diana Alexandra Cherata (1), Ionuț Donoiu (2, *), Rodica Diaconu (2), Adina Glodeanu (1,3), Doina Cârstea (1,3), Constantin Militaru (2), Octavian Istrătoaie (2)

(1) Department of Cardiology, “Filantropia” Municipal Hospital, Craiova, Romania;
(2) Department of Cardiology, University of Medicine and Pharmacy, Craiova, Romania;
(3) Department of Medical semiology, University of Medicine and Pharmacy, Craiova, Romania;

*Corresponding author: Ionuț Donoiu, MD, PhD, University of Medicine and Pharmacy of Craiova, Department of Cardiology, Petru Rareș Street no. 2, Craiova, 200349, Romania; Phone: +40746126669; Fax: +40251426688; Email: ionut.donoiu@umfcv.ro

Abstract

Background: This study was designed to assess right ventricular systolic function in cancer patients.

Methods and Results: 68 consecutive patients receiving potentially cardiotoxic agents were followed for 6 months in a single-center, observational, cohort-study. Left ventricle and free-wall right ventricular longitudinal strain were analyzed prior and after 6 months of treatment, using a vendor-independent software, together with left ventricle ejection fraction, tricuspid annulus plane systolic excursion and right ventricular fractional area change. Cancer therapy-related cardiac dysfunction was defined as a left ventricle ejection fraction drop of >10% to <53%. Both left ventricle ejection fraction (59±7% vs. 55±8%, p<0.0001) and left ventricle longitudinal strain (−19.7±2.5% vs. −17.1±2.6%, p<0.0001) were reduced at follow up, along with free-wall right ventricular longitudinal strain (−24.9±4.5% vs. −21.6±4.9%, p<0.0001). Cancer therapy-related cardiac dysfunction was detected in 20 patients (29%). In 15 out of these 20 patients (75%), a concomitant relative reduction in free-wall right ventricular longitudinal strain magnitude by 17±7% was detected. Moreover, there was a significant correlation between left ventricle and free-wall right ventricular longitudinal strain at follow-up examinations (r=0.323, p<0.0001). A relative drop of right ventricular longitudinal strain >17% had a sensitivity of 55% and a specificity of 70% (AUC=0.75, 0.7-0.8, 95% CI) to identify patients with cancer treatment related cardiac dysfunction. Neither tricuspid annulus plane systolic excursion (24±5 vs. 23±4 mm, p=0.07), nor right ventricular fractional area change (45±8% vs. 44±7%, p=0.6) showed any significant change between examinations.

Conclusions: Longitudinal strain analysis allows the identification of subclinical right ventricular dysfunction appearing in the course of cancer treatment when conventional indices of right ventricular dysfunction function are unaffected.


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References

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