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Contribution of stent underexpansion to recurrence after sirolimus-eluting stent implantation for in-stent restenosis Histopathologic validation of the intravascular ultrasound diagnosis of calcified coronary artery nodules 3-Year Outcomes of the ULTIMATE Trial Comparing Intravascular Ultrasound Versus Angiography-Guided Drug-Eluting Stent Implantation Comparison of inhospital mortality, length of hospitalization, costs, and vascular complications of percutaneous coronary interventions guided by ultrasound versus angiography Combined use of OCT and IVUS in spontaneous coronary artery dissection Use of IVUS guided coronary stenting with drug eluting stent: a systematic review and meta-analysis of randomized controlled clinical trials and high quality observational studies Comparison of plaque characteristics in narrowings with ST-elevation myocardial infarction (STEMI), non-STEMI/unstable angina pectoris and stable coronary artery disease (from the ADAPT-DES IVUS Substudy) Usefulness of intravascular ultrasound to predict outcomes in short-length lesions treated with drug-eluting stents Role of intravascular ultrasound in patients with acute myocardial infarction undergoing percutaneous coronary intervention Intravascular ultrasound predictors of angiographic restenosis after sirolimus-eluting stent implantation

Clinical TrialVolume 11, Issue 8, August 2018

JOURNAL:JACC Cardiovasc Imaging. Article Link

Anthracycline Therapy Is Associated With Cardiomyocyte Atrophy and Preclinical Manifestations of Heart Disease

Ferreira de Souza T, Quinaglia A C Silva T, Coelho-Filho OR et al. Keywords: T1 mapping techniques; anthracycline; cardiac troponin T; fibrosis; left ventricular remodeling; magnetic resonance imaging

ABSTRACT


OBJECTIVESThe goal of this study was to demonstrate that cardiac magnetic resonance could reveal anthracycline-induced early tissue remodeling and its relation to cardiac dysfunction and left ventricular (LV) atrophy.


BACKGROUNDSerum biomarkers of cardiac dysfunction, although elevated after chemotherapy, lack specificity for the mechanism of myocardial tissue alterations.

METHODSA total of 27 women with breast cancer (mean age 51.8 ± 8.9 years, mean body mass index 26.9 ± 3.6 kg/m2), underwent cardiac magnetic resonance before and up to 3 times after anthracycline therapy. Cardiac magnetic resonance variables were LV ejection fraction, normalized T2-weighted signal intensity for myocardial edema, extracellular volume (ECV), LV cardiomyocyte mass, intracellular water lifetime (τic; a marker of cardiomyocyte size), and late gadolinium enhancement.

RESULTSAt baseline, patients had a relatively low (10-year) Framingham cardiovascular event risk (median 5%), normal LV ejection fractions (mean 69.4 ± 3.6%), and normal LV mass index (51.4 ± 8.0 g/m2), a mean ECV of 0.32 ± 0.038, mean τic of 169 ± 69 ms, and no late gadolinium enhancement. At 351 to 700 days after anthracycline therapy (240 mg/m2), mean LV ejection fraction had declined by 12% to 58 ± 6% (p < 0.001) and mean LV mass index by 19 g/m2 to 36 ± 6 g/m2 (p < 0.001), and mean ECV had increased by 0.037 to 0.36 ± 0.04 (p = 0.004), while mean τic had decreased by 62 ms to 119 ± 54 ms (p = 0.004). Myocardial edema peaked at about 146 to 231 days (p < 0.001). LV mass index was associated with τic (β = 4.1 ± 1.5 g/m2 per 100-ms increase in τic, p = 0.007) but not with ECV. Cardiac troponin T (mean 4.6 ± 1.4 pg/ml at baseline) increased significantly after anthracycline treatment (p < 0.001). Total LV cardiomyocyte mass, estimated as: (1 - ECV) × LV mass, declined more rapidly after anthracycline therapy, with peak cardiac troponin T >10 pg/ml. There was no evidence for any significant interaction between 10-year cardiovascular event risk and the effect of anthracycline therapy.

CONCLUSIONSA decrease in LV mass after anthracycline therapy may result from cardiomyocyte atrophy, demonstrating that mechanisms other than interstitial fibrosis and edema can raise ECV. The loss of LV cardiomyocyte mass increased with the degree of cardiomyocyte injury, assessed by peak cardiac troponin T after anthracycline treatment. (Doxorubicin-Associated Cardiac Remodeling Followed by CMR in Breast Cancer Patients; NCT03000036).

Copyright © 2018 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.