Longitudinal Assessment of Concurrent Changes in Left Ventricular Ejection Fraction and Left Ventricular Myocardial Tissue Characteristics After Administration of Cardiotoxic Chemotherapies Using T1-Weighted and T2- Weighted Cardiovascular Magnetic Resonance Jordan et al: Qualitative CMR Changes after Chemotherapy

Background—In a murine anthracycline-related cardiotoxicity model, increases in cardiovascular magnetic resonance (CMR) myocardial contrast-enhanced T1-weighted signal intensity are associated with myocellular injury and decreases in left ventricular ejection fraction (LVEF). We sought to determine if T1and T2-weighted measures of signal intensity associate with decreases in LVEF in human subjects receiving potentially cardiotoxic chemotherapy. Methods and Results—In 65 individuals with breast cancer (n=51) or a hematologic malignancy (n=14), we measured left ventricular volumes, EF, and contrast-enhanced T1-weighted and T2weighted signal intensity prior to and 3 months after initiating potentially cardiotoxic chemotherapy using blinded, unpaired analysis of CMR images. Participants were aged 51±12 years of whom 55% received an anthracycline, 38% received a monoclonal antibody, and 6% received an antimicrotubule agent. Overall, LVEF decreased from 57±6% to 54±7% (p<0.001) due to an increase in end-systolic volume (p<0.05). T1-weighted signal intensities also increased from 14.1±5.1 to 15.9±6.8 (p<0.05) with baseline values trending higher among individuals who received chemotherapy prior to study enrollment (p=0.06). Changes in T1-weighted signal intensity did not differ within the 17 LV myocardial segments (p=0.97). Myocardial edema quantified from T2-weighted images did not change significantly after 3 months (p=0.70). Conclusions—Concordant with previous animal studies, CMR measures of contrast-enhanced T1-weighted signal intensity occur commensurate with small but significant LVEF declines 3 months after receipt of potentially cardiotoxic chemotherapy. These data indicate that changes in T1-weighted signal intensity may serve as an early marker of subclinical injury related to the administration of potentially cardiotoxic chemotherapy in human subjects.