Key result
Potentially cardiotoxic chemotherapy led to a decrease in left ventricular ejection fraction from 57% to 54% (P<0.001) and an increase in T1-weighted signal intensity (P<0.05) at 3 months.
Why the study?
Does potentially cardiotoxic chemotherapy alter left ventricular ejection fraction and myocardial tissue characteristics measured by CMR in individuals with cancer?
Cohort (n=65)
Blinded
Does potentially cardiotoxic chemotherapy alter left ventricular ejection fraction and myocardial tissue characteristics measured by CMR in individuals with cancer?
Changes in T1-weighted signal intensity on CMR occur alongside small declines in LVEF 3 months after cardiotoxic chemotherapy, suggesting its potential as an early marker of subclinical injury.
Answers are grounded in this paper and cite their sources.
May support T1-weighted CMR for early subclinical cardiotoxicity detection; hypothesis-generating and should not yet change practice.
BACKGROUND: In a murine anthracycline-related cardiotoxicity model, increases in cardiovascular magnetic resonance myocardial contrast-enhanced T1-weighted signal intensity are associated with myocellular injury and decreases with left ventricular ejection fraction. We sought to determine whether T1- and T2-weighted measures of signal intensity associate with decreases in left ventricular ejection fraction 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, ejection fraction, and contrast-enhanced T1-weighted and T2-weighted signal intensity before and 3 months after initiating potentially cardiotoxic chemotherapy using blinded, unpaired analysis of cardiovascular magnetic resonance 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, left ventricular ejection fraction decreased from 57 ± 6% to 54 ± 7% (P<0.001) because of 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 before 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, cardiovascular magnetic resonance measures of contrast-enhanced T1-weighted signal intensity occur commensurate with small but significant left ventricular ejection fraction declines 3 months after the 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.
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Jordan et al. (2014) conducted a cohort in Breast cancer or hematologic malignancy (n=65). Potentially cardiotoxic chemotherapy was evaluated on Changes in left ventricular ejection fraction and contrast-enhanced T1-weighted signal intensity (p=<0.001). Potentially cardiotoxic chemotherapy led to a decrease in left ventricular ejection fraction from 57% to 54% (P<0.001) and an increase in T1-weighted signal intensity (P<0.05) at 3 months.
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