CMR procedures were accomplished in less than 30 minutes in all participants; demographic data are displayed in . The time between the first and second examinations for participants receiving (cases) versus not receiving (controls) cancer therapy were similar (3.5 ± 1 months and 4 ± 1 months, respectively; P
= .12). Our study population included eight African American participants (representing 15% of the study population), among whom seven received cancer treatment and one was a control participant; the remaining participants were white. All control and cancer participants had normal renal function (). As shown in , participants treated for cancer exhibited trends toward having more hypertension, hyperlipidemia, diabetes, and anemia than participants in the control group. Participants receiving cancer treatments were diagnosed with breast cancer (n = 19), lymphoma (n = 11), or leukemia (n = 10). Therapies received by participants for treatment of their malignancy included doxorubicin (n = 30), daunorubicin (n = 10), cyclophosphamide (n = 35), and trastuzumab (n = 2), according to established protocols.16–24
Five participants received one of these agents, 33 received two of these agents, and two received three of these agents during the follow-up period. The median cumulative doses of cancer therapy at 3 to 4 months (roughly at the midpoint of the standard prescribed regimens) included doxorubicin 215.3 mg/m2
(range, 60 to 320 mg/m2
), daunorubicin 265 mg/m2
(range, 100 to 600 mg/m2
), trastuzumab 919.8 mg (range, 820 to 1,020 mg), and cyclophosphamide 54.6 mg/kg and 4,585.7 mg (range 1,080 to 9,980 mg). Additional chemotherapeutic agents administered to the patients included the antimetabolites fluorouracil, cytarabine, and methotrexate; the alkylating agent cisplatin; and plant alkaloids including vincristine and vinblastine. None of the participants received biologicals such as bevacizumab or rituximab or radiation therapy.
Demographic Data for Control Group and Cancer Therapy Recipients (mean ± standard error of the estimate)
Findings regarding AoD and PWV are shown in and 3, as well as in . Participants receiving cancer therapy demonstrated a higher baseline PWV (P < .0001), and tended toward a lower baseline AoD (P = .06) compared with control participants. At the follow-up visit, arterial stiffness (AoD and PWV) remained similar to the baseline value in the control participants; however, in those receiving cancer therapy, aortic stiffness notably increased (as evidenced by a decrease in AoD and an increase in PWV) relative to baseline when compared with that of the control group participants ( and ).
Results of ascending aortic distensibility for the control participants (A) and the participants receiving cancer therapy (B). As shown, the aortic distensibility decreased in participants receiving cancer therapy.
Pulse wave velocity (PWV) results for the control participants (A) and the participants receiving cancer therapy (B). PWV increased in participants receiving cancer therapy.
After adjusting for baseline measures of aortic stiffness, AoD and PWV remained different between the two groups at the follow-up sample point in the study (P < .0001 for both). We also performed analyses to assess the effects on our results of age, sex, body mass index, systolic BP (baseline), heart rate (baseline), pulse pressure (PP; baseline), serum hemoglobin (baseline), medical comorbidities (hypertension, diabetes, hyperlipidemia), resting cardiac output, and cardioactive medications. Importantly, after adjusting for all of these conditions, the differences in AoD and PWV between cancer therapy and control participants persisted at the 4-month follow-up visit (P < .0001 for both AoD and PWV).
There were no significant associations between cancer diagnoses (breast cancer versus hematologic malignancies) and baseline PWV and AoD (P = .86 and P = .78, respectively). Four months after receiving anthracyclines, both breast cancer and hematologic malignancy participants experienced an increase in PWV (P < .0001 for both) and a decrease in AoD (P = .0004 for those treated for breast cancer, and P < .0001 for those treated for a hematologic malignancy).
White (n = 33) and African American (n = 7) cancer participants had similar baseline measures of PWV and AoD (P = .36 and P = .35, respectively). Four months after receipt of anthracyclines, both whites and African Americans experienced an increase in PWV (P = .29 for comparison of differences in increased PWV, and a decrease in AoD; P = .11 for comparison of differences in decrease of AoD).
For cancer participants, both men (n = 12) and women (n = 28) had similar baseline measures of PWV and AoD (P = .62 and P = .42, respectively). Four months after receipt of anthracyclines, both men and women experienced an increase in PWV (P < .0001 for men and P = .004 for women compared with control participants), and a decrease in AoD (P = .0002 for men and P = .0003 for women compared with control participants).
The cumulative doses of anthracyclines administered in this study correlated with higher reduction of ascending thoracic AoD (Pearson correlation coefficient r = 0.34; P = .02). The addition of trastuzumab or cyclophosphamide to anthracyclines was not associated with a greater increase in aortic stiffness, relative to receipt of anthracyclines alone (P = .76).
The baseline hemodynamic data, LVV, and LVEF were not different between the two groups (). However, at the follow-up CMR, there was a decrease in diastolic BP, an increase in PP, a decrease in LVEF, and an increase in LVESV (and LVESV index) in participants receiving cancer therapy compared with the control group (P = .04, P = .02, P = .0003, P = .002, and P = .008, respectively). The cardiac output for both cases and controls remained similar between the baseline and follow-up exams (P = .86 and P = .95, respectively). The LVESV was not correlated with AoD or PWV (r = 0.09, P = .51; and r = 0.18, P = .24, respectively).
Hemodynamic Data and Left Ventricular Volume (mean ± standard error of the estimate)