Key result
Paclitaxel and carboplatin combination chemotherapy significantly reduced peak strain (from -17.5% to -16.2%, P<0.02), indicating subtle myocardial mechanical impairment.
Why the study?
Does paclitaxel and carboplatin combination chemotherapy impair left ventricular mechanical and coronary microvascular functions in patients with gynecologic malignancies?
Cohort (n=56)
Does paclitaxel and carboplatin combination chemotherapy impair left ventricular mechanical and coronary microvascular functions in patients with gynecologic malignancies?
Paclitaxel and carboplatin combination chemotherapy induces subtle impairment in myocardial mechanical function detectable by advanced deformation imaging, without impairing coronary flow reserve.
May warrant strain monitoring in gynecologic cancer patients on paclitaxel-carboplatin; hypothesis-generating for clinical cardiotoxicity.
AIM: Paclitaxel and carboplatin are frequently used chemotherapy drugs in the treatment of gynecologic malignancies. Little is known about their effects on left ventricular mechanical and coronary microvascular functions. METHODS: Thirty consecutive patients were prospectively enrolled. Patients underwent transthoracic echocardiography (TTE) before and after chemotherapy, to evaluate left ventricular mechanical functions and coronary flow reserve (CFR). A comprehensive TTE, tissue Doppler and two-dimensional (2D) strain imaging were performed and coronary flow velocity was measured at baseline and after dipyridamole infusion. CFR was calculated as the ratio of hyperemic to baseline diastolic peak flow velocities. Mitral annular velocities by tissue Doppler, peak strain, and systolic strain rate by velocity vector imaging (VVI) were measured. Baseline measurements were compared with healthy controls (n = 26). RESULTS: No patient developed heart failure (HF) symptoms, no significant change occurred in left ventricular ejection fraction or cardiac output and no significant difference was observed in CFR after chemotherapy. Baseline mean longitudinal peak strain and systolic stain rate were similar between patients and controls: -17.5 ± 2.6% versus -17.6 ± 2.2% (P = NS) and -1.04 ± 0.14/sec versus -1.05 ± 0.12/sec (P = NS). Peak strain and systolic strain rate decreased significantly after chemotherapy (from -17.5 ± 2.6% to -16.2 ± 2.5%, P < 0.02; and from -1.05 ± 0.12/sec to -0.96 ± 0.11/sec, P = 0.01, respectively). However, mean longitudinal velocity did not change significantly. CONCLUSION: Paclitaxel and carboplatin combination did not impair CFR; however, this chemotherapy combination could induce subtle impairment in myocardial mechanical function which can be detected by advanced deformation imaging techniques rather than by tissue Doppler imaging or conventional 2D and Doppler echocardiography.
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Altın et al. (2014) conducted a cohort in Gynecologic malignancies (n=56). Paclitaxel and carboplatin combination vs. Baseline / Healthy controls was evaluated on Peak strain (p=<0.02). Paclitaxel and carboplatin combination chemotherapy significantly reduced peak strain (from -17.5% to -16.2%, P<0.02), indicating subtle myocardial mechanical impairment.
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