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Early detection of mild pulmonary arterial hypertension (PAH) based on clinical evaluation and echocardiography remains quite challenging. In addition to enhanced right ventricular (RV) assessment, cardiac magnetic resonance (CMR) imaging may accurately reflect deleterious remodeling and increased stiffness of the central pulmonary arteries based on pulsatility, or percent change of the PA during the cardiac cycle. The purpose of this study is to assess the utility of measuring PA pulsatility by CMR as a potential early maker in PAH. We hypothesize that pulsatility may help discriminate mild PAH from normal control subjects. Consecutive patients with PAH (n = 51) were prospectively enrolled to receive same day CMR and right heart catheterization (RHC). PA stiffness indices including pulsatility, distensibility, compliance, and capacitance were calculated. Comparisons were made between patients with varying severities of PAH and normal controls (n = 18). Of the 51 subjects, 20 had mild PAH, and 31 moderate-severe based on hemodynamic criteria. PA pulsatility demonstrated a progressive decline from normal controls (53%), mild PAH (22%), to moderate-severe PAH (17%; p

Background/Aims: Doxorubicin (DOX) and trastuzumab (TRA) are associated with cardiac dysfunction. Method: High-sensitivity troponin T (hs-TnT) and brain natriuretic peptide attached to the amino acid N-terminal fragment in the prohormone (NT-proBNP) were measured before and on days +1, +2, +3, and +7 during cycles 1 and 2 of therapy with DOX or TRA in breast cancer patients. Results: Five of eleven DOX-treated women, compared with 2/11 TRA-treated women, had undetectable baseline hs-TnT. By day +1 of cycle 2, all the DOX-treated women (p = 0.03) but only 7/11 TRA-treated women (p = ns) had detectible hs-TnT. Time to peak was 1-2 days for both groups. In the DOX-treated women, hs-TnT showed significant peaks from precycle baseline, increases in precycle 1 to precycle 2 levels, and a cycle 1 to cycle 2 peak and area under the curve (AUC). hs-TnT increased from precycle (1, 4.6 ± 6.3 pg/mL) to a cycle 2 peak of 16.1 ± 15.0 pg/mL (p < 0.002). No increases were seen with the TRA treatment. Transient posttreatment increases in NT-proBNP were seen after both therapies. Conclusion: DOX was associated with increased pretreatment baseline, peak, and AUC hs-TnT levels. Both DOX and TRA acutely perturb NT-proBNP. Assessment of pre- and posttreatment hs-TnT could be a means of quantifying cumulative myocardial injury in the course of chemotherapy.

Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA Introduction: A and T are associated with the development of cardiac dysfunction. The kinetics of cardiac biomarkers early after A or T treatment (Rx) is undefined. Methods: We studied hs-TnT (detection limit: 3 ng/ml, myocardial infarction threshold 14 ng/ml) and nt-proBNP (detection limit: 5 pg/ml) levels just prior to (baseline), and on days +1, +2, +3 and +7 during the first and second cycle in breast cancer pts treated with A (n = 11) or T (n = 11). Baseline and peak values for each cycle, baseline to baseline, peak to peak, time to peak, and baseline corrected area under the curve (AUC) were calculated. Study No. [NCT01771549][1] Results: Group (grp) A pts were younger, 51 ± 18 years, than T grp pts, 60 ± 13 years. Three pts in A grp and 4 pts in T grp used antihypertensives. Baseline ejection fraction (EF) was 52-68% (A grp) and 56-69% (T grp). Hs-TnT was undetectable in 5/11 A grp, and 2/11 T grp pts at baseline. By cycle 2 day +1, all A pts had a detectable level of hs-TnT (p = 0.03) compared to 7/11 T pts. Median time to peak level for hs-TnT was 1.5 days for the A grp and 1.2 days for the T grp (NS). In the A grp, significant transient increase in nt-proBNP were also seen (Table). In the T grp, a significant rise in nt-proBNP was not seen in cycle 1 but was seen on cycle 2 day +1 and cycle 2 peak. AUC values were positive for hs-TnT in A pts but not in T pts, and were positive for nt-proBTNP for both A and T. Only 1 pt in A grp had symptomatic EF decline (47%) three months from start of A. None of T grp pts had EF decline. Conclusion: A, but not T was associated with increase in pre-Rx (cycle 2 only), peak, and AUC hs-TnT levels for cycles 1 and 2 with peak values occurring 1.5 days post-Rx. This study evaluating serial kinetics of cardiac biomarker in pts receiving A or T therapy, suggests that assessment of pre- and day +2 post-Rx values could be a means of quantifying cumulative myocardial injury over the chemotherapy course. *Roche Diagnostics Corp, Indianapolis, IN provided assay reagent kits. | hs-TnT, ng/ml | A, cycle 1 | A, cycle 2 | P-val | T, cycle 1 | T, cycle 2 | P-val | | ------------------ | ---------- | ----------- | ------------------------------------------- | ---------- | ---------- | ----- | | Baseline | 4.6 | 9.3