BackgroundAnthracycline chemotherapy remains an integral part of the care for curative intent chemotherapy in breast cancer and non-Hodgkin lymphoma patients. Better tools need to be identified to predict cardiac complications of anthracycline chemotherapy.Materials and methodsWe investigated the utility of high-sensitivity cardiac troponin T (hscTnT), N-terminal pro-B-type natriuretic peptide, cardiac troponin T and I, and creatine kinase (CK)-MB in cancer patients receiving anthracycline-based chemotherapy, in order to determine whether baseline levels or changes in these biomarkers may help predict the onset of congestive heart failure.ResultsEighteen consecutive patients with a pathologic diagnosis of breast cancer or non-Hodgkin lymphoma were enrolled. The median dose of doxorubicin exposure was 240 mg/m2 (range 240–400 mg/m2). After treatment with doxorubicin, the hscTnT increased to 19.1 pg/mL (P<0.001). CKMB and N-terminal pro-B-type natriuretic peptide levels increased to 1.1 ng/mL and 88.3 pg/mL, respectively (P=0.02). When subjects who had a decline in left ventricular ejection fraction (LVEF) by equilibrium radionuclide ventriculography were compared to those who did not have a change in LVEF, there was a suggestion that those subjects with an elevated baseline hscTnT were more likely to have a decline in LVEF (2.7 pg/mL and 0.1 pg/mL, respectively; P=0.07). Spearman correlation demonstrated that patients with higher baseline hscTnT and CKMB tended to have a greater decline in LVEF (Spearman correlation −0.54, 95% confidence interval −0.80 to −0.08 [P=0.02], and −0.49, 95% confidence interval −0.77 to −0.01 [P=0.04], respectively).ConclusionElevations in baseline hscTnT levels are suggestive of an oncology subgroup at high risk of developing cardiac complications from their chemotherapy. Early detection by oncologists with the use of baseline biomarkers may be clinically important in designing interventions to prevent serious anthracycline-based chemotherapy complications.

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Pulmonary embolism (PE) remains one of the leading causes of cardiovascular mortality. The safety and efficacy of thrombolytic therapy using tissue-type plasminogen activator (tPA) for acute PE in clinical practice remain unclear. We describe a case of life-threatening submassive PE causing extreme refractory hypoxaemia, where thrombolysis was successfully administered. Current consensus suggests that patients with features of hemodynamic instability as a result of an acute PE, that is, massive PE, should receive thrombolysis. Patients, not in shock however, but with evidence of right-ventricular (RV) dysfunction echocardiographically, that is, submassive PE may also benefit. Serum troponin and brain-type natriuretic peptide have been suggested as biomarkers of RV injury that may identify a subset of submassive PE patients who may particularly benefit from thrombolytic therapy. The clinical response of this patient to thrombolysis is important, as it may identify a subgroup of patients with submassive PE who warrant this intervention.

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