Heart Drug May Halt Chemotherapy-Induced Cardiotoxicity

Nebivolol shows promise blocking anthracycline-induced cardiotoxicity in breast cancer patients.

A cardioprotective drug, nebivolol, was found to prevent cardiotoxicity in breast cancer patients undergoing chemotherapy.

Anthracyclines are a class of anti-cancer drugs commonly used to treat breast cancer, but have a toxic effect on the cardiovascular system that induces heart failure. In a new study, researchers sought to identify a method that could accurately detect cardiotoxicity early, and determine whether a cardioprotective drug could prevent heart failure as well.

The findings were presented at ESC Congress 2016.

Traditionally, physicians will use an echocardiography, based on the estimation of left ventricular ejection fraction (LVEF) and fraction shortening (FS), to diagnose depressed myocardial contractility. However, the parameters are affected in the advanced stages of cardiotoxicity, according to the study.

New echocardiographic techniques, such as strain rate imaging, speckle tracking, and tissue Doppler, have the ability to recognize myocardial dysfunction before heart failure symptoms occur, and before classical echocardiographic parameters are impaired.

In the current study, researchers used nebivolol, which has a cardioselective beta blocker with anti-oxidant, anti-apoptotic, and vasodilator properties. nebivolol is typically used to treat heart failure and hypertension.

Sixty women with HER-2 negative breast cancer scheduled to start chemotherapy with doxorubicin were enrolled in the study. The mean age of participants was 52 ± 13 years.

Participants were randomized into 2 even groups, with 30 women divided into the control group, and the other 30 women in the nebivolol-treatment group. A dose of 5-mg nebivolol was administered daily for the duration of chemotherapy.

Cytostatic treatment was performed with doxorubicin 70-mg/m2 administered alone intravenously every 21 days. Cytotoxic therapy lasted 6 cycles, and the average cumulative dose of doxorubicin was 520 ± 8 mg/m2.

Researchers performed an echocardiography, which included conventional 2-dimensional echocardiography, tissue Doppler imaging, and speckle tracking imaging, at baseline and after 6 months of chemotherapy.

No significant differences were found between the groups in baseline clinical and echocardiographic characteristics. The cumulative dose of doxorubicin was similar in the group, and none of the patients discontinued chemotherapy or died during the experiment.

The results of the study showed that after 6 cycles of doxorubicin chemotherapy, the diameters of LVEF, FS, and left ventricular (LV) did not significantly change in either of the groups. For the control group, the tissue Doppler imaging showed there were significant alterations of LV diastolic function, while the speckle-tracking imaging showed a significant alteration of the LV systolic function and strain rates.

For the nebivolol treatment group, researchers found no significant changes in heart function.

“Conventional echocardiography showed no change in heart function in either group following chemotherapy,” said researcher Mirela Cleopatra Tomescu. “But the newer, more sensitive echocardiographic techniques showed heart damage after chemotherapy. Patients who received nebivolol were protected and had normal heart function. Our study demonstrates the utility of new echocardiographic methods such as tissue Doppler and speckle tracking imaging in the early detection of ventricular dysfunction induced by cytostatic treatment.”

The study authors concluded that, although the study results are promising, more research needs to be done.

“Our finding that nebivolol treatment prevented anthracycline-induced cardiotoxicity is encouraging, but larger studies with a longer follow-up period are needed to confirm the results,” Tomescu said.