A Biomarker Discovered for Early Diagnosis of Heart Damage During Cancer Treatment

One uncommon but difficult-to-manage adverse effect of cancer treatment is cardiotoxicity (heart damage). Approximately 25 percent of patients receiving cancer treatment develop cardiac toxicity, mostly mild. This damage causes chronic heart disease and premature (early) deaths in cancer patients. In this context, Journal of the American College of Cardiology’ published a study in patients receiving anthracycline cancer drugs that discovered a “radiological biomarker” capable of predicting heart damage. This discovery may allow drug-related heart injury to be recognized at early stages, thereby preventing damage and enabling better management of the patient’s clinical condition.

The advanced specialty addressing heart problems in cancer is called cardio-oncology . There are 3 main challenges in cardio-oncology:

1. The mechanisms of heart damage caused by effective cancer drugs are not clearly known. 
2. There is also no biomarker to diagnose cardiac damage early. 
3. Finally, specific treatments for cardiotoxicity have not yet been developed.

In the study, a new animal model was developed for anthracycline (doxorubusin) -related cardiac toxicity. Pig and human hearts are structurally very similar. Pigs received increasing doses of doxorubicin, an anthracycline drug, over 10 weeks. This strategy ensured accumulation only in heart muscle rather than other organs.

Multiple parameters were examined weekly using magnetic resonance imaging, investigating biomarkers that could provide early signs of cardiac toxicity.

- Related Topic: As Important as the Discovery of the Compass: Magnetic Resonance Imaging and Functional MRI

According to the research results;

The earliest cardiac magnetic resonance sign of doxorubicin cardiotoxicity occurred at week 6.—that is, 2 weeks after the third chemotherapy dose—as prolonged T2 relaxation time. In other words, myocardial edema on T2-weighted magnetic resonance images was identified as an early sign of heart damage.

Doxorubicin damages mitochondria in heart muscle cells, causing cellular edema. Mitochondria are our cells’ energy production centers, and permanent mitochondrial damage prevents heart cells from functioning.

What does this study mean for us?

• Detecting myocardial edema on T2-weighted images (termed disrupted T2 mapping in the study) may be an early marker of anthracycline-related drug toxicity. Cancer medication could thus be used to a safe level before permanent heart damage occurs. In other words, we can use an effective cancer drug much more precisely. 
• This discovery may enable the development of new heart-protective treatment approaches.
• A clinical trial involving 100 patients is planned soon.
• In people who develop heart damage, mitochondrial transplantation is also being considered. This has not yet been successfully accomplished. Experimental studies continue.