Stevens Biomedical Engineering Student Contributes to Cardiac Disease Research
Birva Pinto conducted summer research at the University of Washington on the effects of protein mutations on cardiac disease
Birva Pinto is an international Biomedical Engineering student from Angola, a Portuguese-speaking country in Southern Africa. Pinto initially came to the United States five years ago to study chemistry, beginning her academic journey at Hudson Community College as an English as a Second Language (ESL) student.
Having witnessed the impact of limited medical technology in her home country—especially with her mother battling hypertension—Pinto was inspired to change her field of study to biomedical engineering.
After earning an associate’s degree in engineering science at Hudson Community College, Pinto transferred to Stevens Institute of Technology due to the school’s emphasis on innovation and research, which aligned with her passion for developing medical technologies to improve patient care.
Researching dilated cardiomyopathy
In the summer of 2024, Pinto completed an internship at the Institute for Stem Cell & Regenerative Medicine at the University of Washington. While working in the Moussavi-Harami Lab, which focuses its research on cardiology, Pinto contributed to studying the genetic factors of dilated cardiomyopathy (DCM), a condition that enlarges the heart, making it too weak to pump blood.
DCM arises from a mix of familial and environmental factors. The team focused on the G159D mutation in the cardiac troponin C protein and its role in DCM progression. Troponin C is critical in regulating muscle contraction by binding calcium and mutations in proteins such as troponin, which account for 20-30 percent of DCM cases.
By examining the mutation’s effects, the researchers aimed to contribute valuable insights to the diagnosis and treatment of DCM and related cardiac disorders.
Unexpected findings
The study revealed surprising results: the G159D mutation increased calcium sensitivity in troponin, contradicting the team’s hypothesis. These findings suggest that the mutation may be linked to hypertrophic cardiomyopathy (HCM), a condition that causes the heart muscle, especially in the left ventricle, to thicken (hypertrophy), stiffening the heart muscle. This reduces blood flow and increases the risk of cardiac arrhythmias.
"Understanding this mutation is critically important because mutations like G159D directly impact how troponin C functions in the heart," Pinto explained. "And clarifying the disease mechanisms helps link genetic profiles to physical symptoms, improving diagnosis."
Recognizing the effects of this mutation is a crucial step toward developing targeted treatments to restore normal calcium sensitivity, potentially preventing severe complications such as heart failure and sudden cardiac death.
Presenting the findings
Pinto presented the team’s findings at a Yale Biomedical Engineering Conference in November 2024. She was inspired by the enthusiasm of her peers, all of whom were making unique contributions to advancing science.
"I learned that research is not just about generating data but about working with others to tackle complex problems and translate findings into meaningful solutions," Pinto said. She expressed her hopes of contributing to future interdisciplinary teams in which collaboration and diversity drive research and innovation.
Going forward
Collaborative research experiences at Stevens within the Biomedical Engineering curriculum has strengthened Pinto’s passion for biomedical engineering and fueled her aspirations for a career in translational medicine. She hopes to leverage her experiences in higher education and industry work where she can continue exploring cardiac events and how genetics play a factor in their treatment and, ultimately, create new therapies that improve patient care.