NIH awards $2.5M to study pulmonary hypertension
The National Institutes of Health (NIH) has granted a biomedical engineer $2.5 million to establish how various health factors add up to pulmonary arterial hypertension (PAH). From this, she and her team will develop a way to separate PAH patients who will be helped by regular exercise from those whom it might harm.
Naomi C. Chesler, PhD, an associate professor of biomedical engineering at the University of Wisconsin-Madison, will lead an investigation into the relationships between small artery narrowing, large artery stiffening and their interactions with the right side of the heart in patients with PAH, according to a satement.
"Most patients with pulmonary hypertension die from right heart failure, so even though the disease may be initiated in the small arteries of the lung, the impact on heart function is what's really critical," said Chesler.
Prescribing an appropriate exercise regimen is essential to managing the condition, as activity is a key part of the protocol in spite of PAH patients’ proneness to overexertion. The objective will be finding identifiers that separate PAH patients who will benefit from exercise from those whose condition it will worsen.
The new study builds upon Chesler's work on a previous NIH grant in which she researched how the presence of excess collagen, a fibrous protein found in connective tissues throughout the body, might contribute to pulmonary hypertension.
The new study will be particularly concerned with patients who have scleroderma, or systemic sclerosis (SSc), a disease caused by excess collagen accumulation throughout the body, including blood vessels. Patients with SSc-related PAH don't have many effective treatment options, but focusing on such patients in the study might identify their best treatment options.
Naomi C. Chesler, PhD, an associate professor of biomedical engineering at the University of Wisconsin-Madison, will lead an investigation into the relationships between small artery narrowing, large artery stiffening and their interactions with the right side of the heart in patients with PAH, according to a satement.
"Most patients with pulmonary hypertension die from right heart failure, so even though the disease may be initiated in the small arteries of the lung, the impact on heart function is what's really critical," said Chesler.
Prescribing an appropriate exercise regimen is essential to managing the condition, as activity is a key part of the protocol in spite of PAH patients’ proneness to overexertion. The objective will be finding identifiers that separate PAH patients who will benefit from exercise from those whose condition it will worsen.
The new study builds upon Chesler's work on a previous NIH grant in which she researched how the presence of excess collagen, a fibrous protein found in connective tissues throughout the body, might contribute to pulmonary hypertension.
The new study will be particularly concerned with patients who have scleroderma, or systemic sclerosis (SSc), a disease caused by excess collagen accumulation throughout the body, including blood vessels. Patients with SSc-related PAH don't have many effective treatment options, but focusing on such patients in the study might identify their best treatment options.