A new study lead by Dutch researchers at the Erasmus MC University Medical Center in Rotterdam has just uncovered evidence that increased levels of a peptide in the blood associated with heart disease are also linked to early-stage brain damage. The findings from the new study, which was published recently in the journal Radiology in an article entitled “N-Terminal Pro-B-Type Natriuretic Peptide and Subclinical Brain Damage in the General Population,” imply a close link between the heart and brain even in presumably healthy individuals.
Heart and brain disease inflict a toll on the healthcare system, and incidence rates are expected to increase significantly due to the rapidly aging population. Damage to both organs often occurs at a subclinical stage or before signs and symptoms of disease are evident. Biomarkers in the blood indicative of subclinical heart disease and brain diseases, such as stroke and dementia, could speed the initiation of treatments and lifestyle changes—potentially slowing or even reversing the disease's course.
In the new study, the Dutch investigators found that a protein released into the blood in response to cardiac wall stress, called N-terminal pro-B-type natriuretic peptide (NT-proBNP), could be a new disease marker with promising potential. Blood serum levels of NT-proBNP rise when heart failure worsens and drop when it gets better. While previous studies have shown a link between heart disease and brain disease, less is known about the association between NT-proBNP and the entire spectrum of imaging markers of subclinical brain damage, like brain volume and white matter integrity.
The investigators looked at the relationship between the heart and brain in 2397 community-dwelling middle-aged and elderly nondemented people without a clinical diagnosis of cardiovascular disease. The patients were drawn from the landmark Rotterdam Study, an ongoing, population-based study of more than 10,000 people from a suburb of Rotterdam, The Netherlands.
“We found that higher serum levels of NT-proBNP were associated with smaller brain volumes, in particular with smaller gray matter volume, and with poorer organization of the brain's white matter,” noted senior study investigator Meike Vernooij, M.D., Ph.D., assistant professor and neuroradiologist at Erasmus MC University Medical Center.
NT-proBNP is currently used in a clinical setting to rule out heart failure, yet it is too early to say if it can play a similar role for subclinical brain damage, because the new study only looked at people at one point in time.
Moreover, there are several hypotheses to explain the link between cardiac dysfunction and subclinical brain damage. For instance, decreases in blood flow could lead to cerebral microvascular damage or problems in the function of the blood–brain barrier. Inflammatory factors associated with cardiac stress could also harm the barrier, leading to increased permeability and damage to the brain. Further research, including follow-up brain magnetic resonance imaging (MRI) studies and measurements of NT-proBNP, will be needed to clarify the relationship between cardiac dysfunction and subclinical brain disease.
“We cannot rule out that the observed subclinical brain damage led to increased levels of NT-proBNP,” Dr. Vernooij stated. “However, from a biological perspective, and based on animal studies, it is more likely that cardiac dysfunction affects brain changes rather than vice versa.”