Brain-Heart Connection: Implications for stroke patients

Approximately 50,000 individuals in Canada experience a stroke each year – that’s about one stroke every 10 minutes. Although that’s just over 0.1% of the population, stroke is the leading cause of adult disability and the third leading cause of death in Canada. Studies have shown that getting to the hospital within 3 hours of the first symptoms of a stroke is critical to treatment success. However, we lack an effective treatment plan for those that do not get to the hospital quickly enough. While most stroke-induced disability and death is a result of brain injury, cardiac complications are the second leading cause of post-stroke death.

Ischemic stroke accounts for the majority of stroke cases and occurs when a blood vessel in the brain becomes blocked. This blockage restricts blood flow to a portion of the brain causing brain tissue death and inflammation. Importantly, this damage to the brain can also result in significant damage to the heart. Post-stroke heart damage can manifest in several ways, such as an irregular heartbeat, heart attack, or heart failure. Further, approximately 2-6% of stroke patients will die of cardiac causes within the first 3 months post-stroke. A link between stroke and cardiac consequences has been established but these mechanisms are not well understood. Furthering our understanding of the brain-heart connection in the context of stroke is critical to improvement of treatment plans and patient outcomes.

A team of researchers at Western University aimed to interrogate the mechanisms involved in post-stroke cardiac dysfunction by investigating cardiac outcomes in a rodent model of stroke. The 2019 study was led by post-doctoral fellow Dr. Brittany Balint and PhD student Victoria Jaremek. They examined post-stroke cardiac outcomes by analyzing heart tissue from rodents 28 days following an induced stroke.

In their study, the stroke targeted the insula, a tiny structure in the brain that is implicated in a wide array of functions; one of which being heart rate regulation. Previous research has shown that strokes affecting the insula are associated with an increased risk of cardiac complications. For this reason, the researchers used an animal model of stroke that specifically targeted the insula. Broadly, their analysis then focused on two main cardiac changes: fibrosis and inflammation.

Cardiac fibrosis refers to abnormal scarring that occurs in the heart muscle and can impair heart function; it is characterized by an increase in collagen, the most abundant protein in the human body. Normally, collagen provides structural support throughout the whole body; the word collagen comes from the Greek word kolla, which appropriately translates to glue. However, in the case of cardiac fibrosis, the increased collagen in the heart can then disrupt normal heart functioning. In this study, cardiac fibrosis was analyzed in the heart tissue post-stroke by identifying collagen accumulation. Importantly, the researchers demonstrated that inducing a stroke in the insula resulted in a significant increase in cardiac fibrosis.

While post-stroke brain inflammation has been well evaluated, this study provided critical evidence that stroke can also cause an increase in cardiac inflammation. This is important because cardiac inflammation can affect the heart’s ability to effectively pump blood which can cause heart failure. In this study, the researchers identified four different inflammatory cells in the heart: pan-leukocytes, neutrophils, T lymphocytes and B lymphocytes. They found an increase in all four inflammatory cells in post-stroke heart tissue, providing important confirmation that stroke induces inflammation outside of the brain.

Altogether, the researchers discovered critical evidence of specific cardiac changes that occur post-stroke, but there are still many unanswered questions about the brain-heart connection following stroke. For example, this study only examined cardiac changes at 28 days post-stroke. Future studies could assess these changes more precisely across time to develop a timeframe for intervention that could slow down cardiac inflammation and fibrosis. Further, the results of this study are specific to strokes that affect the insula, these findings may not be applicable to strokes that occur in other brain regions. With cardiac complications being the second leading cause of post-stroke death, a better understanding of post-stroke heart injury is essential for improvement of patient outcomes.