Introduction
Traumatic brain injury (TBI) can cause disability and premature death. TBI may be commonly seen among military personnel and individuals playing contact sports. Research has found that TBI may have an association with cardiovascular diseases. Understanding the link between TBI and cardiovascular diseases may help prevent disability and premature death.
What Is Traumatic Brain Injury?
The injury caused to the brain due to a blow or a hit is known as TBI. This condition is considered to be the major reason for death and disability in the U.S. TBI causes many short-term and long-term medical issues, and they can affect every part of life.
Thousands of individuals are affected by TBI every year in the U.S. It was estimated that 2,14000 people needed in-patient care for TBI in 2020, and more than 69000 individuals died due to TBI.
Whenever trauma to the brain occurs, there is damage to the brain and its blood vessels. There may be chemical changes that occur due to TBI. The symptoms may vary according to their severity. These include physical, altered thinking or memory, and social or emotional issues. Symptoms appear similar in both adults and children.
TBI causes many complications, and this depends on the severity of TBI. Some complications include
-
Bleeding in the brain.
-
Permanent brain damage and disability.
-
Life expectancy is reduced.
-
Alzheimer’s disease may develop.
-
Anxiety may appear.
-
Chronic traumatic encephalopathy.
-
Depression may occur.
-
Disorders related to movements occur.
-
Post-traumatic stress disorder may develop.
What Is the Link Between TBI and Cardiovascular Disease?
TBI is more commonly seen among military personnel and those playing contact sports. Research has probed into the acute and chronic neurological consequences of TBI, its association with cardiovascular diseases, and a group of other non-neurological conditions.
A group of researchers has found from various studies that there may be nervous system dysfunction, neuroinflammation, changes in the brain-gut connection, and post-injury comorbidities that tend to increase the risk of cardiovascular and cognitive dysfunction among survivors of TBI when compared to the general population.
Long-term medical issues like neurologic and psychiatric issues are well established. Growing researchers have found a sequelae called cardiovascular disease (CVD) because of TBI. A recent review has probed, and they have found the studies and mechanisms involved in relating CVD as a sequelae to TBI.
Complications of CVD after TBI include,
-
Hypotension.
-
Changes in electrocardiogram.
-
Cardiac arrhythmias.
-
Release of biomarkers of cardiac injury.
-
Left ventricular (LV) dysfunction.
These abnormalities are reversible, and this can be achieved with general supportive care and by treating the underlying TBI.
Pathophysiology of Complications of CVD Due to TBI:
Catecholamine Effect:
TBI and subarachnoid hemorrhage (SAH) cause a catecholamine storm. The central neuroendocrine axis drives this catecholamine storm. This axis increases sympathetic outflow and activates the adrenal glands.
Damage to the insular and hypothalamus also causes the complications of CVD. This may activate and be followed by dysfunction of the autonomic nervous system and intense inflammatory responses. These can have major adverse effects on the heart.
A high sympathetic tone can be observed for some time after TBI. This causes catecholamine levels to be high and remain for up to 10 days. Though this is considered a protective mechanism to maintain cerebral perfusion in increased intracranial pressure, it causes many adverse effects of CVD.
Systemic Circulatory Effects:
A catecholamine storm causes intense systemic vasoconstriction. This, in turn, may lead to increased cardiac afterload, myocardial workload, and oxygen demand. There may be simultaneous coronary vasoconstriction, but the increase in oxygen demand is not associated with oxygen delivery. Because of this, it may lead to subendocardial ischemia and impaired ventricular function. This may, again, cause or lead to cardiogenic pulmonary edema and systemic hypotension. Hypertension may be possible because of head injury-related disruption of brain stem centers related to hemodynamic control.
Neurogenic Stunned Myocardium (NSM) Syndrome:
NSM is a reversible cardiac injury characterized by a change in ECG, arrhythmias, LV dysfunction, and the release of biomarkers of cardiac injury. This condition is caused due to increased norepinephrine release from the myocardial nerve terminals. It is independent of plasma catecholamine levels.
The release of catecholamines into the myocardial interstitium may result in the prolonged opening of beta 1-adrenergic receptors-controlled calcium channels and rapid depletion of adenosine triphosphate. This may further lead to mitochondrial dysfunction and cell death. This is also related to the histologic picture of myocardial contraction band necrosis. The severity of NSM and degree of myocardial injury may be related to the severity of the underlying brain injury.
Neuroinflammation:
TBI and SAH activate a neuroinflammatory response. This causes the release of immunologically active mediators, like cytokines, adhesion molecules, and other multifunctional peptides, from the brain to the systemic circulation. This leads to systemic inflammatory response syndrome. This, in turn, causes systemic organ dysfunction and failure after the brain injury. This change was also observed in the pathogenesis of ventricular arrhythmias after SAH.
It was observed that there is a complex interaction between the brain, immune system, and autonomic nervous system. It is thought that parasympathetic dysfunction and activation of the sympathetic nervous system play a role in cardiac damage through modulation of the myocardial inflammatory response through acetylcholine receptors. Unchecked myocardial inflammation may result in myocardial dysfunction and cell death.
Neurogenic cardiovascular dysfunction may exhibit minimal clinical effects, but in severe cases, it may lead to cardiogenic shock and pulmonary edema.
Studies have found that there is a potential link between TBI, CVD, and cognitive dysfunction. It was thought that neuroinflammatory pathways triggered by TBI could be responsible for the cause of atherosclerosis. Weight gain and disturbances in sleep after injury may be responsible for independent or additive risks.
There may be disruptions in the connections between the nervous and gastrointestinal systems, leading to distortion of the balance in the microbes present in the gut. This may be responsible for cognitive and cardiovascular effects.
A study on football players found that many systems may interact to produce multilevel dysfunction after TBI. Many studies have shown that individuals without any preexisting comorbidities sustain TBI, and TBI is associated with a higher risk for CVD than those without TBI.
Conclusion
The brain is an important organ that regulates many functions of the body. Traumatic brain injury may disrupt many functions of the body, including cardiovascular function. TBI may result in disability and premature death. Many researchers have found an association between TBI and CVD. Hence, it becomes important to know about TBI, its pathophysiology, and its link with CVD. Knowing about this may help in finding ways to understand the condition, its treatment, and prevention. This may, in turn, help improve the quality of life of an individual.
