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The neurogenic cardiac injury in patients with or without pre-existing heart disease 

Cardiac dysfunction can occur after a variety of neurological pathologies. The main cause of neurogenic stress cardiomyopathy is a subarachnoid hemorrhage (SAH), but other neurological pathologies that could be a cause include traumatic brain injury (TBI), hemorrhagic and ischemic stroke, infections of the central nervous system (CNS), and epilepsy. The review article by Ziaka M and Exadaktylos A. discussed the pathophysiology of neurogenic cardiac injury and cardiac dysfunction in stroke. The authors described the brain-heart axis and highlighted the main pathophysiological mechanisms of stroke-heart interactions. They also analyzed the main pathophysiological mechanisms leading to secondary and delayed cerebral injury in patients with hemorrhagic or ischemic stroke and neurogenic stress cardiomyopathy.

The association between stroke and a greater propensity for adverse cardiac events has attracted growing interest over the past decades. Stroke is a good model to study neuro-cardiac influences because the location of the lesion can be precisely identified.

About brain-heart interaction

For many years, animal or clinical studies have shown a major influence of the brain on cardiac structure and function. Data from historical sources, such as the study by Beattie et al. (1930) demonstrated that chloroform-induced ventricular tachyarrhythmia was abolished by the mid-collicular, but not higher, diencephalic section. Later, in 1960 the scientists reported intriguing changes in the electrocardiogram (ECG) after SAH.

The anatomical structures involved in cardiac regulation extend from the spinal cord to the cortex. The CNS directly affects cardiac function via sympathetic and parasympathetic efferents from the brainstem cardio-regulatory centers.

According to neuroimaging and electrophysiological studies, the insula, an anatomical structure in the temporal lobe, plays a cardinal role in autonomic nervous system regulation at the cortical level. The lesions in the CNS, particularly of the insular cortex, can change the balance of sympathetic and parasympathetic tone, increase plasma catecholamine concentrations, cause myocardial damage, and increase the incidence of cardiac arrhythmias. The right insula is considered to be the center of sympathetic autonomic control, while the left insula is considered to be the center of parasympathetic autonomic control.

About the study

The authors described the heart-brain axis and highlighted the main pathophysiological mechanisms of stroke-heart interaction. 

 

The pathophysiology of neurogenic cardiac injury 

Acute brain injury can induce cardiac dysfunction in the absence of cardiac disease. Factors that could explain this relationship include hemodynamic disorders and subsequent cerebral hypoperfusion, development of secondary cerebral cardioembolic complications, disturbances of oxygenation, neurohormonal mechanisms, systemic and cerebral inflammation, disruption of the blood-brain barrier (BBB), and activation of glial cells.

The most prevailing theory is that sympathetic hyperstimulation, due to physical or emotional triggers, leads to direct catecholamine toxicity, epicardial and microvascular coronary vasoconstriction, and adrenoreceptor-mediated damage.

At the cellular level, the local action of catecholamines is facilitated by the proximity of cardiomyocytes and nerve endings. This leads to changes in calcium homeostasis and β-adrenergic signal transduction. The result is necrosis of the myocardial contraction band and impairment of coronary microcirculation. The systemic inflammation and the excessive release of interleukin-1 with neurohormonal mechanisms seem to play an important role in neurogenic stress cardiomyopathy development. Cardiac dysfunction caused by brain injury can lead to potentially long-lasting cardiac complications, such as heart failure.

 

Clinical presentations of neurogenic stress cardiomyopathy 

In general, cardiac manifestations are highly variable and associated with ECG signs and echocardiographic findings. Acute ECG changes are more frequently associated with intracerebral hemorrhage or SAH than with acute ischemic stroke. The two major categories of ECG changes during neurogenic heart disease are dysrhythmias (e.g., atrial and ventricular tachyarrhythmias, sinus bradycardia, and tachycardia) and repolarization changes. The most common repolarization changes are found in the anterolateral and inferolateral leads, including prolongation of the QT interval and changes in ST-T. In patients with neurogenic stress cardiomyopathy, the most frequent ECG findings are prolongation of the QT-interval and T-wave inversion.

The most frequent echocardiographic findings are abnormalities in the left ventricular wall motion. Cardiac systolic impairment is not uncommon after a severe neurologic injury.

Notably, in patients with SAH, the incidence of cardiac dysfunction, if ECG criteria are used, is 100%. If echocardiographic criteria are used, 10%–15% of patients develop global systolic dysfunction with a left ventricular ejection fraction lower than 50%, while almost 30% of patients present abnormalities in wall motion. In patients with acute ischemic stroke, the clinical spectrum of cardiac dysfunction includes ischemic and non-ischemic myocardial injury with cardiac troponin elevation, heart failure, arrhythmias, and sudden cardiac death. Cardiac systolic impairment occurs in 13% to 29% of patients with ischemic stroke and in 22% of patients with TBI.

 

The coexistence of “heart and brain failure” following a heart disease

If the brain complications are the consequence of cardiac dysfunction, they are related to cerebral hypoperfusion, oxygenation disturbance, activation of the hypothalamic-pituitary-adrenal axis, and systemic inflammation. The term “cardiogenic dementia” has been used to describe the coexistence of “heart and brain failure” following a heart disease.

Conclusion

Concerning clinical management and therapeutic implications, the authors concluded that therapeutic management of neurogenic cardiac dysfunction is conservative, with an emphasis on the improvement of cardiac function, adequate oxygenation, prevention of further neuroinflammation,  and maintenance of cerebral homeostasis and perfusion pressure.

 

This article was published in the Journal of Stroke.

 

Journal Reference

 

Ziaka M, Exadaktylos A. The Heart Is at Risk: Understanding Stroke-Heart-Brain Interactions with Focus on Neurogenic Stress Cardiomyopathy—A Review. Journal of Stroke 2023; 25(1): 39-54. (Open Access)  https://doi.org/10.5853/jos.2022.02173

 

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