User:Lisa M Johnson/sandbox

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Overview[edit]

Neurocardiology refers to the pathophysiological interplays of the nervous and cardiovascular systems. [1] It is an emerging field in medicine over the last decade. The constant communication between the heart and the brain have proved invaluable to interdisciplinary fields of neurological and cardiac diseases.[2]

The fundamental understanding of the communication between the heart and the brain via the nervous system has led scientists into understanding its elaborate circuitry.[3] The brain emits neurological signals of oscillating frequencies. The neural rhythms provide information on steady state conditions of healthy individuals. Variation in the neural rhythms provide evidence that a problem is present regarding physiologic regulation.[4]

Links between the cardiovascular system and the nervous system along the cardiac axis have been shown to cause many problems on the body including: arrhythmias, epilepsy, and stroke, all relating to the fundamental factor of stress. As stated previously, the changes in neural oscillations can contribute to the knowledge of what a steady state in an individual looks like, as well as contributing to the imbalance of the nervous system and physiological function. In addition, the brain can also control the heart rate through the sympathetic nervous system and a few other areas of the heart.[4]

Map between Cardiovascular System to Nervous System[edit]

The cardiovascular system is regulated by the autonomic nervous system, which includes the sympathetic and parasympathetic nervous systems. A distinct balance between these systems is crucial for the pathophysiology of cardiovascular disease. An imbalance can be caused by hormone levels, lifestyle and environmental stressors, and injuries.[5]

The complicated link between the brain and the heart can be mapped out from the complex of higher nervous influences descending down to the heart. It innervates key autonomic structures from the brain's cortex all the way to the heart, the source of cardiac arrhythmias and complications. The information originates in the cortex and descending down to the hypothalamus. The neural signals are then transferred to the brainstem, followed by the spinal cord and ganglia, which is where the heart receives all its signals. In more detail, the heart receives its neural input through parasympathetic and sympathetic ganglia and intermediolateral gray column of the spinal cord. [6]

Problems[edit]

The neurocardiac axis has been a link to many problems regarding the physiological functions of the body. This includes cardiac ischemia, stroke, epilepsy, and most importantly, heart arrhythmias cardiac myopathies. Many of these problems are due to the imbalance of the nervous system, resulting in symptoms that effect both the heart and the brain. This link between the cardiovascular and nervous system has brought up a concern in our nonintegrated specialty training process for doctors. Doctors are trained for specifically one specialty and as a result not as knowledgeable about the others, even though they all related to the same thing, the human body. Individual physicians review patient's symptoms based on their own specific system of interest, without considering the ways in which one system interacts with another. Consequently, this delays correct diagnosis for the patient and in return, the appropriate treatment.

Stress[edit]

The physiological effects of stress on the body

Cardiovascular systems are regulated by the autonomic nervous systems, which includes the sympathetic and parasympathetic nervous systems. A distinct balance between these two systems is crucial for the pathophysiology of cardiovascular disease. Chronic stress has been widely studied on its effects of the body resulting in an elevated heart rate (HR), reduced HR variability, elevated sympathetic tone, and intensified cardiovascular activity. Consequently, stress promotes an autonomic imbalance in favor of the sympathetic nervous system. The activation of the sympathetic nervous system contributes to endothelial dysfunction, hypertension, atherosclerosis, insulin resistance, and increased incidence of arrhythmias.[5] An imbalance in the autonomic nervous system has been documented in mood disorders; It is commonly regarded as a mediator between mood disorders and cardiovascular disorders.

Your hypothalamus is the part of the brain that regulates function and responds to stress. When the brain perceives environmental danger, the amygdala fires a nerve impulse to the hypothalamus to initiate the body's fight-or-flight mode through the sympathetic nervous system. The stress response starts with the hypothalamus stimulating the pituitary gland, which releases the adrenocorticotropic hormone. This signals the release of cortisol, the stress hormone, initiating a multitude of physical effects on the body to aid in survival. The negative feedback loop is then needed to return the body to its resting state by signaling the parasympathetic nervous system.[7]

Prolonged stress leads to many hazards within your nervous system. Various hormones and glands become overworked, chemical waste is produced resulting in degeneration of nerve cells. The result of prolonged stress is the breakdown of the body and the nervous system. Stress alone does not produce potentially deadly arrhythmias in normal healthy hearts, however studies do appear to show that stress causes cardiac damage that may lead to arrhythmias.

Arrhythmias[edit]

In a study relating to relationship of neurocardiology of arrhythmias and sudden cardiac death, they hypothesized that the individual with a diseased heart has a greater likelihood of experiencing cardiac arrhythmias and sudden cardiac death when the neurocardiac axis is activated.[6] An arrhythmia is defined as any disturbance in the cardiac activation sequence or any deviation from accepted limits of rate or regularity of the normal impulse. The main types of arrhythmia leading to sudden cardiac death are tachyarrhythmias and bradyarrhythmias. Tachyarrhythmias are associated with ventricular fibrillation and ventricular tachycardia. Bradyarrhythmias are associated with complete atrioventricular blockage and sudden asystole. The underlying cause of sudden cardiac death is unclear, despite the understanding that heart disease causes arrhythmias, which in turn produce sudden cardiac death.[6] Lown describes the heart as the target, and the brain is called the trigger. Sudden cardiac death is triggered by an electrical accident, which can be treated with ventricular defibrillation.[8]

Stroke[edit]

Stroke activates the neurocardiac axis, producing arrhythmias, cardiac damage, and sudden death. In a recent study on patients with already diseased hearts and electrocardiographic abnormalities, there was evidence of lost hypothalamic-medullary integration at the midbrain. This resulted in the fact that overactivity in the parasympathetic nervous system may also cause sudden death with asystole after stroke. Catecholamine medications have been studied to mediate the effects of electrocardiographic changes and heart damage [6].

Epilepsy[edit]

Sudden death from epilepsy is not very common, with a rate of approximately 2 in a thousand. The present understanding about how sudden cardiac death can result from epilepsy is that the brain is stimulating an arrhythmia. Recordings during seizures report that the onset of tachycardia just prior to the seizure is common, with both atrial and ventricular ectopy [6]. The sudden epileptic death may be a result of the sympathetic activation or autonomic imbalance of the nervous system as described earlier.

Emotions[edit]

The relationship between emotions and their effect on the destabilization of the heart continues to be a mystery. It is considered that both the spatial and temporal patterns of autonomic input to the heart play a key role in altered electrophysiological parameters. The body continually attempts to maintain homeostasis through the baroreflex. This balance in the autonomic neural input to the heart in response to the pressure and volume changes leads to alterations in the baroreceptors [9] .

Treatments[edit]

Medications[edit]

Drugs with both antidepressant and cardiometabolic actions are in the process of being studied. Most of the medications work on stressors of the heart, and some also work to treat the neuropsychiatric diseases. Antidepressant medications have shown to be insufficient to induce normalization of the of the cardiovascular dysfunctions that are associated with the psychiatric conditions.[10]

  • Hypercatecholaminergic medications[10]
  • Adrenoreceptor blockers (alpha and beta)
They are most commonly used to treat hypercatecholaminergic states. Overall the blockers reduce incidences of long-term disease. The blockade not only affects cardiomyocytes directly but also works to reduce the risks of heart failure and hypertension. One side effect is that it can activate pulmonary edema with patients who already have unstable hearts. In particular, beta-blockers are used for the management of cardiac arrhythmias. They link the brain and the cardiovascular system in cardiovascular diseases [5]. Beta-blockers have also been studied in depressed patients. A meta-analysis concluded that with anti-depressant medication, the percentage of patients in remission from depressed symptoms significantly increased from just anti-depressants alone [5]. This suggests that this type of medication might be beneficial for both behavioral and cardiovascular symptoms of depression. Further studies need to be conducted to determine results along the overall neurocardiac axis.
This medication, known as spironolactone, acts by blocking its binding to spironolactone receptors. This has shown positive feedback in tackling both cardiovascular and activation of the main feature of stress-related disorders.
  • Adrenoreceptor agonist
Acts on the central nervous system to inhibit the sympathetic nervous system, leading to a decrease in blood pressure. It is commonly used to reduce the risk of stroke and heart attacks by treating high blood pressure, anxiety, and panic disorders. It also leads to the decreased activity of norepinephrine release from the sympathetic nerve terminals [10].

Physical Activity and Diet[edit]

Lifestyle modifications play a crucial role in management of cardiovascular and neurological diseases. Physical activity and a well-balanced diet favor cardiovascular conditioning and improves performance and capacity. Exercise has a positive effect on the metabolism, which controls glucose levels, especially for stress-related pathology and brain disorders such as depression, which impose a heavy burden on the cardiovascular system. Many studies are currently being done for more information and knowledge regarding the common mediators for cardiovascular disease and the central nervous system. The brain-heart interaction is considered bidirectional, however the majority of times the central nervous system is regulated more over the heart and blood vessels [5].

References[edit]

  1. ^ Van Der Wall, E. E.; Van Gilst, W. H. (2013). "Neurocardiology: close interaction between heart and brain". Netherlands Heart Journal. 21 (2): 51–52. doi:10.1007/s12471-012-0369-4. PMC 3547430. PMID 23239452. {{cite journal}}: Check date values in: |year= / |date= mismatch (help); Unknown parameter |month= ignored (help)
  2. ^ Carrero, Milton (12 February 2011). "One Vital Organ: Heart is More than a Pump". The Morning Call. Retrieved 11 November 2013.
  3. ^ Madurasinghe, Lakshman. "Neurocardiology: The Brain in the Heart". Retrieved 11 November 2013.
  4. ^ a b Fallen, Ernest (December 2000). "Hidden rhythms in the heart record: a primer on neurocardiology". Clin Invest Med. 23 (6): 387–394. PMID 11152408.{{cite journal}}: CS1 maint: date and year (link)
  5. ^ a b c d e Pereira, Vitor Hugo; Cerqueira, João José; Palha, Joana Almeida; Sousa, Nuno (5). "Stressed brain, diseased heart: a review on the pathophysiologic mechanisms of neurocardiology". International Journal of Cardiology. 166 (1): 30–37. doi:10.1016/j.ijcard.2012.03.165. hdl:1822/24143. PMID 22521375. Retrieved 24 Aug. 2013. {{cite journal}}: Check date values in: |accessdate=, |date=, and |year= / |date= mismatch (help); Unknown parameter |month= ignored (help)
  6. ^ a b c d e Davis, Alan (1993). "Brain-Heart Interactions: The Neurocardiology of Arrhythmia and Sudden Cardiac Death". Texas Heart Institute Journal. 20 (3): 158–169. PMC 325088. PMID PMC325088. {{cite journal}}: Check |pmid= value (help)
  7. ^ "How Your nervous System Gets Out of Sync" (PDF). Retrieved 28 Octoberr 2013. {{cite web}}: Check date values in: |accessdate= (help)
  8. ^ Lown, B (May 1977). "Neural and Psychologic Mechanisms and the Problem of Sudden Cardiac Death". American Journal of Cardiology. 39 (6): 890–902. doi:10.1016/S0002-9149(77)80044-1. PMID 860697. Retrieved 28 October 2013. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: date and year (link)
  9. ^ Taggart, P.; Boyett, M. R.; Logantha, S. J.; Lambiase, P. D. (2011). "Anger, Emotion, and Arrhythmias: from Brain to Heart". Frontiers in Physiology. 2: 67. doi:10.3389/fphys.2011.00067. PMC 3196868. PMID PMC3196868. {{cite journal}}: Check |pmid= value (help); Unknown parameter |month= ignored (help)CS1 maint: date and year (link)
  10. ^ a b c Goldstein, David S. (2012). "Neurocardiology: Therapeutic Implications for Cardiovascular Disease". Cardiovascular Therapeutics. 30 (2): 89–106. doi:10.1111/j.1755-5922.2010.00244.x. PMC 4893308. PMID 21108771.

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