This review focuses on Andrade, et al’s. (2014). “The clinical profile and pathophysiology of atrial fibrillation: relationships among clinical features, epidemiology, and mechanisms” published in Circulation research, 114(9). The nature of Atrial Fibrillation notes significance in the growing risks of morbidity and the commonality of the disease as an arrhythmia. Scholarship has identified the common risks factors of morbidity with growing evidence into numerous other risks that may result to occurrence.
As such, there is significance in the determination of the pathophysiological process of the event in order to determine the most effective interventions. The event is related to general decline in the population quality of life, increased rates of hospitalization which is antecedent to the increased costs of healthcare, and general decline of social health quality. It is this significance in terms of risks and potential consequence that the article under review was selected. The development of the understanding into the pathophysiology of Atrial Fibrillation would allow the advancement of knowledge into how best to contribute to scholarship and research on both preventive and curative preventions.
The authors point to similarly identified significance of the disease pointing to the growing risks of comorbidity and occurrence. More specifically, the authors note that current research is continually unearthing more risks of occurrence including hypertrophic cardiomyopathy, increased pulse pressure, obstructive sleep apnea, diastolic dysfunction, high-level physical training, predisposing gene variants, and congenital heart disease among others. As such, the objective of the authors was to develop better understanding of the disease’s pathophysiology in order to be able to establish interventions which would be preventive and curative. Accordingly, they note four types of disturbances that promote the occurrence of the disease; ion channel dysfunction, Ca2+-handling abnormalities, structural remodeling and autonomic neural dysregulation. The inference of the author’s opinion is that, the occurrence of the disease is primarily as a result of the imbalances of caused in the blood system. This means that the disease is as a result of improper blood functions in the body of the patient.
Given the risks factors of the disease, the authors sought to understand the relationship between the pathophysiology of those factors and of Atrial Fibrillation. From the understanding of the authors, the risk factors cause one or more of the aforementioned disturbances which triggers the fibrillation. As such, the inference is that any disease or condition that results in ion channel dysfunction, Ca2+-handling abnormalities, structural remodeling or autonomic neural dysregulation, would inevitably cause atrial fibrillation. The context of the supposition is based on the relationship between diseases and their comorbid concerns. Where a condition causes ion channel dysfunction, it would become a risk factor to atrial fibrillation. For instance, with hypertension, the systolic blood pressure that usually occurs at the pre-hypersensitive phase causes widening of pulse pressure which increases the risks of arrhythmia. As such, following from the inferences of the authors, it is easily understandable that the higher the risks of conditions resulting in the occurrence of disturbances in the vascular system, the higher the risks of atrial fibrillation occurrence.
The Ca2+-handling abnormalities occur as an outcome of delayed afterdepolarizations or early afterdepolarizations. The Exchange between Ca2+ allows for the control of the function of the arteries as such, where there is a disturbance in the handling of positively charged calcium ions, the cell physiology is affected. This results in the affecting the operations of the valves and results to dysfunctional exchanges of the oxygenated and deoxygenated blood. The fault in the opening and closing of the valves results in the ineffective operations of the atria. As a result, atrial fibrillation occurs. Therefore, any disturbances in the control of the opening and closing of cells would ultimately result in occurrence of the disease. From the author’s perspective the Ca2+-handling abnormalities are common in delayed afterdepolarizations and these, result in focal ectopic firing.
The second disturbance is dysfunction in the ion channel. The ion channel is responsible for the passage of ions and electrical charge which sends information through the membranes. The disturbance of effective passage and electrical charge through the cells results in delayed responses of some of the cells in the body. This results in hyperpolarization and causes reentry of substrate. The disturbance in this case follows from the ineffective activation of the channel through impaired autonomic neural controls. From this perspective, it is possible to understand the argument of the authors regarding the cognitive dysfunction causes of atrial fibrillation. The absence of correct neural functions results in ineffective operations of the ion channels. This dysfunction causes ineffective control of ions and electrical charges which causes the occurrence.
The basic pathophysiology of atrial fibrillation is as a function of improper movement of ions, electrical charges, and charged calcium between the cell membranes. This dysfunctional movement occurs as a result of different factors which contribute to physiological difficulties to process the information required to process the exchange process. As a result of the cell operation dysfunction, the movement of valves, and membranes within the vascular system are affected. From this perspective, the authors’ arguments are evident. There are a number of factors which cause the improper exchange of information in the cellular system. Given the cells are responsible for the autonomic responses, there is delayed information between the neural system and the cellular system. As such, all diseases that affect the exchange of information may result in atrial fibrillation. It is therefore vital to develop preventive responses to the triggers of the disturbances in order to develop preventive interventions to atrial fibrillation.