Clinical fi ndings associated with cardiovascular autonomic dysfunction in adult sickle cell anaemia patients

Oguanobi, Nelson I; Onwubere, Bjc; Anisiuba, BC; Ike, SO; Ejim, EC; Ibegbulam, Obike

doi:10.1080/ac.67.2.2154207

Cited by 10 publications

(11 citation statements)

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“…Although the effect size for STAI Y1 was small in the multivariate analysis, it was significant, suggesting that treatments directed at relieving anxiety may help reduce vascular reactivity. Baseline HRV was lower in SCD, as reported by others, [39][40][41][42][43] but there were no differences between controls and patients with SCD in the direct measures of cardiac autonomic activity in response to thermal stimuli. Cardiac autonomic activity and peripheral vascular autonomic reactivity are related to each other via complex neural mechanisms, but are not equivalent.…”

Section: Discussionsupporting

confidence: 79%

Progressive vasoconstriction with sequential thermal stimulation indicates vascular dysautonomia in sickle cell disease

Veluswamy

Shah

Khaleel

et al. 2020

Blood

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Sickle cell disease (SCD) subjects exhibit subjective hypersensitivity to cold and heat perception in experimental settings, and triggers such as cold exposure are known to precipitate vaso-occlusive crisis by still unclear mechanisms. Decreased microvascular blood flow (MBF) increases the likelihood of vaso-occlusion by increasing entrapment of sickled red blood cells in the microvasculature. As SCD subjects have dysautonomia, we anticipated that thermal exposure would induce autonomic hypersensitivity of their microvasculature with an increased propensity towards vasoconstriction. We exposed 17 SCD and 16 control subjects to a sequence of predetermined threshold temperatures for cold and heat detection as well as cold and heat pain via a thermode placed on the right hand. MBF was measured on the contralateral hand using photo-plethysmography, and cardiac autonomic balance was assessed using heart rate variability. Thermal stimuli at both detection and pain thresholds caused significant decrease in MBF in the contralateral hand within seconds of stimulus application, with SCD subjects showing significantly stronger vasoconstriction (p=0.019). Furthermore, SCD subjects showed greater progressive decrease in blood flow than controls, with poor recovery between episodes of thermal stimulation (p=0.042). SCD subjects had faster vasoconstriction than controls (p=0.033), especially with cold detection stimulus; individuals with higher anxiety also vasoconstricted faster (p=0.007). Augmented vasoconstriction responses and progressive decrease in perfusion with repeated thermal stimulation in SCD is indicative of autonomic hypersensitivity in the microvasculature. This is likely to increase red cell entrapment in response to clinical triggers like cold or stress that have been associated with vaso-occlusive crisis in SCD.

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Section: Discussionsupporting

confidence: 79%

Progressive vasoconstriction with sequential thermal stimulation indicates vascular dysautonomia in sickle cell disease

Veluswamy

Shah

Khaleel

et al. 2020

Blood

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“…The role of hypoxemia/hypoxia on ANS dysfunction has been reinforced by studies in rats showing that chronic hypoxia causes cell loss in the nucleus ambiguous, a structure from which several vagal efferent axons innervate ganglionated plexuses in the dorsal surface of cardiac atria, which in turn may have different functional roles in cardiac regulation [34]. SCA patients with the most severe form of the disease [10], at risks for developing frequent vaso-occlusive crises [11] or acute chest syndrome [12], or with leg ulcers and erectile dysfunction [35], have a depressed ANS activity and a reduced parasympathetic activity. These findings suggest a role of parasympathetic withdrawal and sympathetic predominance in the pathophysiology of several sickle cell complications.…”

Section: Discussionmentioning

confidence: 99%

Acute Moderate Exercise Does Not Further Alter the Autonomic Nervous System Activity in Patients with Sickle Cell Anemia

et al. 2014

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A decreased global autonomic nervous system (ANS) activity and increased sympathetic activation in patients with sickle cell anemia (SCA) seem to worsen the clinical severity and could play a role in the pathophysiology of the disease, notably by triggering vaso-occlusive crises. Because exercise challenges the ANS activity in the general population, we sought to determine whether a short (<15 min) and progressive moderate exercise session conducted until the first ventilatory threshold had an effect on the ANS activity of a group of SCA patients and a group of healthy individuals (CONT group). Temporal and spectral analyses of the nocturnal heart rate variability were performed before and on the 3 nights following the exercise session. Standard deviation of all normal RR intervals (SDNN), total power, low frequencies (LF) and high frequencies powers (HF) were lower but LF/HF was higher in SCA patients than in the CONT group. Moderate exercise did not modify ANS activity in both groups. In addition, no adverse clinical events occurred during the entire protocol. These results imply that this kind of short and moderate exercise is not detrimental for SCA patients.

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“…In one of the earliest studies evaluating HRV in SCD, Romero et al found that 58% of SCD subjects had abnormal cardiac autonomic balance, implying a role for dysautonomia in the high frequency of sudden death in SCD patients [44]. More recently, autonomic activity has been associated with disease severity in SCD [45,46,47]. Reduced parasympathetic activity at baseline has been associated with increased risk of VOC [46] and acute chest syndrome [48].…”

Section: Autonomic Dysfunction and Peripheral Vasoreactivity In Scdmentioning

confidence: 99%

Vaso-Occlusion in Sickle Cell Disease: Is Autonomic Dysregulation of the Microvasculature the Trigger?

Veluswamy

Shah

Denton

et al. 2019

JCM

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Sickle cell disease (SCD) is an inherited hemoglobinopathy characterized by polymerization of hemoglobin S upon deoxygenation that results in the formation of rigid sickled-shaped red blood cells that can occlude the microvasculature, which leads to sudden onsets of pain. The severity of vaso-occlusive crises (VOC) is quite variable among patients, which is not fully explained by their genetic and biological profiles. The mechanism that initiates the transition from steady state to VOC remains unknown, as is the role of clinically reported triggers such as stress, cold and pain. The rate of hemoglobin S polymerization after deoxygenation is an important determinant of vaso-occlusion. Similarly, the microvascular blood flow rate plays a critical role as fast-moving red blood cells are better able to escape the microvasculature before polymerization of deoxy-hemoglobin S causes the red cells to become rigid and lodge in small vessels. The role of the autonomic nervous system (ANS) activity in VOC initiation and propagation has been underestimated considering that the ANS is the major regulator of microvascular blood flow and that most triggers of VOC can alter the autonomic balance. Here, we will briefly review the evidence supporting the presence of ANS dysfunction in SCD, its implications in the onset of VOC, and how differences in autonomic vasoreactivity might potentially contribute to variability in VOC severity.

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Clinical fi ndings associated with cardiovascular autonomic dysfunction in adult sickle cell anaemia patients

Abstract: Significant cardiac morbidity is associated with abnormal cardiovascular autonomic function in sickle cell anaemia.

Cited by 10 publications

References 0 publications

Progressive vasoconstriction with sequential thermal stimulation indicates vascular dysautonomia in sickle cell disease

Progressive vasoconstriction with sequential thermal stimulation indicates vascular dysautonomia in sickle cell disease

Acute Moderate Exercise Does Not Further Alter the Autonomic Nervous System Activity in Patients with Sickle Cell Anemia

Vaso-Occlusion in Sickle Cell Disease: Is Autonomic Dysregulation of the Microvasculature the Trigger?

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