Determinants of Cardiac Autonomic Dysfunction in ESRD

Chan, Christopher T.; Levin, Nathan W.; Chertow, Glenn M.; Larive, Brett; Schulman, Gerald; Kotanko, Peter

doi:10.2215/cjn.03080410

Cited by 62 publications

(51 citation statements)

References 28 publications

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“…The magnitude of 25(OH)D increase was directly correlated with the magnitude of increased cardioprotective PNS activity, implying that vitamin D levels may constitute an important role in the development of common CVD-related outcomes in this population by affecting the ANS. Chan et al [28] reported that patients with CKD demonstrated poor cardiac ANS activity, which was characterized by decreased activity of the inhibitory PNS. Furthermore, in patients with end-stage renal disease (ESRD), depressed HRV is extremely common and usually presents as suppressed PNS activity with increased SNS input to the sino-atrial node [14] [28].…”

Section: Discussionmentioning

confidence: 99%

“…Chan et al [28] reported that patients with CKD demonstrated poor cardiac ANS activity, which was characterized by decreased activity of the inhibitory PNS. Furthermore, in patients with end-stage renal disease (ESRD), depressed HRV is extremely common and usually presents as suppressed PNS activity with increased SNS input to the sino-atrial node [14] [28]. For the dissertation by Mann [14], a cross-over study was conducted in which 56 participants with ESRD on hemodialysis were randomized to either conventional (0.25 mg alfacalcidol 3 times per week plus placebo 3 times per week for 6 weeks) or intensive (0.25 mg alfacalcidol 3 times per week plus 50,000 IU ergocalciferol once a week plus placebo 2 days per week for 6 weeks) vitamin D therapy followed by a 12-week washout period and another 6 weeks of vitamin D therapy.…”

Section: Discussionmentioning

confidence: 99%

“…They did not observe significant changes in measures of cardiac autonomic tone, mineral metabolism, or RAAS activity, but an exploratory subgroup analysis found that after treatment, Open Journal of Internal Medicine participants who remained vitamin D deficient (25(OH)D < 20 ng/ml), compared to those who achieved sufficiency (>30 ng/ml), had significant ANS imbalance. In the ESRD population, abnormal HRV and ANS dysfunction are also common in this population; thus, putting them at higher risk of sudden arrhythmic death [28] [29].…”

Section: Discussionmentioning

confidence: 99%

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Vitamin D Status, Autonomic Nervous System Activity, and Cardiometabolic Risk

Lopez¹,

Campa²,

Huffman³

et al. 2017

OJIM

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Vitamin D and its association with cardiovascular disease (CVD) are currently a topic of investigation. The objective of this study was to explore the association between vitamin D status (serum 25-hydroxyvitamin D (25(OH)D)) and a cardiometabolic risk score (CMRS) derived from markers of cardiac autonomic nervous system activity, vascular dynamics, and body composition, using an innovative non-invasive technology. We found that individuals who were vitamin D sufficient ((25(OH)D) ≥ 30 ng/ml, n = 51), compared to those who were vitamin D insufficient (<30 ng/ml, n = 44), had significantly higher heart rate variability (as measured by time and frequency domain variables) and lower photoplethysmography analysis markers and CMRS. These outcomes show that vitamin D insufficient subjects had reduced cardio protective parasympathetic nervous system activity, increased endothelial dysfunction, and hence were at greater cardiometabolic risk, implying vitamin D may play a meaningful role in CVD.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Vitamin D Status, Autonomic Nervous System Activity, and Cardiometabolic Risk

Lopez¹,

Campa²,

Huffman³

et al. 2017

OJIM

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“…Changes in sinus rhythm controlled by the electrical signals passed from the ANS to the heart can be quantified by measuring Heart Rate Variability (HRV) with a typical ambulatory heart monitor [14]. Measures of HRV in CKD patients often demonstrate a dramatic shift in ANS activity, in which the heart is predominantly regulated by excitatory sympathetic signaling couple by extreme withdrawal in inhibitory, cardio-protective parasympathetic control [15,16]. This characteristic imbalance in HRV has been associated with the increased risk of SCD in this patient population [15,16].…”

mentioning

confidence: 99%

“…Measures of HRV in CKD patients often demonstrate a dramatic shift in ANS activity, in which the heart is predominantly regulated by excitatory sympathetic signaling couple by extreme withdrawal in inhibitory, cardio-protective parasympathetic control [15,16]. This characteristic imbalance in HRV has been associated with the increased risk of SCD in this patient population [15,16]. Interestingly, observational studies have shown evidence of a link between vitamin D deficiency and abnormal HRV in humans both with and without CKD [17,18], as well as an improvement in HRV responses to a vascular stressor following 4 weeks of intensive oral vitamin D supplementation [19].…”

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confidence: 99%

Vitamin D Deficiency and Cardiovascular Risk: weÃ¢ÂÂre still in the Dark

Mann¹

2015

J Nutr Food Sci

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For decades, observational studies has provided evidence of the association between reduced levels of 25-hydroxy vitamin D and increased risk of cardiovascular disease. It is generally accepted that vitamin D deficiency is in some way related to adverse cardiovascular outcomes [1,2]. It has been postulated that this association may be a result of reverse causality in which unhealthy and less mobile individuals are less likely to be exposed to sunlight [3], or perhaps due to a physiological chain of events in which low vitamin D concentrations promote downstream vascular remodeling and hemodynamic instability [4,5].And yet, after thousands of studies have been published on the topic, the global medical community remains very much in the dark regarding whether a true relationship exists between vitamin D deficiency and increased cardiovascular risk. A small number of clinical trials which have aimed to assess the possibility of a direct, causal relationship between low vitamin D concentrations and poor cardiovascular outcomes in select patient populations do exist. Unfortunately, metaanalyses of these trials demonstrate widespread inconsistency in trial duration, sample size, type of vitamin D intervention and route of administration, and primary outcomes [6][7][8]. As a result, the medical landscape is barren of vitamin D trials with consistent, pragmatic designs formulated a priori to assess cardiovascular outcomes and thus the depth of knowledge of vitamin D has remained stagnant [6].One large patient population may be able to shine a much-needed spotlight on this topic. Individuals with chronic kidney disease (CKD), specifically those with end-stage kidney disease requiring dialysis, experience dramatically increased risk of cardiovascular disease compared to that of the general population [9]. In addition, the progressive loss of kidney function also results in disruption of regular vitamin D metabolism, thus the prevalence of severe vitamin D deficiency in this patient population is extremely high [10]. The concomitant nature of high cardiovascular risk and severe vitamin D deficiency persistent in CKD provides a unique opportunity to analyze this seemingly complex physiological relationship.In general, approximately 25% of all deaths in CKD are attributed to Sudden Cardiac Arrhythmic death (SCD) [9,11], which results primarily from miscommunication between the sympathetic and parasympathetic branches of the cardiac Autonomic Nervous System (ANS) and the atrio-ventricular and sino-atrial nodes of the heart [12,13]. Changes in sinus rhythm controlled by the electrical signals passed from the ANS to the heart can be quantified by measuring Heart Rate Variability (HRV) with a typical ambulatory heart monitor [14]. Measures of HRV in CKD patients often demonstrate a dramatic shift in ANS activity, in which the heart is predominantly regulated by excitatory sympathetic signaling couple by extreme withdrawal in inhibitory, cardio-protective parasympathetic control [15,16]. This characteristic imbalance in HRV has ...

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