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Genomics of Cardiovascular Measures of Autonomic Tone.

ABSTRACT: The autonomic nervous system exerts broad control over the involuntary functions of the human body through complex equilibrium between sympathetic and parasympathetic tone. Imbalance in this equilibrium is associated with a multitude of cardiovascular outcomes, including mortality. The cardiovascular static state of this equilibrium can be quantified using physiological parameters such as heart rate (HR), blood pressure, and by spectral analysis of HR variability. Here, we review the current state of knowledge of the genetic background of cardiovascular measurements of autonomic tone. For most parameters of autonomic tone, a large portion of variability is explained by genetic heritability. Many of the static parameters of autonomic tone have also been studied through candidate-gene approach, yielding some insight into how genotypes of adrenergic receptors affect variables such as HR. Genome-wide approaches in large cohorts similarly exist for static variables such as HR and blood pressure but less is known about the genetic background of the dynamic and more specific measurements, such as HR variability. Furthermore, because most autonomic measures are likely polygenic, pathway analyses and modeling of polygenic effects are critical. Future work will hopefully explain the control of autonomic tone and guide individualized therapeutic interventions.

SUBMITTER: Sigurdsson MI

PROVIDER: S-EPMC5839974 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature

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Genomics of Cardiovascular Measures of Autonomic Tone.

Sigurdsson Martin I MI Waldron Nathan H NH Bortsov Andrey V AV Smith Shad B SB Maixner William W

Journal of cardiovascular pharmacology 20180301 3

The autonomic nervous system exerts broad control over the involuntary functions of the human body through complex equilibrium between sympathetic and parasympathetic tone. Imbalance in this equilibrium is associated with a multitude of cardiovascular outcomes, including mortality. The cardiovascular static state of this equilibrium can be quantified using physiological parameters such as heart rate (HR), blood pressure, and by spectral analysis of HR variability. Here, we review the current sta ...[more]

PMID: 29300220

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Project description:BackgroundInsomnia disorder is a widespread sleep disorder with a prevalence of approximately 10%. Even though the link between insomnia and cardiovascular activity is not exactly clear, it is generally assumed that cardiovascular autonomic modifications could occur as a result of sleeplessness, or, alternatively, that autonomic alterations could be an expression of a hyper-arousal state. This review investigates whether cardiovascular measures are different between insomniacs and controls.MethodsElectronic databases were systematically searched, and 34 studies were identified. Heart rate variability features, the association of cardiac and EEG activity, physiologic complexity measures, and cardiovascular activity, assessed by measures such as pre-ejection time, blood pressure, and heart rate dynamics were studied. Given the heterogeneity of the studies, a narrative synthesis of the findings was performed.ResultsThis review study found overall differences in cardiovascular activity between insomniacs and controls in most of the observational studies (21/26), while the expression of cardiovascular regulation varied between the examined insomniac groups. All the studies that investigated the association of cardiac activity and EEG power reported an altered relation between autonomic activity and EEG parameters in insomniacs.ConclusionAutonomic regulation tends to be consistent between insomniacs, as long as they are grouped according to their respective phenotype, as shown in the insomnia subgroup with objectively short sleep duration. Our hypothesis is that these differences in the expression of cardiovascular activity could be explained by the heterogeneity of the disorder. Therefore, the determination of insomnia phenotypes, and the study of cardiovascular measures, rather than heart rate variability alone, will give more insight into the link between insomnia and cardiovascular regulation. This study suggests that cardiovascular activity differs between insomniacs and controls. These new findings are of interest to clinicians and researchers for a more accurate insomnia assessment, and the development of personalized technological solutions in insomnia.

Project description:BACKGROUND: Fabry patients have symptoms and signs compatible with autonomic dysfunction. These symptoms and signs are considered to be due to impairment of the peripheral nervous system, but findings indicative of autonomic neuropathy in other diseases, such as orthostatic intolerance and male sexual dysfunction, are infrequently reported in Fabry disease. The aim of our study was to investigate autonomic symptoms and cardiovascular autonomic function in a large cohort of male and female Fabry patients. METHODS: Forty-eight Fabry patients (15 male, 30 treated with enzyme replacement therapy) and 48 sex- and age-matched controls completed a questionnaire on autonomic symptoms (the Autonomic Symptom Profile). Thirty-six Fabry patients underwent cardiovascular function tests. RESULTS: The Autonomic Symptom Profile revealed a significantly higher sum score in Fabry patients than in healthy control subjects (22 versus 12), but a relatively low score compared to patients with proven autonomic neuropathy. Fabry patients scored worse than healthy controls in the orthostatic intolerance domain. Scores in the male sexual dysfunction domain were comparable between healthy controls and male Fabry patients. The cardiovascular autonomic function tests revealed only mild abnormalities in seven patients. None of these seven patients showed more than one abnormal test result. Enzyme replacement therapy was not associated with less severe disease, lower ASP scores or less frequent abnormal cardiovascular function test results. CONCLUSIONS: Male sexual function and autonomic control of the cardiovascular system are nearly normal in Fabry patients, which cast doubt on the general accepted assumption that autonomic neuropathy is the main cause of symptoms and signs compatible with autonomic dysfunction in Fabry disease. Possibly, end-organ damage plays a key role in the development of symptoms and signs in Fabry patients. An exceptional kind of autonomic neuropathy is another but less likely explanation.

Dataset Information

Genomics of Cardiovascular Measures of Autonomic Tone.

Publications

Genomics of Cardiovascular Measures of Autonomic Tone.

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