Interactions Between Autonomic Nervous System Activity and Endothelial Function: A Model for the Development of Cardiovascular Disease

Harris, Kelly F.; Matthews, Karen A.

doi:10.1097/01.psy.0000116719.95524.e2

Cited by 153 publications

(118 citation statements)

References 127 publications

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“…This process presumably becomes outweighed at more advanced stages of HCM. Finally, changes in the autonomic nervous system could also influence microvascular function (12). However, there were no differences in LF/HF or SDNN between control and HCM groups in this study, making the impact of the autonomic nervous system less conceivable.…”

Section: Discussionmentioning

confidence: 47%

Peripheral microvascular function is altered in young individuals at risk for hypertrophic cardiomyopathy and correlates with myocardial diastolic function

Fernlund

Schlegel

Platonov

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Fernlund E, Schlegel TT, Platonov PG, Carlson J, Carlsson M, Liuba P. Peripheral microvascular function is altered in young individuals at risk for hypertrophic cardiomyopathy and correlates with myocardial diastolic function. Am J Physiol Heart Circ Physiol 308: H1351-H1358, 2015. First published March 20, 2015 doi:10.1152/ajpheart.00714.2014.-Hypertrophic cardiomyopathy (HCM) is a major cause of sudden cardiac death in the young. Based on previous reports of functional abnormalities in not only coronary but also peripheral vessels in adults with HCM, we aimed to assess both peripheral vascular and myocardial diastolic function in young individuals with an early stage of HCM and in individuals at risk for HCM. Children, adolescents, and young adults (mean age: 12 yr) with a family history of HCM who either had (HCM group; n ϭ 36) or did not have (HCM-risk group; n ϭ 30) echocardiographydocumented left ventricular (LV) hypertrophy as well as healthy matched controls (n ϭ 85) and healthy young athletes (n ϭ 12) were included in the study. All underwent assessment with 12-lead electrocardiography, two-dimensional echocardiography, tissue Doppler imaging and laser Doppler with transdermal iontophoresis of ACh and sodium nitroprusside. LV thickness and mass were increased in HCM and athlete groups compared with control and HCM-risk groups. The mitral E-to-e= ratio, measured via tissue Doppler, was increased in HCM (P Ͻ 0.0001) and HCM-risk (P Ͻ 0.01) groups compared with control and athlete groups, as were microvascular responses to ACh (HCM group: P ϭ 0.045 and HCM-risk group: P ϭ 0.02). Responses to ACh correlated with the E-to-e= ratio (r ϭ 0.5, P ϭ 0.001). Microvascular responses to sodium nitroprusside were similar in all groups (P Ͼ 0.2). HCM-causing mutations or its familial history are associated with changes in cardiac diastolic function and peripheral microvascular function even before the onset of myocardial hypertrophy. Tissue Doppler can be used to differentiate HCM from physiological LV hypertrophy in young athletes. early diagnosis; myocardial hypertrophy; diastology; endothelium; athletes' heart FAMILIAL HYPERTROPHIC CARDIOMYOPATHY (HCM) is the most common inherited heart disease, being characterized by gradual thickening of cardiac muscle and increased risk for major cardiac events, including ventricular arrhythmias and sudden cardiac death (9, 23). HCM is inherited in an autosomal dominant fashion, with a 50% risk for transmission of the disease-causing mutation to each child of the affected family (23, 24). The risk for HCM-related cardiac events, including sudden cardiac death, appears to be highest in childhood, with a peak incidence of up to 10% during the first decades of life (3,26,29,42). ECGs are often normal through the early phases of hypertrophy (18,25). The diagnosis of HCM, currently based on echocardiographic demonstration of regional or diffuse thickening of the myocardium, is more difficult in younger patients due to the progressive nature of the disease (33, 36). Furthermore, dist...

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Section: Discussionmentioning

confidence: 47%

Peripheral microvascular function is altered in young individuals at risk for hypertrophic cardiomyopathy and correlates with myocardial diastolic function

Fernlund

Schlegel

Platonov

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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“…10,12,15,21 NO is the primary mediator of vasodilation that is released from the vascular endothelium. …”

Section: Discussionmentioning

confidence: 99%

Cervical Ganglion Block Attenuates the Progression of Pulmonary Hypertension via Nitric Oxide and Arginase Pathways

Kim²,

Ryoo³

et al. 2014

Hypertension

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Abstract-It has been recognized that the sympathetic nervous system is activated in pulmonary arterial hypertension (PAH), and abnormal sympathetic hyperactivity leads to worsening of PAH via endothelial dysfunction. The purpose of this study was to examine whether sympathetic ganglion block (SGB) can treat PAH by increasing the availability of nitric oxide (NO). PAH was induced in rats by 50 mg/kg of subcutaneous monocrotaline. After 2 weeks, daily injections of ropivacaine into the left superior cervical ganglion were repeated for 14 days (monocrotaline-SGB group). Monocrotaline group received sham SGB with saline, whereas control group received saline instead of monocrotaline. PAH was evident in monocrotaline group, with right ventricular systolic pressures (47±4 mm Hg) that were higher than those of controls (17±2 mm Hg), whereas SGB significantly attenuated monocrotalineinduced PAH (35±4 mm Hg). The right/left ventricular mass ratios exhibited similar changes to those seen with right ventricular pressures. Heart rate variability showed significantly higher sympathetic activity in the monocrotaline group. Microscopy revealed a higher proportion of muscular arteries with thicker medial walls in the monocrotaline group, which was attenuated by SGB. Monocrotaline induced arginase hyperactivity, which was in turn decreased by SGB-induced endothelial NO synthase activation. SGB restored monocrotaline-induced hypoactivity of superoxide dismutase. In conclusion, SGB could suppress PAH and the remodeling of pulmonary arteries via inactivation of arginase and reciprocal elevation of NO bioavailability, thus attenuating disproportionate hyperactivation of the have been reported to attenuate the severity of symptoms and slow the progression of cardiovascular diseases including coronary artery disease, heart failure, and arrhythmias. According to the previous reports, there is a possibility that direct sympathetic nerve blocks are effective in patients with myocardial ischemia or systemic hypertension. 17,19 Given the relationship between sympathetic nervous system hyperactivity and endothelial dysfunction in patients with PAH, blockade of sympathetic hyperactivity may improve vascular reactivity by preserving endothelial function. To date, however, there is limited amount of data on the therapeutic effects of sympathetic ganglion block (SGB) on PAH. The purpose of the present study is to assess the therapeutic effects of SGB in a monocrotaline-induced PAH rat model. In parallel, we investigated whether SGB could attenuate the changes in arginase and NO bioavailability, as well as oxidative stress caused by monocrotaline. MethodsDetailed methods about animal preparation, experimental design, SGB, heart rate variability, hemodynamic analysis, right ventricular mass, pulmonary vessel morphometry, and NO (synthase)/arginase/ cGMP/oxidative stress assay are described in the online-only Data Supplement. Results Right Ventricular Systolic Pressure and Right Ventricular/Left Ventricular Mass RatioRight ventricular systolic pr...

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“…79) However, the direct effect of the endothelium on alterations in neurotransmitter release, reuptake, or receptor sensitivity requires further investigation. 80) …”

Section: Interaction Between Vascular Function and The Ans In Subjectmentioning

confidence: 99%

The Relationship between Vascular Function and the Autonomic Nervous System

Amiya

Watanabe

Komuro

2014

Annals of Vascular Diseases

108

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Endothelial dysfunction and autonomic nervous system dysfunction are both risk factors for atherosclerosis. There is evidence demonstrating that there is a close interrelationship between these two systems. In hypertension, endothelial dysfunction affects the pathologic process through autonomic nervous pathways, and the pathophysiological process of autonomic neuropathy in diabetes mellitus is closely related with vascular function. However, detailed mechanisms of this interrelationship have not been clearly explained. In this review, we summarize fi ndings concerning the interrelationship between vascular function and the autonomic nervous system from both experimental and clinical studies. The clarifi cation of this interrelationship may provide more comprehensive risk stratifi cation and a new effective therapeutic strategy against atherosclerosis.

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Interactions Between Autonomic Nervous System Activity and Endothelial Function: A Model for the Development of Cardiovascular Disease

Abstract: Although interactions between cardiovascular ANS regulation and endothelial function are likely involved in CVD development, further research is needed to determine whether ANS and endothelium interactions are a plausible pathway linking psychosocial factors with increased CVD risk.

Cited by 153 publications

References 127 publications

Peripheral microvascular function is altered in young individuals at risk for hypertrophic cardiomyopathy and correlates with myocardial diastolic function

Peripheral microvascular function is altered in young individuals at risk for hypertrophic cardiomyopathy and correlates with myocardial diastolic function

Cervical Ganglion Block Attenuates the Progression of Pulmonary Hypertension via Nitric Oxide and Arginase Pathways

The Relationship between Vascular Function and the Autonomic Nervous System

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