Increased Sympathetic Nerve Activity in COPD is Associated with Morbidity and Mortality

Andreas, Stefan; Haarmann, Helge; Klarner, S; Hasenfuß, Gerd; Raupach, Tobias

doi:10.1007/s00408-013-9544-7

Cited by 64 publications

(55 citation statements)

References 45 publications

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“…Furthermore, in patients in whom sympathetic hyperactivity is suspected or confirmed, it is virtually impossible to detect among the multiple potential candidate mechanisms, the one(s) responsible. Finally, the prognostic importance of adrenergic overdrive, especially with respect to its independent impact on cardiovascular morbidity and mortality, has been documented in several diseases [77][78][79][80][81][82] but never studied in hypertension. Despite the disappointing results of a large-scale outcome trial, 120 on the protective effect of an antisympathetic agent in the treatment of hypertension, the large amount of data on the participation of sympathetic hyperactivity in the appearance of a blood pressure elevation, the progressive and increasing severity of hypertension over time, and the determination of hypertension-related cardiovascular risk cardiovascular risk justify addressing this issue in further studies.…”

Section: Discussionmentioning

confidence: 99%

The Autonomic Nervous System and Hypertension

Mancia

Grassı

2014

Circulation Research

509

373

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T hat hypertension is due to a derangement of sympathetic and parasympathetic cardiovascular regulation is one of the most widely accredited and tested hypotheses in cardiovascular research. Its proposal followed from the demonstration that autonomic cardiovascular influences play a fundamental role in homeostatic control of the cardiovascular system. In animal models of hypertension, both an increased sympathetic nerve activity and a reduction of vagal cardiac tone are associated with and responsible for the appearance and maintenance of high blood pressure, with their role expanding to include hypertension-related sequelae.1-3 Albeit through a longer and more difficult journey, evidence is now available that similar autonomic alterations may have a causative or cocausative role also in the generation and maintenance of human hypertension. [4][5][6][7] We begin this review by describing the alterations in autonomic cardiovascular control that characterize human hypertension. We then discuss the possible mechanisms underlying these alterations and the evidence that they contribute to the functional and structural changes of the heart and systemic circulation that accompany a chronic hypertensive state and lead to its clinical complications. Finally, we consider the effects of nonpharmacological and pharmacological treatment of hypertension on autonomic cardiovascular control. Our focus is limited to the condition defined as essential or primary hypertension, with no reference to the secondary forms of high blood pressure because secondary hypertension accounts for only a small fraction of the overall prevalence of hypertension 8 and its causes do not include alterations of central or reflex autonomic drive. In addition, the concomitant alterations of sympathetic and parasympathetic cardiovascular control that develop in secondary hypertension have been less extensively documented and remain somewhat controversial. 1,4,6 Autonomic Dysfunction in PrehypertensionAbnormal increases in circulating plasma levels of the adrenergic neurotransmitters norepinephrine and epinephrine The Autonomic Nervous System and Hypertension Giuseppe Mancia, Guido GrassiThis Review is in a thematic series on The Autonomic Nervous System and the Cardiovascular System, which includes the following articles:

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Section: Discussionmentioning

confidence: 99%

The Autonomic Nervous System and Hypertension

Mancia

Grassı

2014

Circulation Research

509

373

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“…High concentrations of epinephrine is thought of as the main cause of the disease [4][5][6], which was supported by several scholars reported that iatrogenic epinephrine could induce SCM [7,8]. Usually individuals with chronic diseases have higher activity of sympathetic nervous system [9][10][11][12], and the hyperactivation of sympathetic nervous system resulted in high concentrations of catecholamines [13]. So we speculated that the susceptibility to the cardiomyopathy may, in part, be related to the chronic disease.…”

Section: Introductionmentioning

confidence: 77%

“…It has been known that the activity of sympathetic nervous system increased in some chronic diseases (such as, hypertension [9], heart failure [10], chronic kidney disease [11], COPD [12]). The hyperactivation of sympathetic nervous system resulted in high concentrations of catecholamines in circulation [13].…”

Section: Scm Profile In Patients With Chronic Diseasesmentioning

confidence: 99%

Stress Cardiomyopathy was Prone to Occur in Patients with Chronic Diseases: Maybe a Good Thing

Chong¹,

Hou²,

Zhang³

2016

Cardiovasc Pharm Open Access

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Background：Stress Cardiomyopathy (SCM) is an increasingly reported disease as a syndrome of acute, severe, but reversible, which is commonly triggered by an acute strong physical or emotional stress. But little is known whether chronic diseases may contribute to the occurrence of SCM.Method：The case reports about SCM from January 1998 to May 2014 were searched in the PubMed using the Medical Subject Headings: "tako-tsubo cardiomyopathy" or "stress cardiomyopathy" or ''ampulla syndrome'' or ''apical ballooning syndrome'' or ''broken heart syndrome''. The publications were excluded which didn't meet the inclusion criteria. SCM patients with and without chronic diseases were CD group and NCD group, respectively. The CD group was further classified into nine subgroups according to underlying chronic diseases. The circulatory diseases group which had the highest percentage in CD group was analyzed further.Results: 1331 literatures about SCM were collected, in which 1052 documents were eligible. In these documents, 1206 patients were reported, 795 had chronic diseases, 411 had no significant past medical history. The average age in NCD group was younger than that in CD group (57.3 ± 0.9 years versus 62.4 ± 0.6 years, P < 0.01). The number of SCM patients with Circulatory diseases was the most, then was Endocrine, Digestive, Respiratory, etc. The proportion of hypertension was 74.0% in circulatory diseases followed by dyslipidemia 29.3%, arrhythmia 10.1%, coronary artery disease 5.8%, etc.Conclusion：According to our results, the chronic diseases, especially hypertension, rose the rate of occurrence and delayed the onset age of SCM.

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“…Similarly, in the present patient population, activation of the sympathetic nervous system by hypoxaemia could result in changes in bowel perfusion and subsequently contribute to the observed intestinal barrier loss. In stable COPD, it has been shown that an imbalance in auto-regulation of the cardiac rhythm leads to arrhythmias and that sympathetic activation is related to a higher rate of hospitalizations and mortality in COPD [50, 51]. …”

Section: Discussionmentioning

confidence: 99%

Increased Small Intestinal Permeability during Severe Acute Exacerbations of COPD

et al. 2018

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Background: Disturbances of intestinal integrity, manifested by increased gastro-intestinal (GI) permeability, have been found in chronic obstructive pulmonary disease (COPD) patients during physical activity, often associated with intermittent hypoxic periods. Evidence about extrapulmonary organ disturbances, especially of the GI tract, during hospitalised acute exacerbation of COPD (AE-COPD) with hypoxaemic respiratory failure (RF) is lacking. Objective: The aim was to assess changes in GI permeability in patients with AE-COPD and during recovery 4 weeks later. Methods: All patients admitted to our hospital with AE-COPD accompanied by hypoxaemia at admission (PaO₂ <8.7 kPa or O₂ saturation <93%) were screened between October 2013 and February 2014. Patients with a history of GI or renal disease, chronic heart failure, or use of non-steroidal anti-inflammatory drugs in the 48 h before the test were excluded. GI permeability was assessed by evaluating urinary excretion ratios of the orally ingested sugars lactulose/L-rhamnose (L/R ratio), sucrose/L-rhamnose (Su/R ratio) and sucralose/erythritol (S/E ratio). Results: Seventeen patients with severe to very severe COPD completed the study. L/R ratio (×10³) at admission of AE-COPD was significantly higher than in the recovery condition (40.9 [29.4–49.6] vs. 27.3 [19.5–47.7], p = 0.039), indicating increased small intestinal permeability. There were no significant differences in the individual sugar levels in urine nor in the 0- to 5-h urinary S/E and Su/R ratios between the 2 visits. Conclusion: This is the first study showing increased GI permeability during hospitalised AE-COPD accompanied by hypoxaemic RF. Therefore, GI integrity in COPD patients is an attractive target for future research and for the development of interventions to alleviate the consequences of AE-COPD.

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Increased Sympathetic Nerve Activity in COPD is Associated with Morbidity and Mortality

Abstract: Our data suggest that sympathetic activation is related to adverse outcome in COPD. Although this finding has to be replicated in larger studies, it implies that neurohumoral activation could be a potential therapeutic target in COPD.

Cited by 64 publications

References 45 publications

The Autonomic Nervous System and Hypertension

The Autonomic Nervous System and Hypertension

Stress Cardiomyopathy was Prone to Occur in Patients with Chronic Diseases: Maybe a Good Thing

Increased Small Intestinal Permeability during Severe Acute Exacerbations of COPD

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