AsthmaANASTHMANCT02836691
Autonomic Nervous System Role in Uncontrolled ASTHMA and the Paucigranulocitic Phenotype
A study testing EKG (electrocardiogram) in people with Asthma, run by Fundació Institut de Recerca de l'Hospital de la Santa Creu i Sant Pau at 1 site in Spain.
Trial summary
The autonomic nervous system (ANS) plays an important role in asthma, primarily through the parasympathetic (by the cholinergic pathway) promoting bronchoconstriction. Asthma is a chronic inflammatory disease, however, bronchoconstriction is not always caused by bronchial inflammation, as occurs in paucigranulocitic… Read more about this study
- Who is it for?
- Ages 16 to 70 yearsHealthy volunteers can take part
- Conditions the study is for
- Asthma
- What is being tested?
- EKG (electrocardiogram)
- Type of treatment
- Medical device
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 40 participants
- Where
- 1 siteSpain
- Study dates
- May 2016to 26 Jun 2019
- Phase
- Interventional
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 16 to 70 years
- All sexes
- Healthy volunteers accepted
- Child, Adult, Older adult
Who may be able to join
- Patients of both sexes aged over 16 diagnosed with asthma (according to criteria GEMA 4.0). The diagnosis of asthma is assumed when the patient records stating suggestive previous symptoms of asthma with variable airflow obstruction (determined by spirometry or meter peak flow) or positive bronchodilator test (increase of 12% and 200 ml. of FEV1 after inhalation of a bronchodilator) or positive test to unspecific bronchoconstriction.
Who cannot join
- Asthma exacerbations a month before the visit
- Concomitance of other chronic respiratory diseases (bronchiectasis, fibrosis, etc.)
- Other important comorbidities in the opinion of investigators example: cardiovascular, endocrinological (especially diabetes, mental retardation, psychiatric or neurological disease relevant systemic inflammatory or immune disease
Trial locations and contacts
1 site in 1 country.
About this study
The autonomic nervous system (ANS) plays an important role in asthma, primarily through the parasympathetic (by the cholinergic pathway) promoting bronchoconstriction. Asthma is a chronic inflammatory disease, however, bronchoconstriction is not always caused by bronchial inflammation, as occurs in paucigranulocitic phenotype or noninflammatory asthma. The hypothesis of this project is based on the activation of the parasympathetic nervous system (PNS) would be involved in the pathogenesis of noninflammatory asthma (paucigranulocitic phenotype) and emotional stress and poor control of patients with severe asthma. To determine the ANS involvement in the pathogenesis of paucigranulocItic phenotype in asthma and correlate emotional stress, mediated by the ANS, with uncontrolled severe asthma. 30 asthmatics with different clinical severity (mild, severe controlled and uncontrolled severe) will be recruited , along with a control group of 10 healthy people. Descriptive variables, spirometry, inflammatory parameters (FeNO and inflammatory cell count in induced sputum), blood, saliva, urine and hair to obtain stress markers (glucose, copeptin, prolactin, cortisol) will be collected, and be supplied validated questionnaires of asthma control, quality of life and stress. For monitoring the response of the ANS will be done through an electrocardiogram, recording the heart rate variability (HRV). This analysis is carried out with the collaboration of engineers specialized in the characterization of cardiovascular signals for measuring the ANS.
Read the detailed description
- Role of the ANS in asthma For decades it's considered that the autonomic nervous system (ANS) plays an important role in the pathophysiology and symptomatology of asthma. The ANS had important functions besides regulating airway, such as bronchial smooth muscle tone, secretions, blood flow, microvascular permeability, also acts on migration and release of inflammatory mediators. This complex interaction between inflammation and neuronal control of airway, with effects on inflammatory mediators in neurotransmitters, modulates the inflammatory response (hypersecretion, edema and release of pro-inflammatory mediators as mast cell), through the activation of cholinergic reflex. Cholinergic neuronal pathway has a dominant effect on bronchoconstriction, and therefore represents an excellent therapeutic target. Anticholinergics reduce bronchial hyperresponsiveness to a wide range of bronchoconstriction agents, such as prostanoids, histamine, bradykinin, capsaicin, exercise or allergens.
- ANS and non-inflammatory asthma (paucigranulocitic) In asthma can distinguish different inflammatory phenotypes, commonly typified by the presence of eosinophil's or neutrophils, and that can be performed through non invasive techniques of inflammometric such as exhaled nitric oxide and induced sputum. But it's not always bronchoconstriction mediated by bronchial inflammation. There is a significant proportion of patients with asthma, about 40% in those not objective bronchial inflammation, to that asthma is called noninflammatory asthma or paucigranulocitic phenotype, to proceed with normal levels of eosinophil's and neutrophils in sputum. The pathogenesis of the phenotype is not well defined, although suspected to be caused by strictly mechanical mechanisms diameter of the airway induced nervous stimulation. Among these mechanisms, the PNS could play an important role, however there are no studies that have evaluated the activation of the PNS in different clinical inflammatory disease phenotypes.
- Control of asthma and stress Emotional stress affects the appearance and development of asthma by acting directly on the pathogenic mechanisms of airways, since states of great psychological stress have been associated with impaired adrenal sympathetic system and adrenal-pituitary-hypothalamic axis (APH). The argument that psychological stress influences the autonomic control of the airways is based primarily on the fact that many of the same autonomous mechanisms seem to play a role in asthma are involved in the activation and regulation of the physiological response to stress as chronic stress can alter the APH axis, cortisol secretion which is attenuated, leading to an increase in secretion of inflammatory cytokines.
- Non-Invasive methods to measure the role of ANS Some author's suggest that the altered autonomic control of the caliber of airway in asthma can be reflected through a parallel change in heart rate (HR), as it is shown that in the asthmatic population are more likely to elevated resting heart rate compared to asthmatic population. Asthma and allergy has been associated with an increased activity of the PNS and asthma causes an elevation of heart rate variability (HRV), based on the measurement of basal parasympathetic tone. In fact, the authors asthma severity associated with greater impairment of HRV.
Therefore, evaluation of ANS is of great interest for diagnosis, prognosis and monitoring of this respiratory disorder. Direct evaluation of the PNS is infeasible or impractical in these situations. However, non-invasive evaluation of the PNS is proposed through the HRV according to the standards of measurement, physiological interpretation and clinical use of guides working group of the European Society and American Cardiology and Electrophysiology that are made through the electrocardiogram (ECG).
Ultimately, this research project aims to evaluate in a comprehensive manner the role it can play the ANS in the pathogenesis of asthma, namely the uncontrolled and non-inflammatory asthma severe asthma. The results of this study could provide new clues to understand why other mechanisms of asthma that do not pass through inflammatory. And therefore identification or further characterization of the role of ANS in the disease could generate preliminary evidence on which lay further research aimed at developing new molecules with anticholinergic capacity to treat asthma.
- Conditions
- Asthma
- Being tested
- EKG (electrocardiogram)
- Keywords
- Autonomic nervous system, Uncontrolled severe asthma, Paucigranulocitic asthma phenotype, Stress
- Medical subject headings
- Asthma
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
EKG (electrocardiogram)Device
Analysis of the heart rate variability with an electrocardiogram with a commercial device adapted to asthmatic patients using 12 leads, a respiratory band and a pulseoximeter.
| Study group | Role | What they receive |
|---|---|---|
| EKG to Control subjects | Active comparator | healthy controls without asthma or other respiratory disease. Receives: Device: EKG (electrocardiogram) |
| EKG monitoring Mild asthma | Active comparator | The clinical grade of asthma is assessed in terms of the type of current asthma control (as GEMA Guide 4.0) Receives: Device: EKG (electrocardiogram) |
| EKG monitoring severe control asthma | Active comparator | The clinical grade of asthma is assessed in terms of the type of current asthma control (as GEMA Guide 4.0) Receives: Device: EKG (electrocardiogram) |
| EKG monitoring severe uncontrolled asthma | Active comparator | The clinical grade of asthma is assessed in terms of the type of current asthma control (as GEMA Guide 4.0) Receives: Device: EKG (electrocardiogram) |
What is being measured
The primary outcome is the main question the study is designed to answer.
Heart rate variability (HRV)
Comparison of heart rate variability (HRV) through an EKG among the group of non-inflammatory asthma (paucigranulocitic) with the rest of inflammatory phenotypes of severe asthma analyzed.
Measured: 2 years
Secondary outcomes (7)
Stress
Stress will be evaluated with validated questionnaires. Hospital Anxiety and Depression Scale (HADS)
Measured: 2 years
Glucose (mg/dL)
Blood determination of glucose (mg/dl) as biomarker of emotional stress in patients with severe uncontrolled asthma.
Measured: 2 years
copeptin (pmol/L)
Blood determination of copeptin (pmol/L) as biomarker of emotional stress in patients with severe uncontrolled asthma.
Measured: 2 years
Prolactin (ng/mL)
Blood determination of prolactin (ng/mL) as biomarker of emotional stress in patients with severe uncontrolled asthma.
Measured: 2 years
Salivary cortisol (ng/ml)
Salivary determination of cortisol (ng/ml) as biomarker of emotional stress in patients with severe uncontrolled asthma.
Measured: 2 years
Salivary alpha-amylase U/L
Salivary determination of alpha-amylase U/L as biomarker of emotional stress in patients with severe uncontrolled asthma.
Measured: 2 years
Urine cortisol (mcg/24h)
Urine cortisol (mcg/24h) as biomarker of emotional stress in patients with severe uncontrolled asthma.
Measured: 24 hours
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted19 Jul 2016 (estimated)
- Study startMay 2016
- Primary completionMar 2017
- Study completion26 Jun 2019
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (16)Papers the sponsor has linked to this study.
- Other trials for AsthmaStudies of the same condition, open and under way.
- More trials run by Fundació Institut de Recerca de l'Hospital de la Santa Creu i Sant PauThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Basic science
- Allocation
- Non-randomised
- Intervention model
- Parallel groups
- Masking
- None (open label)
- Enrolment
- 40 participants (actual)
Sponsor and investigators
- Sponsor type
- University, hospital or other
- Collaborators
- Universidad de Zaragoza
- Responsible party
- Sponsor
- Investigators
- Lorena Soto-Retes, physician, Principal investigator, Santa Creu i Sant Pau Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02836691
- Sponsor's protocol ID
- IIBSP-SNA-2015-87
- Acronym
- ANASTHMA
- Status last verified
- Feb 2020
- First submitted
- 5 May 2016
- Last updated
- 17 Feb 2020
- Results posted
- No
- Data monitoring committee
- No
- Individual data sharing
- No
Publications
Kaliner M, Shelhamer JH, Davis PB, Smith LJ, Venter JC. Autonomic nervous system abnormalities and allergy. Ann Intern Med. 1982 Mar;96(3):349-57. doi: 10.7326/0003-4819-96-3-349.
PubMed 6277221Barnes PJ. Neuroeffector mechanisms: the interface between inflammation and neuronal responses. J Allergy Clin Immunol. 1996 Nov;98(5 Pt 2):S73-81; discussion S81-3.
PubMed 8939180Gosens R, Bos IS, Zaagsma J, Meurs H. Protective effects of tiotropium bromide in the progression of airway smooth muscle remodeling. Am J Respir Crit Care Med. 2005 May 15;171(10):1096-102. doi: 10.1164/rccm.200409-1249OC. Epub 2005 Feb 1.
PubMed 15695490Peters SP, Kunselman SJ, Icitovic N, Moore WC, Pascual R, Ameredes BT, Boushey HA, Calhoun WJ, Castro M, Cherniack RM, Craig T, Denlinger L, Engle LL, DiMango EA, Fahy JV, Israel E, Jarjour N, Kazani SD, Kraft M, Lazarus SC, Lemanske RF Jr, Lugogo N, Martin RJ, Meyers DA, Ramsdell J, Sorkness CA, Sutherland ER, Szefler SJ, Wasserman SI, Walter MJ, Wechsler ME, Chinchilli VM, Bleecker ER; National Heart, Lung, and Blood Institute Asthma Clinical Research Network. Tiotropium bromide step-up therapy for adults with uncontrolled asthma. N Engl J Med. 2010 Oct 28;363(18):1715-26. doi: 10.1056/NEJMoa1008770. Epub 2010 Sep 19.
PubMed 20979471Malerba M, Ragnoli B, Radaeli A, Tantucci C. Usefulness of exhaled nitric oxide and sputum eosinophils in the long-term control of eosinophilic asthma. Chest. 2008 Oct;134(4):733-739. doi: 10.1378/chest.08-0763.
PubMed 18842911Schleich FN, Manise M, Sele J, Henket M, Seidel L, Louis R. Distribution of sputum cellular phenotype in a large asthma cohort: predicting factors for eosinophilic vs neutrophilic inflammation. BMC Pulm Med. 2013 Feb 26;13:11. doi: 10.1186/1471-2466-13-11.
PubMed 23442497Douwes J, Gibson P, Pekkanen J, Pearce N. Non-eosinophilic asthma: importance and possible mechanisms. Thorax. 2002 Jul;57(7):643-8. doi: 10.1136/thorax.57.7.643.
PubMed 12096210Wright RJ. Exploring biopsychosocial influences on asthma expression in both the family and community context. Am J Respir Crit Care Med. 2008 Jan 15;177(2):129-30. doi: 10.1164/rccm.200710-1526ED. No abstract available.
PubMed 18165380Haldar P, Pavord ID. Noneosinophilic asthma: a distinct clinical and pathologic phenotype. J Allergy Clin Immunol. 2007 May;119(5):1043-52; quiz 1053-4. doi: 10.1016/j.jaci.2007.02.042.
PubMed 17472810Lehrer PM, Isenberg S, Hochron SM. Asthma and emotion: a review. J Asthma. 1993;30(1):5-21. doi: 10.3109/02770909309066375.
PubMed 8428858Wright RJ, Rodriguez M, Cohen S. Review of psychosocial stress and asthma: an integrated biopsychosocial approach. Thorax. 1998 Dec;53(12):1066-74. doi: 10.1136/thx.53.12.1066.
PubMed 10195081Kallenbach JM, Webster T, Dowdeswell R, Reinach SG, Millar RN, Zwi S. Reflex heart rate control in asthma. Evidence of parasympathetic overactivity. Chest. 1985 May;87(5):644-8. doi: 10.1378/chest.87.5.644.
PubMed 3987376Shah PK, Lakhotia M, Mehta S, Jain SK, Gupta GL. Clinical dysautonomia in patients with bronchial asthma. Study with seven autonomic function tests. Chest. 1990 Dec;98(6):1408-13. doi: 10.1378/chest.98.6.1408.
PubMed 2245682Garrard CS, Seidler A, McKibben A, McAlpine LE, Gordon D. Spectral analysis of heart rate variability in bronchial asthma. Clin Auton Res. 1992 Apr;2(2):105-11. doi: 10.1007/BF01819665.
PubMed 1638105Tokuyama K, Morikawa A, Mitsuhashi M, Mochizuki H, Tajima K, Kuroume T. Beat-to-beat variation of the heart rate in children with allergic asthma. J Asthma. 1985;22(6):285-8. doi: 10.3109/02770908509087111.
PubMed 4077809
Study at a glance
From the registry record, last updated by the sponsor on 17 Feb 2020. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Autonomic Nervous System Role in Uncontrolled ASTHMA and the Paucigranulocitic Phenotype
- ClinicalTrials.gov ID
- NCT02836691
- Acronym / sponsor ID
- ANASTHMA / IIBSP-SNA-2015-87
- Conditions
- Asthma
- Keywords
- Autonomic nervous system, Uncontrolled severe asthma, Paucigranulocitic asthma phenotype, Stress
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 40 participants (actual)
- Lead sponsor
- Fundació Institut de Recerca de l'Hospital de la Santa Creu i Sant PauUniversity, hospital or other
- Collaborators
- Universidad de Zaragoza
- Study start
- May 2016
- Primary completion
- Mar 2017 (actual)
- Study completion
- 26 Jun 2019 (actual)
- First posted
- 19 Jul 2016 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The autonomic nervous system (ANS) plays an important role in asthma, primarily through the parasympathetic (by the cholinergic pathway) promoting bronchoconstriction. Asthma is a chronic inflammatory disease, however, bronchoconstriction is not always caused by bronchial inflammation, as occurs in paucigranulocitic phenotype or noninflammatory asthma. The hypothesis of this project is based on the activation of the parasympathetic nervous system (PNS) would be involved in the pathogenesis of noninflammatory asthma (paucigranulocitic phenotype) and emotional stress and poor control of patients with severe asthma. To determine the ANS involvement in the pathogenesis of paucigranulocItic phenotype in asthma and correlate emotional stress, mediated by the ANS, with uncontrolled severe asthma. 30 asthmatics with different clinical severity (mild, severe controlled and uncontrolled severe) will be recruited , along with a control group of 10 healthy people. Descriptive variables, spirometry, inflammatory parameters (FeNO and inflammatory cell count in induced sputum), blood, saliva, urine and hair to obtain stress markers (glucose, copeptin, prolactin, cortisol) will be collected, and be supplied validated questionnaires of asthma control, quality of life and stress. For monitoring the response of the ANS will be done through an electrocardiogram, recording the heart rate variability (HRV). This analysis is carried out with the collaboration of engineers specialized in the characterization of cardiovascular signals for measuring the ANS.
Detailed description
- Role of the ANS in asthma For decades it's considered that the autonomic nervous system (ANS) plays an important role in the pathophysiology and symptomatology of asthma. The ANS had important functions besides regulating airway, such as bronchial smooth muscle tone, secretions, blood flow, microvascular permeability, also acts on migration and release of inflammatory mediators. This complex interaction between inflammation and neuronal control of airway, with effects on inflammatory mediators in neurotransmitters, modulates the inflammatory response (hypersecretion, edema and release of pro-inflammatory mediators as mast cell), through the activation of cholinergic reflex. Cholinergic neuronal pathway has a dominant effect on bronchoconstriction, and therefore represents an excellent therapeutic target. Anticholinergics reduce bronchial hyperresponsiveness to a wide range of bronchoconstriction agents, such as prostanoids, histamine, bradykinin, capsaicin, exercise or allergens.
- ANS and non-inflammatory asthma (paucigranulocitic) In asthma can distinguish different inflammatory phenotypes, commonly typified by the presence of eosinophil's or neutrophils, and that can be performed through non invasive techniques of inflammometric such as exhaled nitric oxide and induced sputum. But it's not always bronchoconstriction mediated by bronchial inflammation. There is a significant proportion of patients with asthma, about 40% in those not objective bronchial inflammation, to that asthma is called noninflammatory asthma or paucigranulocitic phenotype, to proceed with normal levels of eosinophil's and neutrophils in sputum. The pathogenesis of the phenotype is not well defined, although suspected to be caused by strictly mechanical mechanisms diameter of the airway induced nervous stimulation. Among these mechanisms, the PNS could play an important role, however there are no studies that have evaluated the activation of the PNS in different clinical inflammatory disease phenotypes.
- Control of asthma and stress Emotional stress affects the appearance and development of asthma by acting directly on the pathogenic mechanisms of airways, since states of great psychological stress have been associated with impaired adrenal sympathetic system and adrenal-pituitary-hypothalamic axis (APH). The argument that psychological stress influences the autonomic control of the airways is based primarily on the fact that many of the same autonomous mechanisms seem to play a role in asthma are involved in the activation and regulation of the physiological response to stress as chronic stress can alter the APH axis, cortisol secretion which is attenuated, leading to an increase in secretion of inflammatory cytokines.
- Non-Invasive methods to measure the role of ANS Some author's suggest that the altered autonomic control of the caliber of airway in asthma can be reflected through a parallel change in heart rate (HR), as it is shown that in the asthmatic population are more likely to elevated resting heart rate compared to asthmatic population. Asthma and allergy has been associated with an increased activity of the PNS and asthma causes an elevation of heart rate variability (HRV), based on the measurement of basal parasympathetic tone. In fact, the authors asthma severity associated with greater impairment of HRV.
Therefore, evaluation of ANS is of great interest for diagnosis, prognosis and monitoring of this respiratory disorder. Direct evaluation of the PNS is infeasible or impractical in these situations. However, non-invasive evaluation of the PNS is proposed through the HRV according to the standards of measurement, physiological interpretation and clinical use of guides working group of the European Society and American Cardiology and Electrophysiology that are made through the electrocardiogram (ECG).
Ultimately, this research project aims to evaluate in a comprehensive manner the role it can play the ANS in the pathogenesis of asthma, namely the uncontrolled and non-inflammatory asthma severe asthma. The results of this study could provide new clues to understand why other mechanisms of asthma that do not pass through inflammatory. And therefore identification or further characterization of the role of ANS in the disease could generate preliminary evidence on which lay further research aimed at developing new molecules with anticholinergic capacity to treat asthma.
Study design
- Primary purpose
- Basic science
- Allocation
- Non-randomised
- Intervention model
- Parallel groups
- Masking
- None (open label)
- Number of arms
- 4
| Arm | Type | Receives |
|---|---|---|
| EKG to Control subjects | Active comparator | Device: EKG (electrocardiogram)healthy controls without asthma or other respiratory disease. |
| EKG monitoring Mild asthma | Active comparator | Device: EKG (electrocardiogram)The clinical grade of asthma is assessed in terms of the type of current asthma control (as GEMA Guide 4.0) |
| EKG monitoring severe control asthma | Active comparator | Device: EKG (electrocardiogram)The clinical grade of asthma is assessed in terms of the type of current asthma control (as GEMA Guide 4.0) |
| EKG monitoring severe uncontrolled asthma | Active comparator | Device: EKG (electrocardiogram)The clinical grade of asthma is assessed in terms of the type of current asthma control (as GEMA Guide 4.0) |
Who may qualify
- Ages
- 16 to 70 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Child, Adult, Older adult
Key inclusion criteria (1 listed)
- Patients of both sexes aged over 16 diagnosed with asthma (according to criteria GEMA 4.0). The diagnosis of asthma is assumed when the patient records stating suggestive previous symptoms of asthma with variable airflow obstruction (determined by spirometry or meter peak flow) or positive bronchodilator test (increase of 12% and 200 ml. of FEV1 after inhalation of a bronchodilator) or positive test to unspecific bronchoconstriction.
Key exclusion criteria (3 listed)
- Asthma exacerbations a month before the visit
- Concomitance of other chronic respiratory diseases (bronchiectasis, fibrosis, etc.)
- Other important comorbidities in the opinion of investigators example: cardiovascular, endocrinological (especially diabetes, mental retardation, psychiatric or neurological disease relevant systemic inflammatory or immune disease
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| EKG (electrocardiogram)Analysis of the heart rate variability with an electrocardiogram with a commercial device adapted to asthmatic patients using 12 leads, a respiratory band and a pulseoximeter. | Device | EKG monitoring Mild asthma, EKG monitoring severe control asthma, EKG monitoring severe uncontrolled asthma, EKG to Control subjects |
Primary outcome
Heart rate variability (HRV)
Time frame: 2 years
Comparison of heart rate variability (HRV) through an EKG among the group of non-inflammatory asthma (paucigranulocitic) with the rest of inflammatory phenotypes of severe asthma analyzed.
7 secondary outcomes
Stress
Time frame: 2 years
Glucose (mg/dL)
Time frame: 2 years
copeptin (pmol/L)
Time frame: 2 years
Prolactin (ng/mL)
Time frame: 2 years
Salivary cortisol (ng/ml)
Time frame: 2 years
Salivary alpha-amylase U/L
Time frame: 2 years
Urine cortisol (mcg/24h)
Time frame: 24 hours
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 17 Feb 2020.
- Results publication: PubMed 6277221Kaliner M, Shelhamer JH, Davis PB, Smith LJ, Venter JC. Autonomic nervous system abnormalities and allergy. Ann Intern Med. 1982 Mar;96(3):349-57. doi: 10.7326/0003-4819-96-3-349.
- Results publication: PubMed 8939180Barnes PJ. Neuroeffector mechanisms: the interface between inflammation and neuronal responses. J Allergy Clin Immunol. 1996 Nov;98(5 Pt 2):S73-81; discussion S81-3.
- Results publication: PubMed 15695490Gosens R, Bos IS, Zaagsma J, Meurs H. Protective effects of tiotropium bromide in the progression of airway smooth muscle remodeling. Am J Respir Crit Care Med. 2005 May 15;171(10):1096-102. doi: 10.1164/rccm.200409-1249OC. Epub 2005 Feb 1.
- Results publication: PubMed 20979471Peters SP, Kunselman SJ, Icitovic N, Moore WC, Pascual R, Ameredes BT, Boushey HA, Calhoun WJ, Castro M, Cherniack RM, Craig T, Denlinger L, Engle LL, DiMango EA, Fahy JV, Israel E, Jarjour N, Kazani SD, Kraft M, Lazarus SC, Lemanske RF Jr, Lugogo N, Martin RJ, Meyers DA, Ramsdell J, Sorkness CA, Sutherland ER, Szefler SJ, Wasserman SI, Walter MJ, Wechsler ME, Chinchilli VM, Bleecker ER; National Heart, Lung, and Blood Institute Asthma Clinical Research Network. Tiotropium bromide step-up therapy for adults with uncontrolled asthma. N Engl J Med. 2010 Oct 28;363(18):1715-26. doi: 10.1056/NEJMoa1008770. Epub 2010 Sep 19.
- Results publication: PubMed 18842911Malerba M, Ragnoli B, Radaeli A, Tantucci C. Usefulness of exhaled nitric oxide and sputum eosinophils in the long-term control of eosinophilic asthma. Chest. 2008 Oct;134(4):733-739. doi: 10.1378/chest.08-0763.
- Results publication: PubMed 23442497Schleich FN, Manise M, Sele J, Henket M, Seidel L, Louis R. Distribution of sputum cellular phenotype in a large asthma cohort: predicting factors for eosinophilic vs neutrophilic inflammation. BMC Pulm Med. 2013 Feb 26;13:11. doi: 10.1186/1471-2466-13-11.
- Results publication: PubMed 12096210Douwes J, Gibson P, Pekkanen J, Pearce N. Non-eosinophilic asthma: importance and possible mechanisms. Thorax. 2002 Jul;57(7):643-8. doi: 10.1136/thorax.57.7.643.
- Results publication: PubMed 18165380Wright RJ. Exploring biopsychosocial influences on asthma expression in both the family and community context. Am J Respir Crit Care Med. 2008 Jan 15;177(2):129-30. doi: 10.1164/rccm.200710-1526ED. No abstract available.
- Results publication: PubMed 17472810Haldar P, Pavord ID. Noneosinophilic asthma: a distinct clinical and pathologic phenotype. J Allergy Clin Immunol. 2007 May;119(5):1043-52; quiz 1053-4. doi: 10.1016/j.jaci.2007.02.042.
- Results publication: PubMed 8428858Lehrer PM, Isenberg S, Hochron SM. Asthma and emotion: a review. J Asthma. 1993;30(1):5-21. doi: 10.3109/02770909309066375.
- Results publication: PubMed 10195081Wright RJ, Rodriguez M, Cohen S. Review of psychosocial stress and asthma: an integrated biopsychosocial approach. Thorax. 1998 Dec;53(12):1066-74. doi: 10.1136/thx.53.12.1066.
- Results publication: PubMed 3987376Kallenbach JM, Webster T, Dowdeswell R, Reinach SG, Millar RN, Zwi S. Reflex heart rate control in asthma. Evidence of parasympathetic overactivity. Chest. 1985 May;87(5):644-8. doi: 10.1378/chest.87.5.644.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Lorena Soto-Retes, physician principal investigator
Santa Creu i Sant Pau Hospital
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing EKG (electrocardiogram) in people with Asthma, run by Fundació Institut de Recerca de l'Hospital de la Santa Creu i Sant Pau at 1 site in Spain.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 1 inclusion and 3 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 17 Feb 2020. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Spain. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Heart rate variability (HRV) (time frame: 2 years). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT02836691, which also lists 16 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 17 Feb 2020.