Relevant analyses
AltraBio provides statistical expertise to assist with your clinical research projects from inception to publication.
Our statisticians possess extensive experience in analyzing medical data across various therapeutic areas including (but not limited to) neuropsychiatry, neurosciences, pulmonology, immunology, dermatology, cardiology, and rheumatology.
We tailor our solutions to meet the specific needs of our clients, which include human and veterinary pharmaceutical companies, medical device manufacturers, biotechs, cosmetic and nutritional industries, and academic laboratories. Our services span from the development phases to post-market clinical follow-up.
Study design
- Sample size and power calculation
- Writing of the synopsis
- Definition of the analysis methodology
- Development of the Statistical Analysis Plan
Data collection
- Support for writing the Data Management Plan
- Selection of the eCRF
Data processing
- Data extraction
- Formatting in accordance with the standards (CDISC, …)
- Data correction and cleaning (atypical data, missing data, …)
Data Analysis and valorization
- Descriptive methods, comparative analyses, …
- Construction of explanatory or predictive models, …
- Delivery of statistical reports in the form of a pdf or of a dynamic web page, processing algorithms
- Writing of abstracts, posters, research articles
Our Publications In Medical Data Analysis
2020
Patout, Maxime; Gagnadoux, Frédéric; Rabec, Claudio; Trzepizur, Wojciech; Georges, Marjolaine; Perrin, Christophe; Tamisier, Renaud; Pépin, Jean-Louis; Llontop, Claudia; Attali, Valerie; Goutorbe, Frederic; Pontier-Marchandise, Sandrine; Cervantes, Pierre; Bironneau, Vanessa; Portmann, Adriana; Delrieu, Jacqueline; Cuvelier, Antoine; Muir, Jean-François
AVAPS-AE versus ST mode: A randomized controlled trial in patients with obesity hypoventilation syndrome Journal Article
In: Respirology, vol. 25, no. 10, pp. 1073–1081, 2020, ISSN: 1440-1843.
@article{pmid32052923,
title = {AVAPS-AE versus ST mode: A randomized controlled trial in patients with obesity hypoventilation syndrome},
author = {Maxime Patout and Frédéric Gagnadoux and Claudio Rabec and Wojciech Trzepizur and Marjolaine Georges and Christophe Perrin and Renaud Tamisier and Jean-Louis Pépin and Claudia Llontop and Valerie Attali and Frederic Goutorbe and Sandrine Pontier-Marchandise and Pierre Cervantes and Vanessa Bironneau and Adriana Portmann and Jacqueline Delrieu and Antoine Cuvelier and Jean-François Muir},
doi = {10.1111/resp.13784},
issn = {1440-1843},
year = {2020},
date = {2020-10-01},
urldate = {2020-10-01},
journal = {Respirology},
volume = {25},
number = {10},
pages = {1073--1081},
abstract = {BACKGROUND AND OBJECTIVE: Average volume-assured pressure support-automated expiratory positive airway pressure (AVAPS-AE) combines an automated positive expiratory pressure to maintain upper airway patency to an automated pressure support with a targeted tidal volume. The aim of this study was to compare the effects of 2-month AVAPS-AE ventilation versus pressure support (ST) ventilation on objective sleep quality in stable patients with OHS. Secondary outcomes included arterial blood gases, health-related quality of life, daytime sleepiness, subjective sleep quality and compliance to NIV.
METHODS: This is a prospective multicentric randomized controlled trial. Consecutive OHS patients included had daytime P CO > 6 kPa, BMI ≥ 30 kg/m , clinical stability for more than 2 weeks and were naive from home NIV. PSG were analysed centrally by two independent experts. Primary endpoint was sleep quality improvement at 2 months.
RESULTS: Among 69 trial patients, 60 patients had successful NIV setup. Baseline and follow-up PSG were available for 26 patients randomized in the ST group and 30 in the AVAPS-AE group. At baseline, P CO was 6.94 ± 0.71 kPa in the ST group and 6.61 ± 0.71 in the AVAPS-AE group (P = 0.032). No significant between-group difference was observed for objective sleep quality indices. Improvement in P CO was similar between groups with a mean reduction of -0.87 kPa (95% CI: -1.12 to -0.46) in the ST group versus -0.87 kPa (95% CI: -1.14 to -0.50) in the AVAPS-AE group (P = 0.984). Mean NIV use was 6.2 h per night in both groups (P = 0.93). NIV setup duration was shorter in the AVAPS-AE group (P = 0.012).
CONCLUSION: AVAPS-AE and ST ventilation for 2 months had similar impact on sleep quality and gas exchange.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
BACKGROUND AND OBJECTIVE: Average volume-assured pressure support-automated expiratory positive airway pressure (AVAPS-AE) combines an automated positive expiratory pressure to maintain upper airway patency to an automated pressure support with a targeted tidal volume. The aim of this study was to compare the effects of 2-month AVAPS-AE ventilation versus pressure support (ST) ventilation on objective sleep quality in stable patients with OHS. Secondary outcomes included arterial blood gases, health-related quality of life, daytime sleepiness, subjective sleep quality and compliance to NIV.
METHODS: This is a prospective multicentric randomized controlled trial. Consecutive OHS patients included had daytime P CO > 6 kPa, BMI ≥ 30 kg/m , clinical stability for more than 2 weeks and were naive from home NIV. PSG were analysed centrally by two independent experts. Primary endpoint was sleep quality improvement at 2 months.
RESULTS: Among 69 trial patients, 60 patients had successful NIV setup. Baseline and follow-up PSG were available for 26 patients randomized in the ST group and 30 in the AVAPS-AE group. At baseline, P CO was 6.94 ± 0.71 kPa in the ST group and 6.61 ± 0.71 in the AVAPS-AE group (P = 0.032). No significant between-group difference was observed for objective sleep quality indices. Improvement in P CO was similar between groups with a mean reduction of -0.87 kPa (95% CI: -1.12 to -0.46) in the ST group versus -0.87 kPa (95% CI: -1.14 to -0.50) in the AVAPS-AE group (P = 0.984). Mean NIV use was 6.2 h per night in both groups (P = 0.93). NIV setup duration was shorter in the AVAPS-AE group (P = 0.012).
CONCLUSION: AVAPS-AE and ST ventilation for 2 months had similar impact on sleep quality and gas exchange.
METHODS: This is a prospective multicentric randomized controlled trial. Consecutive OHS patients included had daytime P CO > 6 kPa, BMI ≥ 30 kg/m , clinical stability for more than 2 weeks and were naive from home NIV. PSG were analysed centrally by two independent experts. Primary endpoint was sleep quality improvement at 2 months.
RESULTS: Among 69 trial patients, 60 patients had successful NIV setup. Baseline and follow-up PSG were available for 26 patients randomized in the ST group and 30 in the AVAPS-AE group. At baseline, P CO was 6.94 ± 0.71 kPa in the ST group and 6.61 ± 0.71 in the AVAPS-AE group (P = 0.032). No significant between-group difference was observed for objective sleep quality indices. Improvement in P CO was similar between groups with a mean reduction of -0.87 kPa (95% CI: -1.12 to -0.46) in the ST group versus -0.87 kPa (95% CI: -1.14 to -0.50) in the AVAPS-AE group (P = 0.984). Mean NIV use was 6.2 h per night in both groups (P = 0.93). NIV setup duration was shorter in the AVAPS-AE group (P = 0.012).
CONCLUSION: AVAPS-AE and ST ventilation for 2 months had similar impact on sleep quality and gas exchange.
Boussuges, Alain; Rives, Sarah; Marlinge, Marion; Chaumet, Guillaume; Vallée, Nicolas; Guieu, Régis; Gavarry, Olivier
Hyperoxia During Exercise: Impact on Adenosine Plasma Levels and Hemodynamic Data Journal Article
In: Front Physiol, vol. 11, pp. 97, 2020, ISSN: 1664-042X.
@article{pmid32116800,
title = {Hyperoxia During Exercise: Impact on Adenosine Plasma Levels and Hemodynamic Data},
author = {Alain Boussuges and Sarah Rives and Marion Marlinge and Guillaume Chaumet and Nicolas Vallée and Régis Guieu and Olivier Gavarry},
doi = {10.3389/fphys.2020.00097},
issn = {1664-042X},
year = {2020},
date = {2020-01-01},
urldate = {2020-01-01},
journal = {Front Physiol},
volume = {11},
pages = {97},
abstract = {INTRODUCTION: Adenosine is an ATP derivative that is strongly implicated in the cardiovascular adaptive response to exercise. In this study, we hypothesized that during exercise the hyperemia, commonly observed during exercise in air, was counteracted by the downregulation of the adenosinergic pathway during hyperoxic exposure.
METHODS: Ten healthy volunteers performed two randomized sessions including gas exposure (Medical air or Oxygen) at rest and during exercise performed at 40% of maximal intensity, according to the individual fitness of the volunteers. Investigations included the measurement of adenosine plasma level (APL) and the recording of hemodynamic data [i.e., cardiac output (CO) and systemic vascular resistances (SVR) using pulsed Doppler and echocardiography].
RESULTS: Hyperoxia significantly decreased APL (from 0.58 ± 0.06 to 0.21 ± 0.05 μmol L, < 0.001) heart rate and CO and increased SVR in healthy volunteers at rest. During exercise, an increase in APL was recorded in the two sessions when compared with measurements at rest (+0.4 ± 0.4 vs. +0.3 ± 0.2 μmol L for medical air and oxygen exposures, respectively). APL was lower during the exercise performed under hyperoxia when compared with medical air exposure (0.5 ± 0.06 vs. 1.03 ± 0.2 μmol L, respectively < 0.001). This result could contribute to the hemodynamic differences between the two conditions, such as the increase in SVR and the decrease in both heart rate and CO when exercises were performed during oxygen exposure as compared to medical air.
CONCLUSION: Hyperoxia decreased APLs in healthy volunteers at rest but did not eliminate the increase in APL and the decrease in SVR during low intensity exercise.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
INTRODUCTION: Adenosine is an ATP derivative that is strongly implicated in the cardiovascular adaptive response to exercise. In this study, we hypothesized that during exercise the hyperemia, commonly observed during exercise in air, was counteracted by the downregulation of the adenosinergic pathway during hyperoxic exposure.
METHODS: Ten healthy volunteers performed two randomized sessions including gas exposure (Medical air or Oxygen) at rest and during exercise performed at 40% of maximal intensity, according to the individual fitness of the volunteers. Investigations included the measurement of adenosine plasma level (APL) and the recording of hemodynamic data [i.e., cardiac output (CO) and systemic vascular resistances (SVR) using pulsed Doppler and echocardiography].
RESULTS: Hyperoxia significantly decreased APL (from 0.58 ± 0.06 to 0.21 ± 0.05 μmol L, < 0.001) heart rate and CO and increased SVR in healthy volunteers at rest. During exercise, an increase in APL was recorded in the two sessions when compared with measurements at rest (+0.4 ± 0.4 vs. +0.3 ± 0.2 μmol L for medical air and oxygen exposures, respectively). APL was lower during the exercise performed under hyperoxia when compared with medical air exposure (0.5 ± 0.06 vs. 1.03 ± 0.2 μmol L, respectively < 0.001). This result could contribute to the hemodynamic differences between the two conditions, such as the increase in SVR and the decrease in both heart rate and CO when exercises were performed during oxygen exposure as compared to medical air.
CONCLUSION: Hyperoxia decreased APLs in healthy volunteers at rest but did not eliminate the increase in APL and the decrease in SVR during low intensity exercise.
METHODS: Ten healthy volunteers performed two randomized sessions including gas exposure (Medical air or Oxygen) at rest and during exercise performed at 40% of maximal intensity, according to the individual fitness of the volunteers. Investigations included the measurement of adenosine plasma level (APL) and the recording of hemodynamic data [i.e., cardiac output (CO) and systemic vascular resistances (SVR) using pulsed Doppler and echocardiography].
RESULTS: Hyperoxia significantly decreased APL (from 0.58 ± 0.06 to 0.21 ± 0.05 μmol L, < 0.001) heart rate and CO and increased SVR in healthy volunteers at rest. During exercise, an increase in APL was recorded in the two sessions when compared with measurements at rest (+0.4 ± 0.4 vs. +0.3 ± 0.2 μmol L for medical air and oxygen exposures, respectively). APL was lower during the exercise performed under hyperoxia when compared with medical air exposure (0.5 ± 0.06 vs. 1.03 ± 0.2 μmol L, respectively < 0.001). This result could contribute to the hemodynamic differences between the two conditions, such as the increase in SVR and the decrease in both heart rate and CO when exercises were performed during oxygen exposure as compared to medical air.
CONCLUSION: Hyperoxia decreased APLs in healthy volunteers at rest but did not eliminate the increase in APL and the decrease in SVR during low intensity exercise.
2019
Delliaux, Stéphane; Delaforge, Alexis; Deharo, Jean-Claude; Chaumet, Guillaume
Mental Workload Alters Heart Rate Variability, Lowering Non-linear Dynamics Journal Article
In: Front Physiol, vol. 10, pp. 565, 2019, ISSN: 1664-042X.
@article{pmid31156454,
title = {Mental Workload Alters Heart Rate Variability, Lowering Non-linear Dynamics},
author = {Stéphane Delliaux and Alexis Delaforge and Jean-Claude Deharo and Guillaume Chaumet},
doi = {10.3389/fphys.2019.00565},
issn = {1664-042X},
year = {2019},
date = {2019-01-01},
urldate = {2019-01-01},
journal = {Front Physiol},
volume = {10},
pages = {565},
abstract = {Mental workload is known to alter cardiovascular function leading to increased cardiovascular risk. Nevertheless, there is no clear autonomic nervous system unbalance to be quantified during mental stress. We aimed to characterize the mental workload impact on the cardiovascular function with a focus on heart rate variability (HRV) non-linear indexes. A 1-h computerized switching task (letter recognition) was performed by 24 subjects while monitoring their performance (accuracy, response time), electrocardiogram and blood pressure waveform (finger volume clamp method). The HRV was evaluated from the beat-to-beat RR intervals (RRI) in time-, frequency-, and informational- domains, before (Control) and during the task. The task induced a significant mental workload (visual analog scale of fatigue from 27 ± 26 to 50 ± 31 mm, < 0.001, and NASA-TLX score of 56 ± 17). The heart rate, blood pressure and baroreflex function were unchanged, whereas most of the HRV parameters markedly decreased. The maximum decrease occurred during the first 15 min of the task (P1), before starting to return to the baseline values reached at the end of the task (P4). The RRI dimension correlation (D2) decrease was the most significant (P1 vs. Control: 1.42 ± 0.85 vs. 2.21 ± 0.8, < 0.001) and only D2 lasted until the task ended (P4 vs. Control: 1.96 ± 0.9 vs. 2.21 ± 0.9, < 0.05). D2 was identified as the most robust cardiovascular variable impacted by the mental workload as determined by posterior predictive simulations ( = 0.9). The Spearman correlation matrix highlighted that D2 could be a marker of the generated frustration ( = -0.61, < 0.01) induced by a mental task, as well as the myocardial oxygen consumption changes assessed by the double product ( = -0.53, < 0.05). In conclusion, we showed that mental workload sharply lowered the non-linear RRI dynamics, particularly the RRI correlation dimension.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Mental workload is known to alter cardiovascular function leading to increased cardiovascular risk. Nevertheless, there is no clear autonomic nervous system unbalance to be quantified during mental stress. We aimed to characterize the mental workload impact on the cardiovascular function with a focus on heart rate variability (HRV) non-linear indexes. A 1-h computerized switching task (letter recognition) was performed by 24 subjects while monitoring their performance (accuracy, response time), electrocardiogram and blood pressure waveform (finger volume clamp method). The HRV was evaluated from the beat-to-beat RR intervals (RRI) in time-, frequency-, and informational- domains, before (Control) and during the task. The task induced a significant mental workload (visual analog scale of fatigue from 27 ± 26 to 50 ± 31 mm, < 0.001, and NASA-TLX score of 56 ± 17). The heart rate, blood pressure and baroreflex function were unchanged, whereas most of the HRV parameters markedly decreased. The maximum decrease occurred during the first 15 min of the task (P1), before starting to return to the baseline values reached at the end of the task (P4). The RRI dimension correlation (D2) decrease was the most significant (P1 vs. Control: 1.42 ± 0.85 vs. 2.21 ± 0.8, < 0.001) and only D2 lasted until the task ended (P4 vs. Control: 1.96 ± 0.9 vs. 2.21 ± 0.9, < 0.05). D2 was identified as the most robust cardiovascular variable impacted by the mental workload as determined by posterior predictive simulations ( = 0.9). The Spearman correlation matrix highlighted that D2 could be a marker of the generated frustration ( = -0.61, < 0.01) induced by a mental task, as well as the myocardial oxygen consumption changes assessed by the double product ( = -0.53, < 0.05). In conclusion, we showed that mental workload sharply lowered the non-linear RRI dynamics, particularly the RRI correlation dimension.