Office Address

John D. Dingell VA Medical Center
4646 John R.
Detroit, MI 48201

Post Graduate Training

Residency, Internal Medicine, Unity Health System-Affiliate of the University of Rochester School of Medicine and Dentistry, Rochester, NY (2005)                 

Fellowship, Pulmonary/Critical Care Medicine, Wayne State University- Detroit Medical Center, Detroit, MI (2008) 

Clinical & Translational Research Training- Columbia Summer Research Institute, Columbia University Medical Center, NY (2011)

Peer-Reviewed Publications

https://scholar.google.com/citations?hl=en&user=-ALgJnwAAAAJ&view_op=list_works&sortby=pubdate

 

Research

(1) Pathogenesis of sleep disordered breathing in patients with chronic spinal cord injury (SCI):

Sleep disorders are common in patients with SCI, whoever little is known about the mechanism of sleep disordered breathing in this population and the effect of different levels of spinal injuries. The central hypothesis is that cervical SCI predispose to breathing instability during sleep more than thoracic injuries, and that repetitive hypoxia may play a role in the serotonin mechanisms that can be used as therapeutic target for new treatment. With a team of collaborators, I was able to first characterize the sleep disturbances in the SCI population and to ascertain predictors of sleep disordered breathing in chronic SCI patients using quantitative polysomnography. This is the first study to assess sleep disordered breathing and ventilation changes comparing two different levels of SCI (cervical vs. thoracic). To assess the contribution of upper airway collapsibility on mechanism of SDB in SCI, passive pharyngeal closing pressure was measured during sleep and we found SCI (both cervical and thoracic) have increased upper airway collapsibility. In addition to assess the effect of cervical vs. thoracic SCI on susceptibility for central sleep apnea, hypocapnic apneic threshold and CO2 reserved were measured during sleep in 24 subjects and we found that tetraplegic patient have more increased risk to develop hypocapnic central apnea. Finally, to assess the effect of intermittent hypoxia on ventilation and cardiac responses in cervical, thoracic and able-bodied subjects, 15 episodes of intermittent hypoxia were induced during wakefulness and we found that cervical SCI had higher ventilatory long-term facilitation. Findings from these mechanistic studies advanced our understanding of the disease in SCI and led us to test two medications to assess the Role of Enhancing Serotonin receptors activity for Sleep apnea Treatment in patients with SCI [REST-SCI].

a. Sankari A; Bascom A; Oomman S; Badr MS. Sleep disordered breathing in chronic spinal cord injury. J Clin Sleep Med. 2014 Jan 15;10(1):65-72.

b. Sankari A, Bascom-Latin A, Chowdhuri S, Badr MS. Tetraplegia is a risk factor for central apnea. J Appl Physiol 2014 Feb 1;116(3):345-53.

c. Sankari A, Bascom AT, Badr MS. Upper airway mechanics in chronic spinal cord injury during sleep. J Appl Physiol 2014 Jun 1;116(11):1390-5.

d. Sankari A, Martin JL, Bascom AT, Mitchell MN, Badr MS. Identification and treatment of sleep-disordered breathing in chronic spinal cord injury. Spinal Cord 12/2014; 53(2).

e. Sankari A, Bascom AT, Riehani A, Badr MS. Tetrapelgia is associated with enhanced peripheral chemoreflex sensitivity and ventilatory long term facilitation. J Appl Physiol japplphysiol.00088.2015. [Epub ahead of print].

(2) Effect of ventilatory motor output on upper airway mechanics during sleep:
The prevailing theory is that upper airway obstruction is an inspiratory phenomenon caused by reduced upper airway muscle activity. However, pharyngeal narrowing occurs during periods of reduced ventilatory motor output, especially in individuals with unfavorable upper airway anatomy, such as patients with obstructive sleep apnea. The central hypothesis is that central hypopnea can lead to airway narrowing due to reduced ventilatory motor output. Previous studies ignored the relative contribution of ventilatory motor output versus lung volume changes to upper airway patency. Therefore, the purpose of this investigation was to determine the effect of ventilatory drive on upper airway patency during inspiration and expiration in healthy humans during spontaneous sleep using a fiberoptic broncoscope and pressure catheter. In this study my collaborators and I demonstrated that expiratory pharyngeal narrowing occurs at the retropalatal area during central hypocapnic hypopnea indicating a possible role in the pathogenesis of upper airway obstruction during sleep. To determine whether the narrowing was due to the effect of hypocapnia not mechanical changes in pressure only, hypocapnic hypoxia was used during sleep in healthy subjects and upper airway resistance was measured. This study demonstrated that hypocapnic but not isocapnic hypoxia was associated with increased expiratory upper airway resistance. This study adds to the field for the first time that central hypopnea results in pharyngeal narrowing at the retropalatal area and predominantly during the expiratory phase.

a- Sankri-Tarbichi AG, Rowley JA, Badr MS. Expiratory Pharyngeal Narrowing during Central Hypocapnic Hypopnea. Am J Respir Crit Care Med. 2009 Feb 15;179(4):313-9.

b- Sankri-Tarbichi AG, Richardson N, Chowdhuri S, Rowley JA, and Badr MS. Hypocapnia is associated with increased upper airway expiratory resistance during sleep. Respir Physiol Neurobiol. 2011 Jul 31;177(2):108-13.

c- Sankri-Tarbichi AG, Rowley JA, and Badr MS. Inhibition of ventilatory motor output increases expiratory retro palatal compliance during sleep. Respir Physiol Neurobiol. 2011 May 31;176(3):136-43.

(3) Relationship between expiratory upper airway narrowing and obstructive lung disorders:
In addition to the contributions described above, with a team of collaborators, I documented the first case of the relationship between expiratory flow limitations/snoring and the presence of obstructive lung disease in patients with sleep disordered breathing. Subsequently with team of collaborators we confirmed this relationship in nearly 100 patients and demonstrated that the presence of expiratory snoring increases the odds of obstructive ventilatory defect measured by PFT more than 10 times.

a- Sankri-Tarbichi AG and Badr MS. What is the cause of the loud snoring- What should be done?. Am J Respir Crit Care Med: 2011: 183;1730.

b- Alchakaki Abdulrazak, Riehani Anas, Mina Nader, M. S. Badr, and Sankari Abdulghani. Expiratory Snoring Predicts Obstructive Pulmonary Disease In Patients With Sleep-Disordered Breathing. In: D30. NOVEL SCREENING APPROACHES AND THERAPIES FOR SLEEP DISORDERED BREATHING. American Thoracic Society, 2014, p. A5612.

(4) Effect of obesity on cardiac function in patients with sleep disordered breathing:
Obesity and heart failure are strongly associated with sleep-disordered breathing. However, the determinants of cardiac dysfunction in patients with SDB are not known. To answer this question we studied 90 patients suspected of having SDB by polysomnography and echocardiography to measure left heart dimensions. The main findings of this study were that obesity can predict cardiovascular morbidity and nocturnal hypoxemia independent of the severity of the SDB. These findings suggest the independent contribution of excess body weight on cardiac dysfunction and hypoxia in SDB patients.

a. Alkatib S, Sankri-Tarbichi A, Badr MS. The impact of obesity on cardiac dysfunction in patients with sleep-disordered breathing. Sleep Breath. 2014 Mar;18(1):137-42.

b. Abdul Ghani Sankri-Tarbichi, Shetha Alkatib, James A. Rowley, and Safwan Badr. Influence Of Obesity On Left Atrial Dimensions In Patients With Sleep Disordered Breathing. B72. CONSEQUENCES OF SLEEP DISORDERED BREATHING: CLINICAL ASPECTS. May 1, 2010, A3682-A3682.

(5) A new approach for diagnosing sleep disordered breathing:

Scoring of hypopnea requires the presence of physiologic consequences, namely de-saturation or arousal. However, the magnitude of de-saturation may depend on weight and baseline pulmonary function. Therefore more sensitive method is needed to determine whether respiratory events that do not meet the hypopnea definition are associated with physiological consequences and possible adverse long term outcome. I led the development of a new method to detect sleep disordered breathing using cardiac autonomic responses from single lead ECG. Preliminary findings were presented in international meetings such as the American Thoracic Society and SLEEP meetings. In addition this method has pending patent application and currently being validated on the Wisconsin sleep cohort database.

a. Maresh S, Bascom A, Berkowski A, Badr M, and Sankari A. Cardiac Autonomic Control In Patients With Chronic Spinal Cord Injury And Sleep-Disordered Breathing. In: A68. PATHOLOGIC SEQUELAE OF SLEEP DISORDERED BREATHING. American Thoracic Society, 2014, p. A2133.

b. Sankari A, Pranathiageswaran S, Maresh S and Badr M. A New Approach To Scoring Sleep Disordered Breathing. SLEEP abstract Supplement, 2015 Volume 38:p. A167. 
 

 

Education

MD: Aleppo University- Faculty of Medicine, Syria

MSMR: Wayne State University- School of Medicine, Michigan

PhD: Wayne State University- School of Medicine, Michigan
 

Faculty Appointments

Professor, Department of Medicine, Wayne State University- School of Medicine, Detroit, MI (2015)

Associate Faculty, Cardiovascular Research Institute (CVRI), Wayne State University- School of Medicine, Detroit, MI (2010)

Assistant Professor, Department of Medicine, Wayne State University- School of Medicine, Detroit, MI (2008-2015)

 

Clinical Interests

- Sleep Disordered Breathing

- Chronic Obstructive Pulmonary Disease (COPD) & Asthma

- Respiratory and sleep disorders in patient with neuromuscular diseases and SCI

Research Interests

Mechanism of sleep-disordered breathing and upper airway narrowing during sleep; Pathogensis of sleep apnea in heart failure and spinal cord injury patients

← Return to listing