Lia Bittencourt

Dr. Lia Bittencourt

orcid

Research Focus & Metrics

Academic Career Length

48Years (1979-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 May 2010 in Sleep Medicine
Verified
Journal Article
Closed access
STSergio Tufik
Sergio Tufik
RSRogerio Santos-Silva
Rogerio Santos-Silva
JTJose Augusto Taddei
Jose Augusto Taddei
LBLia Bittencourt
Lia Bittencourt

1 September 2016 in The Lancet Respiratory Medicine
Verified
Journal Article
Closed access
HMHelena Marti-Soler
Helena Marti-Soler
CHCamila Hirotsu
Camila Hirotsu
Pedro Marques-VidalPedro Marques-Vidal
Pedro Marques-Vidal
PVPeter Vollenweider
Peter Vollenweider
GWGérard Waeber
Gérard Waeber
RHRaphael Heinzer
Raphael Heinzer

5 January 2018 in SLEEP
Verified
Journal Article
Open access
PDF file
BKBrendan T Keenan
Brendan T Keenan
JKJinyoung Kim
Jinyoung Kim
BSBhajan Singh
Bhajan Singh
LBLia Bittencourt
Lia Bittencourt
NCNing-Hung Chen
Ning-Hung Chen
APAllan I Pack
Allan I Pack
A recent study of patients with moderate–severe obstructive sleep apnea (OSA) in Iceland identified three clinical clusters based on symptoms and comorbidities. We sought to verify this finding in a new cohort in Iceland and examine the generalizability of OSA clusters in an international ethnically diverse cohort. Using data on 972 patients with moderate–severe OSA (apnea–hypopnea index [AHI] ≥ 15 events per hour) recruited from the Sleep Apnea Global Interdisciplinary Consortium (SAGIC), we performed a latent class analysis of 18 self-reported symptom variables, hypertension, cardiovascular disease, and diabetes. The original OSA clusters of disturbed sleep, minimally symptomatic, and excessively sleepy replicated among 215 SAGIC patients from Iceland. These clusters also generalized to 757 patients from five other countries. The three clusters had similar average AHI values in both Iceland and the international samples, suggesting clusters are not driven by OSA severity; differences in age, gender, and body mass index were also generally small. Within the international sample, the three original clusters were expanded to five optimal clusters: three were similar to those in Iceland (labeled disturbed sleep, minimal symptoms, and upper airway symptoms with sleepiness) and two were new, less symptomatic clusters (labeled upper airway symptoms dominant and sleepiness dominant). The five clusters showed differences in demographics and AHI, although all were middle-aged (44.6–54.5 years), obese (30.6–35.9 kg/m2), and had severe OSA (42.0–51.4 events per hour) on average. Results confirm and extend previously identified clinical clusters in OSA. These clusters provide an opportunity for a more personalized approach to the management of OSA.

20 May 2013 in Journal of Dental Research
Verified
Journal Article
Closed access
PDF file
MMM. Maluly
M. Maluly
MAM.L. Andersen
M.L. Andersen
CDC. Dal-Fabbro
C. Dal-Fabbro
SGS. Garbuio
S. Garbuio
LBLia Bittencourt
Lia Bittencourt
STSergio Tufik
Sergio Tufik
The goal of the current study was to estimate the prevalence of sleep bruxism (SB) in the general population using a representative sample of 1,042 individuals who answered questionnaires and underwent polysomnography (PSG) examinations. After PSG, the individuals were classified into 3 groups: absence of SB, low-frequency SB, and high-frequency SB. The results indicated that the prevalence of SB, indicated by questionnaires and confirmed by PSG, was 5.5%. With PSG used exclusively as the criterion for diagnosis, the prevalence was 7.4% regardless of SB self-reported complaints. With questionnaires alone, the prevalence was 12.5%. Of the 5.5% (n = 56) with confirmed SB, 26 were classified as low-frequency SB, and 30 as high-frequency. The episodes of SB were more frequent in stage 2 sleep, and the phasic bruxism events were more frequent than tonic or mixed events in all sleep stages in individuals with SB. A positive association was observed between SB and insomnia, higher degree of schooling, and a normal/overweight body mass index (BMI). These findings demonstrate the prevalence of SB in a population sampled by PSG, the gold standard methodology in the investigation of sleep disorders, combined with validated questionnaires (ClinicalTrials.gov, NCT00596713).

1 April 2014 in Sleep Medicine
Verified
Journal Article
Closed access
WMWalter Moraes
Walter Moraes
RPRonaldo Piovezan
Ronaldo Piovezan
DPDalva Poyares
Dalva Poyares
LBLia Bittencourt
Lia Bittencourt
RSRogerio Santos-Silva
Rogerio Santos-Silva
STSergio Tufik
Sergio Tufik

1 December 2014 in Journal Of Hypertension
Verified
Journal Article
Closed access
IIImran H. Iftikhar
Imran H. Iftikhar
CVChristopher W. Valentine
Christopher W. Valentine
LBLia Bittencourt
Lia Bittencourt
DCDebbie L. Cohen
Debbie L. Cohen
AFAnnette C. Fedson
Annette C. Fedson
UMUlysses J. Magalang
Ulysses J. Magalang
Objective: To systematically analyze the studies that have examined the effect of continuous positive airway pressure (CPAP) on blood pressure (BP) in patients with resistant hypertension and obstructive sleep apnea (OSA). Methods: Design – meta-analysis of observational studies and randomized controlled trials (RCTs) indexed in PubMed and Ovid (All [email protected]). participants: individuals with resistant hypertension and OSA; interventions – CPAP treatment. Results: A total of six studies met the inclusion criteria for preintervention to postintervention analyses. The pooled estimates of mean changes after CPAP treatment for the ambulatory (24-h) SBP and DBP from six studies were −7.21 mmHg [95% confidence interval (CI): −9.04 to −5.38; P < 0.001; I2 58%) and −4.99 mmHg (95% CI: −6.01 to −3.96; P < 0.001; I2 31%), respectively. The pooled estimate of the ambulatory SBP and DBP from the four RCTs showed a mean net change of −6.74 mmHg [95% CI: −9.98 to −3.49; P < 0.001; I2 61%] and −5.94 mmHg (95% CI: −9.40 to −2.47; P = 0.001; I2 76%), respectively, in favor of the CPAP group. Conclusion: The pooled estimate shows a favorable reduction of BP with CPAP treatment in patients with resistant hypertension and OSA. The effects sizes are larger than those previously reported in patients with OSA without resistant hypertension.