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Dive into the research topics where K. Mae Hla is active.

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Featured researches published by K. Mae Hla.


Arteriosclerosis, Thrombosis, and Vascular Biology | 2014

Obstructive Sleep Apnea Is Associated With Future Subclinical Carotid Artery Disease Thirteen-Year Follow-Up From the Wisconsin Sleep Cohort

Sverrir I. Gunnarsson; Paul E. Peppard; Claudia E. Korcarz; Jodi H. Barnet; Susan E. Aeschlimann; Erika W. Hagen; Terry Young; K. Mae Hla; James H. Stein

Objective— To determine the longitudinal associations between obstructive sleep apnea, carotid artery intima-media thickness (IMT), and plaque. Approach and Results— This is a population-based, prospective cohort study conducted from July, 1989, to November, 2012, on 790 randomly selected Wisconsin residents who completed a mean of 3.5 (range, 1–6) polysomnograms during the study period. Obstructive sleep apnea was characterized by the apnea–hypopnea index (AHI, events/h). Common carotid artery IMT and plaque were assessed by B-mode ultrasound. The mean (SD) time from the first polysomnograms to carotid ultrasound was 13.5 (3.6) years. Multivariable regression models were created to estimate the independent associations of baseline and cumulative obstructive sleep apnea exposure with subsequent carotid IMT and plaque. At baseline, the mean age of participants was 47.6 (7.7) years (55% men, 97% white). AHI was 4.4 (9.0) events/h (range, 0–97); 7% had AHI >15 events/h. Carotid IMT was 0.755 (0.161) mm; 63% had plaque. Adjusting for age, sex, body mass index, systolic blood pressure, smoking, and use of lipid-lowering, antihypertensive, and antidiabetic medications, baseline AHI independently predicted future carotid IMT (&bgr;=0.027 mm/unit log10[AHI+1]; P=0.049), plaque presence (odds ratio, 1.55 [95% confidence intervals, 1.02–2.35]; P=0.041) and plaque score (odds ratio, 1.30 [1.05–1.61]; P=0.018). In cumulative risk factor–adjusted models, AHI independently predicted future carotid plaque presence (P=0.012) and score (P=0.039), but not IMT (P=0.608). Conclusions— Prevalent obstructive sleep apnea is independently associated with increased carotid IMT and plaque more than a decade later, indicating increased future cardiovascular disease risk.Objective— To determine the longitudinal associations between obstructive sleep apnea, carotid artery intima-media thickness (IMT), and plaque. Approach and Results— This is a population-based, prospective cohort study conducted from July, 1989, to November, 2012, on 790 randomly selected Wisconsin residents who completed a mean of 3.5 (range, 1–6) polysomnograms during the study period. Obstructive sleep apnea was characterized by the apnea–hypopnea index (AHI, events/h). Common carotid artery IMT and plaque were assessed by B-mode ultrasound. The mean (SD) time from the first polysomnograms to carotid ultrasound was 13.5 (3.6) years. Multivariable regression models were created to estimate the independent associations of baseline and cumulative obstructive sleep apnea exposure with subsequent carotid IMT and plaque. At baseline, the mean age of participants was 47.6 (7.7) years (55% men, 97% white). AHI was 4.4 (9.0) events/h (range, 0–97); 7% had AHI >15 events/h. Carotid IMT was 0.755 (0.161) mm; 63% had plaque. Adjusting for age, sex, body mass index, systolic blood pressure, smoking, and use of lipid-lowering, antihypertensive, and antidiabetic medications, baseline AHI independently predicted future carotid IMT (β=0.027 mm/unit log10[AHI+1]; P =0.049), plaque presence (odds ratio, 1.55 [95% confidence intervals, 1.02–2.35]; P =0.041) and plaque score (odds ratio, 1.30 [1.05–1.61]; P =0.018). In cumulative risk factor–adjusted models, AHI independently predicted future carotid plaque presence ( P =0.012) and score ( P =0.039), but not IMT ( P =0.608). Conclusions— Prevalent obstructive sleep apnea is independently associated with increased carotid IMT and plaque more than a decade later, indicating increased future cardiovascular disease risk. # Significance {#article-title-30}


Journal of Sleep Research | 2015

Minimal nocturnal oxygen saturation predicts future subclinical carotid atherosclerosis: the Wisconsin sleep cohort.

Sverrir I. Gunnarsson; Paul E. Peppard; Claudia E. Korcarz; Jodi H. Barnet; Erika W. Hagen; K. Mae Hla; Mari Palta; Terry Young; James H. Stein

Previous data on the associations between nocturnal oxygen saturation parameters and carotid atherosclerosis are conflicting. We examined the prospective associations of nocturnal oxygen saturation (SaO2) and cardiovascular disease (CVD) risk factors with carotid intima‐media thickness (IMT) and plaques. We used data on 689 Wisconsin sleep cohort participants who had baseline overnight polysomnography followed by carotid ultrasonography a mean (SD) of 7.8 (2.5) years later. Far wall common carotid IMT was measured using B‐mode ultrasound. Bilateral common, bifurcation and internal carotid artery segments were evaluated for plaque score. Participants (8) were aged 56 years (55% male); 32% had hypertension and mean body mass index (BMI) was 31 (7) kg m2. Mean and minimum nocturnal SaO2 were 95% (2) and 86% (7), respectively. Mean percentage sleep time with SaO2 < 90% was 2% (8). Both mean (odds ratio [OR]: 0.60 lower plaque count per 5% higher mean SaO2, 95% confidence interval [CI]: 0.38–0.96, P = 0.033) and minimum SaO2 (OR: 0.88 lower plaque count per 5% higher minimum SaO2, 95% CI: 0.80–0.97, P = 0.013) predicted carotid plaque score after adjusting for age, sex and BMI. Minimum SaO2 predicted future plaque score after adding adjustment for traditional CVD risk factors (OR: 0.90 lower plaque count per 5% higher minimum SaO2, 95% CI: 0.81–0.99, P = 0.038). Mean SaO2 was not associated with carotid IMT after CVD risk factor adjustment. We conclude that minimum nocturnal SaO2 is an independent predictor of future carotid plaque burden. Other nocturnal SaO2 parameters are not associated with future carotid IMT or plaques after adjusting for traditional CVD risk factors.


Journal of the American College of Cardiology | 2014

ASSOCIATION OF NOCTURNAL OXYGEN SATURATION WITH FUTURE SUBCLINICAL CAROTID ARTERY DISEASE: THE WISCONSIN SLEEP COHORT

Sverrir I. Gunnarsson; Paul E. Peppard; Claudia E. Korcarz; Jodi H. Barnet; Erika W. Hagen; K. Mae Hla; Terry Young; James H. Stein

Sleep-disordered breathing (SDB) is associated with increased cardiovascular disease (CVD) risk. However, the contributions of traditional CVD risk factors (e.g., hypertension) relative to SDB are unknown. We evaluated longitudinal associations of nocturnal 02 saturation (SaO2) and CVD risk factors


Arteriosclerosis, Thrombosis, and Vascular Biology | 2014

Obstructive Sleep Apnea Is Associated With Future Subclinical Carotid Artery DiseaseSignificance

Sverrir I. Gunnarsson; Paul E. Peppard; Claudia E. Korcarz; Jodi H. Barnet; Susan E. Aeschlimann; Erika W. Hagen; Terry Young; K. Mae Hla; James H. Stein

Objective— To determine the longitudinal associations between obstructive sleep apnea, carotid artery intima-media thickness (IMT), and plaque. Approach and Results— This is a population-based, prospective cohort study conducted from July, 1989, to November, 2012, on 790 randomly selected Wisconsin residents who completed a mean of 3.5 (range, 1–6) polysomnograms during the study period. Obstructive sleep apnea was characterized by the apnea–hypopnea index (AHI, events/h). Common carotid artery IMT and plaque were assessed by B-mode ultrasound. The mean (SD) time from the first polysomnograms to carotid ultrasound was 13.5 (3.6) years. Multivariable regression models were created to estimate the independent associations of baseline and cumulative obstructive sleep apnea exposure with subsequent carotid IMT and plaque. At baseline, the mean age of participants was 47.6 (7.7) years (55% men, 97% white). AHI was 4.4 (9.0) events/h (range, 0–97); 7% had AHI >15 events/h. Carotid IMT was 0.755 (0.161) mm; 63% had plaque. Adjusting for age, sex, body mass index, systolic blood pressure, smoking, and use of lipid-lowering, antihypertensive, and antidiabetic medications, baseline AHI independently predicted future carotid IMT (&bgr;=0.027 mm/unit log10[AHI+1]; P=0.049), plaque presence (odds ratio, 1.55 [95% confidence intervals, 1.02–2.35]; P=0.041) and plaque score (odds ratio, 1.30 [1.05–1.61]; P=0.018). In cumulative risk factor–adjusted models, AHI independently predicted future carotid plaque presence (P=0.012) and score (P=0.039), but not IMT (P=0.608). Conclusions— Prevalent obstructive sleep apnea is independently associated with increased carotid IMT and plaque more than a decade later, indicating increased future cardiovascular disease risk.Objective— To determine the longitudinal associations between obstructive sleep apnea, carotid artery intima-media thickness (IMT), and plaque. Approach and Results— This is a population-based, prospective cohort study conducted from July, 1989, to November, 2012, on 790 randomly selected Wisconsin residents who completed a mean of 3.5 (range, 1–6) polysomnograms during the study period. Obstructive sleep apnea was characterized by the apnea–hypopnea index (AHI, events/h). Common carotid artery IMT and plaque were assessed by B-mode ultrasound. The mean (SD) time from the first polysomnograms to carotid ultrasound was 13.5 (3.6) years. Multivariable regression models were created to estimate the independent associations of baseline and cumulative obstructive sleep apnea exposure with subsequent carotid IMT and plaque. At baseline, the mean age of participants was 47.6 (7.7) years (55% men, 97% white). AHI was 4.4 (9.0) events/h (range, 0–97); 7% had AHI >15 events/h. Carotid IMT was 0.755 (0.161) mm; 63% had plaque. Adjusting for age, sex, body mass index, systolic blood pressure, smoking, and use of lipid-lowering, antihypertensive, and antidiabetic medications, baseline AHI independently predicted future carotid IMT (β=0.027 mm/unit log10[AHI+1]; P =0.049), plaque presence (odds ratio, 1.55 [95% confidence intervals, 1.02–2.35]; P =0.041) and plaque score (odds ratio, 1.30 [1.05–1.61]; P =0.018). In cumulative risk factor–adjusted models, AHI independently predicted future carotid plaque presence ( P =0.012) and score ( P =0.039), but not IMT ( P =0.608). Conclusions— Prevalent obstructive sleep apnea is independently associated with increased carotid IMT and plaque more than a decade later, indicating increased future cardiovascular disease risk. # Significance {#article-title-30}


Arteriosclerosis, Thrombosis, and Vascular Biology | 2014

Obstructive Sleep Apnea Is Associated With Future Subclinical Carotid Artery Disease

Sverrir I. Gunnarsson; Paul E. Peppard; Claudia E. Korcarz; Jodi H. Barnet; Susan E. Aeschlimann; Erika W. Hagen; Terry Young; K. Mae Hla; James H. Stein

Objective— To determine the longitudinal associations between obstructive sleep apnea, carotid artery intima-media thickness (IMT), and plaque. Approach and Results— This is a population-based, prospective cohort study conducted from July, 1989, to November, 2012, on 790 randomly selected Wisconsin residents who completed a mean of 3.5 (range, 1–6) polysomnograms during the study period. Obstructive sleep apnea was characterized by the apnea–hypopnea index (AHI, events/h). Common carotid artery IMT and plaque were assessed by B-mode ultrasound. The mean (SD) time from the first polysomnograms to carotid ultrasound was 13.5 (3.6) years. Multivariable regression models were created to estimate the independent associations of baseline and cumulative obstructive sleep apnea exposure with subsequent carotid IMT and plaque. At baseline, the mean age of participants was 47.6 (7.7) years (55% men, 97% white). AHI was 4.4 (9.0) events/h (range, 0–97); 7% had AHI >15 events/h. Carotid IMT was 0.755 (0.161) mm; 63% had plaque. Adjusting for age, sex, body mass index, systolic blood pressure, smoking, and use of lipid-lowering, antihypertensive, and antidiabetic medications, baseline AHI independently predicted future carotid IMT (&bgr;=0.027 mm/unit log10[AHI+1]; P=0.049), plaque presence (odds ratio, 1.55 [95% confidence intervals, 1.02–2.35]; P=0.041) and plaque score (odds ratio, 1.30 [1.05–1.61]; P=0.018). In cumulative risk factor–adjusted models, AHI independently predicted future carotid plaque presence (P=0.012) and score (P=0.039), but not IMT (P=0.608). Conclusions— Prevalent obstructive sleep apnea is independently associated with increased carotid IMT and plaque more than a decade later, indicating increased future cardiovascular disease risk.Objective— To determine the longitudinal associations between obstructive sleep apnea, carotid artery intima-media thickness (IMT), and plaque. Approach and Results— This is a population-based, prospective cohort study conducted from July, 1989, to November, 2012, on 790 randomly selected Wisconsin residents who completed a mean of 3.5 (range, 1–6) polysomnograms during the study period. Obstructive sleep apnea was characterized by the apnea–hypopnea index (AHI, events/h). Common carotid artery IMT and plaque were assessed by B-mode ultrasound. The mean (SD) time from the first polysomnograms to carotid ultrasound was 13.5 (3.6) years. Multivariable regression models were created to estimate the independent associations of baseline and cumulative obstructive sleep apnea exposure with subsequent carotid IMT and plaque. At baseline, the mean age of participants was 47.6 (7.7) years (55% men, 97% white). AHI was 4.4 (9.0) events/h (range, 0–97); 7% had AHI >15 events/h. Carotid IMT was 0.755 (0.161) mm; 63% had plaque. Adjusting for age, sex, body mass index, systolic blood pressure, smoking, and use of lipid-lowering, antihypertensive, and antidiabetic medications, baseline AHI independently predicted future carotid IMT (β=0.027 mm/unit log10[AHI+1]; P =0.049), plaque presence (odds ratio, 1.55 [95% confidence intervals, 1.02–2.35]; P =0.041) and plaque score (odds ratio, 1.30 [1.05–1.61]; P =0.018). In cumulative risk factor–adjusted models, AHI independently predicted future carotid plaque presence ( P =0.012) and score ( P =0.039), but not IMT ( P =0.608). Conclusions— Prevalent obstructive sleep apnea is independently associated with increased carotid IMT and plaque more than a decade later, indicating increased future cardiovascular disease risk. # Significance {#article-title-30}


Sleep | 2008

Sleep Disordered Breathing and Mortality: Eighteen-Year Follow-up of the Wisconsin Sleep Cohort

Terry Young; Laurel Finn; Paul E. Peppard; Mariana Szklo-Coxe; Diane Austin; F. Javier Nieto; Robin Stubbs; K. Mae Hla


JAMA Internal Medicine | 1997

Population-Based Study of Sleep-Disordered Breathing as a Risk Factor for Hypertension

Terry Young; Paul E. Peppard; Mari Palta; K. Mae Hla; Laurel Finn; Barbara J. Morgan; James B. Skatrud


JAMA Internal Medicine | 2006

Longitudinal Association of Sleep-Related Breathing Disorder and Depression

Paul E. Peppard; Mariana Szklo-Coxe; K. Mae Hla; Terry Young


Chest | 2002

The Effect of Correction of Sleep-Disordered Breathing on BP in Untreated Hypertension

K. Mae Hla; James B. Skatrud; Laurel Finn; Mari Palta; Terry Young


Sleep | 1996

Snoring as part of a dose-response relationship between sleep-disordered breathing and blood pressure.

Terry Young; Laurel Finn; K. Mae Hla; Barbara J. Morgan; Mari Palta

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Terry Young

University of Wisconsin-Madison

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Paul E. Peppard

University of Wisconsin-Madison

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Claudia E. Korcarz

University of Wisconsin-Madison

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Erika W. Hagen

University of Wisconsin-Madison

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James H. Stein

University of Wisconsin-Madison

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Jodi H. Barnet

University of Wisconsin-Madison

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Laurel Finn

University of Wisconsin-Madison

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Mari Palta

University of Wisconsin-Madison

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Sverrir I. Gunnarsson

University of Wisconsin-Madison

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F. Javier Nieto

University of Wisconsin-Madison

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