The DOI matches its Crossref record; 44 of the 45 references it cites were found in a registry or an index.
Left Ventricular Hypertrophy in Severe Obesity: Interactions Among Blood Pressure, Nocturnal Hypoxemia, and Body Mass
Abstract
Obese subjects have a high prevalence of left ventricular (LV) hypertrophy. It is unclear to what extent LV hypertrophy results directly from obesity or from associated conditions, such as hypertension, impaired glucose homeostasis, or obstructive sleep apnea. We tested the hypothesis that LV hypertrophy in severe obesity is associated with additive effects from each of the major comorbidities. Echocardiography and laboratory testing were performed in 455 severely obese subjects with body mass index 35 to 92 kg/m 2 and 59 nonobese reference subjects. LV hypertrophy, defined by allometrically corrected (LV mass/height 2.7 ), gender-specific criteria, was present in 78% of the obese subjects. Multivariable regression analyses showed that average nocturnal oxygen saturation <85% was the strongest independent predictor of LV hypertrophy ( P <0.001), followed by systolic blood pressure ( P <0.015) and then body mass index ( P <0.05). With regard to LV mass, there were synergistic effects between hypertension and body mass index ( P interaction <0.001) and between hypertension and reduced nocturnal oxygen saturation. Severely obese subjects had normal LV endocardial fractional shortening (35±6% versus 35±6%) but mildly decreased midwall fractional shortening (15±2% versus 17±2%; P <0.001), indicating subtle myocardial dysfunction. In conclusion, more severe nocturnal hypoxemia, increasing systolic blood pressure, and body mass index are all independently associated with increased LV mass. The effects of increased blood pressure seem to amplify those of sleep apnea and more severe obesity.
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In the citing paper
“In addition, the results indicate that both LV cavity size and wall thickness are increased in obese subjects compared with age-matched controls (22, 134, 151, 156, 242, 279, 377).”
From Cardiac remodeling in obesity (2008) · cites this paper as [22]
In the citing paper
“Many published studies have concluded that obesity is independently associated with LV hypertrophy (22, 28, 63, 72, 116, 235, 242, 266, 279, 284, 377).”
From Cardiac remodeling in obesity (2008) · cites this paper as [22]
In the citing paper
“The more recent data confirm the increased prevalence of LV hypertrophy in obese subjects.”
From Cardiac remodeling in obesity (2008) · cites this paper as [22]
In the citing paper
“Many studies have shown increased LA dimensions in obese subjects compared with normal-weight control subjects (16, 17, 22, 140, 274, 371, 375).”
From Cardiac remodeling in obesity (2008) · cites this paper as [22]
In the citing paper
“Various authors have reported depressed LV ejection fraction (EF) (15, 68, 100), normal EF (22, 111, 116, 191, 242, 266, 279, 377), and supernormal EF (28, 155, 274, 375) in obese subjects.”
From Cardiac remodeling in obesity (2008) · cites this paper as [22]
In the citing paper
“More recently, however, several studies have found that LV ejection fraction is normal or even supranormal in the majority of obese subjects, even those with severe obesity (22, 28, 155, 191, 242, 274, 279, 375, 377).”
From Cardiac remodeling in obesity (2008) · cites this paper as [22]
In the citing paper
“Indeed, obese subjects have generally been found to have subclinical contractile abnormalities when assessed with the aforementioned techniques (21, 22, 71, 279, 377).”
From Cardiac remodeling in obesity (2008) · cites this paper as [22]
In the citing paper
“Unfortunately, this relatively straightforward and logical hypothesis is complicated by the fact that multiple recent studies have shown a predominance of concentric geometry in obese patients (22, 63, 72, 279, 377).”
From Cardiac remodeling in obesity (2008) · cites this paper as [22]
In the citing paper
“Higher systolic blood pressures, even if they are not in the hypertensive range, are associated with a greater extent of LV hypertrophy in obesity (22).”
From Cardiac remodeling in obesity (2008) · cites this paper as [22]
In the citing paper
“The presence of diabetes, or measures of insulin resistance, was not predictive of LV mass in the mainly Caucasian, middle-aged women studies by Avelar et al. (22).”
From Cardiac remodeling in obesity (2008) · cites this paper as [22]
In the citing paper
“Several studies have shown synergistic effects between increasing BMI and increasing systolic blood pressure (22, 72).”
From Cardiac remodeling in obesity (2008) · cites this paper as [22]
In the citing paper
“Although some studies have failed to show a relationship between sleep apnea and LV hypertrophy, the majority do support such an association (18, 22, 69, 250, 256–258, 284, 287, 331, 373).”
From Cardiac remodeling in obesity (2008) · cites this paper as [22]
In the citing paper
“Rather, growing data suggest that nocturnal oxygen de-saturation may be the true culprit (22, 69).”
From Cardiac remodeling in obesity (2008) · cites this paper as [22]
In the citing paper
“Avelar et al. (22) reported that in a predominantly Caucasian female population with severe obesity, the degree of LV hypertrophy was related to BMI, systolic blood pressure, and the severity of nocturnal hypoxemia (22).”
From Cardiac remodeling in obesity (2008) · cites this paper as [22]
In the citing paper
“In this study, a diagnosis of hypertension or an average nocturnal O2 saturation <85% each had synergistic interactions with increasing BMI.”
From Cardiac remodeling in obesity (2008) · cites this paper as [22]
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Drazner, M. H. (2011) · Cited by 1
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Cardiovascular Damage in Obesity and Metabolic Syndrome
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Modulation of the Cardiomyocyte Hypertrophic Responses to Endothelin-1 by Adipocytes
Bairwa, S. C. (2014) · Scholarship@Western (Western University)
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Vengethasamy, L. (2010) · University of the Witwatersrand, Johannesburg Institutional Repository on DSpace (University of the Witwatersrand, Johannesburg)
Severe Obesity and Left Ventricular Geometry
SIMONE, G. D. (2015)
Metadata
- Authors
- Avelar, E., Cloward, T. V., Walker, J. M., Farney, R. J., Strong, M., Pendleton, R. C., Segerson, N., Adams, T. D., Gress, R. E., Hunt, S. C., & Litwin, S. E.
- Affiliations
- Intermountain Healthcare (US)
- Venue
- Hypertension
- Published
- 2007-01
- Volume
- 49
- Issue
- 1
- Pages
- 34-39
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2154952676
- Cited by
- 228
- References
- 45
- Citations by year
- 2026: 3 · 2025: 12 · 2024: 10 · 2023: 8 · 2022: 11 · 2021: 12 · 2020: 17 · 2019: 10 · 2018: 7 · 2017: 16 · 2016: 13 · 2015: 9 · 2014: 16 · 2013: 21 · 2012: 6
- FWCI
- 7.38
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (T32-HL-7576, T32HL007576)
- National Institute of Diabetes and Digestive and Kidney Diseases (5R01DK0550006-05, R01DK055006)
- National Center for Research Resources (M01-RR 00064, M01RR000064)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Health Sciences › Medicine › Physiology (medical) › Obstructive Sleep Apnea Research
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- left ventricular hypertrophy, morbid obesity, nocturnal hypoxemia, obstructive sleep apnea, body mass index, left ventricular mass, fractional shortening, cardiac dysfunction, comorbidities
- MeSH terms
- Adult, Hypoxia, Blood Pressure, Body Weight, Circadian Rhythm, Echocardiography, Female, Heart, Humans, Male, Middle Aged, Obesity, Morbid, Prognosis, Sleep Apnea Syndromes, Systole, Hypertrophy, Left Ventricular
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