Small Degree of Lumbar Lordosis as an Overlooked Determinant for Orthostatic Increases in Blood Pressure in the Elderly: The Nagahama Study.


Journal

American journal of hypertension
ISSN: 1941-7225
Titre abrégé: Am J Hypertens
Pays: United States
ID NLM: 8803676

Informations de publication

Date de publication:
01 01 2019
Historique:
received: 14 06 2018
accepted: 09 09 2018
pubmed: 29 9 2018
medline: 31 3 2020
entrez: 29 9 2018
Statut: ppublish

Résumé

Orthostatic hypertension was associated with worse cardiovascular outcomes, although the factors responsible for an orthostatic rise in blood pressure (BP) are uncertain. We investigated a possible relationship between a stooping posture and orthostatic BP change. Study participants consisted of 1,992 older individuals. Orthostatic BP change was calculated by systolic BP measured at sitting position, and again 1 and 3 minutes after standing up. Spinal alignment and curvature was assessed by guiding the SpinalMouse device on the surface of the skin along the spine. Mean lumbar lordosis at standing position was 13.4° ± 12.4°. The degree of lumbar lordosis was significantly smaller in orthostatic hypertensive individuals (systolic BP change, ≥+20 mm Hg: 3.3° ± 15.6°, ≥+10 mm Hg: 10.4° ± 14.3°) than in individuals who were orthostatic normotensive (14.2° ± 11.9°). Multiple linear regression analysis identified lumbar lordosis (β = -0.171, P < 0.001) and thoracic kyphosis (β = 0.062, P = 0.007), but not sacral inclination (β = 0.033, P = 0.303), as independent determinants for orthostatic BP change. As waist circumference was another independent determinant, the frequency of orthostatic hypertensive individuals was linearly increased with the combination of abdominal obesity and small degree of lumbar lordosis (control: 9.9%, abdominal obesity: 17.4%, small degree of lordosis: 19.4%, both: 24.1%, P < 0.001). Participants who sustained orthostatic hypertension for 3 minutes after standing up had the smallest degree of lumbar lordosis (5.2° ± 16.4°). Stooped posture was an overlooked determinant for orthostatic increases in BP.

Sections du résumé

BACKGROUND
Orthostatic hypertension was associated with worse cardiovascular outcomes, although the factors responsible for an orthostatic rise in blood pressure (BP) are uncertain. We investigated a possible relationship between a stooping posture and orthostatic BP change.
METHODS
Study participants consisted of 1,992 older individuals. Orthostatic BP change was calculated by systolic BP measured at sitting position, and again 1 and 3 minutes after standing up. Spinal alignment and curvature was assessed by guiding the SpinalMouse device on the surface of the skin along the spine.
RESULTS
Mean lumbar lordosis at standing position was 13.4° ± 12.4°. The degree of lumbar lordosis was significantly smaller in orthostatic hypertensive individuals (systolic BP change, ≥+20 mm Hg: 3.3° ± 15.6°, ≥+10 mm Hg: 10.4° ± 14.3°) than in individuals who were orthostatic normotensive (14.2° ± 11.9°). Multiple linear regression analysis identified lumbar lordosis (β = -0.171, P < 0.001) and thoracic kyphosis (β = 0.062, P = 0.007), but not sacral inclination (β = 0.033, P = 0.303), as independent determinants for orthostatic BP change. As waist circumference was another independent determinant, the frequency of orthostatic hypertensive individuals was linearly increased with the combination of abdominal obesity and small degree of lumbar lordosis (control: 9.9%, abdominal obesity: 17.4%, small degree of lordosis: 19.4%, both: 24.1%, P < 0.001). Participants who sustained orthostatic hypertension for 3 minutes after standing up had the smallest degree of lumbar lordosis (5.2° ± 16.4°).
CONCLUSION
Stooped posture was an overlooked determinant for orthostatic increases in BP.

Identifiants

pubmed: 30265274
pii: 5108463
doi: 10.1093/ajh/hpy137
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

61-69

Auteurs

Yasuharu Tabara (Y)

Center for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto Japan.

Mitsuhiro Masaki (M)

Department of Physical Therapy, Human Health Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.

Tome Ikezoe (T)

Department of Physical Therapy, Human Health Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.

Kazuya Setoh (K)

Center for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto Japan.

Takehiro Kato (T)

Department of Physical Therapy, Human Health Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.

Takahisa Kawaguchi (T)

Center for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto Japan.

Shinji Kosugi (S)

Department of Medical Ethics and Medical Genetics, Kyoto University School of Public Health, Kyoto, Japan.

Takeo Nakayama (T)

Department of Health Informatics, Kyoto University School of Public Health, Kyoto, Japan.

Noriaki Ichihashi (N)

Department of Physical Therapy, Human Health Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.

Tadao Tsuboyama (T)

Department of Physical Therapy, Human Health Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.

Fumihiko Matsuda (F)

Center for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto Japan.

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