Clustered metabolic abnormalities blunt regression of hypertensive left ventricular hypertrophy: the LIFE study

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Clustered metabolic abnormalities blunt regression of hypertensive left ventricular hypertrophy: the LIFE study. / de Simone, G; Okin, P M; Gerdts, E; Olsen, M H; Wachtell, K; Hille, D A; Dahlöf, B; Kjeldsen, S E; Devereux, R B.

I: Nutrition, Metabolism & Cardiovascular Diseases, Bind 19, Nr. 9, 2009, s. 634-40.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

de Simone, G, Okin, PM, Gerdts, E, Olsen, MH, Wachtell, K, Hille, DA, Dahlöf, B, Kjeldsen, SE & Devereux, RB 2009, 'Clustered metabolic abnormalities blunt regression of hypertensive left ventricular hypertrophy: the LIFE study', Nutrition, Metabolism & Cardiovascular Diseases, bind 19, nr. 9, s. 634-40. https://doi.org/10.1016/j.numecd.2008.12.012

APA

de Simone, G., Okin, P. M., Gerdts, E., Olsen, M. H., Wachtell, K., Hille, D. A., Dahlöf, B., Kjeldsen, S. E., & Devereux, R. B. (2009). Clustered metabolic abnormalities blunt regression of hypertensive left ventricular hypertrophy: the LIFE study. Nutrition, Metabolism & Cardiovascular Diseases, 19(9), 634-40. https://doi.org/10.1016/j.numecd.2008.12.012

Vancouver

de Simone G, Okin PM, Gerdts E, Olsen MH, Wachtell K, Hille DA o.a. Clustered metabolic abnormalities blunt regression of hypertensive left ventricular hypertrophy: the LIFE study. Nutrition, Metabolism & Cardiovascular Diseases. 2009;19(9):634-40. https://doi.org/10.1016/j.numecd.2008.12.012

Author

de Simone, G ; Okin, P M ; Gerdts, E ; Olsen, M H ; Wachtell, K ; Hille, D A ; Dahlöf, B ; Kjeldsen, S E ; Devereux, R B. / Clustered metabolic abnormalities blunt regression of hypertensive left ventricular hypertrophy: the LIFE study. I: Nutrition, Metabolism & Cardiovascular Diseases. 2009 ; Bind 19, Nr. 9. s. 634-40.

Bibtex

@article{f6e67fc064ba11df928f000ea68e967b,
title = "Clustered metabolic abnormalities blunt regression of hypertensive left ventricular hypertrophy: the LIFE study",
abstract = "BACKGROUND AND AIMS: Clusters of metabolic abnormalities resembling phenotypes of metabolic syndrome predicted outcome in the LIFE study, independently of single risk markers, including obesity, diabetes and baseline ECG left ventricular hypertrophy (LVH). We examined whether clusters of two or more metabolic abnormalities (MetAb, including obesity, high plasma glucose without diabetes, low HDL-cholesterol) in addition to hypertension were associated to levels of ECG LVH reduction comparable to that obtained in hypertensive subjects without or with only one additional metabolic abnormality (no-MetAb). METHODS AND RESULTS: We studied 5558 non-diabetic participants without MetAb (2920 women) and 1235 with MetAb (751 women) from the LIFE-study cohort. MetAb was defined by reported LIFE criteria, using partition values from the ATPIII recommendations. Time-trends of Cornell voltage-duration product (CP) over 5 years was assessed using a quadratic polynomial contrast, adjusting for age, sex, prevalent cardiovascular disease and treatment arm (losartan or atenolol). At baseline, despite similar blood pressures, CP was greater in the presence than in the absence of MetAb (p<0.0001). During follow-up, despite similar reduction of blood pressure, CP decreased less in patients with than in those without MetAb, even after adjustment for the respective baseline values (both p<0.002). Losartan was more effective than atenolol in reducing CP independently of MetAb. CONCLUSIONS: Clusters of metabolic abnormalities resembling phenotypes of metabolic syndrome are related to greater initial ECG LVH in hypertensive patients with value of blood pressure similar to individuals without metabolic abnormalities, and are associated with less reduction of ECG LVH during antihypertensive therapy, potentially contributing to the reported adverse prognosis of metabolic syndrome.",
author = "{de Simone}, G and Okin, {P M} and E Gerdts and Olsen, {M H} and K Wachtell and Hille, {D A} and B Dahl{\"o}f and Kjeldsen, {S E} and Devereux, {R B}",
note = "Keywords: Aged; Blood Glucose; Blood Pressure; Cholesterol; Cluster Analysis; Cohort Studies; Diabetes Mellitus; Echocardiography; Electrocardiography; Female; Follow-Up Studies; Humans; Hypertension; Hypertrophy, Left Ventricular; Male; Middle Aged; Obesity; Prevalence; Risk Factors",
year = "2009",
doi = "10.1016/j.numecd.2008.12.012",
language = "English",
volume = "19",
pages = "634--40",
journal = "Nutrition, Metabolism & Cardiovascular Diseases",
issn = "0939-4753",
publisher = "Elsevier",
number = "9",

}

RIS

TY - JOUR

T1 - Clustered metabolic abnormalities blunt regression of hypertensive left ventricular hypertrophy: the LIFE study

AU - de Simone, G

AU - Okin, P M

AU - Gerdts, E

AU - Olsen, M H

AU - Wachtell, K

AU - Hille, D A

AU - Dahlöf, B

AU - Kjeldsen, S E

AU - Devereux, R B

N1 - Keywords: Aged; Blood Glucose; Blood Pressure; Cholesterol; Cluster Analysis; Cohort Studies; Diabetes Mellitus; Echocardiography; Electrocardiography; Female; Follow-Up Studies; Humans; Hypertension; Hypertrophy, Left Ventricular; Male; Middle Aged; Obesity; Prevalence; Risk Factors

PY - 2009

Y1 - 2009

N2 - BACKGROUND AND AIMS: Clusters of metabolic abnormalities resembling phenotypes of metabolic syndrome predicted outcome in the LIFE study, independently of single risk markers, including obesity, diabetes and baseline ECG left ventricular hypertrophy (LVH). We examined whether clusters of two or more metabolic abnormalities (MetAb, including obesity, high plasma glucose without diabetes, low HDL-cholesterol) in addition to hypertension were associated to levels of ECG LVH reduction comparable to that obtained in hypertensive subjects without or with only one additional metabolic abnormality (no-MetAb). METHODS AND RESULTS: We studied 5558 non-diabetic participants without MetAb (2920 women) and 1235 with MetAb (751 women) from the LIFE-study cohort. MetAb was defined by reported LIFE criteria, using partition values from the ATPIII recommendations. Time-trends of Cornell voltage-duration product (CP) over 5 years was assessed using a quadratic polynomial contrast, adjusting for age, sex, prevalent cardiovascular disease and treatment arm (losartan or atenolol). At baseline, despite similar blood pressures, CP was greater in the presence than in the absence of MetAb (p<0.0001). During follow-up, despite similar reduction of blood pressure, CP decreased less in patients with than in those without MetAb, even after adjustment for the respective baseline values (both p<0.002). Losartan was more effective than atenolol in reducing CP independently of MetAb. CONCLUSIONS: Clusters of metabolic abnormalities resembling phenotypes of metabolic syndrome are related to greater initial ECG LVH in hypertensive patients with value of blood pressure similar to individuals without metabolic abnormalities, and are associated with less reduction of ECG LVH during antihypertensive therapy, potentially contributing to the reported adverse prognosis of metabolic syndrome.

AB - BACKGROUND AND AIMS: Clusters of metabolic abnormalities resembling phenotypes of metabolic syndrome predicted outcome in the LIFE study, independently of single risk markers, including obesity, diabetes and baseline ECG left ventricular hypertrophy (LVH). We examined whether clusters of two or more metabolic abnormalities (MetAb, including obesity, high plasma glucose without diabetes, low HDL-cholesterol) in addition to hypertension were associated to levels of ECG LVH reduction comparable to that obtained in hypertensive subjects without or with only one additional metabolic abnormality (no-MetAb). METHODS AND RESULTS: We studied 5558 non-diabetic participants without MetAb (2920 women) and 1235 with MetAb (751 women) from the LIFE-study cohort. MetAb was defined by reported LIFE criteria, using partition values from the ATPIII recommendations. Time-trends of Cornell voltage-duration product (CP) over 5 years was assessed using a quadratic polynomial contrast, adjusting for age, sex, prevalent cardiovascular disease and treatment arm (losartan or atenolol). At baseline, despite similar blood pressures, CP was greater in the presence than in the absence of MetAb (p<0.0001). During follow-up, despite similar reduction of blood pressure, CP decreased less in patients with than in those without MetAb, even after adjustment for the respective baseline values (both p<0.002). Losartan was more effective than atenolol in reducing CP independently of MetAb. CONCLUSIONS: Clusters of metabolic abnormalities resembling phenotypes of metabolic syndrome are related to greater initial ECG LVH in hypertensive patients with value of blood pressure similar to individuals without metabolic abnormalities, and are associated with less reduction of ECG LVH during antihypertensive therapy, potentially contributing to the reported adverse prognosis of metabolic syndrome.

U2 - 10.1016/j.numecd.2008.12.012

DO - 10.1016/j.numecd.2008.12.012

M3 - Journal article

C2 - 19361968

VL - 19

SP - 634

EP - 640

JO - Nutrition, Metabolism & Cardiovascular Diseases

JF - Nutrition, Metabolism & Cardiovascular Diseases

SN - 0939-4753

IS - 9

ER -

ID: 19867658