Changes in left ventricular structure and function in patients with white coat hypertension: cross sectional survey

Muscholl, M.; Hw, Hense; Bröckel, Ulrich; Döring, Angela; Riegger, Günter A.J.; Schunkert, Heribert

doi:10.1136/bmj.317.7158.565

Cited by 75 publications

(47 citation statements)

References 27 publications

(34 reference statements)

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“…[11][12][13] Subjects originated from a gender-and age-stratified random sample of all German residents of the Augsburg area. The third survey represents individuals 25 to 75 years of age and Ϸ300 subjects for each 10-year increment.…”

Section: Study Populationmentioning

confidence: 99%

Association of the T8590C Polymorphism of CYP4A11 With Hypertension in the MONICA Augsburg Echocardiographic Substudy

et al. 2005

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Abstract-Genetic variants of the arachidonic acid monooxygenase CYP4A11 result in decreased synthesis of 20-hydroxyeicostatetraenoic acid and experimental hypertension. Moreover, in humans, the T8590C polymorphism of CYP4A11 displayed association with arterial hypertension. The aim of the present study was to further investigate this association in a large population-based sample. Therefore, the participants of the echocardiographic substudy of the third MONICA (MONitoring trends and determinants In CArdiovascular disease) survey (nϭ1397) were studied by standardized anthropometric, echocardiographic, and biochemical measurements as well as genotyping for CYP4A11 . Consistent with the renal effects of the gene, no blood pressure-independent association between the T8590C polymorphism and echocardiographic parameters of left ventricular function and geometry was found. In conclusion, our data strengthen the association between the T8590C polymorphism of CYP4A11 and hypertension and suggest a recessive mode of inheritance. In contrast, we found no blood pressure-independent modulatory effect of CYP4A11 T8590C on cardiac size, structure, and function. Key Words: genetics Ⅲ polymorphism Ⅲ hypertension, arterial Ⅲ echocardiography A variety of gene variants has shown association with arterial hypertension. However, only small or inconsistent effects on blood pressure were observed for most of the frequent polymorphisms of hypertension-related genes. 1 On the other hand, mutations with profound implications for blood pressure regulation were found predominantly in exceptional families. 2 Thus, despite extensive research, genetic testing for risk assessment in hypertension is not yet advisable for routine patient evaluation. A major challenge for this field will be the identification of genetic variants with reproducible and clinically as well as epidemiologically relevant effects on blood pressure regulation that, in addition, offer the potential of therapeutical intervention.The CYP4A arachidonic acid monooxygenase oxidizes endogenous arachidonic acid to 20-hydroxyeicostatetraenoic acid (20-HETE). Depending on its expression at renovascular or tubular sites, the 20-HETE metabolite can act in a prohypertensive or antihypertensive manner. [3][4][5][6] Holla et al characterized a CYP4A14 (Ϫ/Ϫ) knockout mouse as a model of gender-specific severe hypertension. 7 Evaluation of human homologues as potential novel genetic determinants in hypertension revealed 2 candidate genes: CYP4A11 and CYP4A22 from the CYP4A gene family. 8,9 Recently, CYP4A11 but not CYP4A22 was identified as the functional active protein that catalyzes the metabolism of arachidonic acid to 20-HETE in humans. 10 Screening for genetic variants revealed a cytosine for thymidine transition at nucleotide 8590 in exon 11, which results in a nonsynonymous phenylalanine to serine substitution at residue 434 of CYP4A11. The less frequent 8590C genotype, which corresponds to the 434S variant on protein

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Section: Study Populationmentioning

confidence: 99%

Association of the T8590C Polymorphism of CYP4A11 With Hypertension in the MONICA Augsburg Echocardiographic Substudy

et al. 2005

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“…23 The control population for this group of MI patients was drawn as a subgroup from the third MONICA survey of the general population of the city of Augsburg in 1994/1995 that originated from a sex/age-stratified cluster sample of all German residents of the Augsburg study area (age 25 to 74 years; participating nϭ1674). [23][24][25] All individuals were studied by a standardized interview, clinical examination, and biochemical and molecular analyses.…”

Section: Group 1: MI Cases and Controls From The Augsburg Monica Centermentioning

confidence: 99%

Association of Polymorphisms of the Apolipoprotein(a) Gene With Lipoprotein(a) Levels and Myocardial Infarction

Holmer¹,

Hengstenberg²,

Kraft³

et al. 2003

Circulation

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“…4,6 Many studies indicate that WCH is associated with target organ damage as well as metabolic abnormalities. 9 Increased numbers of metabolic syndrome (MS) components are associated with elevated night-time SBP levels, 10 left ventricular hypertrophy 7,[11][12][13][14] and increased values of intima-media thickness. 15,16 It is known that phosphate balance is essential for various biological activities and biochemical reactions, and the molecular regulation of phosphate homeostasis has enormous clinical and biological importance.…”

Section: Introductionmentioning

confidence: 99%

Serum phosphate in white-coat hypertensive patients: focus on dipping status and metabolic syndrome

Vyssoulis¹,

Karpanou

Tzamou³

et al. 2010

Hypertens Res

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Recent studies indicate an association between serum phosphate levels and blood pressure in hypertensive patients. A growing body of evidence suggests that white-coat hypertension (WCH) is associated with target organ damage. Furthermore, metabolic syndrome (MS) and a non-dipping pattern are associated with increased cardiovascular risk. The purpose of this study was to explore the nocturnal blood pressure fall in patients with WCH according to their serum phosphate levels and number of MS components fulfilled. The study included 2600 patients with WCH who attended our outpatient clinics. All patients underwent repeated office blood pressure measurements, 24-h ambulatory blood pressure monitoring and full clinical and laboratory evaluation. The diagnosis of MS was made according to the Adult Treatment Panel III criteria. Dipping pattern was defined as follows: 'dippers' had a nocturnal systolic blood pressure (NSBP) fall X10% but o20%; 'non-dippers' had an NSBP fall o10%; 'extreme dippers' had an NSBP fall X20% and 'reverse dippers' had an NSBP increase. There were 314 extreme dippers, 1337 dippers, 734 non-dippers and 116 reverse dippers. Reverse dippers presented with significantly lower levels of serum phosphate, whereas extreme dippers had significantly higher levels (3.39 ± 3.29 vs. 3.58 ± 3.52 mg per 100 ml, Po0.0001). The patients were classified according to the number of MS components and the main observation was the inverse relationship of serum phosphate with MS components (3.53±0.36, 3.50±0.38, 3.49±0.38, 3.44±0.36 and 3.35±0.31 mg per 100 ml, respectively, P¼0.003). Patients with WCH and low serum phosphate levels appear to have a higher incidence of a non-dipping NSBP profile and an impaired metabolic profile. This observation may be important for the stratification of the cardiovascular risk in WCH patients.

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Changes in left ventricular structure and function in patients with white coat hypertension: cross sectional survey

Cited by 75 publications

References 27 publications

Association of the T8590C Polymorphism of CYP4A11 With Hypertension in the MONICA Augsburg Echocardiographic Substudy

Association of the T8590C Polymorphism of CYP4A11 With Hypertension in the MONICA Augsburg Echocardiographic Substudy

Association of Polymorphisms of the Apolipoprotein(a) Gene With Lipoprotein(a) Levels and Myocardial Infarction

Serum phosphate in white-coat hypertensive patients: focus on dipping status and metabolic syndrome

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