Assessment of the interaction of heritability of volume load and left ventricular mass

The HyperGEN offspring study

Giovanni De Simone, Weihong Tang, Richard B. Devereux, Steven Hunt, Dalane W. Kitzman, D. C. Rao, Donna K. Arnett

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

BACKGROUND: Left ventricular mass (LVM) is more closely associated with volume load than pressure load. We assessed whether part of the genetic heritability of LVM can be explained by stroke volume (SV) inheritance. METHODS: Echocardiographic LVM, SV and peripheral resistance were measured in 527 families with at least two relatives from the HyperGEN study (51% African-American, 43% men, 44% obese, 53% hypertensive). Included were 1792 subjects without prevalent cardiovascular disease, diabetes and renal failure. Ethnic-specific genetic correlations were estimated using a variance components procedure (SOLAR). RESULTS: Significant genetic correlations existed between LVM and SV after adjusting for age, sex, race, field center, systolic blood pressure, number of antihypertensive medications, and body mass index (ρg = 0.93 in African-Americans and 0.70 in Caucasians; both P < 0.0001). Urinary Na excretion or serum creatinine did not influence these correlations. After adjusting for covariates, heritability of LVM was greater (h = 0.46 in African-Americans and 0.47 in Caucasians; both P < 0.0001) than that for SV (h = 0.18 in African-Americans and 0.29 in Caucasians; both P < 0.02). Heritability of LVM slightly decreased in African-Americans (h = 0.34), but not in Caucasians (h = 0.45; both P < 0.0001) when SV was added to covariates. Heritability of SV almost disappeared by addition of LVM into the model in African-Americans (h = 0.04, P = not significant), whereas it was slightly reduced in Caucasians (h = 0.20, P < 0.005). CONCLUSION: LVM and SV share a common genetic profile, but with only a modest reciprocal influence. Variability of LVM has some effect on calculated heritability of SV, especially in African-Americans, whereas the role of heritable volume load in determining the variability of LVM was modest only in African-Americans.

Original languageEnglish
Pages (from-to)1397-1402
Number of pages6
JournalJournal of Hypertension
Volume25
Issue number7
DOIs
Publication statusPublished - Jul 2007
Externally publishedYes

Fingerprint

African Americans
Stroke Volume
Blood Pressure
Vascular Resistance
Antihypertensive Agents
Renal Insufficiency
Creatinine
Body Mass Index
Cardiovascular Diseases
Pressure
Serum

Keywords

  • Echocardiography
  • Hypertension
  • Hypertrophy
  • Inheritance
  • Race
  • Stroke volume

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology

Cite this

Assessment of the interaction of heritability of volume load and left ventricular mass : The HyperGEN offspring study. / De Simone, Giovanni; Tang, Weihong; Devereux, Richard B.; Hunt, Steven; Kitzman, Dalane W.; Rao, D. C.; Arnett, Donna K.

In: Journal of Hypertension, Vol. 25, No. 7, 07.2007, p. 1397-1402.

Research output: Contribution to journalArticle

De Simone, Giovanni ; Tang, Weihong ; Devereux, Richard B. ; Hunt, Steven ; Kitzman, Dalane W. ; Rao, D. C. ; Arnett, Donna K. / Assessment of the interaction of heritability of volume load and left ventricular mass : The HyperGEN offspring study. In: Journal of Hypertension. 2007 ; Vol. 25, No. 7. pp. 1397-1402.
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abstract = "BACKGROUND: Left ventricular mass (LVM) is more closely associated with volume load than pressure load. We assessed whether part of the genetic heritability of LVM can be explained by stroke volume (SV) inheritance. METHODS: Echocardiographic LVM, SV and peripheral resistance were measured in 527 families with at least two relatives from the HyperGEN study (51{\%} African-American, 43{\%} men, 44{\%} obese, 53{\%} hypertensive). Included were 1792 subjects without prevalent cardiovascular disease, diabetes and renal failure. Ethnic-specific genetic correlations were estimated using a variance components procedure (SOLAR). RESULTS: Significant genetic correlations existed between LVM and SV after adjusting for age, sex, race, field center, systolic blood pressure, number of antihypertensive medications, and body mass index (ρg = 0.93 in African-Americans and 0.70 in Caucasians; both P < 0.0001). Urinary Na excretion or serum creatinine did not influence these correlations. After adjusting for covariates, heritability of LVM was greater (h = 0.46 in African-Americans and 0.47 in Caucasians; both P < 0.0001) than that for SV (h = 0.18 in African-Americans and 0.29 in Caucasians; both P < 0.02). Heritability of LVM slightly decreased in African-Americans (h = 0.34), but not in Caucasians (h = 0.45; both P < 0.0001) when SV was added to covariates. Heritability of SV almost disappeared by addition of LVM into the model in African-Americans (h = 0.04, P = not significant), whereas it was slightly reduced in Caucasians (h = 0.20, P < 0.005). CONCLUSION: LVM and SV share a common genetic profile, but with only a modest reciprocal influence. Variability of LVM has some effect on calculated heritability of SV, especially in African-Americans, whereas the role of heritable volume load in determining the variability of LVM was modest only in African-Americans.",
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T1 - Assessment of the interaction of heritability of volume load and left ventricular mass

T2 - The HyperGEN offspring study

AU - De Simone, Giovanni

AU - Tang, Weihong

AU - Devereux, Richard B.

AU - Hunt, Steven

AU - Kitzman, Dalane W.

AU - Rao, D. C.

AU - Arnett, Donna K.

PY - 2007/7

Y1 - 2007/7

N2 - BACKGROUND: Left ventricular mass (LVM) is more closely associated with volume load than pressure load. We assessed whether part of the genetic heritability of LVM can be explained by stroke volume (SV) inheritance. METHODS: Echocardiographic LVM, SV and peripheral resistance were measured in 527 families with at least two relatives from the HyperGEN study (51% African-American, 43% men, 44% obese, 53% hypertensive). Included were 1792 subjects without prevalent cardiovascular disease, diabetes and renal failure. Ethnic-specific genetic correlations were estimated using a variance components procedure (SOLAR). RESULTS: Significant genetic correlations existed between LVM and SV after adjusting for age, sex, race, field center, systolic blood pressure, number of antihypertensive medications, and body mass index (ρg = 0.93 in African-Americans and 0.70 in Caucasians; both P < 0.0001). Urinary Na excretion or serum creatinine did not influence these correlations. After adjusting for covariates, heritability of LVM was greater (h = 0.46 in African-Americans and 0.47 in Caucasians; both P < 0.0001) than that for SV (h = 0.18 in African-Americans and 0.29 in Caucasians; both P < 0.02). Heritability of LVM slightly decreased in African-Americans (h = 0.34), but not in Caucasians (h = 0.45; both P < 0.0001) when SV was added to covariates. Heritability of SV almost disappeared by addition of LVM into the model in African-Americans (h = 0.04, P = not significant), whereas it was slightly reduced in Caucasians (h = 0.20, P < 0.005). CONCLUSION: LVM and SV share a common genetic profile, but with only a modest reciprocal influence. Variability of LVM has some effect on calculated heritability of SV, especially in African-Americans, whereas the role of heritable volume load in determining the variability of LVM was modest only in African-Americans.

AB - BACKGROUND: Left ventricular mass (LVM) is more closely associated with volume load than pressure load. We assessed whether part of the genetic heritability of LVM can be explained by stroke volume (SV) inheritance. METHODS: Echocardiographic LVM, SV and peripheral resistance were measured in 527 families with at least two relatives from the HyperGEN study (51% African-American, 43% men, 44% obese, 53% hypertensive). Included were 1792 subjects without prevalent cardiovascular disease, diabetes and renal failure. Ethnic-specific genetic correlations were estimated using a variance components procedure (SOLAR). RESULTS: Significant genetic correlations existed between LVM and SV after adjusting for age, sex, race, field center, systolic blood pressure, number of antihypertensive medications, and body mass index (ρg = 0.93 in African-Americans and 0.70 in Caucasians; both P < 0.0001). Urinary Na excretion or serum creatinine did not influence these correlations. After adjusting for covariates, heritability of LVM was greater (h = 0.46 in African-Americans and 0.47 in Caucasians; both P < 0.0001) than that for SV (h = 0.18 in African-Americans and 0.29 in Caucasians; both P < 0.02). Heritability of LVM slightly decreased in African-Americans (h = 0.34), but not in Caucasians (h = 0.45; both P < 0.0001) when SV was added to covariates. Heritability of SV almost disappeared by addition of LVM into the model in African-Americans (h = 0.04, P = not significant), whereas it was slightly reduced in Caucasians (h = 0.20, P < 0.005). CONCLUSION: LVM and SV share a common genetic profile, but with only a modest reciprocal influence. Variability of LVM has some effect on calculated heritability of SV, especially in African-Americans, whereas the role of heritable volume load in determining the variability of LVM was modest only in African-Americans.

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KW - Hypertrophy

KW - Inheritance

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