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CLINICAL STUDIES

Familial predisposition of left ventricular hypertrophy

Heribert Schunkert, MD^a, Ulrich Bröckel, MD^a, Christian Hengstenberg, MD^a, Andreas Luchner, MD^a, Michael W. Muscholl, MD^a, Klaus Kurzidim, MD^a, Bernhard Kuch, MD^*, Angela Döring, MD, G.ünter A. J. Riegger, MD^a and Hans-Werner Hense, MD^*

^a Klinik und Poliklinik für Innere Medizin II, University of Regensburg, Regensburg, Germany
^* Institut für Epidemiologie und Sozialmedizin, University of Münster, Münster, Germany
GSF Forschungszentrum, Institut für Epidemiologie, Munich-Neuherberg, Germany

Manuscript received July 16, 1998; revised manuscript received December 9, 1998, accepted January 20, 1999.

Reprint requests and correspondence: Dr. H. Schunkert, Klinik und Poliklinik für Innere Medizin II, University of Regensburg, D-93042, Regensburg, Germany.
heribert.schunkert{at}klinik.uni-regensburg.de

OBJECTIVES

The study evaluated the contribution of familial predisposition to the risk of left ventricular hypertrophy (LVH).

BACKGROUND

Left ventricular hypertrophy is a multifactorial condition that serves as an important predictor of cardiovascular mortality. At present it is unclear whether familial predisposition contributes to the manifestation of LVH. Thus, we determined whether siblings of subjects with LVH are at increased risk to present with an elevation of LV mass or an abnormal LV geometry.

METHODS

Echocardiographic and anthropometric measurements were performed in 2,293 individuals who participated in the echocardiographic substudies of population-based MONICA Augsburg surveys. In addition, a total of 319 siblings of survey participants with echocardiographic evidence of LVH were evaluated. The risk of these siblings to present with LVH or abnormal LV geometry was estimated by comparison with 636 subjects matched for gender and age that were selected from the entire echocardiography study base.

RESULTS

Blood pressure, body mass index, age, and gender (i.e., known determinants of LV mass) were comparable in LVH-siblings and the matched comparison group. However, septal and posterior wall thicknesses, relative wall thickness as well as LV mass index were significantly elevated in LVH-siblings (p < 0.001, each) whereas LV dimensions did not differ. Likewise, the prevalence of LVH was raised in LVH-siblings, as was the relative risk of LVH after adjustment for confounders (p < 0.05). More specifically, LVH-siblings displayed increased prevalences of concentric remodeling and concentric LVH (p < 0.05) but not of eccentric LVH.

CONCLUSIONS

Familial predisposition appears to contribute to increased LV wall thickness, to the development of LV hypertrophy and abnormal LV geometry.

Abbreviations and Acronyms   BMI = body mass index   EDD = end-diastolic diameter   LVH = left ventricular hypertrophy   LVM(I) = left ventricular mass (index)   PWT = posterior wall thickness   RWT = relative wall thickness   SWT = septal wall thickness

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