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CLINICAL RESEARCH: ATHEROSCLEROSIS RISK

Physical activity reduces genetic susceptibility to increased central systolic pressure augmentation: a study of female twins

Jerry R. Greenfield, MBBS, BSc (Med), FRACP^*,*, Katherine Samaras, MBBS, PhD, FRACP^*, Lesley V. Campbell, MBBS, FRCP, FRACP^*, Arthur B. Jenkins, BSc, PhD, Paul J. Kelly, MBBS, MD, FRACP^||, Tim D. Spector, MSc, MD, FRCP^¶ and Christopher S. Hayward, BMedSc, MBBS, MD, FRACP^#

^* Department of Endocrinology, St. Vincent’s Hospital, Sydney, Australia
Diabetes Centre, St. Vincent’s Hospital, Sydney, Australia
Department of Cardiology, St. Vincent’s Hospital, Sydney, Australia
Department of Biomedical Science, University of Wollongong, Wollongong, Australia
^|| Sequenom, San Diego, California, USA
^¶ Twin Research and Genetic Epidemiology Unit, St. Thomas’ Hospital, London, United Kingdom
^# Victor Chang Cardiac Research Institute, Sydney, Australia

Manuscript received January 19, 2003; revised manuscript received April 10, 2003, accepted April 17, 2003.

^* Reprint requests and correspondence: Dr. Jerry R. Greenfield, Department of Endocrinology, St. Vincent’s Hospital, Darlinghurst, Sydney, NSW 2010, Australia.
j.greenfield{at}garvan.org.au

OBJECTIVES: We sought to examine associations between the augmentation index (AI) and metabolic, adiposity, and lifestyle factors, independent of genetic influences, and to determine whether gene-environment interactions modulate these relationships.

BACKGROUND: Reported associations between AI, an index of systemic arterial stiffness, and metabolic, adiposity, and lifestyle factors remain contradictory. The modulating effect of genetic risk is unknown.

METHODS: We studied 684 female twins (age 18 to 71 years); AI was derived from the pressure waveform measured at the radial artery by applanation tonometry. Percentage of total body fat (TBF) and percentage of central abdominal fat (CAF) were assessed by dual-energy X-ray absorptiometry.

RESULTS: In univariate analysis, age-adjusted AI was significantly associated with fasting triglyceride levels (r = 0.1, p = 0.03), apolipoprotein-B/A1 (r = 0.1, p = 0.04), percentage of TBF (r = 0.11, p = 0.006), and percentage of CAF (r = 0.11, p = 0.004). In co-twin case-control (monozygotic twin) analysis, a 3.1% absolute within-pair difference in percentage of CAF accounted for a 6% within-pair difference in AI, independent of genetic effects. Smokers and subjects with alcohol intakes >15 U/week had higher AI than nonsmokers (p = 0.01) and nondrinkers (p = 0.02), respectively. Forty percent of the variance in AI was explained by age, central mean arterial pressure, heart rate, height, percentage of CAF, and smoking. In gene-environment interaction analysis, subjects at high genetic risk of increased AI participating in regular leisure-time physical activity had AI values similar to low genetic risk subjects.

CONCLUSIONS: Central abdominal adiposity is a significant determinant of AI in female twins, independent of hemodynamic, lifestyle, and, importantly, genetic effects. Smoking is associated with increased AI, even after controlling for abdominal obesity and other AI determinants. Physical activity reduces genetic predisposition to increased AI.

Abbreviations and Acronyms   AI   augmentation index   BMI   body mass index   BP   blood pressure   CAF   central abdominal fat   CMAP   central mean arterial pressure   DXA   dual-energy X-ray absorptiometry   DZ   dizygotic   HOMA   homeostasis model assessment   HRT   hormone replacement therapy   MZ   monozygotic   TBF   total body fat

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