Artery Research (Aug 2013)

Arterial stiffness, wave reflection amplitude and left ventricular afterload are increased in overweight individuals

  • Wilmer W. Nichols,
  • John W. Petersen,
  • Scott J. Denardo,
  • Demetra D. Christou

DOI
https://doi.org/10.1016/j.artres.2013.08.001
Journal volume & issue
Vol. 7

Abstract

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Background: Reflected pressure waves from the lower body to the heart in overweight subjects return early and augment aortic systolic pressure and increase left ventricular (LV) afterload and wasted energy. Methods: Central aortic pressure waves were generated from radial artery pressure waves recorded non-invasively in 176 subjects (age 52 ± 18 years). Augmentation index (Alx), an estimate of wave reflection, and LV wasted energy (Ew) were calculated from the generated aortic pressure wave. Data were collected in 88 non-diabetic, non-renal disease normotensive overweight (BMI 30 ± 5.0 kg/m2) subjects and compared to data collected from 88 normotensive normal weight (BMI 23 ± 2.1, P < 0.01) control subjects matched for gender, age, height, heart rate and ejection duration. Results: Compared to controls, overweight subjects had higher aortic systolic (124 ± 17 vs 114 ± 14 mmHg, P < 0.001) and pulse (44 ± 16 vs 37 ± 12 mmHg, P < 0.001) blood pressures. Also, increased BMI was associated with an increase in Alx (28 ± 9.3 vs 20 ± 12%, P < 0.001), reflected wave duration (176 ± 28 vs 159 ± 30 msec, P < 0.004) and Ew (2527 ± 1732 vs 1498 ± 1375 dsc−2, P < 0.001) and a decrease in pressure wave travel time (133 ± 14 vs 143 ± 15 msec, P < 0.001). These modifications in wave reflection characteristics in overweight subjects were associated with a decrease in pulse pressure amplification (1.3 ± 0.14 vs 1.5 ± 0.29, P < 0.01). Conclusions: Overweight subjects have a stiffer arterial system which decreases wave propagation time and causes the reflected pressure wave to arrive earlier at the heart with increased amplitude and duration. These changes in arterial function and wave reflection characteristics cause an increase in LV afterload, myocardial oxygen demand and wasted LV energy.

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