Author + information
- Received November 28, 1995
- Revision received March 4, 1996
- Accepted March 11, 1996
- Published online July 1, 1996.
- Johannes Soma, MD∗,
- Tor Erik Widerøe, MD, PhD,
- Ketil Dahl, MD,
- Ole Rossvoll, MD and
- Terje Skjærpe, MD, PhD
- ↵∗Address for correspondence: Dr. Johannes Soma, Department of Medicine, Section of Cardiology, University Hospital of Trondheim, N-7006 Trondheim, Norway.
Objectives. The aim of this study was to investigate left ventricular function in subjects with “white coat” hypertension, defined as office arterial diastolic pressure ≥90 and ambulatory daytime pressure < 140/90mm Hg.
Background. The white coat arterial pressure response may, by influencing left ventricular function, have a confounding effect in studies of heart disease.
Methods. Two-dimensional and Doppler echocardiography, combined with the calibrated subclavian arterial pulse tracing, were used to assess variables of left ventricular function in 26 subjects with white coat hypertension, as well as 22 subjects with previously untreated ambulatory hypertension (office arterial diastolic pressure ≥90 and <115 mm Hg and ambulatory daytime diastolic pressure ≥90 mm Hg) and 32 normotensive subjects.
Results. In subjects with white coat hypertension, systolic arterial pressure during the echocardiographic examination was significantly higher than ambulatory daytime systolic pressure. This pressure response was positively related to the ratio of the systolic to diastolic pulmonary venous flow peak velocities and to the peak velocity of flow reversion during atrial systole; it was inversely related to the ratio of early to late mitral flow peak velocities. Left ventricular stroke volume, ejection fraction and velocity of circumferential fiber shortening did not differ in the study groups, but left ventricular external work and end-systolic wall stress were increased in the white coat group.
Conclusions. The arterial pressure response in subjects with white coat hypertension is associated with increased left ventricular external work, increased end-systolic wall stress and alterations of left ventricular filling but normal ejection fraction and velocity of circumferential fiber shortening.
☆ This work was supported by grants from the University of Trondheim, Trondheim and the Norwegian Council on Cardiovascular Diseases, Oslo, Norway.
- Received November 28, 1995.
- Revision received March 4, 1996.
- Accepted March 11, 1996.