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The Effect of Dobutamine Stress on Left Ventricular Outflow Tract Gradients in Hypertensive Patients with Basal Septal Hypertrophy

Bakent University School of Medicine, Department of Cardiology, Medical and Research Center, Adana, Turkey, fyalcin{at}baskent-adn.edu.tr

Haldun Muderrisoglu, MD, FESC

Bakent University School of Medicine, Department of Cardiology, Medical and Research Center, Adana, Turkey

Mehmet Emin Korkmaz, MD, FESC

Bakent University School of Medicine, Department of Cardiology, Medical and Research Center, Adana, Turkey

Bulent Ozin, MD

Bakent University School of Medicine, Department of Cardiology, Medical and Research Center, Adana, Turkey

Mehmet Baltali, MD

Bakent University School of Medicine, Department of Cardiology, Medical and Research Center, Adana, Turkey

Fatma Yigit, MD

Bakent University School of Medicine, Department of Cardiology, Medical and Research Center, Adana, Turkey

Basal septal hypertrophy (BSH), a cause of left ventricular outflow tract (LVOT) obstruction, is thought to occur by increased ventricular dynamics. The aim of the study was to evaluate the effect of pharmacologic stress on LVOT gradients in a group of hypertensive patients with BSH. Dobutamine stress was used in 24 hypertensive patients (mean age 56 ±8 years; 11 women) with BSH and 20 normal controls (mean age 54 ±9 years; 7 women). Ejection fraction and myocardial mass, basal septal dimension, and LVOT diameter were measured with 2-dimensional echocardiography. LVOT velocities and transmitral velocities before and at peak dobutamine infusion were determined by continuous wave Doppler and pulsed Doppler, respectively. There were no differences in mean ejection fraction and myocardial mass between BSH patients (58 ±3%, 204 ±24 g) and normals (56 ±4%, 201 ±32 g). The basal septum was thicker in patients (1.55 ±0.2 cm) than in normals (1.03 ±0.1 cm, p<0.001). Maximum LVOT velocities were similar in BSH (1.2 ±0.4 m/sec) and normals (1.1 ±0.2 m/sec) at rest. At peak stress, maximum LVOT velocities were higher in BSH (3.3 ±0.6 m/sec) than normals (1.7 ±0.4 m/sec, p<0.001). LV rate-pressure product at peak stress was higher in BSH (23,326 ±4,388) than normals (17,592 ±2,409, p<0.001). LV isovolumetric relaxation time was prolonged, and the E/A ratio was decreased in the patients at rest (130 ±14 msec and 0.72 ±0.18, respectively, p<0.001). At peak stress, diastolic function did not significantly change in two groups. The correlations between LVOT velocity change by stress and mean LVOT diameter (r =-0.668, p<0.001) and mean BS thickness (r =0.610; p<0.001) were significant in the whole group. High velocities appeared on LVOT at peak pharmacologic stress in the hypertensive patients with BSH compared with control group. This suggests dynamic ventricular ejection by stress may contribute to hypertrophy of the basal segment, which is the closest part of septum to increased afterload.

Angiology, Vol. 55, No. 3, 295-301 (2004)
DOI: 10.1177/000331970405500309


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