Key result
Dobutamine stress induced higher maximum left ventricular outflow tract velocities in hypertensive patients with basal septal hypertrophy than in normal controls (3.3 vs 1.7 m/sec, p<0.001).
Why the study?
Does dobutamine stress increase LVOT velocities in hypertensive patients with basal septal hypertrophy compared to normal controls?
Observational (n=44)
Does dobutamine stress increase LVOT velocities in hypertensive patients with basal septal hypertrophy compared to normal controls?
Pharmacologic stress with dobutamine provokes significant dynamic LVOT obstruction in hypertensive patients with basal septal hypertrophy compared to normal controls.
Answers are grounded in this paper and cite their sources.
May warrant caution with dobutamine stress in this population; leaves open clinical relevance and need for prospective studies.
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.
No takes yet. Share an insight, caveat, or question.
Yalçın et al. (2004) conducted an observational in Hypertensive patients with basal septal hypertrophy (n=44). Dobutamine stress vs. Normal controls was evaluated on Maximum LVOT velocities at peak stress (p=<0.001). Dobutamine stress induced higher maximum left ventricular outflow tract velocities in hypertensive patients with basal septal hypertrophy than in normal controls (3.3 vs 1.7 m/sec, p<0.001).
Synapse has enriched 10 related papers. Consider them for comparative context: