BACKGROUND: Dobutamine stress echocardiography (DSE) quantified by tissue Doppler (TVI) have improved the diagnostic capacity of the procedure. Quantification of other stress modalities, e.g. adenosine stress echo (ASE) and exercise stress echocardiography (ESE) are necessary for assessing any pathophysiological differences in different forms of stress. METHODS: Ten healthy individuals underwent ASE, DSE, and ESE during a span of 2-5 days. Left ventricular (LV) apical images at rest and peak stress (max) were postprocessed using TVI on a GE System FiVe equipment. ECG-derived QRS duration (QRSD, ms), heart rate (HR, bpm), TVI-estimated basal systolic velocities (S2V, cm s(-1)), ejection time (S2T, ms) and strain (S, %) were computed off-line and compared. Longitudinal displacement imaging, tissue tracking, was also made. RESULTS: Data for ASE, DSE and ESE during peak stress were (HR: 84 +/- 12***, 142 +/- 19, 137 +/- 27; P<0.001) (QRSD: 92 +/- 18**, 74 +/- 13, 79 +/- 9; P<0.05), (S2T: 307 +/- 34***, 175 +/- 53, 192 +/- 25; P<0.001) and (S%: 26.0 +/- 3.0, 21.2 +/- 7.3, 22.1 +/- 5.1; P = n.s.) respectively. Velocity response, registered in the LV septum at max, was lowest during ASE (7.4 +/- 1.4) highest during DSE (13.0 +/- 2.7; P<0.001 versus ASE) and somewhat intermediate during ESE (11.3 +/- 3.5; P<0.001 versus ASE). In contrast, strain and displacement did not differ. CONCLUSION: ASE evokes significantly less LV systolic response compared with both DSE and ESE. Increased velocity (P<0.05 versus rest) and strain (P>0.05) response at a much lower HR indicates that adenosine has minor effects on contraction presumably secondary to vasodilatation. Powerful chronotropic response to DSE and ESE is probably prerequisite for strong velocity response at the expense of strain and displacement. TVI-assisted stress echocardiography thereby shows different LV systolic response in healthy individuals, depending on stress modality.
BACKGROUND:Dobutamine stress echocardiography (DSE) quantified by tissue Doppler (TVI) have improved the diagnostic capacity of the procedure. Quantification of other stress modalities, e.g. adenosine stress echo (ASE) and exercise stress echocardiography (ESE) are necessary for assessing any pathophysiological differences in different forms of stress. METHODS: Ten healthy individuals underwent ASE, DSE, and ESE during a span of 2-5 days. Left ventricular (LV) apical images at rest and peak stress (max) were postprocessed using TVI on a GE System FiVe equipment. ECG-derived QRS duration (QRSD, ms), heart rate (HR, bpm), TVI-estimated basal systolic velocities (S2V, cm s(-1)), ejection time (S2T, ms) and strain (S, %) were computed off-line and compared. Longitudinal displacement imaging, tissue tracking, was also made. RESULTS: Data for ASE, DSE and ESE during peak stress were (HR: 84 +/- 12***, 142 +/- 19, 137 +/- 27; P<0.001) (QRSD: 92 +/- 18**, 74 +/- 13, 79 +/- 9; P<0.05), (S2T: 307 +/- 34***, 175 +/- 53, 192 +/- 25; P<0.001) and (S%: 26.0 +/- 3.0, 21.2 +/- 7.3, 22.1 +/- 5.1; P = n.s.) respectively. Velocity response, registered in the LV septum at max, was lowest during ASE (7.4 +/- 1.4) highest during DSE (13.0 +/- 2.7; P<0.001 versus ASE) and somewhat intermediate during ESE (11.3 +/- 3.5; P<0.001 versus ASE). In contrast, strain and displacement did not differ. CONCLUSION: ASE evokes significantly less LV systolic response compared with both DSE and ESE. Increased velocity (P<0.05 versus rest) and strain (P>0.05) response at a much lower HR indicates that adenosine has minor effects on contraction presumably secondary to vasodilatation. Powerful chronotropic response to DSE and ESE is probably prerequisite for strong velocity response at the expense of strain and displacement. TVI-assisted stress echocardiography thereby shows different LV systolic response in healthy individuals, depending on stress modality.