Background: The aim of this study was to compare the results of dipyridamole-echocardiography test (DET: two-dimensional echo monitoring during dipyridamole infusion up to 0.84 mg/kg over a period of 10 minutes) with both anatomic and physiological parameters of coronary artery disease severity, assessed by computer-assisted quantitative coronary arteriography, and regional coronary flow reserve, measured by [13N]ammonia (13NH3) and dynamic positron emission tomography (PET), respectively. Methods and Results: We studied 31 patients with a history of chest pain and neither previous myocardial infarction nor resting wall motion abnormalities. Eighteen patients had single-vessel disease (>50% stenosis of one major coronary vessel), and 13 had normal coronary arteries. The criterion for DET positivity was the appearance of a new transient regional wall motion abnormality. In patients with a positive DET, two parameters were evaluated: the dipyridamole time (ie, the time from the beginning of drug infusion to the development of obvious dyssynergy) and the wall motion score index (WMSI, a semiquantitative integrated estimation of extent and severity of the stress-induced dyssynergy). WMSI was derived by summation of individual segment scores divided by the number of segments interpreted. Quantification of regional myocardial blood flow was obtained by PET measurements of 13NH3 arterial input function and left ventricular myocardial tissue concentration both at control and after dipyridamole (0.56 mg/kg over 4 minutes). Maximal regional blood flow after dipyridamole in the region supplied by the stenotic vessel was significantly lower in the 11 patients with coronary artery disease and positive DET than in the 7 patients with coronary artery disease and negative DET (1.08±0.33 versus 1.98±0.37 mL · min-1 · g-1, P<.01). In patients with a positive DET, regional coronary flow reserve correlated well with dipyridamole time (r=.87, P<.01) but not with peak WMSI (r=.25, P=NS). Patients with dipyridamole-induced akinesia or dyskinesia (n=6) had a greater reduction in regional coronary flow reserve than did those showing hypokinesia (n=5): 1.38±0.51 versus 2.17±0.42, P<.05. Percent area reduction was more severe in patients with DET positivity than in those with DET negativity (93.7±8.7% versus 77±10.3%, P<.01), and it correlated with regional coronary flow reserve (r=.64, P<.01) and dipyridamole time (r=-.59, P<.01). Conclusions: In patients with single- vessel disease, DET shows an excellent specificity but a limited sensitivity; in these patients, DET positivity is associated with a physiologically important coronary stenosis. Severity of the anatomic stenosis and impairment in regional flow reserve are greater when the dipyridamole-induced dyssynergy appears earlier during the test. Therefore, a stratification of the anatomophysiological severity of coronary artery disease can be obtained with DET, based mainly on the temporal allocation of the transient dyssynergy.

Assessment of anatomic and physiologic severity of single vessel coronary artery lesions by dipyridamole echocardiography: Comparison with positron emission tomography and quantitative arteriography

SAMBUCETI, GIANMARIO;
1994-01-01

Abstract

Background: The aim of this study was to compare the results of dipyridamole-echocardiography test (DET: two-dimensional echo monitoring during dipyridamole infusion up to 0.84 mg/kg over a period of 10 minutes) with both anatomic and physiological parameters of coronary artery disease severity, assessed by computer-assisted quantitative coronary arteriography, and regional coronary flow reserve, measured by [13N]ammonia (13NH3) and dynamic positron emission tomography (PET), respectively. Methods and Results: We studied 31 patients with a history of chest pain and neither previous myocardial infarction nor resting wall motion abnormalities. Eighteen patients had single-vessel disease (>50% stenosis of one major coronary vessel), and 13 had normal coronary arteries. The criterion for DET positivity was the appearance of a new transient regional wall motion abnormality. In patients with a positive DET, two parameters were evaluated: the dipyridamole time (ie, the time from the beginning of drug infusion to the development of obvious dyssynergy) and the wall motion score index (WMSI, a semiquantitative integrated estimation of extent and severity of the stress-induced dyssynergy). WMSI was derived by summation of individual segment scores divided by the number of segments interpreted. Quantification of regional myocardial blood flow was obtained by PET measurements of 13NH3 arterial input function and left ventricular myocardial tissue concentration both at control and after dipyridamole (0.56 mg/kg over 4 minutes). Maximal regional blood flow after dipyridamole in the region supplied by the stenotic vessel was significantly lower in the 11 patients with coronary artery disease and positive DET than in the 7 patients with coronary artery disease and negative DET (1.08±0.33 versus 1.98±0.37 mL · min-1 · g-1, P<.01). In patients with a positive DET, regional coronary flow reserve correlated well with dipyridamole time (r=.87, P<.01) but not with peak WMSI (r=.25, P=NS). Patients with dipyridamole-induced akinesia or dyskinesia (n=6) had a greater reduction in regional coronary flow reserve than did those showing hypokinesia (n=5): 1.38±0.51 versus 2.17±0.42, P<.05. Percent area reduction was more severe in patients with DET positivity than in those with DET negativity (93.7±8.7% versus 77±10.3%, P<.01), and it correlated with regional coronary flow reserve (r=.64, P<.01) and dipyridamole time (r=-.59, P<.01). Conclusions: In patients with single- vessel disease, DET shows an excellent specificity but a limited sensitivity; in these patients, DET positivity is associated with a physiologically important coronary stenosis. Severity of the anatomic stenosis and impairment in regional flow reserve are greater when the dipyridamole-induced dyssynergy appears earlier during the test. Therefore, a stratification of the anatomophysiological severity of coronary artery disease can be obtained with DET, based mainly on the temporal allocation of the transient dyssynergy.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11567/197596
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