TY - JOUR
T1 - Strain echocardiography tracks dobutamine-induced decrease in regional myocardial perfusion in nonocclusive coronary stenosis
AU - Yip, Gabriel
AU - Khandheria, Bijoy
AU - Belohlavek, Marek
AU - Pislaru, Cristina
AU - Seward, James
AU - Bailey, Kent
AU - Tajik, A. Jamil
AU - Pellikka, Patricia
AU - Abraham, Theodore
N1 - Funding Information:
Supported by an American Heart Association (Northland Affiliate) Beginning Grant in Aid Award.
PY - 2004/10/19
Y1 - 2004/10/19
N2 - This study was designed to determine whether strain echocardiography parameters reflect changes in regional myocardial perfusion during dobutamine stress. Strain echocardiography depicts regional myocardial mechanical activity. Ischemia has been shown to reduce systolic strain rate (sSR) and prolong the time to regional lengthening (T RL). In an experimental model, we tested whether sSR and T RL tracked dobutamine-induced changes in regional myocardial perfusion (regional myocardial blood flow [RMBF]), as measured by colored microspheres. We used a closed-chest pig model of nonocclusive coronary stenosis (n = 14) created by inflating an angioplasty balloon in the proximal left anterior descending artery. Invasive hemodynamics, RMBF, and strain parameters were measured at baseline and peak dobutamine stimulation before and during the coronary stenosis. We compared segments with reduced RMBF versus those with preserved RMBF at peak dobutamine stimulation. Peak sSR correlated with RMBF (r = 0.70). In the absence of coronary stenosis, dobutamine stimulation caused a significant increase in RMBF and sSR and a decrease in T RL. This response was blunted during coronary stenosis. Using the "best cutoff" method, the sensitivity and specificity for prediction of reduced RMBF (ischemia) was 81% and 91% for sSR and 65% and 91% for T RL, respectively. These changes occurred in the absence of any change in global systolic and diastolic function (dP/dT max, dP/dT min, and tau). Novel strain parameters that depict regional myocardial mechanics are able to predict changes in RMBF during dobutamine stress. Quantitative strain parameters may complement current echocardiographic techniques for ischemia detection and potentially improve the accuracy and reproducibility of stress echocardiography.
AB - This study was designed to determine whether strain echocardiography parameters reflect changes in regional myocardial perfusion during dobutamine stress. Strain echocardiography depicts regional myocardial mechanical activity. Ischemia has been shown to reduce systolic strain rate (sSR) and prolong the time to regional lengthening (T RL). In an experimental model, we tested whether sSR and T RL tracked dobutamine-induced changes in regional myocardial perfusion (regional myocardial blood flow [RMBF]), as measured by colored microspheres. We used a closed-chest pig model of nonocclusive coronary stenosis (n = 14) created by inflating an angioplasty balloon in the proximal left anterior descending artery. Invasive hemodynamics, RMBF, and strain parameters were measured at baseline and peak dobutamine stimulation before and during the coronary stenosis. We compared segments with reduced RMBF versus those with preserved RMBF at peak dobutamine stimulation. Peak sSR correlated with RMBF (r = 0.70). In the absence of coronary stenosis, dobutamine stimulation caused a significant increase in RMBF and sSR and a decrease in T RL. This response was blunted during coronary stenosis. Using the "best cutoff" method, the sensitivity and specificity for prediction of reduced RMBF (ischemia) was 81% and 91% for sSR and 65% and 91% for T RL, respectively. These changes occurred in the absence of any change in global systolic and diastolic function (dP/dT max, dP/dT min, and tau). Novel strain parameters that depict regional myocardial mechanics are able to predict changes in RMBF during dobutamine stress. Quantitative strain parameters may complement current echocardiographic techniques for ischemia detection and potentially improve the accuracy and reproducibility of stress echocardiography.
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U2 - 10.1016/j.jacc.2004.02.065
DO - 10.1016/j.jacc.2004.02.065
M3 - Article
C2 - 15489101
AN - SCOPUS:5644290755
SN - 0735-1097
VL - 44
SP - 1664
EP - 1671
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 8
ER -