TY - JOUR
T1 - Coronary autoregulation is abnormal in syndrome X
T2 - Insights using myocardial contrast echocardiography
AU - Rinkevich, Diana
AU - Belcik, Todd
AU - Gupta, Nandita C.
AU - Cannard, Elizabeth
AU - Alkayed, Nabil J.
AU - Kaul, Sanjiv
N1 - Funding Information:
This study was supported in part by grants to Dr. Rinkevich from the Bechen Family Foundation and the Alpha Phi Foundation (Portland, OR) and grants R01 NS44313 and NS070837 to Dr. Alkayed and PO1-HD034430 to Dr. Kaul from the National Institutes of Health (Bethesda, MD).
PY - 2013/3
Y1 - 2013/3
N2 - Background: Syndrome X in women is thought to be caused by coronary microvascular dysfunction, the exact site of which is unknown. The aim of this study was to characterize the microvascular site of dysfunction in these patients using myocardial contrast echocardiography. Methods: Women with exertional angina, positive test results on stress imaging, but no coronary artery disease (the study group, n = 18) and age-matched control women also with no coronary artery disease (n = 17) were enrolled. Myocardial contrast echocardiography was performed at rest and during dipyridamole-induced hyperemia. Mean microbubble velocity (β) and myocardial blood volume (A) were measured, and myocardial blood flow (A · β) was computed. In addition, plasma concentrations of eicosanoids, female sex hormones, and C-reactive protein were measured. Results: Rest β and myocardial blood flow (A · β) were higher in the study compared with the control women (1.61 ± 0.68 vs 0.74 ± 0.44, P =.0001, and 157 ± 121 vs 54 ± 54, P = 0.0001, respectively) despite similar heart rates and systolic blood pressures. After the administration of dipyridamole, whereas the changes in A and A · β were not significantly different between the two groups, β reserve (the ratio of stress β to rest β) was markedly lower in the study group (1.48 ± 0.62 vs 2.78 ± 0.94, P =.0001). Blood hematocrit, eicosanoids, female sex hormones, glucose, and C-reactive protein were not different between the two groups. Conclusions: Coronary autoregulation is abnormal in patients with syndrome X (higher resting β and myocardial blood flow and lower β reserve), which suggests that the coronary resistance vessels are the site of microvascular abnormality.
AB - Background: Syndrome X in women is thought to be caused by coronary microvascular dysfunction, the exact site of which is unknown. The aim of this study was to characterize the microvascular site of dysfunction in these patients using myocardial contrast echocardiography. Methods: Women with exertional angina, positive test results on stress imaging, but no coronary artery disease (the study group, n = 18) and age-matched control women also with no coronary artery disease (n = 17) were enrolled. Myocardial contrast echocardiography was performed at rest and during dipyridamole-induced hyperemia. Mean microbubble velocity (β) and myocardial blood volume (A) were measured, and myocardial blood flow (A · β) was computed. In addition, plasma concentrations of eicosanoids, female sex hormones, and C-reactive protein were measured. Results: Rest β and myocardial blood flow (A · β) were higher in the study compared with the control women (1.61 ± 0.68 vs 0.74 ± 0.44, P =.0001, and 157 ± 121 vs 54 ± 54, P = 0.0001, respectively) despite similar heart rates and systolic blood pressures. After the administration of dipyridamole, whereas the changes in A and A · β were not significantly different between the two groups, β reserve (the ratio of stress β to rest β) was markedly lower in the study group (1.48 ± 0.62 vs 2.78 ± 0.94, P =.0001). Blood hematocrit, eicosanoids, female sex hormones, glucose, and C-reactive protein were not different between the two groups. Conclusions: Coronary autoregulation is abnormal in patients with syndrome X (higher resting β and myocardial blood flow and lower β reserve), which suggests that the coronary resistance vessels are the site of microvascular abnormality.
KW - Coronary autoregulation
KW - Myocardial contrast echocardiography
KW - Syndrome X
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U2 - 10.1016/j.echo.2012.12.008
DO - 10.1016/j.echo.2012.12.008
M3 - Article
C2 - 23313388
AN - SCOPUS:84874659680
SN - 0894-7317
VL - 26
SP - 290
EP - 296
JO - Journal of the American Society of Echocardiography
JF - Journal of the American Society of Echocardiography
IS - 3
ER -