Peripheral flow response to transient arterial forearm occlusion does not reflect myocardial perfusion reserve

Background-Ultrasonographic evaluation of systemic arterial function is wid ely available, and a close relation of endothelial function in the coronary and brachial arteries has been documented. It is unknown, however, whether a similar correlation exists for their 2 microcirculatory territories and thus whether assessment of the systemic microcirculation can be used simila rly as a surrogate marker of myocardial perfusion. Methods and Results-Twenty-three patients with documented coronary artery d isease (CAD; 66+/-9 pears old, 18 men), 16 patients with syndrome X (SX; 56 +/-5 years old, 13 women), and 45 healthy control subjects (C; 34+/-9 years old, 22 men) were studied. Myocardial perfusion was measured at rest and a fter dipyridamole (0.56 mg . kg(-1) . min(-1) over 4 minutes) by PET, and b rachial artery blood flow was measured at rest and after transient forearm ischemia by standard Doppler ultrasound techniques, Dipyridamole increased myocardial perfusion in all groups (mL . g(-1) . min(-1): CAD, 0.89+/-0.27 versus 1.62+/-0.67, P<0.001; SX, 0.82+/-0.16 versus 1.67+/-0.49, P<0.001; a nd C, 0.82+/-0.15 versus 2.32+/-0.64, P<0.001), Postocclusion forearm flow increased similarly in all groups (CAD, 52+/-18 versus 174+/-77 mL/min, P<0 .001; SX, 49+/-29 versus 202+/-82 mL/min, P<0.001; and C, 61+/-34 versus 22 9+/-108 mL/min, P<0.001). No significant: correlations were found between p eripheral and myocardial microcirculatory beds for either resting flow, hyp eremic flow, or flow reserve in any of the groups (r(2)<0.1, P=NS). Conclusions-The peripheral perfusion responses to transient forearm ischemi a do not correlate with dipyridamole-induced myocardial hyperemia, The lack of correlation indicates different mechanisms of microvascular activation or regulation and confirms that extrapolations between findings in the 2 va scular beds are not suitable.