Peripheral Flow Response to Transient Arterial Forearm Occlusion Does Not Reflect Myocardial Perfusion Reserve

Abstract

Background —Ultrasonographic evaluation of systemic arterial function is widely 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 similarly as a surrogate marker of myocardial perfusion. Methods and Results —Twenty-three patients with documented coronary artery disease (CAD; 66±9 years 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 after dipyridamole (0.56 mg · kg −1 · min −1 over 4 minutes) by PET, and brachial 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; and 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 229±108 mL/min, P <0.001). No significant correlations were found between peripheral and myocardial microcirculatory beds for either resting flow, hyperemic flow, or flow reserve in any of the groups ( r 2 <0.1, P =NS). Conclusions —The peripheral perfusion responses to transient forearm ischemia 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 vascular beds are not suitable.