 Coronary collateral blood flow occurs almost entirely during diastole. Fluid shear stress FSS is the driving force in the formation, promotion and maintenance of collaterals i.e. arteriogenesis. It is the product of blood viscosity and shear rate, the latter being the fluid velocity change between different fluid layers which is related to the fluid velocity at the endothelium. Prolongation of diastole via reduction of resting heart rate RHR is naturally equal to extension of shear stress at the endothelium. Bradycardia is likely to be the key factor for augmented collateral function: In several animal models, an inverse relation between heart rate and collateral function was found. We have recently confirmed this finding investigating collateral function measurements in normal coronary arteries of our patient population. 