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. 2010;30(6):612-7.
doi: 10.1159/000319891. Epub 2010 Oct 15.

Does External Counterpulsation Augment Mean Cerebral Blood Flow in the Healthy Brain? Effects of External Counterpulsation on Middle Cerebral Artery Flow Velocity and Cerebrovascular Regulatory Response in Healthy Subjects

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Does External Counterpulsation Augment Mean Cerebral Blood Flow in the Healthy Brain? Effects of External Counterpulsation on Middle Cerebral Artery Flow Velocity and Cerebrovascular Regulatory Response in Healthy Subjects

G J Jungehuelsing et al. Cerebrovasc Dis. .

Abstract

Background and purpose: External counterpulsation (ECP) noninvasively improves myocardial and organ perfusion via diastolic augmentation. The effects on cerebral blood flow velocities (CBFV) and hemodynamics are controversial. In this study, the effect of active ECP treatment on CBF in healthy subjects was continuously measured.

Methods: In 9 healthy volunteers (mean age 34.1 ± 11.1 years, 4 females), 20-min active ECP treatment was performed. CBFV in the middle cerebral artery were detected via transcranial Doppler. CBFV were registered continuously before, during and after ECP. The protocol was repeated twice.

Results: At onset of ECP, immediate changes in CBFV were observed: peak diastolic blood flow velocities increased from baseline to treatment (63 vs. 76 cm/s; p < 0.001) and diastolic blood flow augmentation was maintained throughout ECP. Peak systolic (87 vs. 78 cm/s; p < 0.001) and end-diastolic velocities (40 vs. 28 cm/s; p < 0.001) decreased significantly, while mean CBFV maintained constant (59 vs. 58 cm/s; not significant). The pulsatility index and resistance index as indirect parameters for peripheral vascular resistance increased during ECP (pulsatility index 0.79 vs. 0.89, p < 0.001; resistance index 0.54 vs. 0.64; p < 0.001).

Conclusions: ECP did not increase mean CBFV in healthy subjects even though peak diastolic CBFV were significantly augmented. Changes in CBFV and transcranial Doppler waveform characteristics suggest that the mean flow of the middle cerebral artery is maintained stable via cerebrovascular autoregulatory mechanisms.

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