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.

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.

The Berlin 'Cream&Sugar' Study: the prognostic impact of an oral triglyceride tolerance test in patients after acute ischaemic stroke.

RATIONALE: Stratification according to risk factors is crucial for secondary prevention after acute ischaemic stroke. Nonfasting triglyceride levels seem to be associated with stroke in the general population. However, the exact role of triglyceride levels for the risk of recurrent stroke is unknown. HYPOTHESIS: We hypothesise that the results of a standardised oral triglyceride tolerance test in the subacute setting (3-7 days) after the first ischaemic stroke are associated with the risk of recurrent stroke within 12 months after the index event. DESIGN: Prospective observational study. STUDY OUTCOME(S): The primary end-point of the study is recurrent fatal or nonfatal stroke within 12 months. The secondary outcomes are myocardial infarction, coronary revascularisation, cardiovascular death (death due to any cardiovascular or cerebrovascular event), or a transient ischaemic attack within 12 months after the qualifying event. DISCUSSION: The study has the potential to change clinical practice. It will show whether the oral triglyceride tolerance test in the subacute setting is a useful tool to predict the risk of recurrent stroke.