The Impact of Cardiac Contractility on Cerebral Blood Flow in Ischemia

OBJECTIVE In cerebral regions affected by ischemia, intrinsic vascular autoregulation is often lost. Blood flow delivery depends upon cardiac function and may be influenced by neuro-endocrine mediated myocardial suppression. Our objective is to evaluate the relation between ejection fraction (EF) and transcranial doppler (TCD) peak systolic velocities (PSV) in patients with cerebral ischemic events. METHODS We conducted a retrospective cohort study from an existing TCD registry. We evaluated patients admitted within 24 hours of onset of a focal neurological deficit who had an echocardiogram and TCD performed within 72 hours of admission. RESULTS We identified 58 patients from March to October 2003. Eighty-one percent (n=47) had a hospital discharge diagnosis of ischemic stroke and 18.9% (n=11) had a diagnosis of transient ischemic attack. Fourteen patients had systolic dysfunction (EF<50%). The mean PSV in patients with normal systolic function (EF≥50%) compared to those with systolic dysfunction (EF<50%) was as follows: middle cerebral artery 62.0 ± 28.6 cm/s vs. 51.0 ± 23.3 cm/s, p=0.11; anterior cerebral artery 52.1 ± 21.6 cm/s vs. 45.9 ± 22.7 cm/s, p=0.28; internal carotid artery 56.5 ± 20.1 cm/s vs. 46.4 ± 18.4 cm/s, p=0.04; ophthalmic artery 18.6 ± 7.2 cm/s vs. 15.3 ± 5.2 cm/s, p=0.11; vertebral artery 34.0 ± 13.9 cm/s vs. 31.6 ± 15.0 cm/s, p=0.44. CONCLUSION Cerebral blood flow in the internal carotid artery territory appears to be higher in cerebral ischemia patients with preserved left ventricular contractility. Our study was unable to differentiate pre-existing cardiac dysfunction from neuro-endocrine mediated myocardial stunning. Future research is necessary to better understand heart-brain interactions in this setting and to further explore the underlying mechanisms and consequences of neuro-endocrine mediated cardiac dysfunction.