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.