Related Experiment Video
Updated: May 31, 2026
Contractility Measurements on Isolated Papillary Muscles for the Investigation of Cardiac Inotropy in Mice
Published on: September 17, 2015
The impact of cardiac contractility on cerebral blood flow in ischemia
Charles R Wira1, Emanuel Rivers, Brian Silver
1Yale School of Medicine, New Haven, CT.
Insights
Cerebral blood flow may be higher in patients with cerebral ischemia and preserved heart function. Further research is needed to understand the complex heart-brain interactions in these patients.
Area of Science:
- Neurology
- Cardiology
- Vascular Medicine
Background:
- Cerebral ischemia often impairs intrinsic vascular autoregulation, making blood flow dependent on cardiac function.
- Neuro-endocrine mechanisms can influence myocardial function in patients with cerebral events.
Purpose of the Study:
- To evaluate the relationship between ejection fraction (EF) and transcranial Doppler (TCD) peak systolic velocities (PSV) in patients experiencing cerebral ischemic events.
Main Methods:
- Retrospective cohort study using data from a TCD registry.
- Inclusion criteria: patients admitted within 24 hours of focal neurological deficit onset, with echocardiogram and TCD performed within 72 hours.
Main Results:
- 58 patients were analyzed; 81% had ischemic stroke, 18.9% transient ischemic attack.
- Patients with systolic dysfunction (EF<50%) showed lower mean PSV in the internal carotid artery (46.4 ± 18.4 cm/s) compared to those with normal systolic function (EF≥50%) (56.5 ± 20.1 cm/s, p=0.04).
- No significant differences in PSV were observed in other assessed cerebral arteries (MCA, ACA, OPA, VA).
Conclusions:
- Cerebral blood flow in the internal carotid artery territory may be higher in cerebral ischemia patients with preserved left ventricular contractility.
- The study could not distinguish between pre-existing cardiac dysfunction and neuro-endocrine mediated myocardial stunning.
- Further research is essential to elucidate heart-brain interactions and the mechanisms of neuro-endocrine cardiac dysfunction in cerebral 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.
More Related Videos
Related Concept Videos
01:22Cardiac Output II: Effect of Stroke Volume on Cardiac Output
Preload
Preload refers to the initial elongation of the cardiac myocytes before contraction and is related to the volume of blood filling the heart at the end of diastole, or end-diastolic volume. The...
01:29Pathophysiology of Cardiac Performance
01:15Ischemic Stroke ll: Pathophysiology
01:19Cardiac Output I:Effect of Heart Rate on Cardiac Output
Cardiac output (CO) refers to the total amount of blood ejected by one of the ventricles in liters per minute (L/min). In a resting adult, CO ranges from 5 to 6 L/min, adjusting according to the body's metabolic requirements.
Effect of Heart Rate on Cardiac Output
Cardiac output adapts to metabolic demands during stress, physical activity, or illness. The autonomic nervous system regulates heart rate via the sinoatrial node. The parasympathetic nervous system decreases heart rate...
01:27Regulation of Stroke Volume
Preload refers to the degree of stretch on the heart before it contracts. It's analogous to the stretching of a rubber band; the more it's stretched, the more forcefully it snaps back. This concept is encapsulated in the Frank-Starling law of the...
01:26Imbalances in Cardiac Output
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send blood...