Myocardial dysfunction in subarachnoid hemorrhage: prognostication by echo cardiography and cardiac enzymes. A
Prasad Vannemreddy1, Prasanna Venkatesh, Kumar Dinesh
1Department of Neurosurgery, LSUHSC-Shreveport, Shreveport, LA 71103, USA. pvanne@lsuhsc.edu
Insights
Subarachnoid hemorrhage (SAH) can cause myocardial dysfunction, indicated by wall motion abnormalities (WMA). These patients exhibit higher troponin levels and poorer Glasgow Coma Scale (GCS) scores, highlighting significant cardiac impact.
Area of Science:
- Cardiology
- Neurology
- Critical Care Medicine
Background:
- Myocardial dysfunction following non-traumatic subarachnoid hemorrhage (SAH) is not well understood.
- Clinical significance of reported cardiac abnormalities in SAH patients remains uncertain.
Purpose of the Study:
- To prospectively evaluate cardiac dysfunction in patients with non-traumatic SAH.
- To investigate the relationship between cardiac dysfunction, biomarkers, and clinical outcomes in SAH.
Main Methods:
- Serial transthoracic echocardiograms assessed regional wall motion and left ventricular ejection fraction (LVEF).
- Cardiac enzymes (troponin) and Glasgow Coma Scale (GCS) were monitored.
- Patients without prior cardiac disease were included.
Main Results:
- Wall motion abnormalities (WMA) occurred in 20% of patients, predominantly global hypokinesia.
- Patients with WMA had significantly lower LVEF, higher troponin levels, and lower GCS on admission.
- WMA were associated with increased hospitalization duration.
Conclusions:
- Subarachnoid hemorrhage frequently leads to myocardial dysfunction, evidenced by WMA.
- WMA in SAH patients correlate with significant cardiac impairment, elevated troponin, and poorer neurological status.
- Cardiac dysfunction in SAH warrants further investigation due to its clinical implications.
Background:
The myocardial dysfunction in nontraumatic sub-arachnoid hemorrhage (SAH) is not well understood. Borderline elevations of cardiac biomarkers, electrocardiographic repolarization abnormalities and systolic dysfunction have been reported but the clinical significance of these abnormalities is uncertain.
Methods:
Patients without history of cardiac disease were prospectively evaluated for cardiac dysfunction. Myocardial regional wall motion and left ventricular ejection fraction (LVEF) were serially studied by transthoracic echocardiogram along with cardiac enzymes.
Results:
The mean age of the study population was 53 years. Majority of the patients had aneurysms (N = 38). The mean LVEF was 55 +/- 15%. Eight patients had evidence of WMA, mostly global hypokinesia (63%). The mean LVEF of patients with WMA was significantly lower compared to those without WMA (p < 0.001) at day 0. Systolic function recovered in 25% of these patients. The mean value of troponin was significantly higher in those with WMA (p < 0.001) and mean GCS upon admission was significantly lower (p < 0.001). On multivariate analysis, WMA were associated with poor GCS (p < 0.01) and increased hospitalization (P < 0.01).
Conclusions:
WMA with systolic dysfunction occurred in 20% of patients and recovered within 3 days in 25%. Patients with evidence of WMA had a significant myocardial dysfunction, higher troponin levels and poor GCS.
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