University of Texas Health Science Center, USA
Augusto Parra graduated from the University del Bosque Medical School (Bogota-Colombia) in 1988. He obtained an MPH in Biostatistics/Epidemiology from Harvard University in 1992. He pursued clinical training in Neurology and Internal Medicine at Duke University. He completed a Fellowship in Neurocritical Care and Stroke at Duke University in 2001. He is a Neurocritical Care Faculty at Columbia University and at the University of Texas –SA, where he currently directs the Neuro –ICU Program. He has done basic and clinical research, published in the leading scientific medical journals, done editorial peer review, and has been part of the American Heart Association –Brain 1 Basic Science Grant Review Committee for several years. He has special research interest in the repercussions of brain injury into the cardiovascular system and vice versa.
Objective: To study the influence of moderate to severe left ventricular dysfunction [SLVD] from myocardial stunning in increasing the risk of cerebrovascular and cardiovascular events among patients with acute aneurysmal subarachnoid hemorrhage [aSAH].
Methods: A subset of 119 patients (from an prospective cohort of 481 aSAH) with at least one echocardiogram, serial transcranial Doppler [TCD] data, and with no prior history of cardiac disease and or left ventricular dysfunction [LVD] was analysed. LVD’s cutoff was a LVEF of < 40%. The study population for cardio- and cerebrovascular events, and functional outcome and the most predicable Troponin I cut-off for SLVD and role of delayed vasospasmin increasing the likelihood of cerebral ischemic injury in the presence of SLVD were assessed.
Results: SLVD was found in 11% of our study-patients.Younger age, hydrocephalus, and complete filling of the quadrigeminal and fourth ventricles wereassociated with SLVD (all P<0.05). None of the patient's taking antihypertensive medications developed SLVD in our study population. There was a significant association between SLVD and infarction from vasospasm after adjusting for clinical grade, age and peak TCD mean velocities (surrogate for delayed vasospasm severity) (P=0.03). SLVD was also a significant predictor for cardiogenic shock (P=0.001), and pulmonary edema (P=0.002). However, a significant association between SLVD and 14 –day functional outcome in study population was not found.
Conclusions: SLVD after aSAH increases the risk of ischemic cerebrovascular events (especially if significant delayed vasospasm occurs), cardiogenic shock, and pulmonary edema. We were unable to find a significant association of SLVD and 14-day functional outcome or mortality. The later could be explained by the benefits of specialized Neuro-ICU support and an underpowered study population to detect this specific association. Antihypertensive medication appears to be cardio-protective for the development of SLVD after aSAH (myocardial stunning).