机构地区:[1]Department of Neuroscience, Winthrop University Hospital, Mineola, New York, USA
出 处:《World Journal of Cardiovascular Diseases》2015年第11期307-312,共6页心血管病(英文)
摘 要:Acute neurological injuries cause catecholamine-induced cardiac damage and can result in or ex-acerbate preexisting cardiac failure. Milrinone (primacor) has been effective in the treatment of cardiac failure as well as cerebral vasospasm. We would like to present the outcomes of milrinone use in patients with major neurological injuries and preexisting compromised myocardial function. Four patients, age < 60 y/old, three women (two postpartum) and one man, will be presented. Two were diagnosed with a subarachnoid hemorrhage (SAH) coupled with severe vasospasm;one had status epilepticus (SE);and one had cerebral ischemia (CVA) due to carotid artery occlusion. All patients had cardiomyopathy with EF < 35%. All patients were on at least one press or prior to being put on milrinone. Three out of the four patients required an increase in norepinephrine or additional pressors after milrinone was added. All of the patients developed tachycardia, three severe and one mild. In two patients milrinone had to be discontinued due to the persistent hypotension. In our experience, use of milrinone drip in patients with preexisting cardiomyopathy led to hypotension and tachycardia, and brought about the need to increase or add new pressors, which in turn exacerbated catecholamine-induced myocardial injury.Acute neurological injuries cause catecholamine-induced cardiac damage and can result in or ex-acerbate preexisting cardiac failure. Milrinone (primacor) has been effective in the treatment of cardiac failure as well as cerebral vasospasm. We would like to present the outcomes of milrinone use in patients with major neurological injuries and preexisting compromised myocardial function. Four patients, age < 60 y/old, three women (two postpartum) and one man, will be presented. Two were diagnosed with a subarachnoid hemorrhage (SAH) coupled with severe vasospasm;one had status epilepticus (SE);and one had cerebral ischemia (CVA) due to carotid artery occlusion. All patients had cardiomyopathy with EF < 35%. All patients were on at least one press or prior to being put on milrinone. Three out of the four patients required an increase in norepinephrine or additional pressors after milrinone was added. All of the patients developed tachycardia, three severe and one mild. In two patients milrinone had to be discontinued due to the persistent hypotension. In our experience, use of milrinone drip in patients with preexisting cardiomyopathy led to hypotension and tachycardia, and brought about the need to increase or add new pressors, which in turn exacerbated catecholamine-induced myocardial injury.
关 键 词:NEUROGENIC CARDIOMYOPATHY Pressors SUBARACHNOID Hemorrhage
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