Abstract
IntroductionThe occurrence of cardiac dysfunction is common after subarachnoid hemorrhage (SAH) and was hypothesized to be related to the release of endogenous catecholamines. The aim of this prospective study was to evaluate the relationship between endogenous catecholamine and cardiac dysfunction at the onset and during the first week after SAH.MethodsForty consecutive patients admitted for acute SAH without known heart disease were included. Catecholamine plasma concentrations and transthoracic echocardiography (TTE) were documented on admission, on day 1 (D1), and day 7 (D7).ResultsAt baseline, 24 patients had a World Federation of Neurosurgical Societies score (WFNS) of one or two; the remaining 16 had a WFNS between three and five. Twenty patients showed signs of cardiac dysfunction on admission, including six with left ventricle (LV) systolodiastolic dysfunction and 14 with pure LV diastolic dysfunction. On admission, norepinephrine, epinephrine, dopamine, B-type Natriuretic Peptide (BNP) and Troponin Ic (cTnI) plasmatic levels were higher in patients with the higher WFNS score and in patients with altered cardiac function (all P <0.05). Among patients with cardiac injury, heart function was restored within one week in 13 patients, while seven showed persistent LV diastolic dysfunction (P = 0.002). Plasma BNP, cTnI, and catecholamine levels exerted a decrease towards normal values between D1 and D7.ConclusionOur findings show that cardiac dysfunction seen early after SAH was associated with both a rapid and sustained endogenous catecholamine release and WFNS score. SAH-induced cardiac dysfunction was regressive over the first week and paralleled the normalization of catecholamine concentration.
Highlights
The occurrence of cardiac dysfunction is common after subarachnoid hemorrhage (SAH) and was hypothesized to be related to the release of endogenous catecholamines
Our study showed that cardiac alterations associated with SAH included left ventricle (LV) diastolic function and right ventricular function that both require careful hydration
In case echocardiography is not available, our study suggests the possibility to use plasma B-type natriuretic peptide (BNP) as a surrogate marker, and to consider BNP plasma level >300 pg/ ml on admission as being strongly associated with cardiac dysfunction
Summary
The occurrence of cardiac dysfunction is common after subarachnoid hemorrhage (SAH) and was hypothesized to be related to the release of endogenous catecholamines. The aim of this prospective study was to evaluate the relationship between endogenous catecholamine and cardiac dysfunction at the onset and during the first week after SAH. Other studies have shown an association between cTnI [9,11], BNP levels [6], clinical SAH severity, and the presence of cardiac dysfunction [11,12,13]. It has been suggested that the pathophysiology of cardiac injury after SAH is similar to apical ballooning syndrome (Takotsubo or stress cardiomyopathy) that is, in relation to catecholamine endogenous release [14]. Few human studies have shown an association between catecholamine release and cardiac dysfunction at an early stage after SAH, and to our knowledge few human studies have focused on the time course of catecholamine release and cardiac dysfunction during SAH [5,15]
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