Subarachnoid hemorrhage induces an early and reversible cardiac injury associated with catecholamine release: one-week follow-up studyReport as inadecuate

Subarachnoid hemorrhage induces an early and reversible cardiac injury associated with catecholamine release: one-week follow-up study - Download this document for free, or read online. Document in PDF available to download.

Critical Care

, 18:558

First Online: 30 October 2014Received: 07 June 2014Accepted: 29 September 2014


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.

AbbreviationsA velocitylate peak velocity

BNPB-type natriuretic peptide

CNScentral nervous system

CTcomputed tomography

cTnItroponin Ic

DTdeceleration time

E velocityearly peak velocity

ELISAenzyme-linked immunosorbent assay

FiO2inspired oxygen fraction

HPLChigh performance liquid chromatography

ICPintracranial pressure


LVleft ventricular

LVEFleft ventricular ejection fraction

PaO2arterial partial pressure of oxygen

ROCreceiver operator characteristic

RWMAregional wall motion abnormalities

SAHaneurysmal subarachnoid hemorrhage



SPAPsystolic pulmonary artery pressure

TAPSEtricuspid annular plane systolic excursion

TTEtransthoracic electrocardiography

WFNSWorld Federation of Neurosurgical Societies

Electronic supplementary materialThe online version of this article doi:10.1186-s13054-014-0558-1 contains supplementary material, which is available to authorized users.

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Author: Reda Salem - Fabrice Vallée - François Dépret - Jacques Callebert - Jean Pierre Saint Maurice - Philippe Marty - Joaqui


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