Hearing impairment is the most prevalent sensory deficit [1].
Sensorineural hearing loss (SNHL) is the most common type of permanent
hearing loss and it occurswhen there is damage to the inner ear
(cochlea), or to the nerve pathways fromthe inner ear to the brain.Most
of the time, SNHL cannot be medically or surgically corrected.
SNHL can result from genetic, environmental, or combined etiologies
that prevent normal function of hearing, but, despite detailed investigation,
the main cause remains usually unknown. Clinical and experimental
studies have shown that ischemia contributes to several SNHL [2], suchas
sudden sensoneural hearing loss, presbyacusis and noise-induced hearing
loss. All of these SNHL can be related to alteration in blood flow [3].
The aim of the study is finding a relationship between idiopathic
SNHL and endothelial dysfunction

Abbate A.

Bressi E.

Casale M.

Di Sciascio G.

Mangiacapra F.

Moffa A.

Pace A.

Sabatino L.

Salvinelli F.

English

Archivio della ricerca- Università di Roma La Sapienza

IJC Heart & Vasculature 12 (2016) 32–33Contents lists available at ScienceDirectIJC Heart & Vasculaturej ourna l homepage: ht tp : / /www. journa ls .e lsev ie r .com/ i jc -hear t -and-vascu la tureIdiopathic sensorineural hearing loss is associated withendothelial dysfunctionManuele Casale a, Fabio Mangiacapra b, Edoardo Bressi c, Annalisa Pace d, Lorenzo Sabatino e,⁎, Antonio Moffa f,Antonio Abbate g, Germano Di Sciascio h, Fabrizio Salvinelli iUnit of Otolaryngology University Campus Bio-Medico, Rome, ItalyUnit of Cardiovascular Science, University Campus Bio-Medico, Rome, ItalyUnit of Cardiovascular Science, University Campus Bio-Medico, Rome, ItalyUnit of Otolaryngology, University Campus Bio-Medico, Rome, ItalyUnit of Otolaryngology, University Campus Bio-Medico, Rome, ItalyUnit of Otolaryngology, University Campus Bio-Medico, Rome, ItalyDivision of Cardiology, VCU Pauley Heart Center, Virginia Commonwealth University, Richmond, VA, Unites StatesUnit of Cardiovascular Science, University Campus Bio-Medico, Rome, ItalyUnit of Otolaryngology, University Campus Bio-Medico, Rome, Italy⁎ Corresponding author at: Unit of Otolaryngology, DepCampus Bio-Medico di Roma, via Álvaro del Portillo 21, 0E-mail address: l.sabatino@unicampus.it (L. Sabatino)http://dx.doi.org/10.1016/j.ijcha.2016.05.0012352-9067/© 2016 The Authors. Published by Elsevier Irea r t i c l e i n f oArticle history:Received 21 March 2016Accepted 2 May 2016Available online 17 June 2016hearing loss, aural pressure or episodic tinnitus preceding the ISSHLepisode);• Cerebello-pontine angle pathology at MRI;• History of otologic surgery;• Head and/or neck trauma or barotrauma in the 10 weeks prior toaudiological evaluationKeywords:Sensorineural hearing lossInner earHearingOmega 3Endothelial dysfunctionHearing impairment is the most prevalent sensory deficit [1].Sensorineural hearing loss (SNHL) is the most common type of per-manent hearing loss and it occurswhen there is damage to the inner ear(cochlea), or to thenerve pathways from the inner ear to thebrain.Mostof the time, SNHL cannot be medically or surgically corrected.SNHL can result from genetic, environmental, or combined etiologiesthat prevent normal function of hearing, but, despite detailed investiga-tion, themain cause remains usually unknown. Clinical and experimentalstudies have shown that ischemia contributes to several SNHL [2], such assudden sensoneural hearing loss, presbyacusis and noise-induced hear-ing loss. All of these SNHL can be related to alteration in blood flow [3].The aim of the study is finding a relationship between idiopathicSNHL and endothelial dysfunction.52 patients affected by SNHL fromMarch to April 2015 at the Unit ofOtolaryngology of Campus Bio-Medico University of Rome were en-rolled. The exclusion criteria were:artment ofMedicine, Università0128 Rome, Italy..land Ltd. This is an open access articl• Fluctuating cochlea-vestibular dysfunction suggestive of endo-lymphatic hydrops (history of vertigo with either fluctuating• otitis media in the last 10 weeks;• neurologic disorders predisposing to deafness;• recent use of ototoxic medications;• othermajor comorbidities (heart failure, severe pulmonary, hepatic orrenal dysfunction).All included patients underwent to audiological evaluation and tocardiovascular assessment with brachial artery FMD evaluation. Thestudy was approved by the institutional ethics committee.All of the patients underwent a standard pure tone audiometry andthe hearing threshold at each frequencywas calculated. The air conduc-tion pure tone average was obtained by the air conduction at 250, 500,1000, 2000, 4000, and 8000 Hz.Noninvasive endothelial function assessment was performed withultrasound detection of brachial artery reactivity to flow as previouslyreported [4] by a single operator. Patients were asked to abstain fromsmoking, drinking coffee or tea and from physical activity for 60 min,and to discontinue medications for 12 h before endothelial function as-sessment. Two-dimensional brachial artery imaging was obtained onthe dominant forearmwith the patient supine using a 10-MHzmultifre-quency linear array probe attached to a high-resolution ultrasoundma-chine. Straight segments (8 to 10 mm in length) of the artery wereidentified above the antecubital fossa, perpendicular to the ultrasoundbeam and along its long axis. Flow-mediated dilation (FMD) due toshear-induced endothelial nitric oxide release was evaluated after oc-clusion of the forearm circulation. Briefly, a longitudinal image was se-lected to calculate brachial artery diameter (first baseline value), thene under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).Fig. 2.Hearing threshold in patients with (ED) andwithout (nED) endothelial dysfunctionat 8000 Hz: it shows how those ones, who were positive in the FMD, demonstrating anendothelial disease, were also have positive for 8000 Hz hearing loss. Here there werealso a significant correlation (p = 0.008).33M. Casale et al. / IJC Heart & Vasculature 12 (2016) 32–33a blood pressure cuff was inflated on the upper arm to 50mmHg abovethe systolic pressure for 5 min and then deflated. 1 min after cuff defla-tion, a second longitudinal scanwas obtained, and brachial artery diam-eter was measured (post-occlusion value). FMD was expressed aspercent diameter variation. Brachial artery diameters were measuredfrom near-to-far blood-wall interface (intima-media interfaces) atend-diastole in the cardiac cycle (onset of the R-wave at ECG-gatingduring image acquisition). Five cardiac cycles were analyzed and aver-aged for each scan. Intraobserver variationswere 1.25± 0.8% in 10 ran-domly selected patients with two repeated measurements. FMD valuesb11% were considered as indicative of endothelial dysfunction [5,6].All data was taken from medical records of our institution andanalyzed. All the authors were also treating physicians of the includedpatients. Statistical analysis was carried out using STATA/IC 12 (STATACorp., College Station, Texas) and significance was defined as a pvalue b 0.05.At the end of our selection process, 34 patients were prospectivelyincluded and retrospectively analyzed. Patients showed a median ageof 48; (19–65 years).The patients with altered FMD showed a worst hearing level thresh-old for all evaluated frequencies, reaching statistical significance at8000 Hz.The degree of hearing loss, calculated at 8000Hz,was significant cor-related with flow mediated dilatation (FMD)(r = −0.492 and p =0.003)(Fig. 1). That is, patients with higher degrees of hearing loss hadworst FMD (p b 0.05) (Fig. 2).At multivariate analysis, FMD values were independently associatedwith pure tone average at 8000 Hz, even after adjustment for age, gen-der, BMI and cardiovascular risk factors (beta = −3.138, p = 0.036.Sensorineural hearing loss is a common ill-defined clinical condition.Several hypotheses have attempted to explain its pathogenesis. Cochle-ar blood flow impairment has been considered as one of the pathophys-iological mechanism of SNHL.The anterior inferior cerebellar artery (AICA), with its labyrinthineartery, is the supplier of the inner ear. It develops arterioles branchthat radiate running centrifugally over the scala vestibule and acrossthe spiral lamina. Eventually a centripetal system of radiating venulescollects blood.In idiophatic SNHL thebasis of cochlea is typically involved, due to itstonotopic organization, known that the hair cell of basal turn of the co-chlea are more sensitive to noxa pathogena then the apex [7].Basal outer hair cells are also more susceptible to free radical dam-age, because of the lower level of glutathione [8].Our preliminary data show a relationship between SNHL andendothelial dysfunction. Similar studies also confirm the role of endo-thelial dysfunction on other types of hearing loss [9]. This suggests atherapeutic opportunity for patients affected by progressive or earlySNHL; in particular, the ameliorating of microcirculation could slow orFig. 1. Correlation between pure tone average and flowmediated dilatation (FMD). Fromthis inferred a high statistical significance (r = +0.492 and p = 0.003)stop the progression of the disease including omega-3 (omega-3) poly-unsaturated fatty acids (PUFAs). It is known that omega-3 PUFAs im-prove both small and large arteries vasodilatation and compliancereducing the formation of angiotensin II and enhancing nitric oxide(NO) generation. An additional favorable effect on the microcirculationcan be exerted by anti-inflammatorymediators, ameliorating the vascu-larization of small ear vessels that usually cause inner ear injury. If thecorrelation between SNHL and endothelial dysfunction is confirmed instudies on larger scale, SNHL without any evident hearing loss risk fac-tors, especially for high frequencies, could be considered amarker of en-dothelial dysfunction and consequently identify subjects with a majorcardiovascular risk.Conflict of interestThe authors report no relationships that could be construed as a con-flict of interest.References[1] K.P. Steel, New interventions in hearing impairment, BMJ 320 (2000) 622–625.[2] P.R. Thorne, A.L. Nuttall, Laser Doppler measurements of cochlear blood flow duringloud sound exposure in the guinea pig, Hear. Res. 27 (1987) 1–10.[3] M.D. Seidman, W.S. Quirk, N.A. Shirwany, Mechanisms of alterations in the microcir-culation of the cochlea, Ann. N. Y. Acad. Sci. 884 (1999) 226–232.[4] G. Patti, V. Pasceri, R. Melfi, C. Goffredo, M. Chello, et al., Impaired flow-mediated di-lation and risk of restenosis in patients undergoing coronary stent implantation, Cir-culation 111 (2005) 70–75.[5] K.E. Pyke, M.E. Tschakovsky, The relationship between shear stress and flow-mediated dilatation: implications for the assessment of endothelial function, J. Phys-iol. 568 (2005) 357–369.[6] M.C. Corretti, T.J. Anderson, E.J. Benjamin, D. Celermajer, F. Charbonneau, et al., Guide-lines for the ultrasound assessment of endothelial-dependent flow-mediated vasodi-lation of the brachial artery: a report of the International Brachial Artery ReactivityTask Force, J. Am. Coll. Cardiol. 39 (2002) 257–265.[7] T. Nakashima, S. Naganawa, M. Sone, M. Tominaga, H. Hayashi, et al., Disorders of co-chlear blood flow, Brain Res. Brain Res. Rev. 43 (2003) 17–28.[8] F. Scheibe, H. Haupt, C. Ludwig, Intensity-related changes in cochlear blood flow inthe guinea pig during and following acoustic exposure, Eur. Arch. Otorhinolaryngol.250 (1993) 281–285.[9] M.M. Ciccone, F. Cortese, M. Pinto, C. Di Teo, F. Fornarelli, et al., Endothelial functionand cardiovascular risk in patients with idiopathic sudden sensorineural hearingloss, Atherosclerosis 225 (2012) 511–516.

Idiopathic sensorineural hearing loss is associated with endothelial dysfunction

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Idiopathic sensorineural hearing loss is associated with endothelial dysfunction

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