Systemic Hypotension and the Development of Acute Sensorineural Hearing Loss in Young Healthy Subjects

Pirodda, Antonio; Ferri, Gian Gaetano; Modugno, Giovanni Carlo; Borghi, Claudio

doi:10.1001/archotol.127.9.1049

Cited by 54 publications

(24 citation statements)

References 15 publications

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“…There was also one 62-year-old patient who presented a bradycardia syndrome. These results are consistent with those of a previous small case-control study [Pirodda et al, 2001]. In our opinion, severe arterial hypotension or, hemodynamically, a poorly tolerated arterial hypotension may, especially in the case of older adults, be considered a risk factor for iSSNHL.…”

Section: Risk Of Coronary Heart Disease and Issnhlsupporting

confidence: 93%

Idiopathic Sudden Sensorineural Hearing Loss: Classic Cardiovascular and New Genetic Risk Factors

Ballesteros¹,

Tàssies

Reverter

et al. 2012

Audiol Neurotol

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Background: The main causative process in idiopathic sudden sensorineural hearing loss (iSSNHL) has yet to be explained or demonstrated. The clinical picture supports vascular involvement, but obvious limitations of inner ear study make this difficult to corroborate. Objectives: To determine the role of thrombophilic genetic variants that may affect platelet function and to assess the cardiovascular risk profile in a cohort of patients with iSSNHL. Patients and Methods: 118 Caucasian patients with iSSNHL were recruited from the same geographical area and enrolled prospectively in this study. Clinical data were obtained for each patient. Polymorphisms of the platelet glycoprotein subunit IIIa gene, ITGB3 (PLA1/A2, rs5918), and of the platelet glycoprotein subunit Ia gene, ITGA2 (C807T, rs1126643) were analyzed. A control group of 161 age- and gender-matched healthy individuals from the same geographical area was recruited for genetic comparisons. In order to determine the cardiovascular risk profile of each patient and of our cohort, a cross-sectional assessment was performed by means of a calibrated Framingham coronary heart disease risk scale. Risk factor proportions were compared to those recommended in European guidelines for coronary prevention, which are also based on the Framingham function. Results: A significantly high prevalence of the 807T allele of platelet glycoprotein subunit Ia was found in patients compared to controls. There was a significant correlation between the 807TT homozygous genotype and a low probability of recovery. The PLA1/A2 polymorphism of platelet glycoprotein subunit IIIa was not associated with recovery, with a similar genotype prevalence being found in patients and controls. In terms of cardiovascular risk profile, patients did not present an excess of baseline coronary risk factors compared to the general population in the same geographical area. Conclusions: Patients with iSSNHL had a higher prevalence of the 807T thrombophilic polymorphism of platelet glycoprotein Ia/IIa. Patients homozygous for this polymorphism are less likely to recover from iSSNHL. Classical cardiovascular risk factors were not related to iSSNHL.

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Section: Risk Of Coronary Heart Disease and Issnhlsupporting

confidence: 93%

Idiopathic Sudden Sensorineural Hearing Loss: Classic Cardiovascular and New Genetic Risk Factors

Ballesteros¹,

Tàssies

Reverter

et al. 2012

Audiol Neurotol

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“…The low amount of blood flow in the vertebrobasilar system causes ischemia in the cochlea and can lead to In our study, elevated IMT in patients with VBI supports the increased risk for atherosclerosis. Considering these conditions, it is more likely that patients with VBI have sensorineural hearing loss at all frequencies, apparently at bilateral high frequencies, as in our study, rather than hearing loss pattern at unilateral high frequencies as stated in literature (11,12). However, this study should be supported with further studies that will include higher number of patients and be conducted employing tests such as autoacoustic emission or auditory brain stem response audiometry for finding the causes of hearing loss.…”

Section: Discussionsupporting

confidence: 59%

Hearing Thresholds and Serum Apelin Levels in Patients with Vertebrobasilar Insufficiency

Ezerarslan¹,

Çandar²,

Özdemir³

et al. 2014

Turk Arch Otolaryngol

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Objective: Vertebrobasilar insufficiency (VBI) is a clinical entity that results from the decrease in flow volumes due to hemodynamic changes in the vertebral artery and its branches. Herein, we aimed to investigate the hearing thresholds and serum apelin levels in VBI patients who were admitted to our clinics with vertigo. Methods:Patients who were admitted to our clinics with vertigo were included in our study. They underwent bilateral carotid and vertebral artery color Doppler ultrasound investigation to determine VBI. Then, they were grouped into two groups: having VBI or not. Pure tone audiometry tests between 2500-8000 Hertz (Hz) were applied, and plasma levels of apelin, routine biochemistry parameters, and levels of C-reactive protein were studied in these patients.Results: Thirty-eight (47% women, mean age 57.6±9.3) patients with VBI and 24 controls (50% women, mean age 57.0±10.1) were included. In patients with VBI, hearing thresholds were higher in the left ear except at the 500 Hz frequency. Serum apelin levels were not statistically different between the 2 groups. Conclusion:In this study, several abnormalities in hearing tests were determined in VBI patients. The hypothesis was that basilar artery dysfunction caused by asymmetry of vertebral artery flow volumes in VBI might increase apelin levels, which have functions in angiogenesis, hemostasis, and cardiovascular hemodynamics. However, we could not find a significant difference in apelin levels between the 2 groups. This result was thought to be due to the absence of severe hemodynamic abnormalities and atherosclerosis in the study groups.

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“…This involves a reflex mechanism that depends on vagal activation through the transmission of pathological stimuli from vagal afferents to the brainstem, as reported concerning the stomach [11] . This reflex mechanism causes a sequence of hemodynamic changes that can affect the inner ear circulation [12] through a abrupt fall of the systemic blood pressure followed by an altered autonomic response. The vagal activation, causing a sharp hypotension, is subsequently followed by an exaggerated vasoconstriction that results in a transient lack of perfusion to the inner ear.…”

Section: Discussionmentioning

confidence: 99%

“…The vagal activation, causing a sharp hypotension, is subsequently followed by an exaggerated vasoconstriction that results in a transient lack of perfusion to the inner ear. This etiopathogenic model [11,12] suggests an opportunity for a multidisciplinary approach to inner ear dysfunction of uncertain origin and could explain a number of cases which would otherwise be classified as 'idiopathic'. The occurrence of such a kind of phenomenon in the reported case could actually be justified from both physical and psychogenic stimuli.…”

Section: Discussionmentioning

confidence: 99%

Sudden Bilateral Sensorineural Hearing Loss as an Unusual Consequence of Accidental Ingestion of Potassium Hydroxide

Ciorba

Bovo²,

Castiglione³

et al. 2010

Med Princ Pract

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Objective: To discuss the possible etiopathogenetic mechanism of inner ear damage induced by the ingestion of potassium hydroxide (KOH). Clinical Presentation and Intervention: We report the case of a 37-year-old patient with sudden bilateral sensorineural hearing loss after accidental ingestion of a KOH solution. The first ear, nose and throat examination disclosed only mild edema of the upper airways. He was treated in the intensive care unit and prescribed high-dose steroids, proton pump inhibitors and sucralfate for 2 weeks. Unfortunately, there was no recovery of the hearing loss, and no audiogram changes were noticed after 12 months of follow-up.Conclusion: After exploring the possible etiopathogenetic mechanism involved, the authors believe that in this case, a transient severe hemodynamic imbalance can actually be considered to be the most reliable explanation for the inner ear damage and subsequent onset of permanent bilateral sensorineural hearing loss.

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Systemic Hypotension and the Development of Acute Sensorineural Hearing Loss in Young Healthy Subjects

Abstract: Systemic hypotension must be considered as the possible cause responsible for the development of SSHL in young healthy subjects.

Cited by 54 publications

References 15 publications

Idiopathic Sudden Sensorineural Hearing Loss: Classic Cardiovascular and New Genetic Risk Factors

Idiopathic Sudden Sensorineural Hearing Loss: Classic Cardiovascular and New Genetic Risk Factors

Hearing Thresholds and Serum Apelin Levels in Patients with Vertebrobasilar Insufficiency

Sudden Bilateral Sensorineural Hearing Loss as an Unusual Consequence of Accidental Ingestion of Potassium Hydroxide

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