Patients who have an acute onset of hearing loss, in whom examination reveals no underlying condition identifiable by history or examination, are considered to have sensorineural hearing loss (SNHL). SNHL has been known to affect both men and women equally with peak incidences occurring between 50-60% [5]. Though SNHL is very rare in occurrence, between 5 and 30 individuals out of every 100,000 persons annually [6], the etiology still remains largely unknown. There are evidence suggesting its association with an underlying cardiovascular mechanism in some patients [1, 7, 8]. There have been cases reporting that SNHL is associated as an early sign of stroke [9] and another study progressed on in estimating risk of stroke after 5 years of the diagnosis of SNHL [10]. In addition to SNHL, common cardiovascular risk factors have also been suggested to affect the cochlear microvasculature and play an important role in the development of age-related hearing loss [11].

A 49-year-old gentleman with underlying Diabetes Mellitus and Hypertension presented to a regional hospital with a sudden history of typical chest pain associated with shortness of breath, palpitation, and diaphoresis. A diagnosis of acute inferior myocardial infarction was made. Intravenous streptokinase (STK) infusion was commenced as the nearest Hospital with Primary Percutaneous coronary intervention (PCI) was 100 minutes away. During STK infusion he developed acute bilateral hearing loss after 40 mls of STK with minimal gum bleeding. Intravenous STK was stopped immediately, and he was transferred to a tertiary hospital for primary PCI. We referred him to the Ear, Nose, and Throat Specialist on call, and he was diagnosed with acute bilateral SNHL. Primary PCI was performed and noted 2 vessel disease with severe calcification and diffuse disease at Left Anterior Descending (LAD) and Left Circumflex Artery (LCx) with 95% stenosis at Ostial LAD and LCx. His complete hearing loss persisted on discharge.

Many theories have been proposed to explain the unclear etiology of SNHL including vascular occlusion [1], viral infection [2], breaks of labyrinthine membranes [3], immune-mediated mechanisms, and abnormal cellular stress responses within the cochlea [4]. The difficulty of determining the etiology of SNHL can be contributed to the lack of information regarding it. The lack of information can be attributed partly to the fact that it was classified as an “orphan disease” [5]. Due to this, there were many trials being carried out testing a range of treatment goals, but none are able to conclude level 1 evidence due to the lack of case numbers, end – points and study performance. Nevertheless, there is growing evidence that points towards a pathological vascular cause in the development of SNHL, which also helps to explain the association of SNHL with acute myocardial infarction (AMI).

One of the studies that has erred towards the use of corticosteroids showed a non-inferiority outcome when it was adminitstrated via the oral route and with the intratympanic route [12, 13]. This goes to show that even though a potent corticosteroid is used, the outcome is still non inferior.

To date, the most comprehensive study was conducted in Taiwan in 2008, and it was noted among the 1423 SNHL patients that their risk of stroke was 1.64 times higher than in the control group, which favours a vascular association to SNHL [10]. Due to this, there were suggestions that the association between age related hearing loss and cardiovascular risk factors may involve the compromise of the cochlear microvasculature. The contribution of cardiovascular risk factor proceeds in the same fashion in the case of SNHL specifically affecting the stria vascularis which is itself vascular in nature [11].

One class of hearing loss, called strial presbycusis [14], has been linked to increased cardiovascular risk. These affected individuals with strial presbycusis has been demonstrated in cross-sectional analyses to be significantly associated with an increased risk of stroke, coronary artery disease, and myocardial infarction [11].

One of the limitations in this study is the inability to factor in smoking, as smoking has been associated with SNHL as well [15]. The severity of the hearing loss and the extent of recovery also has not been established in this study as well.

Acute bilateral SNHL is rarely reported as a complication of AMI. This study supports an underlying vascular pathomechanism in the development of SNHL. Therefore, clinicians dealing with SNHL patients should be alert to their risk of subsequent AMI.

The authors would like to thank the Director General of Health Malaysia for permission to publish this article.