Peter Torre III
Karen J. Cruickshanks
Barbara E. K. Klein
David M. Nondahl
University of Wisconsin
Medical School, Madison
The Association Between
Cardiovascular Disease and Cochlear
Function in Older Adults
The purpose of this research was to evaluate the relation between self-reported
cardiovascular disease (CVD) and cochlear function in older adults. The
Epidemiology of Hearing Loss Study (EHLS) is an ongoing population-based
study of hearing loss and its risk factors in Beaver Dam, Wisconsin. As part of the
EHLS questionnaire, participants were asked about their cardiovascular medical
history. CVD history was determined from questions regarding history of angina,
myocardial infarction (MI), and stroke. Questions about the use of antihypertensive
medication and blood pressure measurements determined the presence or absence
of hypertension. Among the audiologic measures completed were distortion product
otoacoustic emissions (DPOAEs). Cochlear function was measured using DPOAEs
and participants were categorized as having (a) cochlear impairment, (b) possible
cochlear impairment, or (c) no cochlear impairment. There were 1,501 participants
with complete CVD and DPOAE data from the 1998–2000 examination phase.
Women with a self-reported history of MI were twice as likely (age-adjusted odds
ratio [OR] = 2.00, 95% confidence interval [CI] = 1.15–3.46) to have cochlear
impairment than women without a history of MI. This association was not significant
in men (age-adjusted OR = 0.98, 95% CI = 0.61–1.58). Additionally, no other
CVD variables were associated with cochlear impairment. This study provides data
on a possible sex-specific association between CVD and DPOAEs in older adults.
KEY WORDS: cardiovascular disease, distortion product otoacoustic emissions,
Cruickshanks, Nondahl, Klein, & Klein, 1996; Gates, Cobb, D"Agostino,
& Wolf, 1993; Makishima, 1978; Rosen & Olin, 1965; Rubinstein,
Hildesheimer, Zohar, & Chilarovitz, 1977; Spencer, 1973; Susmano &
Rosenbush, 1988). CVD-related potential risk factors include heart
disease, hypertension, diabetes mellitus, smoking history, and white
blood cell count. Conversely, many researchers have not found an
risk factors (Bunch, 1931; Drettner, Hedstrand, Klockhoff, & Svedberg,
1975; Karamitsos et al., 1996; Miller & Ort, 1966; Parving, Hein,
Suadicani, Ostri, & Gyntelberg, 1993; Saxen, 1952). For example, Bunch
(1931) reported that the average hearing loss in individuals with
arteriosclerosis, hypertension, or chronic cardiac conditions was not
greater than hearing loss in individuals of the same age and in good
general health. No correlations were found between audiometrically
ardiovascular disease (CVD) has been identified as a risk factor
for hearing loss in older adults (Brant et al., 1996; Cocchiarella,
Sharp, & Persky, 1995; Cruickshanks, Klein et al., 1998;
Journal of Speech, Language, and Hearing Research ? Vol. 48 ? 473–481 ? April 2005 ? AAmerican Speech-Language-Hearing Association
assessed hearing loss and CVD risk factors in 1,000
50-year-old men (Drettner et al., 1975). There was no
correlation betweenself-reported hearing problems and
hypertension, angina pectoris, and previous myocardial
infarction (MI) in the Copenhagen Male Study, a pro-
spective, epidemiologic study of CVD (Parving et al.,
1993). Karamitsos et al. (1996) reported no significant
differences in pure-tone audiometry in individuals with
individuals, although there were significant peak audi-
tory brainstem response latency differences between the
In an early study, Rosen and Olin (1965) found that
40–59-year-old individuals with heart disease had
poorer hearing sensitivity than individuals of similar
age without heart disease. Furthermore, Rubinstein
et al. (1977) reported that 65–85-year-old adults (n =
23) with CVD and signs of peripheral circulation dis-
orders had significantly higher mean thresholds (500
to 8000 Hz) than people (n = 23) of comparable age with-
out CVD. The probability of an individual with ische-
mic heart disease having hearing loss was eight times
greater than that for individuals without heart dis-
ease, after adjusting for age, gender, hypertension, and
cigarette smoking (Susmano & Rosenbush, 1988). A
positive relation has been reported for hearing loss and
(a) the degree of stenosis of the internal auditory artery
and (b) the degree of spiral ganglion atrophy based
on histologic studies of temporal bones and brain sec-
tions from older adults with hypertension (Makishima,
1978). In the Framingham Heart Study (Gates et al.,
1993) and the Epidemiology of Hearing Loss Study
(EHLS; Cruickshanks et al., 1996), a significant asso-
ciation was found between history of CVD and in-
creased risk of having hearing loss after adjusting for
age and sex. Also, Cruickshanks, Klein, et al. (1998)
reported that older adults who were smokers were
approximately twice as likely to have a hearing loss as
nonsmokers, after adjusting for age.
These studies establish the possible relation
between CVD and hearing loss. In studies where a
significant association was found between CVD and
hearing loss, researchers used a population-based
approach and more extensive audiologic procedures
(Brant et al., 1996; Cruickshanks et al., 1996; Gates
et al., 1993). Other researchers have studied large
numbers of participants and have not reported a sig-
nificant association (Drettner et al., 1975; Parving
et al., 1993). In these studies, however, men were the
only participants, and Parving et al. (1993) only used
questionnaire data to determine hearing loss. Both
Cruickshanks et al. (1996) and Gates et al. (1993)
reported sex-specific associations. Additionally, research-
ers have speculated that hearing loss (Susmano &
Rosenbush,1988) orimpaired brainstemmicrocirculation
(Karamitsos et al., 1996) were possibly early markers
Most previous studies attempting to establish a
relation between CVD and hearing loss have used pure-
tone audiometry as the auditory measure. Pure-tone
audiometry tests the entire auditory system and re-
quires a behavioral response from the individual. The
measurement of otoacoustic emissions (OAEs) provides
the opportunity to evaluate the outer hair cell (OHC)
function within the cochlea (Brownell, 1982), which is
an important site where age-related changes in hear-
ing occur. OAEs assess the physiologic activity of the
OHCs. The OAE response is recorded with a micro-
phone placedwithintheexternalauditorycanal (Kemp,
1978). A decrease in OAE responses, in the absence of
middle ear disease, usually reflects diminished OHC
function, which may indicate cochlear damage that
precedes changes in pure-tone thresholds. One popular
measure of OAE responses is the distortion product
OAEs (DPOAEs), which are produced when two differ-
ent pure tones, f1and f2where f2> f1, simultaneously
stimulate the cochlea. This activation gives rise to dis-
tortion products that are normally measurable in the
nonlinear cochlear response. Although the human co-
chlea produces many DPOAEs (Pickles, 1988), the most
frequently measured and largest DPOAEs occur at
2f1-f2(e.g., Gaskill & Brown, 1990; Probst, Lonsbury-
Martin, & Martin, 1991). The level of the 2f1-f2DPOAE
affords an optimal measure to assess cochlear function
and can be used to investigate CVD-related changes in
There is no research that has directly evaluated the
association between CVD and cochlear function in older
adults. To date, researchers have used animal models
to investigate the restriction of cochlear blood flow and
its effect on DPOAEs (Mom, Avan, Romand, & Gilain,
Telischi, Stagner, Widick, Balkany, & Lonsbury-
Martin, 1998; Widick, Telischi, Lonsbury-Martin, &
promised, a reduction in DPOAE level was noted in a
rabbit model (Mom et al., 1999; Telischi et al., 1998;
Widick et al., 1994) and in a gerbil model (Mom et al.,
1997). Once the blood flow was restored, DPOAE levels
returned to precompromise levels. The results from
animal models suggest that maintaining adequate
blood flow to the cochlea is critical to cochlear function
and any reduction in blood supply will have a corre-
sponding reduction in cochlear function.
An understanding of the relations between DPOAEs
and cardiovascular function is needed in order to de-
termine those risk factors that may be associated with
changes in human cochlear function. For example, a
decrease in blood supply to the cochlea because of some
degree of CVD may cause cochlear degeneration with a
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Received October 17, 2003
Accepted July 6, 2004
Contact author: Peter Torre III, School of Speech, Language,
and Hearing Sciences, San Diego State University,
5500 Campanile Drive, San Diego, CA 92182-1518.
Torre et al.: Cardiovascular Disease and Cochlear Function