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Possible influence on heart rate on tinnitus
Abstract
Assuming the possibility of the inner ear damage due to a hemodynamic imbalance essentially due to an abnormal vasomotor regulatory response, the possibility that heart rate (HR) has a correlation with the onset and/or the enhancement of tinnitus is hypothesized. In fact, recent studies have drawn the influence of other factors than blood pressure, in normotensive subjects, in taking part to the regulation of peripheral resistance, outlining the importance of both cardiac output (CO) - which is a function of heart rate (HR) and stroke volume (SV) and SV itself as a dynamic component to baroreflex control of muscle sympathetic nerve activity (MSNA). From this point of view, it could be possible that a condition of bradycardia can enhance tinnitus regardless of its cause, and conversely that a more elevated HR can be related to a relief of this symptom.
... We found that heart rate was lower among the patients with tinnitus, which may have been because tinnitus occurs more among the elderly and may be related to dysfunction of the autonomic nervous system. Piroddaa et al. [17] reported that hemodynamic imbalance caused internal ear damage among the group with abnormal vasomotor function, which resulted in tinnitus. In this study, it was noted that bradycardia was prevalent among the patient group with tinnitus. ...
Background
We aimed to examine the correlation among nighttime blood pressure, heart rate variability, and left atrium peak systolic global longitudinal strain among patients with subjective tinnitus.
Material/Methods
Eighty patients with tinnitus were assigned to Group 1 and 80 healthy individuals were assigned to Group 2. Clinical blood pressure measurements, ambulatory blood pressure monitoring, and Holter electrocardiography monitoring were performed. All of the cases included in the study were examined with conventional echocardiography and 2-dimensional speckle tracking echocardiography.
Results
Mean nighttime systolic blood pressure (130.3±5.4) and mean nighttime diastolic blood pressure (82.8±3.9) in Group 1 were higher than in Group 2 (125.1±5.4 and 80.7±4.7, respectively) (p<0.05). Mean heart rate in Group 1 was significantly lower than in Group 2 but there was no statistically significant difference between the groups in terms of heart rate variability parameters and left atrium peak systolic global longitudinal strain values (p>0.05).
Conclusions
Nighttime systolic blood pressure and nighttime diastolic blood pressure were higher among the patients with tinnitus. In light of these results, we can conclude that both clinical blood pressure measurement and ambulatory blood pressure monitoring are important for patients with tinnitus.
... A recent research suggests to investigate all the causes of hemodynamic imbalance and autonomic dysregulation which could be responsible of a circulatory impairment of the labyrinth and consequently of tinnitus [13]. ...
Tinnitus is a perception of sound in absence of sound stimulation. Tinnitus in many cases cannot be eliminated by conventional medical treatment with drugs or surgery. Some people who begin to notice tinnitus, whether spontaneous or induced by noise, trauma or other insult, will experience spontaneous resolution, but many patients will have persistent tinnitus. For some of them, tinnitus sensation will be joined by tinnitus suffering, with many adverse effects like anxiety, depression and sleep disorders. For these tinnitus sufferers the psychological and acoustic approach proposed by the Tinnitus Retraining Therapy and Acoustic Desensitization Protocol may be helpful. Periodically new treatments are suggested like low-frequency repetitive transcranial magnetic stimulation and sequential phase shift sound cancellation treatment based on the frequency and loudness matching of the tinnitus. The aim of this work is to review modern considerations for the treatment of tinnitus.
... Moreover, if in some cases a particular cardiovascular/autonomic profile can be postulated as a basis for explaining this phenomenon [6,7], analogous conditions of imbalance could derive from an insufficient cardiac activity, possibly represented by heart failure [8] or, in a wider population, from a pharmacologic treatment: this is to be considered when planning an antihypertensive therapy. ...
A number of labyrinthine disorders with sensorineural hearing loss, vertigo, and tinnitus are known to occur to young people without vascular risk factors, thus being classified as “idiopathic” in the absence of satisfactory explanations; in the last decade, this phenomenon has found a reliable explanation by the adverse effect of a sharp decrease of blood pressure values followed by an abnormal vasomotor regulation. This model may not only be applied to healthy subjects, but even had some confirmation in conditions possibly affecting hemodynamic changes, such as heart failure or treated hypertension. In particular, the results of a recent study on the impact of different antihypertensive therapies, which was analyzed by monitoring the onset or enhancement of tinnitus as a symptom of inner ear sufferance, unequivocally demonstrated an increased prevalence of tinnitus in subjects submitted to more “aggressive” treatments. This seems in agreement with recent observations about the model of fluid homeostasis of the inner ear, and suggests, when possible, to resort to treatments with modulatory effects in order to maintain a steady perfusion to the labyrinth thus protecting its function.
Objective : To evaluate autonomic nerve balance and sympathetic nerve activity in patients with inner ear dysfunction as examined by heart rate variability(HRV) Research Methods and Procedures : One hundred and twenty three patients(between 15 to 59 years old) who visited Dept. of Oriental medical Opthalmology & Otolaryngology, Kyunghee university and had an examination of HRV test, were selected as subjects of our study. We checked items of HRV test(such as SDNN, RMSSD, LF, HF, TP, norm-LF, norm-HF, LF/HF ratio), and analyzed time and frequency domain differences between three groups classified as tinnitus, hearing loss and vertigo. And we compared HRV items(such as SDNN,RMSSD, TP and LF/HF ratio) with standard levels. Results and Conclusion : Our results showed no significant differences between three groups in HRV items except for mean heart rate. Patients with inner ear dysfunction showed significant lower TP than 2000(p
Internet-based claims suggest that physical activity may help to relieve tinnitus symptoms. The purpose of this study was to empirically investigate the association between accelerometer-assessed physical activity and tinnitus (i.e., ringing, roaring, or buzzing in the ears).
Data were obtained from the 2005-2006 National Health and Nutrition Examination Survey on 963 adolescents (aged 12-19 years old) and 473 older adults (aged 70-85 years old). Physical activity was measured using an accelerometer, and participants were asked several tinnitus-related questions.
The weighted prevalence of tinnitus was 8.9% and 25.3% for adolescents and older adults, respectively. For every 1-min increase in moderate-to-vigorous physical activity, adolescents were 4% less likely to have tinnitus lasting more than 3 months compared with less than 3 months (OR = 0.96, 95% CI [0.93, 0.99]). For older adults with hypertension, for every 60-min increase in light-intensity physical activity, they were 21% less likely to have tinnitus zcompared with not having tinnitus (OR = 0.790, 95% CI [0.649, 0.963]).
Overall, we conclude that physical activity was associated with tinnitus status in a nationally representative sample of adolescents and older adults. If additional studies confirm these findings, then audiologists and other hearing specialists are encouraged to promote physical activity among their patients to help treat and prevent tinnitus.
It has been widely outlined by our group the possibility that a sufferance of the inner ear can take place as a consequence of hemodynamic imbalance which could affect young and healthy people and recognize a merely functional origin. As reported in previous papers, an altered reaction of the autonomic nervous system could actually jeopardize the labyrinthine perfusion even in absence of other damages. From this standpoint, the hypothesis that a hyperactivity of the vagal response to an acute sympathetic drive may result in an inner ear sufferance deserves to be explored. A mechanism which appears to fit to this model is represented by the Bezold-Jarisch reflex (BJR), which is considered to be responsible for vasovagal syncope and is characterized by a dynamic reasonably compatible with our findings. According to these premises, especially considering that the inner ear has a less active protective mechanism against ischemia as compared to brain, in predisposed subjects tinnitus, when considered as an initial symptom of inner ear hypoperfusion, can represent a warning able to prevent the lack of consciousness related to the syncope.
In order to find out any possible cause of an alteration of the vasomotor reactivity which can be responsible for a more or less severe sufferance of the inner ear, announced by the onset or the enhancement of sensorineural hearing loss, tinnitus, and some kind of dizziness and vertigo, a multidisciplinary approach should be considered. The possibility of an influence of hemodynamic imbalance due to hypotensive changes followed by vasomotor changes affecting the microcirculation of the inner ear has already been widely discussed; moreover, an increase in prevalence of tinnitus (which in many cases can be considered as a symptom of sufferance of the inner ear) has been found in subjects submitted to an "aggressive" antihypertensive therapy as well as in patients with severe heart failure, thus demonstrating a relationship between hemodynamic changes and inner ear dysfunction. For the same reason, the research for this mechanism of imbalance could concern other conditions possibly activating an abnormal response of the autonomic nervous system, which could in turn lead to a circulatory impairment of the labyrinth: among these, affections concerning central nervous system, endocrine system, metabolism, renal apparatus and even gastroenteric diseases with a functional component and any other factor which could interfere with vasomotor regulation should be considered. Thus, the absence of reliable causes for a sufferance of the inner ear should not lead to catalogue it as a disorder of "idiopathic" nature, but should represent a reason for a multidisciplinary investigation on all the possible causes of hemodynamic imbalance and/or autonomic dysregulation.
Vasomotor sympathetic activity plays an important role in arterial pressure maintenance via the baroreflex during acute orthostasis in humans. If orthostasis is prolonged, blood pressure may be supported additionally by humoral factors with a possible reduction in sympathetic baroreflex sensitivity. We tested the hypothesis that baroreflex control of muscle sympathetic nerve activity (MSNA) decreases during prolonged upright posture. MSNA and haemodynamics were measured supine and during 45 min 60 deg upright tilt in 13 healthy individuals. Sympathetic baroreflex sensitivity was quantified using the slope of the linear correlation between MSNA and diastolic pressure during spontaneous breathing. It was further assessed as the relationship between MSNA and stroke volume, with stroke volume derived from cardiac output (C2H2 rebreathing) and heart rate. Total peripheral resistance was calculated from mean arterial pressure and cardiac output. We found that MSNA increased from supine to upright (17+/-8 (S.D.) versus 38+/-12 bursts min-1; P<0.01), and continued to increase to a smaller degree during sustained tilt (39+/-11, 41+/-12, 43+/-13 and 46+/-15 bursts min-1 after 10, 20, 30 and 45 min of tilt; between treatments P<0.01). Sympathetic baroreflex sensitivity increased from supine to upright (-292+/-180 versus -718+/-362 units beat-1 mmHg-1; P<0.01), but remained unchanged as tilting continued (-611+/-342 and -521+/-221 units beat-1 mmHg-1 after 20 and 45 min of tilt; P=0.49). For each subject, changes in MSNA were associated with changes in stroke volume (r=0.88+/-0.13, P<0.05), while total peripheral resistance was related to MSNA during 45 min upright tilt (r=0.82+/-0.15, P<0.05). These results suggest that the vasoconstriction initiated by sympathetic adrenergic nerves is maintained by ongoing sympathetic activation during sustained (i.e. 45 min) orthostasis without obvious changes in vasomotor sympathetic neural control.
Tinnitus is a common symptom in audiology and neurologypatients. Controversial data have been reported in the literature about the prevalence of tinnitus in hypertensive patients, whereas its relationship with the extent of blood pressure (BP) control has not been substantially explored.
The aim of this study was to determine the prevalence of tinnitus in hypertensive patients, and the impact of different antihypertensive drugs on the incidence of tinnitus in these patients.
This prospective, single-blind, observational study was conducted at the Hypertension Clinic, St. Orsola-Malpighi Hospital, Bologna, Italy. Patients aged 18 to 75 years with uncontrolled hypertension and receiving antihypertensive therapy were enrolled. Patients were asked to complete a standardized questionnaire to assess the presence, frequency, and duration of tinnitus and the apparent effect of their antihypertensive treatment on it. Patients considered by the investigator to have tinnitus, regardless of their audiologic condition, underwent a complete clinical cardiovascular examination, including supine systolic BP (SBP) and diastolic BP measurement and standard 12-lead electrocardiography. Twelve-hour ambulatory BP monitoring was also performed, and patients were asked to record, using patient diaries, times of the onset and resolution of tinnitus that occurred during those 12 hours. From these data, correlations between the onset of tinnitus and BP were calculated.
A total of 476 patients participated in the study (283 men, 193 women). Of these, 84 (17.6%) patients reported occasional or prolonged spontaneous tinnitus, whereas 392 (82.4%) reported no tinnitus. The incidence of tinnitus was significantly higher in patients receiving diuretics (72/265 [27.2%]) compared with those receiving angiotensin lI receptor blockers (5/37 [13.5%]), α-blockers (12/55 [21.8%]), or 3-hydroxy-3-methylglutaryl coenzyme A reduc tase inhibitors (9/73 [12.3%]) (all, P < 0.05). Mean (SD) SBP was significantly higher in patients without tinnitus compared with those with it (143.2 [11.1 ] vs 140.6 [10.3] mm Hg; P < 0.005). In 10 (11.9%) patients with tinnitus, the onset was correlated with a sudden decrease in SBP (<140 mm Hg).
In this study of tinnitus in patients receiving antihypertensivetherapy, tinnitus was found in 17.6% of patients. Tinnitus was associated with the use of diuretics and with low SBP. Further studies are needed.
We have over the last 15 years seen some important developments in our understanding of tinnitus generation, the distress it can lead to, and more importantly how it can be mitigated. The neurophysiological model introduced by Jastreboff (1) has provided us with a model where the central nervous system is the main factor in tinnitus suffering, and subsequently also central to the rehabilitation of the patients. This paper addresses the medical aspect of tinnitus suffering in general, and presents an introduction to the kind of information with which we provide our patients as part of rehabilitation.
Resting human sympathetic vasoconstrictor traffic displays large reproducible inter‐individual differences which are similar in nerves to muscle, heart and kidney. In spite of this there is no correlation between levels of blood pressure and sympathetic traffic. To test the hypothesis that the pressor effect of the vasoconstrictor activity is counteracted by a circulating dilating factor we measured muscle nerve sympathetic activity (MSA) and an indicator of nitric oxide release (plasma nitrate) in healthy young males.
Sympathetic activity was recorded with the microneurographic technique in the peroneal nerve and a forearm venous plasma sample was obtained in twenty‐one normotensive males aged 21–28 years. Plasma nitrate was analysed by gas chromatography and mass spectrometry.
There was a positive linear correlation between the plasma nitrate concentration and the strength of MSA both when the nerve activity was expressed as bursts per minute and bursts per 100 heart beats ( r = 0.51, P = 0.02 and r = 0.46, P = 0.04, respectively).
The data suggest that the stronger the sympathetic activity the higher the release of the dilating substance, nitric oxide. This would be expected to counteract vasoconstrictor effects of the nerve traffic and thereby contribute to the lack of relationship between resting levels of MSA and blood pressure. We speculate that altered coupling between sympathetic traffic and nitric oxide release may cause abnormal peripheral resistance, e.g. in hypertension.
1. Recordings of multi‐unit sympathetic activity were made from median or peroneal muscle nerve fascicles in thirty‐three healthy subjects, resting in recumbent position. Simultaneous recordings of intra‐arterial blood pressure were made in seventeen subjects. The neural activity, quantified by counting the number of pulse synchronous sympathetic bursts in the mean voltage neurogram (burst incidence), was plotted against the arterial blood pressure level and the age of the subjects. The effects of spontaneous temporary blood pressure fluctuations were studied by correlating different pressure parameters of individual heart beats to the probability of occurrence of a sympathetic burst and to the amplitude of the occurring burst.
2. Between different subjects there were marked differences in burst incidence, from less than 10 to more than 90 bursts/100 heart beats. No correlation was found to interindividual differences in the arterial blood pressure level but there was a slight tendency for increasing burst incidence with increasing age.
3. Irrespective of the magnitude of the burst incidence, the bursts always occurred more frequently during spontaneous transient blood pressure reductions than during transient increases in blood pressure. When, for each heart cycle, the occurrence of a sympathetic burst was correlated with different blood pressure parameters there was regularly a close negative correlation to diastolic pressure, a low correlation to systolic and an intermediary negative correlation to mean blood pressure. There was a positive correlation to pulse pressure and to pulse interval.
4. When measured for individual heart beats, not only the occurrence but also the mean voltage amplitude of the sympathetic bursts tended to increase with decreasing diastolic pressure.
5. In a given subject when comparing heart beats with the same diastolic pressure, the occurrence as well as the amplitude of the sympathetic bursts was higher for heart beats occurring during falling than for heart beats occurring during rising blood pressure. For a given change in diastolic blood pressure, sympathetic activity changed more if pressure was falling than if it was rising.
6. The findings suggest that the sympathetic outflow is modulated by arterial baroreflex mechanisms and that transient variations in the strength of the activity are, to a large extent, determined by diastolic blood pressure fluctuations. The intimate correlation with ‘dynamic’ variations in blood pressure and the absence of correlation to the ‘static’ blood pressure level suggests that the sympathetic outflow to skeletal muscles is of importance for buffering acute blood pressure changes but has little influence on the long term blood pressure level. The difference in reflex sensitivity between falling and rising pressure indicates that acute blood pressure decreases may be buffered more efficiently than acute blood pressure increases.
7. In twenty‐seven subjects baroreflex latency was calculated from the QRS‐complexes in the e.c.g. to the appropriate systolic inhibition in the sympathetic activity. When recording in the peroneal nerve, the latency ranged between 1·16 and 1·49 sec and there was a positive correlation with the height of the subjects. It is suggested that such latency measurements may be used clinically to evaluate conduction in sympathetic fibres.
The generic term 'sudden hearing loss' indicates the lack of knowledge about the etiology and pathogenesis of this phenomenon. In most cases it would seem feasible to consider infections or organic circulatory defects, but there are cases, generally affecting young subjects in whom the damage is often reversible, in which a functional origin is possible. We therefore investigated the possible effect of systemic arterial pressure in a retrospective study in a group of 36 patients aged not more than 40 years, treated for sudden hearing loss, comparing the mean values of their arterial pressure with those of a control group of 25 subjects, of similar age, admitted for other disorders. The significantly lower mean values of arterial pressure in the group affected by sudden hearing loss and the easier reversibility of the damage in these patients suggests that, at least in some cases, the cochlear damage may be caused by a perfusion deficit due to the combined effect of hypotension and imperfect vasomotor regulation.
1. Resting human sympathetic vasoconstrictor traffic displays large reproducible inter-individual differences which are similar in nerves to muscle, heart and kidney. In spite of this there is no correlation between levels of blood pressure and sympathetic traffic. To test the hypothesis that the pressor effect of the vasoconstrictor activity is counteracted by a circulating dilating factor we measured muscle nerve sympathetic activity (MSA) and an indicator of nitric oxide release (plasma nitrate) in healthy young males. 2. Sympathetic activity was recorded with the microneurographic technique in the peroneal nerve and a forearm venous plasma sample was obtained in twenty-one normotensive males aged 21-28 years. Plasma nitrate was analysed by gas chromatography and mass spectrometry. 3. There was a positive linear correlation between the plasma nitrate concentration and the strength of MSA both when the nerve activity was expressed as bursts per minute and bursts per 100 heart beats (r = 0.51, P = 0.02 and r = 0.46, P = 0.04, respectively). 4. The data suggest that the stronger the sympathetic activity the higher the release of the dilating substance, nitric oxide. This would be expected to counteract vasoconstrictor effects of the nerve traffic and thereby contribute to the lack of relationship between resting levels of MSA and blood pressure. We speculate that altered coupling between sympathetic traffic and nitric oxide release may cause abnormal peripheral resistance, e.g. in hypertension.
Sudden sensorineural hearing loss (SSHL) is an acute disorder whose origin is often unclear. A vascular disorder may be a causative factor.
To determine whether hypotension influences the genesis of SSHL in healthy subjects.
To investigate the role of a 24-hour blood pressure (BP) profile in a population of young subjects with SSHL from January 1, 1996, to December 31, 1999, by a nonrandomized controlled trial.
The Ear, Nose and Throat Section of the Department of Surgical and Anaesthesiological Sciences and the Department of Internal Medicine, S. Orsola Hospital, University of Bologna, Bologna, Italy.
The study population consisted of 23 untreated healthy patients diagnosed as having SSHL compared with 20 age- and sex-matched normotensive control subjects. Both groups underwent 24-hour BP monitoring, and their BP profiles were analyzed and compared with routine BP values. The data were analyzed with the Statistical Package for the Social Sciences, version 7.1, and the results are expressed as mean +/- SD.
The mean BP values were expected to be lower in the study population.
The average clinic and ambulatory BP values were significantly lower in patients with SSHL, for systolic (clinic, P =.004; ambulatory BP, P =.02) and diastolic (clinic, P =.03; ambulatory BP, P =.03) values. The occurrence of persistent hypotension (the presence of >2 consecutive recordings of systolic BP of < or =105 mm Hg and/or diastolic BP of < or =60 mm Hg) was increased in the population with SSHL.
Systemic hypotension must be considered as the possible cause responsible for the development of SSHL in young healthy subjects.
We investigated the possible role of hypotension and related autonomic phenomena in the pathogenic mechanism of sudden sensorineural hearing loss.
Forty-nine patients belonging to the ASA I-II classes of anaesthesiological risk and submitted to a non-otological surgical procedure were examined. Each operation was performed under general anaesthesia by controlled hypotension technique. Hearing function of the patients was evaluated before and after surgery by means of a pure tone audiometry recorded by the same clinician with the same instrument.
No cases of bilateral hearing worsening were recorded after surgery.
An induced and controlled steady hypotension under general anaesthesia did not affect the hearing function of any of the patients. It may be supposed, therefore, that an adverse effect on the cochlear oxygenation is more likely to be caused by the sympathetic changes induced by a consistent decrease of blood pressure rather than to hypotension itself.
Large, reproducible interindividual differences exist in resting sympathetic nerve activity among normotensive humans with similar arterial pressures, resulting in a lack of correlation between muscle sympathetic nerve activity (MSNA) and arterial pressure among individuals. Although it is known that the arterial pressure is the main short-term determinant of MSNA in humans via the arterial baroreflex, the lack of correlation among individuals suggests that the level of arterial pressure is not the only important input in regulation of MSNA in humans. We studied the relationship between cardiac output (CO) and baroreflex control of sympathetic activity by measuring MSNA (peroneal microneurography), arterial pressure (arterial catheter), CO (acetylene uptake technique) and heart rate (HR; electrocardiogram) in 17 healthy young men during 20 min of supine rest. Across individuals, MSNA did not correlate with mean or diastolic blood pressure (r<0.01 for both), but displayed a significant negative correlation with CO (r=-0.71, P=0.001). To assess whether CO is related to arterial baroreflex control of MSNA, we constructed a baroreflex threshold diagram for each individual by plotting the percentage occurrence of a sympathetic burst against diastolic pressure. The mid-point of the diagram (T50) at which 50% of cardiac cycles are associated with bursts, was inversely related to CO (r=-0.75, P<0.001) and stroke volume (SV) (r=-0.57, P=0.015). We conclude that dynamic inputs from CO and SV are important in regulation of baroreflex control of MSNA in healthy, normotensive humans. This results in a balance between CO and sympathetically mediated vasoconstriction that may contribute importantly to normal regulation of arterial pressure in humans.
The possible genesis of some damage of the inner ear from a hemodynamic imbalance of functional origin, possibly linked to hypotension followed by an abnormal vasomotor regulatory activity, has been pointed out by our group over the years. As tinnitus, which is often referable to an inner ear origin, can represent a signal of incoming sufferance of the organ of Corti and may not necessarily be linked to hearing impairment, it seemed of some utility to investigate on the prevalence of tinnitus under various well monitored hemodynamic conditions. This led to observe that the prevalence of this symptom, regardless of audiological features, was increased under "aggressive" antihypertensive therapy as well as in particularly severe degree of heart decompensation. These data represent a first step and encourage in searching for a profile of subject who could be more prone to the development of tinnitus with respect to the normal population, even in absence of pathological conditions. With this aim, echocardiography is thought to be able to yield useful informations in addition to standard and ambulatory blood pressure monitoring, in order to obtain a better definition of the correlations between cardiovascular function (and related changes) and inner ear insufficient perfusion.
Tinnitus and blood pressure values in heart failure patients
- Degli Esposti
- D Cosentino
- E R Santi
- De Sanctis
- D Dormi
- A Bacchelli
Degli Esposti D, Cosentino ER, Santi F, De Sanctis D, Dormi A, Bacchelli S, et al. Tinnitus and blood pressure values in heart failure patients. In: Proceedings of the 17th European meeting on hypertension, milan 2007; p. S171.