Determination of Correlation Among Heart Rate Variability, Left Atrium Global Strain, and Nighttime Blood Pressure Among Patients with Tinnitus

Background

Tinnitus affects nearly 10% of the population and may be caused by many factors. It can be divided into 2 types: subjective types with underlying causes in the inner ear (increased damage in the ear with divided stapedial tendons) or auditory pathway; and objective types with underlying vascular and muscular disorders, osseous diseases, or neoplasia. Subjective tinnitus is often associated with sensorineural hearing loss [1,2]. Tinnitus prevalence increases with old age due to autonomous nervous system dysfunction. When tinnitus is severe, it may negatively affect concentration, work performance, and social life. Studies have reported that 71% of the patients developed depression due to tinnitus [3,4]. Psychological conditions such as depression and anxiety may lead to changes in nighttime blood pressure [5]. Thus, diurnal blood pressure changes and some autonomous nervous system dysfunctions occur [6]. Autonomous nerve system dysfunctions exacerbate tinnitus and cause a vicious cycle. Thus far, no study has investigated the correlation between autonomous nerve system dysfunctions and changes in diurnal blood pressure and heart rate variability. Two-dimensional speckle tracking echocardiography, which has recently become widely used, is very important in discovering myocardial deformation, practically assessing heart beat variability, investigating cardiac effects of diurnal blood pressure, and uncovering the correlation between these cardiac effects with tinnitus. We hypothesized that nighttime blood pressure and heart rate variability play a key role in the etiology of tinnitus among those who have clinically normal blood pressure. In the present study, we aimed to examine the correlation among heart rate variability, left atrium (LA) global strain, and nighttime blood pressure among patients with tinnitus.

Material and Methods

STUDY POPULATION:

Eighty patients with tinnitus complaints and 80 healthy individuals were included in the study. Tinnitus was diagnosed by an otorhinolaryngologist. Patients with hypertension, otologic disorders, neurologic disorders, metabolic disorders, pharmacologic causes, psychological diseases, or vascular pathologies were excluded from the study because these conditions cause tinnitus.

STUDY DESIGN:

The study included 2 groups: those with tinnitus (Group 1, n=80) and the control group (Group 2, n=80). Tinnitus was diagnosed by an otorhinolaryngologist. Patients were examined by a neurology specialist and psychiatry specialist in terms of secondary tinnitus causes. Conventional echocardiography images and 2-dimensional speckle tracking echocardiography images of the patients were taken, and ambulatory blood pressure monitoring and Holter electrocardiography monitoring were performed. Echocardiographic measurements were performed by another observer blind to the study.

CLINICAL BLOOD PRESSURE MEASUREMENT:

Blood pressure measurements of the patients were performed using a sphygmomanometer following the rules of standard blood pressure measurements, in the sitting position after resting at least for 5 minutes. Those patients in whom the mean of 3 subsequent blood pressure measurements was ≤140/90 mm Hg in the first clinic visit were included in the study.

ASSESSMENT OF AMBULATORY BLOOD PRESSURE: Following casual systolic blood pressure (SBP) and diastolic blood pressure (DBP) measurements, 24-hour ambulatory blood pressure monitoring (ABPM) was obtained automatically in the nondominant arm by an oscillometric portable monitor (SpaceLabs, Medical Inc., Model: 92512, Redmond, WA, USA) every 20 minutes from 07.00 to 22.00 hours and every 30 minutes from 22.00 to 07.00 hours. Daytime was defined as the time interval between 07.00 to 22.00 hours and nighttime as the time interval between 22.00 to 07.00 hours. Cuff size was selected in accordance with the arm circumference of the subjects. All the patients and controls were advised to maintain their daily activities and avoid vigorous exercise during ABPM monitoring. The recordings of the monitor were downloaded to a computer and the ABPM data were analyzed for: (i) SBP and DBP during awake and sleep times, and (ii) percentage decline in nocturnal SBP and DBP calculated using the formula [(mean daytime BP – mean night-time BP)/mean daytime BP]×100, with normal values being ≥10% [7].

DETERMINATION OF HEART RATE VARIABILITY:

A 24-hour Holter electrocardiography monitoring was performed. During the monitoring period, ‘Holter WIN-PV plus’ software was used. The Holter registries of all of the cases were manually evaluated in order to leave artefacts out of the assessment, and then ‘time-domain’ heart rate variability parameters were automatically established. For the assessments, the following parameters were selected: 24-hour SDNN (standard deviation of all normal R-R intervals), SDNN-i (the mean of the standard deviation of normal 5-minute RR intervals), SDANN (standard deviation of sequential 5-minute R-R interval means in registries), pNN₅₀ (consecutive R-R intervals differ by more than 50 msec), RMSSD (root mean square of the successive differences), and NN (RR interval between 2 adjacent QRS). The patients were asked not to take drugs before 48 hours prior to Holter electrocardiography monitoring and not to drink caffeinated beverages.

Determination of Body Mass Index was formulated as follows:

CONVENTIONAL ECHOCARDIOGRAPHIC ASSESSMENT: Transthoracic echocardiographic examinations were performed with a Vivid 7 Dimension® (GE Vingmed Ultrasound AS N-3190 Horten, Norway) echocardiography instrument and 2.5 MHz transducer. Patients were assessed in a left side decubitus position after a 5-minute rest. We first assessed pericardia, valve morphologies, and wall movements using M mod and 2-dimensional echocardiography. LV ejection fraction (LVEF) was measured using parasternal long axis. In the apical 4-chamber view with Pulsed-wave (PW) Doppler echocardiography in relation with LV inflow, Doppler sample volume was measured parallel to the long axis of the LV and mitral annulus plane and means were obtained. For the assessments, early diastolic flow velocity (E), late diastolic flow velocity (A), and deceleration time (DT) were registered. In the apical 4-chamber view, 5-mm PW Doppler sample volume was performed in the junction of posterior wall and mitral annulus. With sample volume parallel to the wall axis, peak early (E1) diastolic flow rate was registered. All of the measurements were repeated during the subsequent 3 heart beats and means were taken. All of the measurements were performed based on American Echocardiography Association standards [8].

TWO-DIMENSIONAL SPECKLE TRACKING ECHOCARDIOGRAPHIC ASSESSMENT: Apical 4-chamber view and apical 2-chamber view were recorded with grey-scale. Later on, the records were processed using acoustic tracking software (EchoPAC version 7.0, GE Vingmed). Means of the global strain 15 atrial segment measurements were calculated. Frame frequency was 50–90 frames per second. LAGLSs was measured during LV systole (Figure 1).

STATISTICAL ANALYSES:

Results are reported as the mean ±SD and statistical analysis of clinical data between 2 groups consisted of unpaired t-tests for parametric data and Mann-Whitney U test analysis for nonparametric data, and analysis of variance for repeated measures for parametric data. To analyze the correlation between variables, Pearson correlation coefficient was used. Statistical analysis was performed using PASW 18 (SPSS/IBM, Chicago, IL, USA) and the level of significance was established at the 0.05 (2-sided).

REPRODUCIBILITY:

Intra- and inter-observer reproducibility for the LAGLSs were evaluated. For intra-observer evaluation, views from 30 randomly selected patients were reassessed after a week. The Bland-Altman analysis and the intra-class correlation coefficient (ICC) demonstrated good inter- and intra-observer agreement; for interobserver agreement for LAGLSs, the mean difference was 1.9 (−1.9, 4.5) and ICC 0.88; and for intraobserver agreement, the mean difference was 1.4 (−2.1, 3.2) and ICC 0.92.

Results

COMPARISON OF DEMOGRAPHIC, CLINICAL, AND BLOOD PRESSURE CHARACTERISTICS OF THE GROUPS:

Table 1 includes comparisons of the groups in terms of demographic, clinical, and blood pressure characteristics. Eighty cases with tinnitus (Group 1) and 80 healthy individuals (Group 2) were included in the study. Group 1 included 38 men and 42 women and Group 2 included 40 men and 40 women. The groups were similar in terms of sex. Mean age was 65.1±11.8 years in Group 1 and 56.1±10.1 years in Group 2. There were 25.9% of the participants in Group 1 and 24.2% of the participants in Group 2 who actively smoked cigarettes. There was no significant difference between the groups in terms of BMI. Mean heart rate in Group 1 (66.3±8.1) was significantly lower than in Group 2 (77.5±12.1) (p<0.05). There was no statistically significant difference between the groups in terms of cholesterol and keratin values. Mean duration of tinnitus was 3.4 months. There was no statistically significant difference between the groups in terms of clinical BP, 24-hour BP, or daytime BP (p>0.05). Nighttime SBP in Group 1 was significantly higher than in Group 2 (p<0.0001). DBP measured in Group 1 was considerably higher than in Group 2 (p<0.05).

COMPARISON OF HEART RATE VARIABILITY, LEFT ATRIUM GLOBAL LONGITUDINAL STRAIN, AND ECHOCARDIOGRAPHIC CHARACTERISTICS OF THE GROUPS:

Table 2 shows characteristics of the groups in terms of HRV, LAGLSs, and echocardiographic parameters. There was no significant difference between Group 1 and Group 2 in terms of LAGLSs values. There was no significant difference between Group 1 and Group 2 in terms of LVSD, LVDD, LVEF, DT, E, A, or E/E1 (p>0.05).

CORRELATION ANALYSES:

In Group 1, there was: a positive and strong correlation between nighttime SBP and nighttime DBP (p<0.0001, r: 0.77); a negative and weak correlation between nighttime SBP and NN (p: 0006, r: −0.27); a negative and weak correlation between nighttime SBP and SDNN-i (p: 0.002, r: −0.31); a negative and moderate correlation between nighttime DBP and NN (p: 0.0001, r: −0.45); a negative and weak correlation between nighttime DBP and SDNN-i (p: 0.0001, r: −0.38); a positive and weak correlation between SDNN-i and LAGLSs; and a positive and strong correlation between SDNN-i and LAGLSs (p: 0.009, r: 0.26). In Group 2, there was a positive and strong correlation between nighttime SBP and nighttime DBP (p: 0.0001, r: 0.78); a negative and weak correlation between nighttime SBP and LAGLSs (p: 0.0001, r: −0.25); and a negative and weak correlation between nighttime DBP and LAGLSs (p: 0.0001, r: −0.27).

Discussion

LIMITATION OF STUDY:

Group 1 was older than group 2, but this is not an important result.

Conclusions

Our study will help understand the etiology of tinnitus. Measuring only clinic blood pressure may cause wrong diagnoses among patients with tinnitus. Therefore, we recommend that ambulatory blood pressure be followed in order to assess nighttime blood pressure.