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Original Research: SLEEP MEDICINE |

Decreased Right and Left Ventricular Myocardial Performance in Obstructive Sleep Apnea* FREE TO VIEW

Abel Romero-Corral, MD, MSc; Virend K. Somers, MD, PhD; Patricia A. Pellikka, MD; Eric J. Olson, MD; Kent R. Bailey, PhD; Josef Korinek, MD; Marek Orban, MD; Justo Sierra-Johnson, MD, MSc; Masahiko Kato, MD, PhD; Raouf S. Amin, MD; Francisco Lopez-Jimenez, MD, MSc
Author and Funding Information

*From the Divisions of Cardiovascular Diseases (Drs. Romero-Corral, Somers, Pellikka, Korinek, Orban, Sierra-Johnson, and Lopez-Jimenez) and Pulmonary and Critical Care Medicine (Dr. Olson), and the Department of Biostatistics (Dr. Bailey), Mayo Clinic College of Medicine, Mayo Foundation, Rochester, MN; Aerodigestive and Sleep Center (Dr. Amin), Pediatric Pulmonary Medicine, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH; and the Department of Cardiovascular Medicine (Dr. Kato), Graduate School of Medical Science, Tottori University, Yonago, Japan.

Correspondence to: Francisco Lopez-Jimenez, MD, MSc, Division of Cardiovascular Diseases, Gonda 5–368, Mayo Clinic, 200 First St SW, Rochester MN 55905; e-mail: lopez@mayo.edu



Chest. 2007;132(6):1863-1870. doi:10.1378/chest.07-0966
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Background: Obstructive sleep apnea (OSA) may predispose patients to congestive heart failure (CHF), suggesting a deleterious effect of OSA on myocardial contractility.

Methods: A cross-sectional study of 85 subjects with suspected OSA who had undergone their first overnight polysomnogram, accompanied by an echocardiographic study. Patients were divided according to the apnea-hypopnea index as follows: < 5 (control subjects); 5 to 14 (mild OSA); and ≥ 15 (moderate-to-severe OSA). Right and left ventricular function was evaluated using the myocardial performance index (MPI) and other echocardiographic parameters. For the right ventricle analyses, we excluded patients with a Doppler pulmonary systolic pressure of ≥ 45 mm Hg, while for the left ventricle we excluded patients with an ejection fraction of ≤ 45%.

Results: The mean (± SD) age was 60 ± 15 years, and 83% were men. Right and left ventricular function were altered in patients with OSA, especially in those with the moderate-to-severe OSA, even after adjustment for potential confounders. The mean right MPI was 0.23 ± 0.10 in control subjects, 0.26 ± 0.16 in patients with mild OSA, and 0.37 ± 0.11 in patients with moderate-to-severe OSA (p value for trend, < 0.01). The mean left MPI values were 0.28 ± 0.05, 0.27 ± 0.07, and 0.41 ± 0.14, respectively (p value for trend, 0.04). Right and left MPI correlated positively and significantly with the apnea-hypopnea index (ρ = 0.40, p = 0.002; and ρ = 0.27, p = 0.02, respectively). Mean left atrial volume index was increased in patients with OSA (control subjects, 26.8 ± 11; patients with mild OSA, 32.5 ± 15; and patients with moderate-to-severe OSA, 30.4 ± 11; p value for trend, 0.04).

Conclusions: OSA, particularly when moderate to severe, is associated with impaired right and left ventricular function and increased left atrial volume. These findings support the notion that OSA may contribute to the development of atrial fibrillation and CHF.

Figures in this Article

Obstructive sleep apnea (OSA) is highly prevalent, affecting an estimated 20% of the adult population and as many as 40% of people with obesity.14 In addition, OSA is acknowledged as a common cause of secondary hypertension,5and has been implicated in atrial fibrillation,6coronary artery disease,7congestive heart failure (CHF),8pulmonary hypertension,9stroke,10and increased risk of sudden cardiac death during sleep.11 These findings suggest that OSA by itself may significantly affect myocardial contractility.

In clinical practice, ventricular function is commonly evaluated using echocardiography to measure systolic and diastolic function. The myocardial performance index (MPI) incorporates parameters of both systolic and diastolic function, and therefore might be a more accurate and reflective measure of global ventricular function.12The MPI has been shown to be a valid, reproducible, and simple noninvasive method to estimate global right and left ventricular function, with important prognostic implications.1314

We sought to estimate right and left ventricular myocardial performance and other commonly used echocardiographic parameters in patients with OSA. We hypothesized that patients with OSA have impaired right and left ventricular myocardial performance when compared with control subjects, independent of potential confounders.

Study Design and Patient Population

A cross-sectional evaluation of 155 patients who underwent their initial polysomnogram at the Mayo Sleep Disorders Center from January 1, 1996, to September 1, 2005, for suspected OSA and who also had undergone a complete transthoracic echocardiogram within 2 months of their sleep study. Different inclusion criteria were used for right and left ventricular assessments. To assess whether OSA affects right ventricular function independently of pulmonary pressure, we excluded patients with an estimated pulmonary systolic pressure of ≥ 45 mm Hg. To assess whether OSA affects left ventricular performance in subjects with preserved ejection fraction, we excluded patients with CHF who had an ejection fraction of ≤ 45%. General exclusion criteria were as follows: age < 18 years; previous organ transplantation; history of bariatric surgery, severe left ventricular dysfunction (ie, ejection fraction, < 25%), and cardiac surgery (except coronary artery bypass graft surgery); presence of a permanent pacemaker; moderate-to-severe valvular diseases; cardiomyopathies; pulmonary hypertension due to identifiable causes (except OSA); previous use of continuous positive airway pressure; cancer and/or other important comorbidities with an expected survival < 2 years; suboptimal echocardiographic images for measurements; and lack of patient authorization for clinical research. This study was approved by the Institutional Review Board at Mayo Clinic Rochester, MN.

Polysomnography

All subjects underwent attended, laboratory-based, digitally recorded polysomnography (NCI-LAMONT Medical Inc; Madison, WI). The following variables were recorded: electrooculogram; EEG; chin and lower extremity electromyogram; oronasal airflow using a thermocouple (until Spring 2004) or nasal pressure transducer; snoring detected via neck microphone; thoracoabdominal impedance plethysmography; one-channel ECG; and pulse oximetry. Sleep staging and arousals were scored using standard methods.1516 Obstructive apneas were defined as a cessation of airflow for at least 10 s in the presence of thoracoabdominal efforts, and hypopneas were defined as significant reductions in airflow for at least 10 s accompanied by oxyhemoglobin desaturation of ≥ 2% from baseline. All studies were interpreted by a board-certified sleep specialist. The exposure groups were defined a priori using the apnea-hypopnea index (AHI), which was defined as the total number of apnea and/or hypopnea episodes divided by the number of hours of sleep. The groups were defined as control subjects (AHI, < 5), mild OSA (AHI, 5 to 14), and moderate-to-severe OSA (AHI, ≥ 15).

Echocardiographic Measurements

We used videotaped or digitally stored transthoracic echocardiographic studies to calculate the right and left MPI and the fractional area of change. Using Doppler echocardiography, right and left ventricular MPI were calculated as follows: (isovolumic contraction time of the right/left ventricle + isovolumetric relaxation time of right/left ventricle)/pulmonary/aortic ejection time.1314 The MPI calculation was feasible in 65 of 85 patients (79%) for the right ventricle and in 72 of 85 patients (85%) for the left ventricle. Fractional area change was calculated as (end-diastolic area − end-systolic area)/end diastolic area for the right and left ventricle in the apical four-chamber view. Three consecutive beats were measured and averaged for each measurement, and five consecutive beats were measured in patients with atrial fibrillation. Other more commonly used variables were measured according to the recommendations of the American Society of Echocardiography.17 In this protocol, five random measurements were repeated 1 week after the first measurements to calculate the intraobserver variability (by Dr. Romero-Corral) of the MPI and fractional area change, while for the interobserver variability five random measurements of the MPI and fractional area change were made by two persons (Drs. Romero-Corral and Korinek). The percentage of variation in the means and SEs of the measurement were compared using a paired t test. Both investigators were blinded to the OSA status of the patients.

Abstraction of Clinical Data

Data on the demographic characteristics, medical history, medications, laboratory values, and anthropometric measures were extracted from medical records. Height and weight were recorded at the time of polysomnography and were used to calculate the body mass index (weight in kilograms divided by height in square meters). Clinical information included a history of hypertension, defined as a documented diagnosis, treatment of such, or whether the recorded BP was ≥ 125/85 mm Hg. Dyslipidemia was defined as a mean total cholesterol level of ≥ 240 mg/dL, a low-density lipoprotein of ≥ 160 mg/dL, the use of lipid-lowering therapy, or a documented diagnosis of dyslipidemia. Diabetes was defined as a fasting glucose level of ≥ 126 mg/dL or receiving therapy with insulin and/or oral hypoglycemic agents. Coronary artery disease was defined as previous myocardial infarction, percutaneous coronary intervention, or coronary artery bypass graft surgery. Smoking status was classified as current, past, or never. Other diagnoses including COPD were considered if they were documented in the medical history.

Statistical Analysis

To assess baseline differences across AHI groups, we used the independent t test for continuous variables and the χ2 or Fisher exact test for categoric variables. We explored normal distribution across the recorded variables, and we used the logarithm of right and left MPI and fractional area change due to the skewness of these variables. We used one-way analysis of variance and test for trends across OSA severity. We performed multivariate analyses to obtain adjusted p values for trend and for group comparison across AHI groups, and to obtain adjusted correlation coefficients between AHI and both MPI and fractional area change. Two models for adjustment were created for each ventricle. For the right ventricle, model 1 included age, gender, body mass index, and estimated pulmonary systolic pressure. Model 2 included the same variables as model 1 plus COPD and smoking status. For the left ventricle, model 1 included age, gender, body mass index, hypertension, dyslipidemia, diabetes, coronary artery disease, and smoking status. Model 2 included the same variables as model 1 plus ejection fraction. Finally, due to the nonlinearity found in the AHI, MPI, and fractional area, we used a Spearman test to assess the correlations between these variables. Two-tailed p values of ≤ 0.05 were considered to be significant in advance. Statistical analyses were performed using a statistical software package (JMP, version 6.0; SAS Institute; Cary, NC).

We identified 155 patients who fulfilled the inclusion criteria. After applying the exclusion criteria, we studied a total of 85 subjects (27 control subjects, 18 patients with mild OSA, and 40 patients with moderate- to-severe OSA). For the right ventricular measures, we excluded eight more patients (9.4%) due to an estimated pulmonary systolic pressure of ≥ 45 mm Hg. For analyses of the left ventricle, we excluded another 11 patients (12.8%) with an ejection fraction of ≤ 45%. Sensitivity analyses were performed including these patients, and the results remained similar.

Table 1 presents the baseline characteristics of the patients included in the study. The mean (± SD) age was 60 ± 15 years, and 83% were men. There was a significant trend for OSA patients to be older, to have hypertension, and to be less likely to be current smokers. Table 2 compares the polysomnographic parameters and laboratory values across OSA groups.

Reproducibility of Echocardiographic Measures

For patients with right ventricular MPI, the interobserver and intraobserver variability were 7.5% and 6.1%, respectively, while they were 4.4% and 2.1%, respectively, for patients with left ventricular MPI. For the right ventricular fractional area change, the interobserver and intraobserver variabilities were 3.4% and 7.2%, respectively, while for the left ventricular fractional area change they were 6.7% and 3.1%, respectively.

Association Between OSA and Right Ventricular Function

Echocardiographic measurements in the right ventricle and the unadjusted and adjusted p values for trend and for comparisons among AHI groups for both models are displayed in Table 3 . There was an impaired global right ventricular function measured by the MPI across severity of OSA that remained significant after the adjustment of covariates in models 1 and 2 (p < 0.01 for both). Figure 1 shows the significant and positive correlation between right ventricular MPI and AHI (ρ = 0.40; p = 0.002) after adjustment for variables in model 2.

Systolic function measured by the fractional area change was impaired across the severity of OSA in the unadjusted analyses (p = 0.01) but was no longer significant in models 1 and 2 (p > 0.05 for both). After adjustment for variables in model 2, there was a statistical trend for significance for the fractional area change to be negatively correlated with AHI (ρ = −0.20; p = 0.06) [data not shown].

Association Between OSA and Left Ventricular Function

Echocardiographic measurements in the left ventricle, and the unadjusted and adjusted p values for trend and for comparisons among AHI groups for both models are shown in Table 4 . There was an impaired global left ventricular function measured by the MPI across the severity of OSA that remained significant after the adjustment of covariates in models 1 and 2 (both p < 0.05). Figure 2 shows the significant and positive correlation between left ventricular MPI and AHI (ρ = 0.27; p = 0.02) after adjustment for the variables in model 2. The systolic function measured by ejection fraction percentage and fractional area change showed no differences across AHI groups in either model (p > 0.05). However, diastolic function was impaired in patients with OSA, as noted by the significantly increased left atrial volume index across OSA severity that remained significant after adjusting for variables in models 1 and 2 (both p < 0.05). The mean and lowest oxyhemoglobin saturation percentages were not related to any of the echocardiographic measures of the right and left ventricle across AHI groups (p > 0.05 for all).

Our study demonstrates an association between the severity of OSA and decreased right and left ventricular performance in patients with normal diurnal pulmonary pressure and preserved ejection fraction. The association remained significant after adjustment for clinical parameters known to affect right or left ventricular function. The impairment in left and right ventricular myocardial performance was most evident in patients with moderate-to-severe OSA. Finally, we also showed that the left atrial volume index was significantly increased in patients with OSA.

Association Between OSA and Right Ventricular Dysfunction

There are several factors closely related to OSA that can affect right ventricle structure and function, including obesity, elevations in the intrathoracic negative pressure related to apneic events, and nocturnal increases in pulmonary vascular resistance, all of which have been related to impaired right ventricular filling and diastolic dysfunction.67,11,18Previous studies1925 assessing right ventricular function in patients with OSA have been controversial and have had important limitations, including the use of right ventricular measurements with poor reproducibility, nonblinded measures, lack of a control group for comparisons, and inadequate adjustment for known confounders.

In a previous study, Dursunoglu et al26 studied global right ventricular function using the MPI in patients with OSA who had no history of cardiac and lung diseases. This study26reported an excellent correlation between right ventricular MPI and AHI (r = 0.84; p < 0.001), similar to the one obtained in our study without adjustment for pulmonary systolic pressure and body mass index (data not shown). After adjusting for these known confounders, the correlation between global right ventricular dysfunction and AHI diminished but remained significantly correlated (ρ = 0.40; p = 0.002), supporting the notion that obesity and pulmonary pressures are also important contributors to right ventricular dysfunction in patients with OSA. For the association between OSA and right ventricular ejection fraction, Sanner and colleagues27 have previously reported in a sample of patients without cardiovascular and pulmonary diseases, a significant negative correlation between AHI and right ventricular ejection fraction measured by radionuclide ventriculography (r = −0.24; p < 0.01). Although our study did not reach statistical significance, this correlation is very similar to the one we noted between right fractional area change and AHI (ρ = −0.20; p = 0.06).

To our knowledge, this is the first study showing that OSA severity is associated with impaired right ventricular function after the careful consideration of potential confounders, especially elevated body mass index and pulmonary systolic pressure. Interestingly, our data showed that right ventricular function was inversely related to the AHI but not to the mean and lowest oxyhemoglobin saturation, suggesting that the pathophysiologic interactions between OSA and right ventricular function could be related more to the number of apneic events and the changes in the intrathoracic negative pressure, rather than primarily to oxygen desaturation.28

Association Between OSA and Left Ventricular Dysfunction

In the present study, we found that global left ventricular function, measured by the MPI, and the diastolic dysfunction, measured by left atrial volume index, are impaired across the severity of OSA after adjustment for cardiovascular risk factors and even after adjustment for ejection fraction. Our findings confirm and extend the results from previous investigators22,2931 who have found that left ventricular structure and function are affected in patients with OSA. Global left ventricular function in patients with OSA has been previously reported. This study found a significant and positive correlation between the left ventricular MPI and AHI (r = 0.63; p < 0.001).32 However, this study did not include a control group, and the echocardiographic measures and analyses were not conducted blinded to polysomnography results. Nevertheless, this study is supportive of the notion that OSA affects left ventricular function. In a small sample of patients, Noda and colleagues22 reported that OSA is associated with left ventricular hypertrophy, possibly due to long-standing hypertension associated with OSA. Furthermore, Fung et al,29 comparing patients with an AHI of ≥ 40 to those with an AHI of < 40, found that diastolic function reflected by a prolonged isovolumic relaxation time measured by echocardiography, is impaired in patients with an AHI of ≥ 40. Other parameters, including systolic function, were not different between groups. These results are consistent with our present study in which global and diastolic functions were impaired, even when systolic function was not. Furthermore, we have previously reported that otherwise healthy obese patients with OSA, when compared to similarly obese control subjects without OSA, have impaired diastolic function measured by tissue Doppler echocardiography as well as increased left atrial volume index.33Overall, these findings suggest that OSA initially affects diastolic function rather than systolic function. We further speculate that the left atrial enlargement found in patients with OSA could be the reason for the higher prevalence of atrial fibrillation in this patient population.34

Strengths and Limitations

The strengths of our study include the availability of polysomnography data, which is the “gold standard” for OSA diagnosis, and the existence of a control group without OSA. In addition, we obtained good reproducibility of measurements of MPI and fractional area change, which were performed blinded to the polysomnography results. Finally, we adjusted for potential confounders and excluded patients with pulmonary hypertension (for right ventricle measurements) or with reduced left ventricular ejection fraction (for left ventricle measurements). The limitations of this study include the fact that five of our patients (14%) with moderate-to-severe OSA were receiving CPAP treatment at the time of the echocardiogram. However, this would direct our results toward the null hypothesis, meaning that ventricular function could be improved in these patients, possibly masking a greater ventricular dysfunction in this group, as has been suggested by some studies.3536 In addition, the possibility of a prevalence-incidence bias is present in our study. OSA may not have been diagnosed for many years in some patients in our sample. To minimize this problem, we included only first-time evaluations for suspected sleep apnea (incident cases). Another limitation is that the Mayo Clinic is a tertiary care facility; this, in addition to our inclusion and exclusion criteria, which reduced the sample by 50%, limits the extrapolation of our results to the general population. Finally, due to the nature of the cross-sectional design, we cannot assess cause and effect.37

Implications

This study suggests that OSA is associated with impaired right and left ventricular performance and increased left atrial volume independent of several known confounders. Ventricular performance and atrial size should be assessed in patients with OSA even in the absence of comorbidities known to affect heart function.

OSA, particularly the severe form of the disease, is associated with impaired right ventricular function despite normal diurnal pulmonary systolic pressures. OSA patients also have decreased left ventricular myocardial performance and an increased left atrial volume even in the setting of a preserved ejection fraction. These findings support the notion that OSA may contribute to the development of right and left ventricular dysfunction, and, ultimately, to development of atrial fibrillation and CHF.

Abbreviations: AHI = apnea-hypopnea index; CHF = congestive heart failure; MPI = myocardial performance index; OSA = obstructive sleep apnea

Dr. Somers is supported by National Institutes of Health grants HL-65176, HL-70302, HL-73211, and M01-RR00585. Dr. Lopez-Jimenez is a recipient of a Clinical Scientist Development Award from the American Heart Association.

The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Table Graphic Jump Location
Table 1. Baseline Characteristics*
* 

Values are given as the mean ± SD or No. (%), unless otherwise indicated. MI = myocardial infarction; PCI = percutaneous coronary intervention; CABG = coronary artery bypass graft surgery; NS = not significant.

 

p < 0.05 (control subjects vs patients with moderate-to-severe OSA).

 

p < 0.05 (control subjects vs patients with mild OSA).

Table Graphic Jump Location
Table 2. Polysomnography and Laboratory Measures*
* 

Values are given as the mean ± SD, unless otherwise indicated. LDL = low-density lipoprotein; HDL = high-density lipoprotein. See Table 1 for abbreviation not used in the text.

 

p = 0.06 (control subjects vs patients with moderate-to-severe OSA).

 

p < 0.05 (control subjects vs patients with moderate-to-severe OSA).

§ 

p < 0.05 (control subjects vs patients with mild OSA).

 

p < 0.001 (patients with mild OSA vs patients with moderate-to-severe OSA).

Table Graphic Jump Location
Table 3. Association Between OSA Severity and Right Ventricular Echocardiographic Measures*
* 

Values are given as the mean ± SD, unless otherwise indicated. EPSP = estimated pulmonary systolic pressure; FAC = fractional area change. See Table 1 for abbreviation not used in the text.

 

p Values are given as unadjusted/model 1/model 2. Additional models incorporating other alternative comorbidities, such as hypertension, diabetes, dyslipidemia, coronary artery disease, and ejection fraction, did not alter the significance of the p values.

 

p < 0.01 in models 1 and 2 when compared to control subjects.

Figure Jump LinkFigure 1. Positive and significant correlation between right ventricular MPI and AHI after adjustment for confounders known to affect right ventricular function (ie, age, gender, body mass index, COPD, and smoking status).Grahic Jump Location
Table Graphic Jump Location
Table 4. Association Between OSA Severity and Left-Sided Echocardiographic Measures*
* 

Values are given as the mean ± SD, unless otherwise indicated. MV = mitral valve; E = early diastolic velocity; A = late diastolic velocity; e′ = mitral annular early diastolic velocity; E/A ratio = ratio between early and late diastolic velocity; E/e′ ratio = ratio between early diastolic velocity and mitral annular early diastolic velocity. See Tables 1and 3 for abbreviations not used in the text.

 

p Values are given as unadjusted/model 1/model 2.

 

p < 0.05 in models 1 and 2 vs control subjects.

Figure Jump LinkFigure 2. Positive and significant correlation between left ventricular MPI and AHI after adjustment for confounders known to affect left ventricular function (ie, age, gender, body mass index, dyslipidemia, hypertension, diabetes mellitus, coronary artery disease, smoking status, and ejection fraction).Grahic Jump Location
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Figures

Figure Jump LinkFigure 1. Positive and significant correlation between right ventricular MPI and AHI after adjustment for confounders known to affect right ventricular function (ie, age, gender, body mass index, COPD, and smoking status).Grahic Jump Location
Figure Jump LinkFigure 2. Positive and significant correlation between left ventricular MPI and AHI after adjustment for confounders known to affect left ventricular function (ie, age, gender, body mass index, dyslipidemia, hypertension, diabetes mellitus, coronary artery disease, smoking status, and ejection fraction).Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1. Baseline Characteristics*
* 

Values are given as the mean ± SD or No. (%), unless otherwise indicated. MI = myocardial infarction; PCI = percutaneous coronary intervention; CABG = coronary artery bypass graft surgery; NS = not significant.

 

p < 0.05 (control subjects vs patients with moderate-to-severe OSA).

 

p < 0.05 (control subjects vs patients with mild OSA).

Table Graphic Jump Location
Table 2. Polysomnography and Laboratory Measures*
* 

Values are given as the mean ± SD, unless otherwise indicated. LDL = low-density lipoprotein; HDL = high-density lipoprotein. See Table 1 for abbreviation not used in the text.

 

p = 0.06 (control subjects vs patients with moderate-to-severe OSA).

 

p < 0.05 (control subjects vs patients with moderate-to-severe OSA).

§ 

p < 0.05 (control subjects vs patients with mild OSA).

 

p < 0.001 (patients with mild OSA vs patients with moderate-to-severe OSA).

Table Graphic Jump Location
Table 3. Association Between OSA Severity and Right Ventricular Echocardiographic Measures*
* 

Values are given as the mean ± SD, unless otherwise indicated. EPSP = estimated pulmonary systolic pressure; FAC = fractional area change. See Table 1 for abbreviation not used in the text.

 

p Values are given as unadjusted/model 1/model 2. Additional models incorporating other alternative comorbidities, such as hypertension, diabetes, dyslipidemia, coronary artery disease, and ejection fraction, did not alter the significance of the p values.

 

p < 0.01 in models 1 and 2 when compared to control subjects.

Table Graphic Jump Location
Table 4. Association Between OSA Severity and Left-Sided Echocardiographic Measures*
* 

Values are given as the mean ± SD, unless otherwise indicated. MV = mitral valve; E = early diastolic velocity; A = late diastolic velocity; e′ = mitral annular early diastolic velocity; E/A ratio = ratio between early and late diastolic velocity; E/e′ ratio = ratio between early diastolic velocity and mitral annular early diastolic velocity. See Tables 1and 3 for abbreviations not used in the text.

 

p Values are given as unadjusted/model 1/model 2.

 

p < 0.05 in models 1 and 2 vs control subjects.

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