Abstract
Background and Aim:
Pulmonary pulse transit time (pPTT) is a new marker of pulmonary hypertension (PH), which shows the time needed for the pulse wave to propagate from the right ventricular outflow tract to the left atrium (LA), but the relationship between pPTT and diastolic-LA function is almost unknown. In this study, we investigated the relationship between pPTT and LA-diastolic functions without PH.
Materials and Methods:
One hundred and fifty-six patients were included in this prospectively designed study. Comprehensive echocardiographic evaluation was performed and pPTT was recorded as the time from the beginning of the R-wave on the electrocardiogram to the peak of the S-wave in the pulmonary veins.
Results:
We found a statistically significant correlation between LA total stroke volume, passive stroke volume, LA max area, LA volume (LAV) max and LA volume index (LAVi) max, and pPTT (r = 0.263** P = 0.003, r = 0.240** P = 0.007, (r = 0.339** P < 0.001, r = 0.307** P < 0.001 r = 0.199*, P = 0.024, LA total stroke volume, passive stroke volume, LA max area, LAV max, LAVi max respectively). Heart rate (HRt) and LAVi were detected as independent predictors of pPTT (hazard ratio: −2.290 P < 0.001, 95% confidence interval (CI): −3.274–1.306, HR: 0.461, P = 0.028, 95% CI: 0.050–0.873, HRt and LAVi, respectively).
Conclusion:
LAVi and HRt also affected pPTT. The dominant effect of HRt on pPTT should be considered in future studies. Larger studies are needed to determine the change and clinical significance of pPTT in left heart disease.
Keywords: Heart rate, left atrial volume index, pulmonary pulse transit time
INTRODUCTION
Pulmonary pulse transit time (pPTT) is the time from the right ventricular outflow tract of the pulse wave to the left atrium (LA).[1] Although the underlying mechanism is not completely understood, it was suggested as a novel variable for the evaluation of pulmonary hemodynamics, showing a decrease in patients with pulmonary arterial hypertension.[2] Different factors affect pulmonary pulse wave velocity, such as pulmonary capillary wedge pressure LA pressure, pulmonary artery pressure, and pulmonary vascular resistance. Therefore, it may not be a parameter related only to pulmonary hypertension (PH). Only one study showed that pPTT increased with significant mitral stenosis.[3] As such, pPTT was demonstrated to be a possible surrogate marker of pulmonary hemodynamic alterations in HIV-infected patients. pPTT levels were alleviated as well as inversely correlated with disease severity and duration in patients with scleroderma and systemic lupus erythematosus,[4,5] but prior studies about the relationship of pPTT with left heart diseases were insufficient. In this study, we investigated the relationship between pPTT and LA-diastolic functions without PH.
MATERIALS AND METHODS
Study group and clinical data collection
One hundred and fifty-six (156) consecutive patients admitted to the cardiology outpatient clinic between January and June 2021 were included in this prospectively designed study. Exclusion criteria included the presence of PH, any lung disease, tricuspid regurgitation velocity >2.8 ms, right heart dilatation, left ventricular (LV) ejection fraction <50%, severe valvular disease, inflammatory disease, malignancy, obstructive sleep apnea, and atrial fibrillation. Demographic data, medical history, laboratory data, and patient medication history were obtained from the first admission before echocardiographic assessment. This prospective observational study was approved by the local ethics committee and performed according to the Declaration of Helsinki. Informed consent was obtained from all patients before echocardiographic evaluation. Echocardiographic measurements were taken by one echocardiography specialist. Final values were taken as the mean of three measurements.
Echocardiographic assessment
Comprehensive echocardiographic evaluation of patients included 2D, M-mode, pulse wave Doppler, and pulse tissue Doppler imaging. LV diameters were obtained from the parasternal long axis window by M-mode echocardiography, such as LV end diastolic diameter (LVEDD), interventricular septum diameter (IVS), and posterior wall diameter (PWd). LV mass index was calculated as LV mass/body surface area (BSA).
LV mass and relative wall thickness (RWT) values were calculated with the following formulas:
LV mass (g) = 0.8 × (1.04[([LVEDD + IVSd + PWd] 3-LVEDD3)]) + 0.6
RWT = 2 × PWd/LVEDD
Moreover, pPTT was recorded as the time from the beginning of the R-wave on the electrocardiogram (ECG) to the peak of the S-wave in the pulmonary veins [Figure 1].
Figure 1.
Calculation of pPTT (time required for A-B). pPTT = Pulmonary pulse transit time
E values were recorded as transmitral blood flow velocity by pulse wave Doppler, while e’ values were obtained from both septal and lateral LV walls by tissue Doppler and used as the average. The e/e’ ratio, which yields information about diastolic dysfunction, was expressed by dividing the transmitral blood flow velocity by the e’ value.
TLV myocardial performance index (Tei index) was calculated with this formula: ([mitral valve closure to opening time – LV ejection time]/[LV ejection time]).
LA measurements: LA diameters and areas were recorded at different times (end diastolic: maximum, end systolic: minimum, measurement during the onset of the P-wave in the ECG: precontraction) from A4C and A2C windows (A4C: apical 4 chamber, A2C: apical 2 chamber).
The biplane area-length method was used to calculate the LA volume (LAV) using the formula: (0.85) × (A1 × A2)/L. Here, A1 indicates maximum LA area in the apical 4-chamber (A4C) view, A2 indicates maximum LA area in the apical 4-chamber (A4C) view, and L indicates length measured from mitral valve hinge points to the top of the atrium. In addition, LA volume index (LAVi) values were estimated by LAV values divided into BSA.
LA total stroke volume: LAV (max) – LAV (min).
LA active stroke volume: LAV (prec) – LAV (min).
LA passive stroke volume: LAV (max) – LAV (prec).
LA total emptying fraction was calculated with 100 × (LA total stroke volume/LAV [max]).
LA active emptying fraction was calculated as 100 × (LA active stroke volume/LAV [prec]).
LA passive emptying fraction: LA active emptying fraction was calculated as 100 × (LA passive stroke volume/LAV [max]).
LA expansion index was equal to 100× (LA total stroke volume/LAV [min]).
Statistical analysis and sample size determination
Continuous variables were expressed as mean ± standard deviation and categorical variables as numbers and percentages in the manuscript. For a normality check, Shapiro–Wilk and Kolmogorov–Smirnov tests were used. In correlation tests, Spearmen and Pearson correlation tests were used based on the normality distribution, and correlation coefficients and P values were analyzed. Variables with a potential clinical effect on pPTT values were evaluated with univariate and multivariate linear regression analysis. P < 0.05 was considered statistically significant. G*Power 3.1.9.4 version (Denizli, Turkey and Karaman, Turkey) was used for sample size analysis. In the power analysis with the two-way hypothesis, it was calculated that at least 122 patients should be included in the study with 95% power and 5% alpha error. For sample size analysis, moderate correlation (r = 0.432) and Cohen's effect size were defined as 0.5 and observed in the reference study.[3]
RESULTS
A total of 159 patient data were included in the study, with patients’ mean age being 45.05 ± 16.82. There were 29 (18.6%) hypertensive and 30 (19.2%) diabetic patients in the study. The mean ejection fraction values were 63.88 ± 3.96: LAVi (max) values were recorded as 29.57 ± 10.24 mL/m2. The clinical and demographic data of patients are summarized in Table 1.
Table 1.
Table 1: Demographic, clinical features, left ventricular measurements, and left atrial indices of the study population
| Variables | Patients (n=159) | Variables | Patients (n=159) | Variables | Patients (n=159) |
|---|---|---|---|---|---|
| Age (years) | 45.05±16.82 | Heart rate (bpm) | 79.7±13.16 | LA horizontal diameter (mm) | 38.09±4.36 |
| Height (cm) | 167.09±9.34 | LVEF (%) | 63.88±3.96 | LA vertical diameter (mm) | 49.45±6.44 |
| Weight (kg) | 93.12±27.67 | LVEDD (mm) | 47.35±4.43 | LA maximum area (cm2) | 16.28±3.74 |
| BSA (m2) | 2.06±0.32 | LVESD (mm) | 32.12±24.85 | LA precontraction area (cm2) | 11.89±2.78 |
| BMI (kg/m2) | 33.50±9.94 | IVS (mm) | 9.88±1.43 | LA minimum area (cm2) | 8.89±2.61 |
| HT, n (%) | 29 (18.6) | PWT (mm) | 9.5±1.39 | LA maximum volume (mL) | 60.83±23.8 |
| DM, n (%) | 30 (19.2) | LV mass (g) | 161.43±40.33 | LA precontraction volume (mL) | 32.42±13.57 |
| HL, n (%) | 13 (8.3) | RWT | 0.4±0.07 | LA minimum volume (mL) | 18.81±9.86 |
| CAD, n (%) | 8 (5.1) | LVMI (g/m2) | 79.61±16.99 | LAVI maximum (mL/m2) | 29.57±10.24 |
| CCB, n (%) | 11 (7.1) | LVESV (mL) | 29.68±12.48 | LAVI minimum (mL/m2) | 9.2±4.72 |
| ACEI, n (%) | 3 (1.9) | e/e’ ratio | 7.57±2.59 | LA total stroke volume (mL) | 40.73±19.03 |
| ARB, n (%) | 7 (4.5) | MPI | 0.53±0.16 | LA active stroke volume (mL) | 13.85±7.78 |
| Beta blockers, n (%) | 9 (5.8) | Stroke volume (mL) | 71.39±21.71 | LA passive stroke volume (mL) | 26.87±17.05 |
| Alpha blockers, n (%) | 2 (1.3) | Cardiac output (L/min) | 5.65±1.87 | LA active emptying fraction | 43.02±17.3 |
| Anti-platelet treatment, n (%) | 8 (5.2) | Cardiac index (L/min/m2) | 2.76±0.89 | LA passive emptying fraction | 43.39±16.15 |
| Anti-coagulant treatment, n (%) | 1 (0.7) | LA expansion index | 2.73±1.74 |
BSA=Body surface area, HT=Hypertension, DM=Diabetes mellitus, HL=Hyperlipidaemia, CAD=Coronary artery disease, CCB=Calcium channel blockers, ACEI=Angiotensin converting enzyme inhibitors, ARB=Angiotensin receptor blockers, LV=Left ventricle, LVEF=Left ventricular ejection fraction, LVEDD=Left ventricular end-diastolic diameter, LVESD=Left ventricular end-systolic diameter, IVS=Interventricular septum thickness, PWT=Posterior wall thickness, RWT=Relative wall thickness, LVMI=LV mass index, LVESV=LV end-systolic volume, MPI=Myocardial performance index, LA=Left atrium, LAVI=Left atrial volume index, BMI=Body mass index
There was a low correlation between the pPTT and MPI values of patients (r = −0.193*, P = 0.026), and also a correlation between LA total stroke volume, passive stroke volume values, and pPTT (r = 0.263, P = 0.003, r = 0.240, P = 0.007, LA total stroke volume and passive stroke volume, respectively). Similarly, there was a statistically consistent correlation between LA max area, LAV max and LAVi max values, and pPTT (r = 0.339, P < 0.001, r = 0.307, P < 0.001 r = 0.199, P = 0.024, LA max area, LAV max, and LAVi max, respectively). Correlations between pPTT and LA/LV indices are revealed in Table 2. Univariate linear regression analysis showed that LA area, LAV, and LAVi values were among factors affecting pPTT (hazard ratio: 4.977 P < 0.001, confidence interval [CI]: 2.440–7.514, hazard ratio [HR]: 0.651 P = 0.003, CI: 0.232–1.071, HR: 1.126, P = 0.032, CI: 0.096–2.156, LA area, LAV, and LAVi values, respectively). In addition, deceleration time (DT), LV end systolic volume (LVESV), and LA total stroke volume were also predictors of pPTT (HR: 0.273, P = 0.046, CI: 0.005–0.541, HR: 1.244, P = 0.002, CI: 0.446–2.042, HR: 0.551 P = 0.043, CI: 0.018–1.085, DT, LVESV and LA total stroke volume, respectively). Analysis of clinical parameters as predictors for pPTT was presented in Table 3. Heart rate (HRt), and LAVi and DT were evaluated as a multivariate linear regression analysis shown in Table 4: We observed that HRt and LAVi were independent predictors of pPTT (HR: −2.290 P < 0.001, 95% CI: −3.274–1.306, HR: 0.461, P = 0.028, 95%CI: 0.050–0.873, HRt and LAVi, respectively) [Table 4, Model 1]. However, in this analysis, it was determined that the standardized beta value of the HRt was 0.467, indicated in the table, while the pPTT value was strongly determined by the HRt. When factors that may have impacted pPTT were included in the multivariate linear regression model, HRt was an independent predictor of pPTT [Table 4 Model 2] (HR: −1.968 P < 0.001, 95% CI: −3.011–0.925, standardized beta value 0.407).
Table 2.
Correlations between pulmonary pulse transit time, left atrial, and left ventricular indices
| Variables | r/P |
|---|---|
| e/e’ ratio | −0.052/0.528 |
| MPI | −0.193*/0.026 |
| LA total stroke volume | 0.263**/0.003 |
| LA active stroke volume | 0.079/0.378 |
| LA passive stroke volume | 0.240**/0.007 |
| LA active emptying fraction | −0.016/0.857 |
| LA passive emptying fraction | 0.146/0.103 |
| LA expansion index | 0.057/0.524 |
| LA maximum area | 0.339**/0.000 |
| LA minimum area | 0.153/0.076 |
| LA precontraction area | 0.213*/0.013 |
| LA maximum volume | 0.307**/0.000 |
| LA minimum volume | 0.087/0.327 |
| LA precontraction volume | 0.161/0.069 |
| LAVI maximum | 0.199*/0.024 |
| LAVI minimum | −0.017/0.859 |
| LAVI precontraction | 0.036/0.696 |
*P<0.05, **P<0.001. MPI=Myocardial performance index, LA=Left atrium, LAVI=Left atrial volume index
Table 3.
Univariate linear regression analysis of the factors affecting on pulmonary pulse transit time
| HR | P | 95% CI for HR | ||
|---|---|---|---|---|
|
| ||||
| Lower bound | Upper bound | |||
| Age (years) | −0.437 | 0.178 | −1.075 | 0.202 |
| Heart rate (bpm) | −2.098 | 0.000* | −2.878 | −1.318 |
| BSA (m2) | 40.522 | 0.012* | 8.976 | 72.069 |
| LA area (mm2) | 4.977 | 0.000* | 2.440 | 7.514 |
| LA volume (mL) | 0.651 | 0.003* | 0.232 | 1.071 |
| LAVI (mL/m2) | 1.126 | 0.032* | 0.096 | 2.156 |
| Stroke volume (mL) | 0.842 | 0.000* | 0.403 | 1.282 |
| Cardiac output (L/min) | 2.833 | 0.326 | −2.854 | 8.520 |
| LVESV (mL) | 1.244 | 0.002* | 0.446 | 2.042 |
| DT (ms) | 0.273 | 0.046* | 0.005 | 0.541 |
| e/e’ ratio | 0.968 | 0.638 | −3.093 | 5.029 |
| MPI | −36.732 | 0.245 | −98.939 | 25.474 |
| Cardiac index (L/min/m2) | −2.112 | 0.738 | −14.585 | 10.361 |
| LA total stroke volume (mL) | 0.551 | 0.043* | 0.018 | 1.085 |
| LA active stroke volume (mL) | 0.595 | 0.384 | −0.751 | 1.940 |
| LA passive stroke volume (mL) | 0.583 | 0.059 | −0.022 | 1.188 |
| LA active emptying fraction (%) | −0.044 | 0.886 | −0.657 | 0.568 |
| LA passive emptying fraction (%) | 0.416 | 0.208 | −0.234 | 1.066 |
| LA expansion index (%) | 2.100 | 0.479 | −3.752 | 7.952 |
*P<0.05. BSA=Body surface area, LA=Left atrium, LAVI=Left atrial volume index, LV=Left ventricle, LVESV=Left ventricular end-systolic volume, DT=Deceleration time, MPI=Myocardial performance index, HR=Hazard ratio, CI=Confidence interval
Table 4.
Multivariate linear regression analysis of the factors affecting on pulmonary pulse transit time
| Factors | HR | Standardized β | P | 95% CI for HR | |
|---|---|---|---|---|---|
|
| |||||
| Lower bound | Upper bound | ||||
| Model 1 | |||||
| Heart rate (bpm) | −2.290 | −0.467 | 0.000* | −3.274 | −1.306 |
| LA volume (mL) | 0.461 | 0.102 | 0.028* | 0.050 | 0.873 |
| DT (ms) | −0.222 | −0.153 | 0.183 | −0.550 | 0.106 |
| Model 2 | |||||
| Heart rate (bpm) | −1.968 | −0.407 | 0.000* | −3.011 | −0.925 |
| LAVI (mL/m2) | −0.658 | −0.102 | 0.552 | −2.848 | 1.532 |
| DT (ms) | −0.248 | −0.142 | 0.186 | −0.618 | 0.122 |
| LVESV (mL) | 0.485 | 0.101 | 0.307 | −0.452 | 1.422 |
| Stroke volume (mL) | 0.511 | 0.175 | 0.087 | −0.076 | 1.098 |
| LA total stroke volume (mL) | 0.427 | 0.138 | 0.416 | −0.611 | 1.465 |
| e/e’ ratio | −1.295 | −0.049 | 0.611 | −6.339 | 3.748 |
*P<0.05. LA=Left atrium, LAVI=Left atrial volume index, LV=Left ventricle, LVESV=Left ventricular end-systolic volume, HR=Hazard ratio, CI=Confidence interval, DT=Deceleration time
DISCUSSION
The most important findings in our study were as follows: first, pPTT was a parameter that can be affected by HRt and second, pPTT was correlated with LA total, passive stroke volume, and LAVI max. Although LAVI, HRt, DT, and LA total stroke volume were detected as effective parameters on pPTT without PH, the dominant effect of HRt may have been an important issue to consider in future studies.
Studies show that pPTT is a marker related to pulmonary arterial stiffness and decreases in patients with PH.[2] In addition, pPTT was studied in patients with scleroderma and systemic lupus erythematosus, and it was found that pPTT was inversely correlated with disease severity and duration.[4,6] Recently, diastolic dysfunction was seen as a common reason for PH with increased age. The clinical significance of pPTT changes in patients is still unclear. Since pPTT shows the time passed from the right ventricular outflow tract to the LA, it is thought that it may be affected by LA functions, regardless of the presence of PH. Gurbuz et al. demonstrated that pPTT was prolonged with significant mitral stenosis and a positive correlation was found between pPTT and LAVi-systolic pulmonary arterial pressure.[3] The effect of decreased LA compliance may explain the relationship between LAVi and pPTT.[3]
Increased LAV was a useful parameter reflecting chronic elevations of LA pressures.[7,8] LAVi max has emerged as an important biomarker for adverse cardiac events in a variety of conditions.[9] According to our results, the e/e’ ratio and LA active and passive emptying fraction were not correlated with pPTT values. While we could not observe a clear relationship with LA mechanical functions, LAVi has been effective on pPTT without PH.
The results of our study suggest that pPTT should not be considered an independent variable of HRt. HRt increases cardiac output, while another study suggests that corrected A-wave VTI and peak A-wave should be used when the E- and A-waves merge at higher HRts.[10] Therefore, it seems more beneficial to use HRt-adjusted values of pPTT in future studies.
MPI is considered a reliable parameter for global LV function, but is relatively independent of HRt and volume loading conditions.[11,12] However, MPI was not detected as an effective parameter for pPTT, although we found a negative correlation between MPI and pPTT values.
One study with obese patients demonstrated that pPTT was reduced in them compared to healthy controls and strongly correlated with the severity of obesity.[13] Conversely, our patient population was primarily obese, and no similar effect of obesity on pPTT was found in the absence of PH. In addition, E-wave DT is a significant parameter in differential diagnosis of diastolic dysfunction, as its normal values fall between 160 and 200 ms and increase with age.[14] Univariate regression analysis shows that DT is a positive effective parameter on pPTT, but this effect was not observed with multivariate regression analysis, due to the dominant effect of HRt on pPTT. Our study population consisted of young patients with a low rate of additional comorbidity, but even in this population, pPTT was affected by many parameters, such that this may be insufficient to conclude that pPTT may be the only marker associated with PH.
This study has some limitations. This is a single-center study with a relatively small group of patients. More comprehensive methods, such as strain imaging and stress echocardiography, could not be performed; only echocardiography with a specialist may have reduced the objectivity of the measurements. Finally, our study has not assessed the clinical significance of pPTT with invasive measurements.
CONCLUSION
We show the relationship for the first time between pPTT and LA-diastolic function without PH. LAVi and HRt also affected pPTT. The dominant effect of HRt on pPTT should be considered in future studies. Larger studies are needed to determine the change and clinical significance of pPTT in left heart disease.
Ethical statement
This study is approved by the institutional Ethics Committee of Pamukkale University approvel number: E_60116787-020-69618.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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