Tricuspid annular plane systolic excursion (TAPSE) in chronic obstructive pulmonary disease patients: a systematic review and meta-analysis

Article information

Clin Exp Emerg Med. 2025;12(2):121-131

Publication date (electronic) : 2024 September 6

doi : https://doi.org/10.15441/ceem.24.228

Maria Groussis ¹

, Quincy K. Tran ²^,³

, Megan Hoffer ¹, Jalil Ahari ⁴, Ali Pourmand^,¹

¹Department of Emergency Medicine, George Washington University School of Medicine and Health Sciences, Washington, DC, USA

²Department of Emergency Medicine, University of Maryland School of Medicine, Baltimore, MD, USA

³Program in Trauma, R Adams Cowley Shock Trauma Center, University of Maryland School of Medicine, Baltimore, MD, USA

⁴Pulmonary and Critical Care Medicine, George Washington University School of Medicine and Health Sciences, Washington, DC, USA

Correspondence to: Ali Pourmand Department of Emergency Medicine, George Washington University School of Medicine and Health Sciences, 2120 L St, Washington, DC 20037, USA Email: Pourmand@gwu.edu

Received 2024 April 3; Revised 2024 July 15; Accepted 2024 July 15.

Abstract

Objective

Tricuspid annular plane systolic excursion (TAPSE) is an echocardiographic parameter that serves as a prognostic indicator for the severity of chronic obstructive pulmonary disease (COPD) clinical course. This study, consisting of a systematic review and meta-analysis, evaluates the current literature to elucidate the relationship between TAPSE measurement in COPD patients versus control subjects to discern baseline evidence of right heart strain.

Methods

PubMed, Scopus, CINAHL, Web of Science, and Cochrane Library databases were searched from their beginnings through November 1, 2023, for eligible studies. Outcomes included the difference of TAPSE measurement and right ventricular (RV) wall thickness between COPD patients and control patients. The Newcastle-Ottawa Scale was applied to assess risk of bias, Q-statistics and I² values were used to assess for heterogeneity, and Egger and Begg tests were used to assess publication bias.

Results

The search yielded 11 studies reporting TAPSE values involving 1,671 patients, 800 (47.9%) of which had COPD. The unadjusted mean TAPSE value for COPD patients was 18.9±4.0 mm, while the mean TAPSE value for control patients was 22.2±0.8 mm. The presence of COPD was significantly associated with decreased TAPSE values, with the meta-analysis reporting the mean difference in TAPSE value at –3.0 (95% confidence interval, –4.3 to –1.7; P=0.001) between COPD and control patients. Six studies reported the RV free wall thickness [19,21,22,26–28]. The unadjusted mean RV free wall thickness for COPD patients was 4.9±1.2 mm, and for control patients was 3.4±0.7 mm.

Conclusion

This meta-analysis demonstrated statistically significant lower TAPSE values and thicker RV free wall among COPD patients as compared with control patients.

Keywords: Tricuspid annular plane systolic excursion (TAPSE); Chronic obstructive pulmonary disease; Pulmonary disease; Chronic obstructive; Ultrasonography

INTRODUCTION

Chronic obstructive pulmonary disease (COPD) affects an estimated 16.4 million adults in the United States; COPD is also a common reason for visits to the emergency department (ED) [1]. The incidence of pulmonary hypertension (PH) and cor pulmonale in these patients is a significant predictor of mortality; however, the true prevalence is unknown. In one large study the prevalence was reported to be 47.6% [2], but other studies have reported incidence anywhere from 20% to 90% [3]. Currently, there are limited medical therapies for PH in this group of patients (categorized as group III PH), and as such, the management of the underlying condition in conjunction with supportive care is the main treatment approach.

COPD exacerbation is a frequent cause of ED visit in patients with COPD associated PH. The US Department of Health and Human Services reports that there are about 101.6 ED visits per 10,000 adults [4]. While the pathophysiology behind the PH in this group of patients is complex, the main reason is believed to be chronic hypoxia leading to chronic vasoconstriction. This phenomenon ultimately leads to pulmonary vascular remodeling and permanent increase in pulmonary vascular resistance, leading to PH. Further increase in pulmonary vasoconstriction can occur with physical exertion and during COPD exacerbations where there is more hypoxia. Overcoming high pulmonary arterial pressure places strain on the right ventricle, leading to right ventricular (RV) hypertrophy and eventually dilation/RV failure. The presence of PH on computed tomography has been shown to be a predictor of hospitalization for COPD [5].

Echocardiogram has been shown to be a useful noninvasive tool for evaluation of RV strain and this may be a useful adjuvant when applied to patients with COPD [6]. Tricuspid annular plane systolic excursion (TAPSE) and pulmonary artery systolic pressure (PASP) have been used conventionally to assess for right heart dysfunction secondary to PH. A decreased TAPSE/PASP ratio has been shown to correlate with RV-arterial uncoupling, which occurs when RV contraction cannot overcome RV afterload in advanced PH [7]. In one recent retrospective cohort, a decreased TAPSE/PASP ratio was associated with mortality in COPD exacerbations [8]. A recent study of 110 patients found TAPSE alone to be an equally effective surrogate marker for RV-PA uncoupling in patients with heart failure with reduced ejection fraction [9].

Although typically used to evaluate right heart strain secondary to acute conditions such as pulmonary embolism, TAPSE could also be used to evaluate and measure right heart strain in COPD, where it can be used as an objective marker of the severity of exacerbation and as a major long term prognostic factor. The aim of this review is to investigate TAPSE measurement in COPD patients versus control subjects, to determine if COPD patients have baseline evidence of right heart strain. RV free wall measurement will also be assessed as a surrogate marker for chronicity of patients’ existing lung disease.

METHODS

Ethics statement

This systematic review and meta-analysis did not require institutional review board approval as it did not contain any studies with human participants or animals. The study was registered in PROSPERO (No. CRD42023486939)

Search strategy

Our systematic review and meta-analysis followed 2020 PRISMA (Preferred Reporting Items for Systematic Review and Meta-Analyses) guidelines [10]. PubMed, Scopus, CINAHL (Cumulative Index to Nursing and Allied Health Literature), Web of Science, and Cochrane Library databases were searched from their beginnings to November 1, 2023. Our study followed the PICO (patient, intervention, control, and outcome) format as in the following. (1) Patient: patients with COPD; (2) intervention: any patients who received echocardiogram to measure TAPSE, thickness of RV free wall; (3) control: patients without COPD; and (4) outcome: TAPSE, thickness of RV wall at any time of follow-up by the studies’ authors.

The search terms were “chronic obstructive pulmonary disease” AND "tricuspid annular plane systolic excursion" (Supplementary Material 1). Observational studies (retrospective or prospective), clinical trials, and quasi-experimental trials were eligible. We included any studies in an English language and involving adult patients (age ≥18 years) with COPD and with echocardiographic data. Non–full-text articles (conference proceedings, abstracts), non–original studies (reviews, meta-analysis), and case reports were excluded. We contacted five authors identified in the systematic review (Cuttica et al. [11], Cherneva et al. [12], Avesta et al. [13], Masson Silva et al. [14], Armentaro et al. [15]) to clarify their methods sections but we received no response.

Study selection and data extraction

Two investigators independently screened individual titles and abstracts from the search results. All abstracts required agreement between at least two investigators to move forward to the full-text screening step or to be excluded. Therefore, when there was a discrepancy between the two investigators, a third and senior investigator would serve as a tiebreaker to exclude or move the abstract to the next step. The same tiebreaker approach was utilized as necessary at the full-text screening step.

Data were extracted to a standardized spreadsheet (Microsoft Excel, Microsoft Corp) that included demographic and clinical data. First authors’ names, year of publication, study settings (outpatient vs. inpatient), study design (retrospective vs. prospective), patient population (both control population and COPD patients), age, percentage of female sex, and clinical data (echocardiogram information) were collected. The extracted data were presented as a consensus between investigators, and consequently, we did not calculate inter-rater agreement.

Outcome measurements

The primary outcome was the difference of TAPSE between COPD patients and control patients. Secondary outcome was the difference in the thickness of the RV wall between COPD and control patients.

Quality assessment and heterogeneity

Two investigators independently assessed each included study to assess each study’s quality. The Newcastle-Ottawa Scale [16] was used for all observational studies. The Newcastle-Ottawa Scale assesses observational studies across three domains: quality of outcomes, comparability of groups, and cohort selection. Based on the score from each domain, studies achieving scores ≥7 were ranked as high quality, 4 to 6 as moderate quality, and ≤3 scores as low quality.

For heterogeneity assessment, both the I² value and Q-statistic were used. These tests, while assessing different aspects of heterogeneity, are still complementary to each other. The I² value demonstrates the percentage in which the meta-analysis’ effect size was due to true difference between the studies. The Q-statistic tests for the null hypothesis that all studies within our meta-analysis would be similar to the true effect size.

Statistical analysis

Descriptive analyses were used to report data. Continuous variables were reported as mean±standard deviation, and categorical variables as percentages. When continuous variables were reported as median and interquartile range, they were converted to mean±standard deviation for analysis [17,18]. Weighted averages from different subgroups were also used to estimate the population means. A random-effects meta-analysis was used to compare the differences between TAPSE or RV wall thickness when at least three studies reported the same outcome. The mean difference and 95% confidence interval (CI) were reported as the outcome of the random-effects meta-analysis.

Sensitivity analyses with one-study-removed meta-analysis were used to assess whether any one individual study would have undue effect on overall outcome. For this sensitivity analysis, meta-analysis was performed without the first study, then it was performed without the second study, and so on. Thus, if any one study would change the overall effect size, there would be a fluctuation of the overall effect size in the absence of that particular study. To investigate the potential sources of heterogeneity, moderator analyses using categorical variables were performed. The demographic variables most commonly reported by study authors’ (retrospective vs. prospective, outpatient vs. inpatient, and sample size) were collected and used for moderator analyses. Since the sample size of the study was reported using continuous variables, we examined the histograms of the sample sizes and dichotomized it, according to the distribution.

We used Egger and Begg tests to identify the presence of publication bias. When the P-values for both Egger and Begg tests both exceeded 0.05, there was low likelihood of publication bias. We assessed publication bias further by using the funnel plots for both outcomes of TAPSE and RV wall thickness between control and COPD patients. The funnel plot shows the association between study size (y-axis as standard error) and effect size (x-axis). When every study is included, and hence no publication bias, the studies will be spread out evenly on both sides of the central axis, indicating the presence of both negative result and positive result studies. Additionally, smaller studies which would have more sampling variation and more likelihood of statistical significance due to less rigorous methodology, would appear toward the bottom of the funnel plot.

Random-effects meta-analysis, one-study-effect meta-analysis, and moderator analysis were performed by Comprehensive Meta-Analysis ver. 4 (Biostat). All statistical analyses with P<0.05, except the Egger and Begg tests, were considered statistically significant.

RESULTS

Study description

After screening 499 titles and 59 full-text articles, 11 studies [19–29] were included in our analysis (Fig. 1). Among the studies, 10 were prospective observational [19–28], while one was a retrospective study [29] (Table 1). Eight of the studies were conducted in the outpatient setting [19,21–26,28] and three were done in the inpatient setting [20,27,29]. Six studies were considered small studies because they included less than 100 patients total (for both COPD and control patients) [19,23–27], while five studies involved more than 100 patients in total [20–22,28,29]. All studies reported TAPSE values between COPD and control patients at the initial evaluation. Ozben et al. [24] reported the TAPSE values at initial presentation during patients’ exacerbation period, and the TAPSE values after patients’ resolution of symptoms. Pavasini et al. [28] also reported the TAPSE values at patients’ first presentation and then 6 months later. However, the 6-month TAPSE values were not included in our analysis, for consistency with most other studies. Five studies did not report values for RV free wall thickness [20,23–25,29].

Fig. 1.

PRISMA (Preferred Reporting Items for Systematic Review and Meta-Analyses) flowchart for study selection. CINAHL, Cumulative Index to Nursing and Allied Health Literature; PH, pulmonary hypertension.

Table 1.

Characteristics of the studies used in the analysis

The 11 studies included in this meta-analysis involved 1,671 patients, 800 patients (47.9%) with COPD. Of the 1,671 patients, 531 (31.8%) were female, although this number slightly underrepresents the actual number because Vitarelli et al. [19] did not report the number of female patients among the 22 patients in their control group.

Study quality

Since all included studies were observational, the Newcastle-Ottawa Scale was used to assess their qualities. Most studies were graded as having high quality [19–21,23–29], although one study was graded as having moderate quality [22] (Supplementary Table 1).

Primary outcome: comparison of TAPSE values between COPD and control patients

All 11 studies reported TAPSE values. The unadjusted mean TAPSE value for COPD patients was 18.9± 4.0 mm, while the mean TAPSE value for control patients was 22.2±0.8 mm. The meta-analysis reported the mean difference of TAPSE value between COPD and control patients was –3.0 (95% CI, –4.31 to –1.72; P<0.001). The I² value was high at 95%, which indicated high variance between studies within this meta-analysis. Since the P-value for the Q-statistic was 0.001, we rejected the null hypothesis that our meta-analysis would have an effect size similar to the true effect size (Fig. 2) [19–29].

Fig. 2.

Forest plot of tricuspid annular plane systolic excursion (TAPSE) in chronic obstructive pulmonary disease (COPD) patients versus control patients. CI, confidence interval.

Sensitivity analysis with one-study-removed meta-analysis showed that the effect size (mean difference of TAPSE) ranged from –3.3 to –2.5 (Fig. 3) [19–29], which was narrower than the 95% CI of the study, which indicated that there were no individual studies affecting the overall effect size. The P-value for Begg test was 0.280 but for Egger test was 0.048. This result demonstrated that there was publication bias in our meta-analysis. The funnel plot showed that there were smaller numbers of studies to the right of the plot (Fig. 4), indicating TAPSE values in COPD patients would be higher than control patients, which also confirmed the presence of publication bias.

Fig. 3.

Sensitivity analysis on tricuspid annular plane systolic excursion (TAPSE) in chronic obstructive pulmonary disease (COPD) patients versus control patients. CI, confidence interval.

Fig. 4.

Funnel plot of tricuspid annular plane systolic excursion (TAPSE) in chronic obstructive pulmonary disease patients versus control patients.

The moderator analyses, using three categorical variables that were consistently reported by all studies, showed that I² values were high across all subgroups (Table 2). The mean difference of TAPSE values was less between COPD and control patients among studies involving inpatient settings (mean difference, –1.55; 95% CI, –2.95 to 0.76; P=0.180), than the mean difference of TAPSE values for studies in outpatient settings (mean difference, –3.6; 95% CI, –5.19 to –1.78; P=0.001), although the difference between inpatient versus outpatient TAPSE was not statistically significant (P=0.170).

Table 2.

Moderator analyses, using studies’ demographic information that was most consistently reported by studies’ authors

Similarly, studies involving less than 100 total patients reported a larger effect size (mean difference, –4.24; 95% CI, –6.04 to –2.45; P=0.001) than studies involving over 100 patients (mean difference, –1.70; 95% CI, –3.55 to 0.15; P=0.071). Although the differences in effect size did not reach statistical significance (between-group comparison, P=0.053), it illustrated the phenomenon where studies with smaller sample sizes tend to show a misleadingly larger mean difference.

Secondary outcome: comparison of RV free wall thickness between COPD and control patients.

Six studies reported the RV free wall thickness. The unadjusted mean RV free wall thickness for COPD patients was 4.9±1.2 mm, and for control patients was 3.4±0.7 mm (Fig. 5) [19,21,22,26–28]. Sensitivity analysis showed the range of RV free wall thickness extended from 0.54 to 0.85 (Fig. 6) [19,21,22,26–28], which was within the 95% CI of the group. As a result, no individual studies disproportionately impacted the overall effect size of this meta-analysis.

Fig. 5.

Forest plot of right ventricular wall thickness in chronic obstructive pulmonary disease (COPD) patients versus control patients. CI, confidence interval.

Fig. 6.

Sensitivity analysis on right ventricular wall thickness in chronic obstructive pulmonary disease (COPD) patients versus control patients. CI, confidence interval.

The P-value for Begg test was 0.26 but for Egger test was 0.009. A larger number of studies were positioned to the right of the funnel plot center (Fig. 7). This finding indicated that there were more studies reporting thicker RV free wall among COPD patients than among control patients. This finding also indicated that there was publication bias involving reports of RV free wall thickness between COPD and control patients.

Fig. 7.

Funnel plot of right ventricular wall thickness chronic obstructive pulmonary disease patients versus control patients.

Moderator analyses demonstrated that I² values were consistently high among all subgroups (Table 2). The effect size (mean difference of RV free wall thickness between COPD and control patients) was larger among studies in the outpatient setting (mean difference, 1.85; 95% CI, 1.30 to 2.62; P=0.001) than among studies in the inpatient setting (mean difference, 0.81; 95% CI, –2.17 to 2.57; P=0.280). Studies with less than 100 total patients also reported a larger effect size (mean difference, 2.04; 95% CI, 1.59 to 3.24; P=0.001) than studies involving over 100 total patients (mean difference, 1.46; 95% CI, 0.58 to 2.5; P=0.002).

DISCUSSION

This meta-analysis demonstrated a statistically significant decrease in TAPSE in patients with COPD, as well as an increase in RV free wall thickness, indicating right heart dysfunction in these patients compared with control patients. TAPSE and RV free wall thickness can be measured in the ED population and may help determine severity of exacerbation and disposition.

The decrease in TAPSE values observed in this meta-analysis demonstrates the presence of right heart dysfunction in COPD patients. Our results showed a significant difference in TAPSE values between non-COPD patients and COPD patients. Therefore, although a TAPSE value <21 mm does not indicate acute right heart strain, it may be used to identify high risk COPD patients, as a previous study suggested that each mm of increase in TAPSE value was associated with a 33% reduction in the odds of a major cardiovascular event [15]. Management of COPD exacerbation varies considerably based on severity of underlying disease and response to treatment. Inclusion of TAPSE in ED decision-making may provide an objective measurement to ED physicians and admitting hospitalists to help risk stratify these patients and identify those at increased risk for morbidity and mortality. TAPSE has been used serially in patients with PH to monitor for response to treatment [30]. Adoption of routine TAPSE measurement in these patients would additionally provide a baseline for subsequent ED visits, allowing for more objective monitoring of exacerbations and progression of disease.

As evidenced in this systematic review, there is a high rate of comorbid conditions in patients with COPD. Incorporation of bedside ultrasound in the routine management of COPD patients, with inclusion of TAPSE screening, will facilitate correct identification of underlying cause of symptoms, identification of concomitant causes of shortness of breath, and allow the ED physician to identify those at high risk for hospitalization and mortality. RV dysfunction and decreased TAPSE values can also be found in other conditions such as pulmonary embolism. Therefore, understanding whether the measurement of RV free wall thickness in conjunction with TAPSE can aid clinicians in differentiating between acute and chronic disease pathologies is crucial. For instance, the presence of RV dysfunction and decreased TAPSE, coupled with increased RV free wall thickness, is more likely indicative of chronic lung disease than an acute condition like PE.

There are several limitations to this meta-analysis. There was high heterogeneity between the studies, and in the subgroups of comorbidities (PH, cardiovascular disease, and COPD exacerbations). Furthermore, the high heterogeneity and broad prediction intervals indicate that it is still unclear whether TAPSE values in COPD patients are consistently lower than in control patients. Therefore, future studies with a more well-defined patient population are needed to confirm the relationships between TAPSE values and RV free wall thickness. The studies chosen also did not consistently report common study demographics, thus preventing us from performing more thorough moderator analyses. Due to publication bias, it is also possible that studies with COPD patients having normal TAPSE and normal RV measures were not reported.

In conclusion, COPD patients had lower TAPSE values with increased RV free wall thickness. Understanding these measures in relation to individual concomitant comorbidities and changes in values based on acute versus chronic COPD disease are useful next steps to better utilizing limited echocardiography in the ED.

Notes

Author contributions

Conceptualization: QKT, AP; Data curation: MG, QKT, MH, AP; Formal analysis: QKT; Investigation: MG, MH, AP; Methodology: QKT, MH, AP; Project administration: AP; Supervision: JA; AP; Writing–original draft: all authors; Writing–review & editing: all authors. All authors read and approved the final manuscript.

Conflicts of interest

The authors have no conflicts of interest to declare.

Funding

The authors received no financial support for this study.

Data availability

Data analyzed in this study are available from the corresponding author upon reasonable request.

Supplementary materials

Supplementary Material 1.

Search strategy.

ceem-24-228-supplementary-Material-1.pdf

Supplementary Table 1.

Newcastle-Ottawa Quality Assessment Scale for cohort studies

ceem-24-228-supplementary-Table-1.pdf

Supplementary materials are available from https://doi.org/10.15441/ceem.24.228.

References

1. Centers for Disease Control and Prevention (CDC). About COPD [Internet]. CDC; 2024. [cited 2023 Nov 27]. Available from: https://www.cdc.gov/copd/about/index.html.

2. Cuttica MJ, Kalhan R, Shlobin OA, et al. Categorization and impact of pulmonary hypertension in patients with advanced COPD. Respir Med 2010;104:1877–82.

3. Nathan SD, Barbera JA, Gaine SP, et al. Pulmonary hypertension in chronic lung disease and hypoxia. Eur Respir J 2019;53:1801914.

4. Office of Disease Prevention and Health Promotion (OASH), ; US Department of Health and Human Services. Healthy People 2030: reduce emergency department visits for COPD in adults: RD-06: data methodology and measurement [Internet]. OASH; [cited 2023 Nov 26]. Available from: https://health.gov/healthypeople/objectives-and-data/browse-objectives/respiratory-disease/reduce-emergency-department-visits-copd-adults-rd-06/data-methodology.

5. Wells JM, Washko GR, Han MK, et al. Pulmonary arterial enlargement and acute exacerbations of COPD. N Engl J Med 2012;367:913–21.

6. Fukuda Y, Tanaka H, Sugiyama D, et al. Utility of right ventricular free wall speckle-tracking strain for evaluation of right ventricular performance in patients with pulmonary hypertension. J Am Soc Echocardiogr 2011;24:1101–8.

7. Tello K, Wan J, Dalmer A, et al. Validation of the tricuspid annular plane systolic excursion/systolic pulmonary artery pressure ratio for the assessment of right ventricular-arterial coupling in severe pulmonary hypertension. Circ Cardiovasc Imaging 2019;12e009047.

8. Yogeswaran A, Kuhnert S, Gall H, et al. Relevance of cor pulmonale in COPD with and without pulmonary hypertension: a retrospective cohort study. Front Cardiovasc Med 2022;9:826369.

9. Schmeisser A, Rauwolf T, Groscheck T, et al. Pressure-volume loop validation of TAPSE/PASP for right ventricular arterial coupling in heart failure with pulmonary hypertension. Eur Heart J Cardiovasc Imaging 2021;22:168–76.

10. Page MJ, McKenzie JE, Bossuyt PM, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ 2021;372:n71.

11. Cuttica MJ, Bhatt SP, Rosenberg SR, et al. Pulmonary artery to aorta ratio is associated with cardiac structure and functional changes in mild-to-moderate COPD. Int J Chron Obstruct Pulmon Dis 2017;12:1439–46.

12. Cherneva ZV, Denchev SV, Cherneva RV. Echocardiographic predictors of stress induced right ventricular diastolic dysfunction in non-severe chronic obstructive pulmonary disease. J Cardiol 2020;76:163–70.

13. Avesta L, Aslani MR, Parham P, Sadeghieh-Ahari S, Ghobadi H. The relationships between serum heart-type fatty acid-binding protein and right ventricular echocardiographic indices in chronic obstructive pulmonary disease. Clin Respir J 2021;15:628–36.

14. Masson Silva JB, Tannus Silva DG, Furtado RG, et al. Correlation between 2D strain and classic echocardiographic indices in the diagnosis of right ventricular dysfunction in COPD. Int J Chron Obstruct Pulmon Dis 2021;16:1967–76.

15. Armentaro G, Pelaia C, Cassano V, et al. Association between right ventricular dysfunction and adverse cardiac events in mild COPD patients. Eur J Clin Invest 2023;53e13887.

16. Wells G, Shea B, O’Connell D, et al. The Newcastle-Ottawa Scale (NOS) for assessing the quality of nonrandomised studies in meta-analyses [Internet]. Ottawa Hospital Research Institute; [updated 2021 May 3; cited 2023 Nov 26]. Available from: https://www.ohri.ca/programs/clinical_epidemiology/oxford.asp.

17. Lowry R. Estimation of a sample’s mean and variance from its median and range [Internet]. Richard Lowry; [cited 2023 Nov 26]. Available from: http://vassarstats.net/median_range.html.

18. Luo D, Wan X, Liu J, Tong T. Optimally estimating the sample mean from the sample size, median, mid-range, and/or mid-quartile range. Stat Methods Med Res 2018;27:1785–805.

19. Vitarelli A, Conde Y, Cimino E, et al. Assessment of right ventricular function by strain rate imaging in chronic obstructive pulmonary disease. Eur Respir J 2006;27:268–75.

20. Iversen KK, Kjaergaard J, Akkan D, et al. Chronic obstructive pulmonary disease in patients admitted with heart failure. J Intern Med 2008;264:361–9.

21. Tayyareci Y, Tayyareci G, Tastan CP, Bayazit P, Nisanci Y. Early diagnosis of right ventricular systolic dysfunction by tissue Doppler-derived isovolumic myocardial acceleration in patients with chronic obstructive pulmonary disease. Echocardiography 2009;26:1026–35.

22. Hilde JM, Skjorten I, Grotta OJ, et al. Right ventricular dysfunction and remodeling in chronic obstructive pulmonary disease without pulmonary hypertension. J Am Coll Cardiol 2013;62:1103–11.

23. Kazmierczak M, Ciebiada M, Pekala-Wojciechowska A, Pawlowski M, Pietras T, Antczak A. Correlation of inflammatory markers with echocardiographic parameters of left and right ventricular function in patients with chronic obstructive pulmonary disease and cardiovascular diseases. Pol Arch Med Wewn 2014;124:290–7.

24. Ozben B, Eryuksel E, Tanrikulu AM, et al. Acute exacerbation impairs right ventricular function in COPD patients. Hellenic J Cardiol 2015;56:324–31.

25. Geyik B, Tarakci N, Ozeke O, et al. Right ventricular outflow tract function in chronic obstructive pulmonary disease. Herz 2015;40:624–8.

26. Faludi R, Hajdu M, Vertes V, et al. Diastolic dysfunction is a contributing factor to exercise intolerance in COPD. COPD 2016;13:345–51.

27. Kanar BG, Ozmen I, Yildirim EO, Ozturk M, Sunbul M. Right ventricular functional improvement after pulmonary rehabilitation program in patients with COPD determined by speckle tracking echocardiography. Arq Bras Cardiol 2018;111:375–81.

28. Pavasini R, Fiorencis A, Tonet E, et al. Right ventricle function in patients with acute coronary syndrome and concomitant undiagnosed chronic obstructive pulmonary disease. COPD 2019;16:284–91.

29. Goedemans L, Hoogslag GE, Abou R, et al. ST-segment elevation myocardial infarction in patients with chronic obstructive pulmonary disease: prognostic implications of right ventricular systolic dysfunction as assessed with two-dimensional speckle-tracking echocardiography. J Am Soc Echocardiogr 2019;32:1277–85.

30. Ghio S, Pica S, Klersy C, et al. Prognostic value of TAPSE after therapy optimisation in patients with pulmonary arterial hypertension is independent of the haemodynamic effects of therapy. Open Heart 2016;3e000408.

Article information Continued

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/).

Notes

Capsule Summary

What is already known

Tricuspid annular plane systolic excursion (TAPSE), and pulmonary artery systolic pressure (PASP) have been used conventionally to assess for right heart dysfunction secondary to pulmonary hypertension. A decreased TAPSE/PASP ratio has been shown to correlate with right ventricular (RV)-arterial uncoupling, which occurs when RV contraction cannot overcome RV afterload in advanced pulmonary hypertension.

What is new in the current study

Chronic obstructive pulmonary disease (COPD) patients had lower TAPSE values with increased RV free wall thickness. Understanding these measures in relation to individual concomitant comorbidities, their changes based on acute versus chronic COPD disease, are next steps to better utilizing limited echocardiography in the emergency department.

Study	Study design	Setting	Sample size	COPD				Control
Study	Study design	Setting	Sample size	No. of patients	Age (yr)	Female sex	TAPSE^a) (mm)	No. of patients	Age (yr)	Female sex	TAPSE^a) (mm)
Vitarelli et al. [19] (2006)	Cross-sectional	Outpatient	61	39	54±13	12 (30.8)	19±6^b)	22	-	-	21±3
							6±4^c)
Iversen et al. [20] (2008)	Prospective	Inpatient	527	182	73.7±1.5	64 (35.2)	17	345	71.2	128 (37.1)	18
Tayyareci et al. [21] (2009)	Cross-sectional	Outpatient	130	90	61.9±9.03	23 (25.6)	20.5±2.6	40	60.8±10.7	9 (22.5)	21.9±2.1
					61.9±5.90^c)
Hilde et al. [22] (2013)	Prospective	Outpatient	132	98	63±7	49 (50.0)	22±3^b)	34	63±7	19 (55.9)	27±3
							19±4^c)
Kazmierczak et al. [23] (2014)	Cross-sectional	Outpatient	60	44	65.05±8.0^b)	13 (29.5)	26.66±2.61	16	53.1±7.0	12 (75.0)	28.31±1.66
					67.75±9.3^c)
Ozben et al. [24] (2015)	Prospective	Outpatient	60	30	64.2±10.9	8 (26.7)	14.47±2.40	30	61.3±7.8	9 (30.0)	16.33±1.97
							15.27±2.24^d)
Geyik et al. [25] (2015)	Prospective	Outpatient	76	55	62±9	0 (0)	21.7±6.4	21	58±11	0 (0)	27.5±3.5
Faludi et al. [26] (2016)	Cross-sectional	Outpatient	99	65	60.8±9.0	26 (40.0)	20.8±2.5	34	58.0±8.3	16 (47.1)	25.1±3.5
Kanar et al. [27] (2018)	Prospective	Inpatient	78	46	60.8±10.2	18 (39.1)	16.6±2.6^e)	32	58.5±8.9	19 (59.4)	20.4±3.1
							17.2±3.1^f)
Pavasini et al. [28] (2019)	Prospective	Outpatient	137	39	69±8	7 (18.0)	20±4	98	63±11	15 (15.3)	20±4
							19±7^g)				22±3^d)
Goedemans et al. [29] (2019)	Retrospective	Inpatient	311	112	69±10	29 (25.9)	17.9±3.8	199	68±10	55 (27.6)	18.1±3.8

Moderator variable (outcome)	Meta-analysis				Heterogeneity				P-value^a)
Moderator variable (outcome)	No. of studies	Mean difference	95% CI	P-value	Q-statistic	D(f)	P-value	I² (%)	P-value^a)
TAPSE
Study design									0.190
Prospective	10	–3.38	–4.80 to 1.87	0.001	200	9	0.001	95
Retrospective	1	–0.20	–1.12 to 0.73	0.930	NA	NA	NA	NA
Study setting									0.170
Inpatient	3	–1.55	–2.95 to 0.76	0.180	19	2	0.001	89
Outpatient	8	–3.64	–5.19 to 1.78	0.001	107	7	0.001	93
Sample size (no. of patients)									0.053
<100	6	–4.24	–6.04 to –2.45	0.001	45	5	0.001	89
>100	5	–1.70	–3.55 to 0.15	0.071	112	4	0.001	96
RV free wall thickness
Study design									NA
Prospective	6	1.47	0.84 to 2.10	0.001	280	5	0.001	98
Retrospective	0	NA	NA	NA	NA	NA	NA	NA
Study setting									0.160
Inpatient	1	0.81	–2.17 to 2.57	0.280	NA	NA	NA	NA
Outpatient	5	1.85	1.30 to 2.62	0.001	37	4	0.001	89
Sample size (no. of patients)									0.460
<100	3	2.04	1.59 to 3.24	0.001	34	2	0.001	94
>100	3	1.46	0.58 to 2.54	0.002	13	2	0.001	85