Assessment of Left Atrial Strain in Patients with and without Chronic Obstructive Airway Disease

Abstract

Background:

The cardiac abnormality related with chronic obstructive pulmonary disease (COPD) has traditionally been right ventricular (RV) dysfunction, publications in the last century already reporting pathological left atrial (LA) changes due to increased (LV) end diastolic pressure which increases the LA strain.

Aim:

To evaluate left atrium (LA) strain by two-dimensional (2D)- STE in patients with chronic obstructive pulmonary disease (COPD).

Patients and Methods:

This prospective study was carried out on 39 subjects divided into (Group I) including 14 normal persons and (Group II) including 25 COPD patients with typical symptoms and signs and typical radiological features of COPD. All subjects were subjected to resting transthoracic echocardiography and left atrial strain analysis.

Results:

Left atrium, aorta, pulmonary artery systolic pressure (PASP), E/A were significantly higher in group 2 than group left atrial strain rate (LA sr) (apical 4 and 2 chamber) were significantly higher in group 1 than group 2 (P<0.05). LAScd (apical 4 chamber) was significantly lower in group 1 than group 2 (P<0.001). There was a negative correlation between (smoking index) and (LA sr, LAScd in apical 4 and 2 chambers) (P<0.05). There was a negative correlation between (smoking index) and LASct (apical 2 chambers) (P<0.05). There was negative correlation but statistically insignificant between TAPSE and PASP.

Conclusions:

LA sr was affected in COPD patients.

INTRODUCTION

Chronic obstructive pulmonary disease (COPD) is a common, preventable, and treatable disease characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and lungs to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individual patients. Cardiovascular events are more common in patients with COPD compared to smokers without the disease. However, whether this is simply due to the higher prevalence of traditional cardiovascular risk factors (hypertension, diabetes mellitus, reduced physical activity, and dyslipidemia) in COPD patients or whether there is a particular pathophysiological connection is widely debated.[1]

The cardiac abnormality associated with COPD has traditionally been right ventricular (RV) dysfunction, with publications already reporting pathological left atrial (LA) changes due to increased left ventricle (LV) end-diastolic pressure, which increases LA strain. Speckle-tracking echocardiography (STE) is a noninvasive ultrasound imaging technique that enables an objective and quantitative evaluation of global and regional myocardial function independent of the angle of insonation and cardiac translational movements.[2]

In the fields of cardiology and medical imaging, STE is an echocardiographic imaging technique that analyzes the motion of tissues in the heart using the naturally occurring speckle pattern in the myocardium (or motion of blood when imaged by ultrasound).[3] This method of documentation of myocardial motion is a noninvasive method of definition for both vectors and velocity. When compared to other technologies seeking a noninvasive definition of ischemia, speckle tracking seems a valuable endeavor. The speckle pattern is a mixture of interference patterns and natural acoustic reflections. These reflections are also described as speckles or markers.[4]

The pattern is random; each region of the myocardium has a unique speckle pattern (also called patterns, features, or fingerprints) that allows the area to be traced. The speckle pattern is relatively stable, at least from one frame to the next. In postprocessing, this can be tracked consecutively from frame to frame and ultimately resolved into angle-independent two-dimensional (2D) and three-dimensional strain-based sequences.

We hypothesized that LA strain parameters would be significantly impaired in patients with COPD compared to healthy individuals.

This study aimed to evaluate LA strain using 2D-STE in patients with COPD.

PATIENTS AND METHODS

This prospective study was conducted on 25 patients, both sexes, with COPD admitted to the Chest Department at Menoufia University, who exhibited typical symptoms, signs, and radiological features of COPD, as confirmed by chest consultants, and were compared with 14 healthy individuals as Group I. The study was conducted from August 2022 to February 2023, following approval from the Ethical Committee of Menoufia University Hospitals, Menoufia, Egypt. Informed written consent was obtained from the patient or the patient’s relatives.

All subjects were in normal sinus rhythm without atrial fibrillation (AF).

Exclusion criteria were history suggestive of ischemic heart disease by electrocardiogram (ECG) and Echo, any signs or symptoms suggestive of left-sided heart failure, relevant regional wall motion abnormalities (RWMA) at rest by 2D conventional echocardiography, dilated RV dimensions and impaired function, significant valvular heart disease and patients with cardiomyopathy whatever its cause and rhythm other than sinus rhythm.

All patients were subjected to complete history taking, clinical examination, and radiological investigations (resting standard 12-lead ECG and resting transthoracic echocardiography).

Resting transthoracic echocardiography

Conventional echocardiography was performed to exclude any RWMA or valvular heart disease. All patients were examined at rest in the left lateral decubitus position to obtain adequate images in different standard views. All images were obtained from standard parasternal and apical positions using 2D and M-mode echocardiographic techniques. LV ejection fraction was calculated from parasternal M-mode measurements. Assessment of the right side was done by tricuspid annular plane systolic excursion (TAPSE), pulmonary artery systolic pressure (PASP), and tricuspid annular diameter. The assessment of LA morphology and function was paramount in evaluating left ventricular filling among a variety of cardiovascular conditions, including hypertension, heart failure, valvular heart disease, and cardiomyopathies. The LA carries out three discrete functional phases, each accounting for approximately 50%, 30%, and 20% of the left ventricle (LV) filling in healthy subjects, respectively. The “reservoir” phase of the LA transpires during the isovolumetric contraction, ejection, and relaxation phase of the LV, with the mitral valve in a closed state. During this phase, the LA serves as a storage unit for potential energy. The “conduit” phase occurs in the initial phase of ventricular diastole, beginning with the opening of the atrioventricular valves and continuing until the commencement of LA contraction. Throughout this phase, the LA functions as a pathway for blood from the pulmonary veins to the left ventricle (LV). Finally, during the “contraction” or “pump” phase, the contraction of the LA aids in augmenting left ventricular filling. The LA function is vital in averting heart failure, as it initiates its inherent compensatory mechanisms in the event of left ventricular dysfunction. LA dilatation, as signified by a volume index exceeding 34 mL/m², is a crucial indicator of LV filling and diastolic function. STE can be used to investigate LA function, and the LA strain curve, with two positive peaks corresponding to LA reservoir and LA pump function, serves as a sensitive indicator of LV filling pressure, superior to LA volume, and is utilized for the early detection of preclinical LV dysfunction and remodeling. Recent research suggests that atrial fibrosis precipitates impaired atrial contractility, preceding atrial remodeling, which forecasts cardiovascular morbidity and mortality. The evaluation of the left atrial (LA) strain was conducted in accordance with the most recent consensus recommendations published by the European Association of Cardiovascular Imaging (EACVI), ensuring adherence to standardized protocols for image acquisition, analysis, and interpretation of LA deformation parameters. They advocate that it should be executed through dedicated image acquisition from an LA-focused view (4 chambers or two chambers), with a narrow image sector, ensuring nonforeshortened images of the LA and acquiring 3–5 consecutive, regular beats. A high-quality ECG trace with a visible p-wave is essential, and the acquisition of mitral and aortic valve Doppler waves can provide a better retrospective definition of time intervals. Dedicated software should be utilized whenever possible. The region of interest is defined by delineating the endocardial contour and encompassing the LA myocardium while avoiding the strong signal of the pericardium. Common tracking issues should be corrected by manual adjustment if necessary. The LA strain was measured as the Global Longitudinal Strain of the entire wall, and the segmental strain was not considered. The zero reference is end diastole, corresponding to mitral valve closure; following recommendations, we defined it by R wave at ECG (or simply the nadir of the atrial strain curve). Phasic strain calculation involves assessing the deformation of the left atrial (LA) wall during three distinct functional phases: reservoir strain (LA strain during reservoir phase, LAS), conduit strain (LA strain during conduit phase, LAScd), and contraction strain (LA strain during contraction phase, LASc). Left arterial reservoir strain (LASr), always positive, was calculated as the difference between the strain value at the curve peak and the end-diastolic value. LAScd, consistently negative, was calculated as the difference between the strain value at the onset of atrial contraction (p-wave) and the peak value (in AF patients, LAScd has the same value as LASr but with a negative sign). LASc was calculated from the difference between the strain value at the end-diastole (R-wave) and the value at the onset of the p-wave. It consistently exhibits a negative value and only occurs in sinus rhythm. Image quality is ensured via LA-focused views, a narrow sector, and a visual tracking quality check (≥90% tracking acceptance).

Statistical analysis

Statistical analysis was done by SPSS v26 (IBM Inc., Chicago, IL, USA). Quantitative variables were presented as means and standard deviations and compared between the two groups using an unpaired Student’s t-test. Qualitative variables were presented as frequency and percentage (%) and were analyzed utilizing the Chi-square. A two-tailed P < 0.05 was considered statistically significant. Pearson’s correlation was done to estimate the degree of correlation between two quantitative variables. Spearman correlation was used to estimate the degree of correlation between quantitative and qualitative variables.

RESULTS

Age, sex, medical history, and clinical examination were not significantly different between the two groups. The smoking index was significantly higher in Group 2 than in Group 1 [Table 1].

Table 1.

Demographic data and clinical examination of the studied groups

	Group 1 (n=14)	Group 2 (n=25)	P
Age	44.79±5.82	47.48±4.99	0.139
Sex
Male	11 (78.57)	20 (80.0)	0.298
Female	3 (20.0)	5 (20.0)
Smoking index	40±48.04	436.8±177.32	<0.001*
Medical history
HTN	5 (35.71)	10 (40.0)	0.792
DM	0	1 (4.0)	0.448
HTN and DM	0	4 (16.0)	0.276
Clinical examination
Wheezes	0	4 (16.0)	0.098
Barrel chest	0	2 (8.0)
No	14 (100)	19 (76)

*Significant P value ≤0.05. Data are presented as mean ± SD or frequency (%). HTN=Hypertension, DM=Diabetes mellitus, ECG=Echocardiogram, NRS=Normal sinus rhythm, SD=Standard deviation

Tricuspid annulus diameter and E/É (apical 4 and 2 chambers) were insignificantly different between both groups. EF, TAPSE, and E/A were significantly higher in Group 1 than Group 2 (P < 0.05). The measurements of left atrial (LA) diameter, aortic root (AO) diameter, and pulmonary artery systolic pressure (PASP) were significantly lower in Group 1 compared with Group 2, with a highly statistically significant difference (P < 0.001), indicating better cardiac structural and hemodynamic profiles in Group 1 [Table 2].

Table 2.

Conventional echocardiogram (left atrium and aorta) and Doppler imaging of the studied groups

	Group 1 (n=14)	Group 2 (n=25)	P
LA (mm)	3.54±0.33	3.98±0.45	0.002*
AO (mm)	2.54±0.45	2.76±0.21	0.037*
EF (%)	69.71±4.32	62.12±6.23	<0.001**
PASP (mmHg)	29.33±6.66	39.91±7.4	0.028*
TAPSE (mm)	2.71±0.52	2.21±0.3	<0.001*
Tricuspid annulus diameter	2.99±0.3	3.2±0.45	0.136
Doppler tissue imaging
E/A	1.66±0.52	0.96±0.38	<0.001*
E/É	7.45±1.91	6.64±1.68	0.179

*Significant P≤0.05. **Highly significant. Data are presented as mean ± SD or frequency (%). LA=Left atrium, AO=Aorta, EF=Ejection fraction, ECG=Echocardiogram, NRS=Normal sinus rhythm, EF=Ejection fraction, PASP=Pulmonary artery systolic pressure. TAPSE=Tricuspid annular plane systolic excursion, NRS=Normal sinus rhythm, SD=Standard deviation

LASct (apical 4 and 2 chambers) was insignificantly different between both groups. LAsr (apical 4 and 2 chambers) was significantly higher in Group 1 than in Group 2 (P < 0.05). LAScd (apical four chambers) was significantly lower in Group 1 than in Group 2 (P < 0.001) [Table 3].

Table 3.

Strain analysis (left atrial reservoir strain, left atrial conduit strain and left atrial conduit strain contractile reservoir) of the studied groups

Strain analysis	Group 1 (n=14)	Group 2 (n=25)	P
LASr
Apical 4 chamber	34.79±5.26	28.2±7.23	0.005*
Apical 2 chamber	32.29±5.92	23.92±7.37	<0.001**
LAScd
Apical 4 chamber	−22.21±4.35	−16.04±4.73	<0.001**
Apical 2 chamber	−2.57±19.27	−11.48±10.32	0.067
LASct
Apical 4 chamber	−13.14±9.71	−13.16±3.88	0.994
Apical 2 chamber	−0.64±18.62	−9.68±9.86	0.054

*Significant P≤0.05. **Highly significant. Data are presented as mean±SD. LASr=Left atrial reservoir strain, LAScd=Left atrial conduit strain, LASct=Left atrial contractile strain, SD=Standard deviation

There was no correlation between medical history and (LAsr, LAScd, apical 4, and 2 chambers). There was a negative correlation between smoking index and LAsr, LAScd in apical 4 and 2 chambers (P < 0.05). There was no correlation between the smoking index and LASct (apical four chambers). There was a negative correlation between the smoking index and LASct (apical two chambers) (P < 0.05) [Table 4 and Figures 1-4].

Table 4.

Correlation between apical 4 chambers of left atrial reservoir strain, left atrial conduit strain, and left atrial contractile strain and medical history and smoking index and between apical 2 chambers of left atrial reservoir strain, left atrial conduit strain, and left atrial contractile strain and medical history of the studied groups

	DM	HTN	DM and HTN	Smoking index
Apical 4 chambers
LASr
r	0.03	0.05	−0.237	−0.703
P	0.853	0.759	0.146	0.001*
LAScd
r	0.068	−0.072	0.286	−0.503
P	0.680	0.661	0.077	0.001*
LASct
r	−0.212	0.065	0.219	0.119
P	0.196	0.693	0.181	0.467
Apical 2 chambers
LASr
r	0.129	0.021	0.021	−0.449
P	0.433	0.895	0.895	0.004*
LAScd
r	−0.085	−0.181	−0.181	−0.342
P	0.609	0.27	0.27	0.033*
LASct
r	−0.047	0.065	0.065	−0.363
P	0.776	0.694	0.694	0.023*

*Significant P<0.05. r=Pearson coefficient, LASr=Left atrial reservoir strain, LAScd=Left atrial conduit strain, LASct=Left atrial contractile strain, HTN=Hypertension, DM=Diabetes mellitus

Figure 1.

Correlation between smoking index and apical 4-chamber of left arterial reservoir strain. LA sr: Left arterial reservoir strain

Figure 2.

Correlation between smoking index and apical 4-chamber of LAScd

Figure 3.

Correlation between smoking index and apical 2-chamber of left arterial reservoir strain. LA sr: Left arterial reservoir strain

Figure 4.

Correlation between smoking index and apical 2-chamber of LAScd

There was a statistically insignificant negative correlation between TAPSE and PASP [Table 5].

Table 5.

Correlation between tricuspid annular plane systolic excursion and pulmonary artery systolic pressure of the studied groups

TAPSE	PASP
r	−0.363
P	0.074

r=Pearson coefficient, TAPSE=Tricuspid annular plane systolic excursion, PASP=Pulmonary artery systolic pressure

DISCUSSION

COPD is currently considered a pulmonary component of systemic endothelial disease in which many cellular and humoral inflammatory processes simultaneously affect multiple organs, leading to a state of multimorbidity.

In the present study, the age was significantly higher in the case group than in Group I. The smoking index was significantly higher in the case group than in Group I. Medical history was insignificantly different between the two groups. In line with our result, Grebe et al.[5] found that age was significantly higher in Group II than in Group I. Confirming our result, Pelà et al.[6] reported that age was significantly higher in Group II than in Group I.

In the current study, LA (3.54 ± 0.33 in Group I vs. 3.98 ± 0.45 in cases P < 0.002), AO (2.54 ± 0.45 in Group I vs. 2.76 ± 0.21 in cases P = 0.037), and PASP (29.33 ± 6.66 in Group I vs. 39.91 ± 7.4 in cases P = 0.028) were statistically significantly higher in case group than Group I. EF (69.71 ± 4.32 in Group I vs. 62.12 ± 6.23 in cases P < 0.001), E/A (1.66 ± 0.52 in Group I vs. 0.96 ± 0.38 in cases P < 0.001), and TAPSE (2.71 ± 0.52 in Group I vs. 2.21 ± 0.3 in cases P < 0.001) were statistically significantly lower in the case group than Group I. E/É (7.45 ± 1.91 in Group I vs. 6.64 ± 1.68 in cases P = 0.179) and tricuspid annulus diameter (2.99 ± 0.3 in Group I vs. 3.2 ± 0.45 in cases P = 0.136) were insignificantly different between both groups. Supporting our result, Grebe et al.[5] showed that LA was significantly higher in Group II than in Group I, and EF was significantly lower in Group II than in Group I. In agreement with our result, Cengiz Elçioğlu et al.[7] revealed that TAPSE was significantly lower in Group II than in Group I. PASP was significantly higher in Group II than in Group I.

In addition, in disagreement with our results, Pizarro et al.[8] reported that PASP and TAPSE were not significantly different between COPD patients and the control group. This discrepancy may be due to differences in COPD severity or patient selection criteria.

In the present study, LA strain (apical 4 and 2 chambers) was statistically significantly lower in the case group than in Group I (28.2 ± 7.23 vs. 34.79 ± 5.26 and 23.92 ± 7.37 vs. 32.29 ± 5.92, respectively). Regarding LAScd, apical four-chamber was significantly lower in the case group than Group I (−16.04 ± 4.73 vs. −22.21 ± 4.35), while LAScd (apical two-chamber) was insignificantly different between both groups. Regarding LA strain during the contractile phase (LASct) in (apical 4 and 2 chambers) was insignificantly different between both groups. COPD leads to early LA stiffening and pressure elevation, impairing active filling and reducing reservoir strain (LASr), while LAScd remains preserved until more advanced disease stages.[9]

In agreement with our result, Grebe et al.[5] revealed that LASr% was significantly lower in Group II than Group I. LAScd% was significantly lower in Group II than Group I. However, the LASct percentage was significantly lower in Group II than in Group I. This difference was attributed to the variation in the number of patients.

In the current study, a significant negative correlation was found between the LA strain (apical 4 and 2 chambers) and the smoking index. There was a negative correlation between TAPSE and PASP, but it was statistically nonsignificant. There were no correlations between (LA strain apical 4 and 2 chambers and LA Scd apical 4) and medical history.

Limitations of the study included a relatively small sample size. The study was in a single center. There was lack of follow-up. The lack of assessment of inter- and intraobserver variability in strain analysis. Additional limitations include the absence of adjustment for multiple comparisons due to the exploratory nature of the study, as well as the lack of assessment for inter- and intra-observer variability in strain measurements.

CONCLUSIONS

LAsr was affected in COPD patients.

Ethical statement

The study was done from August 2022 to February 2023 after approval from the Ethical Committee Menoufia University Hospitals, Menoufia, Egypt. An informed written consent was obtained from the patient or relatives of the patients.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.