Association of type-D personality and left-ventricular remodelling in patients treated with primary percutaneous intervention after ST-segment elevation myocardial infarction

Abstract

Background

Type-D personality is an established predisposing factor for various diseases. Type-D traits have been shown to pose a 26% increased risk of coronary artery disease after controlling for other confounding factors. Significant associations have been reported between type-D personality traits and dyslipidaemia, impaired endothelial function, coronary heart disease (CAD), acute myocardial infarction, and other adverse cardiovascular events.

Objective

To assess the association between type-D personality and left-ventricular adverse remodelling in patients treated with percutaneous coronary intervention following index ST-segment elevation myocardial infarction.

Methods

All patients hospitalized and treated with percutaneous coronary intervention (PCI) after their index ST-segment elevation myocardial infarction (STEMI) between 1 January 2022 to 31 December 2023 were prospectively enrolled. Type-D personality traits in the study population were determined at baseline using type-D Scale-14 (DS14) instrument, whereas any positive change in left ventricular end diastolic volume (LVEDV) ≥ 20% at follow up period of 12-months from baseline was defined as left-ventricular adverse remodelling (LVAR). Univariate and multivariate analysis was done to establish the independent predictors of LVAR. The area under receiver-operating characteristic curve (AUROC) was employed to assess the sensitivity and specificity of the identified independent predictors.

Results

A total of 124 patients were enrolled in the study. The mean age of the study population was 67 ± 10 years and the overall incidence of LVAR was found to be 25%. Multivariate regression analysis revealed that type-D personality is a significant independent predictor of LVAR apart from the already established independent predictors Killip Class, baseline Global Longitudinal strain (GLS), and 3-vessel CAD. In ROC curve analysis type-D personality as an independent predictor of LVAR achieved a sensitivity of 41.4% and a specificity of 87.1%, p < 0.02.

Conclusion

Type-D personality trait is a significant independent predictor of LVAR in patients treated with PCI after their index-STEMI.

Introduction

Type-D personality is characterized by a combination of two key traits: a tendency to experience negative emotions, known as negative affectivity, and a tendency to suppress emotional expression, referred to as social inhibition [1]. Type-D individuals have also been found to be more susceptible to various diseases [2] and and may experience negative effects on their recovery process [3]. Type-D personality has been shown to be significantly prevalent among patients with heart disease [4]. Studies have reported a strong association between type-D personality traits and various cardiovascular conditions, including coronary artery disease (CAD) [5, 6], peripheral artery disease (PAD) [7], cardiac arrythmia [8], congestive heart-failure (CHF) [9], and a 4-fold risk of developing ischaemic heart disease [6]. It has also been shown that type-D personality independently predicts cardiac events in CAD patients over 5 years (OR = 2.90, p = .003) [10], increasing the risk of mortality [11]. Strong associations have also been demonstrated between type-D personality and increased risk of adverse cardiac events [12–14], severe coronary artery calcification [15], impaired endothelial function [16], and dyslipidaemia [17], emphasizing the connection between this personality type and more advanced forms of cardiovascular disease. Type-D personality has been linked to higher levels of anxiety, stress, and depression [18–22], which contribute to an increased risk of developing CAD [23], poorer cardiovascular outcomes, and higher mortality, as confirmed by multiple meta-analyses [24].

A significant association exists between Type D personality and acute myocardial infarction (AMI) [25]. One major consequence of AMI is left-ventricular adverse remodelling (LVAR), which involves changes in heart muscle that affect ventricular volume, geometry, and function, leading to a higher risk of heart failure and poorer prognosis [26–28]. While primary percutaneous intervention (PCI) has reduced LVAR incidence and improved AMI outcomes, it still occurs in 30–35% of patients [29]. Post-AMI LVAR increases left ventricular (LV) systolic and diastolic volumes and is a strong predictor of adverse clinical events [30]. Various conventional 2D echocardiographic parameters, such as left-ventricular ejection fraction (LVEF), left-ventricular end-systolic volume (LVESV), and left-ventricular end-diastolic volume (LVEDV), have been used to detect left-ventricular adverse remodelling (LVAR) [31, 32], but global longitudinal strain (GLS) from 2D-speckle tracking echocardiography (2D-STE) offers greater predictive accuracy for LVAR and cardiovascular events after ST-segment elevation myocardial infarction (STEMI) [33–36].

However, to the best of our efforts on literature survey we could not trace any investigation studying association and predictive significance of type-D personality in forecasting LVAR, in patients successfully treated with PCI following index STEMI.

Therefore, the aim of the present study was to assess any possible association of type-D personality with LVAR post index acute-STEMI.

Materials and methods

Study design and setting

This single centre, prospective observational study was carried out at Prince Faisal bin Khalid Cardiac Centre (PFKCC), Abha, Kingdom of Saudi Arabia.

Study subjects and duration

Patients hospitalized for index acute STEMI and successfully treated with percutaneous PCI between 1 January 2022 and 31 December 2022, who met the inclusion and exclusion criteria, were eligible for enrolment. The last enrolment occurred in December 2022, with follow-up continuing through December 2023.

Inclusion criteria

Patients were enrolled if:

• They were older than 18 years.

• It was their index acute STEMI.

• They met defined electrographic criteria for acute STEMI.

• They were successfully treated with PCI within 90–120 min from first medical contact.

• They provided written informed consent and completed the provided psychological questionnaires either themselves or with help from an attending nurse.

Exclusion criteria

Patients were excluded if:

• They refused to participate in the study.

• They had history of prior AMI.

• They had severe valvular disease.

• They did not complete the provided psychological questionnaires.

Study and ethical approval

The study was approved by the Research Ethics Committee at King Khalid University (HAPO-06-B-001) vide approval No: ECM #2023–3328 and carried out in-line with the 2013 revision of the principles of Declaration of Helsinki [37].

Study procedure

The relevant data regarding demographics (age, gender), predisposing factors for cardiovascular disease (Diabetes Mellitus, Obesity, Hypertension, history of smoking, hyperlipidaemia), clinical evaluation data, resting 12-lead electrocardiography (ECG), 2D-echocardiography and angiography was recorded on admission.

Confirmation of STEMI

STEMI was confirmed as per the criteria established by the European Society of Cardiology [38].

Determination of Killip class

With respect to their clinical presentation, confirmed acute STEMI patients were stratified to one of the Killip classes, as per the set criteria [39].

Laboratory parameters

On admission peripheral blood samples taken were assayed for serial troponin I, CK-MB, hs-CRP, lipid profile (Cholesterol, Triglycerides, HDL, LDL), creatinine, sodium, potassium, eGFR, CBC, Hb1AC and NT-proBNP.

PCI

The PCI was performed within 90–120 min after acute STEMI was established. The identification of the culprit vessel / vessels and the corresponding extent of stenosis was done as per the set criteria [40]. A thrombolysis in Myocardial infarction (TIMI) flow of grade 3 at the culprit vessel signalled successful PCI [41].

Echocardiography

Conventional and 2D-Spackle tracking echocardiography(2D-STE) was done at 24 ± 4 h following PCI (baseline) and at follow-up (12 Months). LVEF, LVESV, and LVEDV were calculated using Simpson’s biplane method, and GLS determined using 2D-STE, as per the procedures and standards laid down by American Society of Echocardiography [42]. At a follow-up period of 12-months, every enrolled study subject was contacted to have a follow-up visit and echocardiographic evaluation. The operators who performed the follow-up echocardiographic evaluation were blinded to baseline data.

Defining LVAR

Any positive change in LVEDV ≥ 20% from baseline was defined as LVAR [27].

Determining type-D personality

Type-D personality was determined at baseline using the type-D Scale-14(DS14), which is a 14-item scale consisting of 7-item negative affectivity (NA) and 7-item social inhibition (SI) subscales [43]. Items are rated on a 5-point Likert scale, ranging from 0 = False to 4 = True. Individuals with a cut-off score ≥ 10 on both the scales are categorized as type-D. Both the NA and SI subscales are internally consistent with respect to our study (Cronbach’s [44] α = 0.84 / 0.87).

With reference to type-D personality the study population was divided into two groups:

• Group I: Study subjects with type-D personality traits.

• Group II: Study subjects not showing type-D personality traits.

Statistical analysis

All statistical analysis was performed using R [45] scripting language and the accompanying R studio [46] (Version 1.2.5033, Orange Blossom). Sample size calculation was done based on the results of an earlier study [12] using the finite population corrections for proportions version of Cochran’s equation [47]. Continuous variables were reported as mean ± standard deviation (SD), whereas categorical data in numbers and percentages (%). Continuous variables following Gaussian distribution were compared using student’s t-test, whereas continuous variables with non-Gaussian distribution were compared using Mann-Whitney U-test. Chi-Square tests were used to compare categorical variables. Independent predictor variables of LVAR were uncovered using univariate and multivariate analysis. The sensitivity and specificity of the identified predictors were assessed utilizing the area under receiver operating characteristic curve (AUROC). Significance level was set at p < 0.05.

Results

Study population

Initially a total of 140 successfully reperfused acute-STEMI patients were included in the study. Sixteen patients were excluded from the study as 8 refused to participate, 5 underwent a second PCI, and 3 were lost during the follow-up period. Consequently, 124 patients were included in the final analysis. The mean age of the study population was 67 ± 10 years, with the mean age in Group I (subjects with type-D traits) being significantly higher compared to Group II (p = 0.002). Group I was predominantly male (55%), however compared to Group II the difference was not statistically significant (p = 0.059). Majority of subjects in Group I had Killip class III (p = 0.010), 2-vessel and 3-vessel CAD (p = 0.012 and (p = 0.006 respectively). Regarding laboratory parameters, subjects in Group I reported higher baseline values of peak CPK-MB levels (p = 037), NT-proBNP levels (p .041), cTnI levels (p = 0.011), and peak cTnI levels (p < 0.001). More importantly, LVAR was significantly prevalent in Group I compared to Group II (p < 0.0001). For clinical variates diabetes mellitus, smoking status, dyslipidaemia, Killip Classes I and II, culprit vessel, laboratory variate hs-CRP, and medications at discharge, no significant intergroup differences were observed (Table 1).

Table 1.

Baseline data

(N = 124)	Group I (n = 56)	Group II (n = 68)	p-value
Age, Years ± SD	69 ± 9	63 ± 12	0.002**
Male, n (%)	31(55)	26(38)	0.059
Hypertension, n (%)	44(78.6)	40(59)	0.020**
Diabetes Mellitus, n (%)	27(48.21)	35(51.5)	0.716
Current Smoker, n (%)	42(75)	40(58.8)	0.058
Obesity, n (%)	14(25)	23(33.82)	0.288
Dyslipidemia, n (%)	36(64.28)	33(48.53)	0.080
Killip Class
I, n (%)	16(28.57)	26(38.23)	0.259
II, n (%)	23(35.7)	37(54.41)	0.140
III, n (%)	12(21.4)	4(5.8)	0.010**
IV, n (%)	5(9.5)	1(1.5)	0.054
LVAR	26(46.5)	05(7.35)	< 0.0001**
Culprit Vessel
LAD n (%)	29(51.78)	47(69.12)	0.049
LCX n (%)	13(23.21)	11(16.17)	0.325
RCA n (%)	14(25)	22(32.35)	0.371
CAD
1-Vessel n (%)	28(50)	56(82.35)	0.0001**
2-Vessel n (%)	20(35.71)	11(16.17)	0.012**
3-Vessel n (%)	08(14.3)	01(1.5)	0.006**
Peak CPK-MB (IU/L) median (Q1, Q3)	294(153,637)	201(87, 312)	0.037**
NT-proBNP (ng/L) median (Q1, Q3)	597(167, 1691)	347(101, 453)	0.041**
cTnI (µg/L), median (Q1,Q3)	5.94(0.45–73.63)	2.63(0.36–17.87)	0.011**
Peak-cTnI (µg/L), median (Q1,Q3)	97.89 (5.46–160.34)	21.6 (3.7–61.57)	< 0.001**
hs-CRP (mg/L), median (Q1,Q3)	6.4(5.2–8.6)	5.8 (4.3–7.6)	0.432
Medications at Discharge, n(%)
Antiplatelet	56(100)	68(100)	0.999
β-blockers	52(92.86)	64(94.11)	0.778
ACEi’s /ARB’s	46(82.14)	53(79.42)	0.703
SGLT-2i	27(48.21)	35(51.47)	0.719
Statins	56(100)	68(100)	0.999
MRA	04(7.14)	03(4.41)	0.513

Categorical variables are presented as number (percentage); Normally distributed continuous variables are presented as mean ± standard deviation, and non-normally distributed continuous variable as median (25th Quartile, 75th Quartile); Abbreviations: SD, standard deviation; CAD, coronary artery disease; LAD, left anterior descending artery; LCX, left circumflex artery; RCA, right coronary artery; CPK-MB, creatine kinase MB-isoenzyme; BNP, brain natriuretic peptide; cTnI, cardiac troponin I; hs-CRP, high sensitivity c-reactive protein; ACEi, angiotensin converting enzyme inhibitor; ARB, angiotensin receptor blockers; MRA, mineralocorticoid receptor antagonists; Statistical significance shown (p < 0.05) as **

Echocardiography

The difference in Group I and Group II was highly significant in terms of both the baseline GLS (-13.37 ± 2.21 vs -19.11 ± 3.4; p < 0.0001) and GLS at 1-year follow-up (-11.23 ± 2.19 vs -13.47 ± 1.84; p < 0.0001). The mean baseline LVESV was higher in Group I compared to Group II (p. = 0.037). No significant differences were observed between the two groups (Group I and Group II) in terms of other baseline echocardiographic parameters-EF, LVESVI, and LVEDV. However, differences in EF (p. = 0.002), LVEDV(p. = 0.004), EVSI(p. = 0.011), and LVEDVI(p. = 0.028) values at 1-year follow-up were significant between Group I and Group II. Echocardiographic data presented in Table 2.

Table 2.

Echocardiographic parameters at Baseline and Follow-up

(N = 124)		Group I (n = 56)	Group II (n = 68)	p-value
EF (%, Mean ± SD)
Baseline		55.03 ± 6.21	56.31 ± 8.40	0.345
1-Year Follow-up		45.98 ± 8.67	50.79 ± 8.48	0.002**
LVESV (mL, Mean ± SD)
Baseline		51.62 ± 8.96	48.43 ± 7.89	0.037**
1-Year Follow-up		58.27 ± 14.13	54.18 ± 9.17	0.054
LVESVI (mL/m2,Mean ± SD)
Baseline		30.91 ± 7.58	29.02 ± 6.68	0.143
1-Year Follow-up		36.39 ± 11.97	32.44 ± 7.77	0.028**
LVEDV (mL, Mean ± SD)
Baseline		113.35 ± 23.77	108.27 ± 24.83	0.250
1-Year Follow-up		139.76 ± 28.24	125.65 ± 14.23	0.004**
LVEDVI (mL/m2,Mean ± SD)
Baseline		67.87 ± 20.14	64.83 ± 21.04	0.416
1-Year Follow-up		83.68 ± 23.82	75.23 ± 12.05	0.011**
GLS (%, Mean ± SD)
Baseline		-13.37 ± 2.21	-19.11 ± 3.4	< 0.0001**
1-Year Follow-up		-11.23 ± 2.19	-13.47 ± 1.84	< 0.0001**

Categorical variables are presented as number (percentage); Normally distributed continuous variables are presented as mean ± standard deviation; Abbreviations: SD, standard deviation; EF, Ejection Fraction, LVESV, Left-ventricular end systolic Volume; LVESVI, Left-ventricular end Systolic Volume Indexed; LVEDV, Left-ventricular end Diastolic Volume; LVEDVI, Left-ventricular end Diastolic Volume Indexed; GLS, Global Longitudinal Strain; Statistical significance shown (p < 0.05) as **

Predictors of left ventricular adverse remodelling

The association of type-D personality with LVAR and covariates age, baseline hypertension, Killip class, 2- and 3-vessel CAD, Peak CPK-MB levels, cTnI levels, peak cTnI levels, LVESV, and LV GLS assumed statistical significance. To find the level of association between LVAR and type-D personality, tables 1 and 2 were pivoted with respect to LVAR (as dependent variable). Multivariate logistic regression analysis revealed that type-D personality, Killip Class, LV GLS, and 3-vessel CAD are independent predictors of LVAR (Table 3). The receiver-operating characteristic (ROC) curve analyses was used to compare the identified independent predictors of LVAR (Fig. 1).

Table 3.

Independent Predictors of LVAR based on Multivariate Logistic Regression

Independent predictor	Crude results			Adjusted resultsη
	Crude Odds Ratio	95% CI	p-value	Adjusted Odds Ratio	95% CI	p-value
Killip Class	7.39	2.59–23.04	< 0.0001**	7.30	3.03–17.55	< 0.0001**
Baseline GLS (%)	2.74	1.81–6.24	< 0.0001**	2.69	1.19–6.61	0.01**
Type-D Personality	3.06	2.31–7.43	0.001**	2.51	1.16–5.77	0.03**
3-Vessel CAD	2.40	1.1- 6.37	0.01**	2.27	1.10- 5.33	0.04**

^η Adjusted for age, sex, peak TnI, baseline LVEDV, and medication use. Abbreviations: CAD, Coronary Artery Disease; GLS, Global Longitudinal Strain. Statistical significance shown (p < 0.05) as **

Fig. 1.

Receiver-Operating characteristic curve (ROC) analyses of the identified independent predictors

The ROC curve analyses showed cutoff values for the identified predictors are Killip Class greater than II (sensitivity 81.9%, specificity 84.7%, p < 0.001), baseline GLS < |-12.3| % (sensitivity 69.5%, specificity 88.6%, p < 0.001), presence of 3-vessel CAD(sensitivity 43.3%, specificity 80.9%, p < 0.007), and establishment of type-D personality trait (sensitivity 41.4%, specificity 87.1%, p < 0.02).

Discussion

This is a novel study as to the best of our knowledge it is the first study which examined the impact and significance of type-D personality trait on LVAR in patients successfully reperfused with PCI after their index STEMI. This study showed that the type-D personality trait is an independent predictor of LVAR, with patients exhibiting type-D traits who underwent PCI following an initial STEMI having a 2.51 times higher risk of developing LVAR compared to those without type-D personality traits (. Despite, extensive survey of relevant literature, we could not trace any previous study investigating the impact and predictive usefulness of type-D personality on LVAR in patients successfully reperfused with PCI after index STEMI. However, previous research has reported type-D trait as an established risk factor for coronary heart disease (CHD) [11]. Sixth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of 10 societies and by invited experts) have recommended to screen for type-D personality type in cardiovascular preventive screening [48]. Type-D personality type has also been shown to be related more to cardiovascular adverse events and cardiac death in comparison to non-cardiac adverse events and death [12]. The association of type-D personality trait and LVAR can be traced to multiple physiological pathways that get al.tered due to sustained psychosocial stress, which always accompanies type-D personality types. Personality traits of type-D may modulate the normal working of body’s stress hormones (cortisol and norepinephrine). The hypothalamus-pituitary-adrenal (HPA) axis and the sympatho-adrenal medullary (SAM) axis, constituting the neurohormonal system, along with the autonomic nervous system (ANS) are the primary output pathways of the brain to the heart. The HPA axis secretes cortisol, which controls the response to stress as well as other important physiological functions such as the regulation, production and, release of pro-inflammatory cytokines from cytotoxic t cells. In this backdrop, cortisol assumes a very important role in the mechanism of promoting chronic inflammation, transitively triggering a cascade of other processes such as atherosclerosis, increased blood pressure, endothelial dysfunction, obesity, and hyperlipidaemia, all of which are central to the aetiology, and pathophysiology of cardiovascular diseases [49]. Investigations have also reported increased diurnal cortisol output in acute coronary syndrome patients with type-D personality traits compared to non-type D patients [50, 51]. Moreover, the cortisol induced pro-inflammatory state has been demonstrated to affect availability of nitric oxide synthase [51] resulting in subclinical atherosclerosis [52], and coronary calcification [53]. All of these mechanisms strongly suggest that increased cortisol levels in type-D personality types might induce and catalyse cardiovascular risks. The second significant stress neurohormone is norepinephrine, which is secreted in response to stress by the sympatho-adrenal medullary (SAM) axis. Norepinephrine also plays a role as neurotransmitter of the sympathetic part of the autonomic nervous system. Individuals with Type D personality often face heightened psychological stress due to their tendency to focus on negative emotions and excessive worry. Their social inhibition limits their ability to seek support, further amplifying stress. In a previous study [54], elevated stress levels have been identified as a strong predictor of moderate to high SYNTAX and SYNTAX II scores, which are linked to a poorer prognosis in patients undergoing PCI. Investigations exposing young adults to endurance stressors have demonstrated that individuals with type-D personality traits responded with an exaggerated blood pressure response and male individuals with type-D traits showed sympathetic hyperactivation as well as autonomic co-activation pattern compared to non-type D individuals and females [55]. Autonomic co-activation, in which both the sympathetic and parasympathetic nervous systems show hyperactivation, have previously been linked with increased odds of cardiovascular risks [56]. All of the discussed stress-response mechanisms may affect the pathophysiological pathways linked to LVAR and other cardiovascular risks.

The other significant results with respect to LVAR of this study demonstrate the predictive significance of Killip Class (Odds ratio 7.30, 95% CI 3.03-17.55, p < .0001), 3-vessel CAD (Odds ratio 2.27,95% CI 1.10-5.33, p = .04) and, baseline GLS (Odds ratio 2.69,95% CI 1.19-6.61, p = .01) measured using 2D-STE in patients successfully reperfused with PCI after their index STEMI. Traditionally, LVEF and wall motion score index (WMSI) have been used to evaluate the quantum of myocardial injury, with WMSI being regarded as an independent predictor of LVAR [57, 58]. However, both the LVEF and WMSI have been shown to be fraught with limitations in assessing the extent of myocardial damage as well as their risk stratification value after acute myocardial infarction (AMI) [59]. In contrast, 2D-STE, is not only capable of estimation the myocyte motion but it can also assess the active and passive motility of left ventricular segments, thus making it more sensitive to measure left ventricular function [60]. The results of the current study show that GLS measured using 2D-STE, and not the LVEF and WMSI is an independent predictor of LVAR sensitivity: 69.5%, specificity: 88.6%, cutoff value < |-12.3%|, p < .001). An earlier study has reported similar cutoff value ( [61]. This suggests that strain can better differentiate between active and passive motion of left ventricular segments, hence GLS seems to be more predictive of LVAR. Several other studies have reported GLS to be an independent predictor of LVAR [34, 62, 63]. The present study also demonstrated that 3-vessel CAD is an independent predictor of LVAR . These findings are similar to an earlier investigation [64], which reported 3-vessel CAD as an independent predictor of LVAR . Moreover, it was unexpected to find that dyslipidaemia, a recognized risk factor for cardiovascular disease, did not differ significantly between the two groups (Table 1). This suggests that dyslipidaemia, which is typically associated with adverse cardiac outcomes, may not have had a noticeable influence on the development of LVAR in this study. However, this finding should be interpreted with caution due to the small sample size, which may have limited the study’s ability to detect a true association. The lack of a significant difference may not necessarily mean that dyslipidaemia has no impact on LVAR, but rather that the study might have been underpowered to reveal its true effect. A larger sample size could provide a more accurate understanding of the relationship between dyslipidaemia and LVAR, as the small cohort in this study might mask any potential influence of dyslipidaemia on left ventricular function and remodelling. Further research with more robust sample sizes is required to draw definitive conclusions about the role of dyslipidaemia in LVAR outcomes.

The present study adds valuable information to the limited information pool regarding LVAR post-STEMI, after successful revascularization by PCI, in conjunction with type-D personality traits. However, we are of the firm belief and advocate that further studies including randomised trials are needed to further investigate and understand the underlying diversified mechanistic associations between type-D personality traits and LVAR.

Limitations

The primary limitations of this study include its single-center design and relatively small sample size, which may reduce the statistical power and limit the robustness of the conclusions. Additionally, the demographic component is largely drawn from a specific geographic region—the Aseer region in the Kingdom of Saudi Arabia—where cultural, genetic, and environmental factors may differ from other populations. This regional focus restricts the ability to generalize the results to broader or more diverse populations. Furthermore, potential biases related to patient selection and the lack of external validation in a multicentre or international context should be considered when interpreting the findings.

Conclusions

The study highlights that type-D personality, along with Killip Class, baseline GLS, and 3-vessel CAD, is a significant independent predictor of LVAR in AMI patients who have undergone successful PCI reperfusion. By considering these factors at baseline, clinicians can achieve efficient risk stratification, plan preventive strategies, and reduce the likelihood of pathological LVAR and subsequent heart failure.

Author contributions

Z.S., S.A., and J.I. majorly contributed to the conceptualization and Design. B.A., I.R., and H.D. contributed towards data acquisition, analysis, and interpretation of data. A.P., S.W., and SA.A. contributed to manuscript writing. All authors read and approved the final manuscript.

Funding

The authors extend their appreciation to the Deanship of Scientific Research at King Khalid University, Abha, Saudi Arabia for funding this work through Large Group Project under grant number [RPG 2/571/45].

Data availability

The data used during the current study are available from the corresponding author on reasonable request.

Declarations

Ethical approval

This study was approved by the Research Ethics Committee at King Khalid University (HAPO-06-B-001) vide approval No: ECM #2023–3328 and written informed consent was obtained from all the participants.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.