The influence of white-coat hypertension on left atrial phasic function

Abstract

We aimed to investigate the association between white-coat hypertension (WCH) and left atrial (LA) phasic function assessed by the volumetric and speckle tracking method. This cross-sectional study included 52 normotensive individuals, 49 subjects with WCH and 56 untreated hypertensive patients who underwent a 24-h ambulatory BP monitoring and complete two-dimensional echocardiographic examination (2DE). WCH was diagnosed if clinic blood pressure (BP) was elevated and 24-h BP was normal. We obtained that maximum, minimum LA and pre-A LAV volumes and volume indexes gradually and significantly increased from the normotensive subjects, throughout the white-coat hypertensive individuals to the hypertensive patients. Passive LA emptying fraction (EF), representing the LA conduit function, gradually reduced from normotensive to hypertensive subjects. Active LA EF and the parameter of the LA booster pump function increased in the same direction. Similar results were obtained by 2DE strain analysis. The LA stiffness index gradually increased from normotensive controls, throughout white-coat hypertensive subjects to hypertensive patients. Clinic systolic BP was associated with LA passive EF (β= −0.283, p = 0.001), LA active EF (β = 0.342, p < 0.001), LA total longitudinal strain (β= −0.356, p < 0.001), LA positive longitudinal strain (β= −0.264, p = 0.009) and LA stiffness index (β = 0.398, p < 0.001) without regard to age, BMI, left ventricular structure and diastolic function in the whole study population. In the conclusion, WCH significantly impacts LA phasic function and stiffness. Clinic systolic BP was associated with functional and mechanical LA remodeling in the whole study population.

Key Words:

• Left atrium
• stiffness
• two-dimensional strain
• white-coat hypertension

Introduction

The impact of white-coat hypertension (WCH) on total and cardiovascular morbidity and mortality has not been established yet. Although the majority of studies imply an unfavorable influence of WCH,[1–3] not all agree with this.[4] Recent meta-analysis that included 4806 with WCH reported that cardiovascular morbidity and mortality associated with WCH is slightly higher compared with normotensive subjects, but has significantly lower risks associated with sustained hypertension.[5]

The cardiac remodeling, especially left ventricular (LV) impairment, in WCH subjects is the matter of debate in the last couple of decades. Our recent meta-analysis, which included 1705 WCH individuals, showed that LV mass (LVM) index was significantly increased, while mitral E/A ratio was significantly reduced in WCH.[6] This indicates significant impairment of LV structure and diastolic function in WCH. In the same analysis we demonstrated significant enlargement of the left atrium (LA) in WCH individuals. Additionally, we have shown that WCH simultaneously impacts the left and right ventricular structure, function and mechanics.[7,8]

Studies reveal a significant role of LA size, function and mechanics on mortality and morbidity in patients with and without cardiovascular diseases.[9–11] The data regarding LA function and mechanics in WCH are scarce. Ermiş et al. have recently published a very interesting study regarding three-dimensional volumetric assessment of LA phasic function in a limited number of WCH and normotensive subjects.[12] However, the authors did not use LA strain analysis and did not include a comparison with sustained hypertensive subjects.

The purpose of the present study is to evaluate LA phasic function using two-dimensional volumetric and strain methods in subjects with WCH and sustained hypertension.

Methodology

This cross-sectional study included 157 consecutive untreated patients (52 normotensive individuals, 49 subjects with WCH and 56 untreated hypertensive patients) referred to our outpatient clinic due to echocardiographic examination or ambulatory blood pressure (BP) monitoring in the period between June 2014 and January 2016. Patients included in this study are referred to our outpatient clinic by general practitioners, cardiologists and as a part of the primary prevention program. During this period 2720 patients were examined and screened for this study. However, the majority of patients had some exclusion criteria (mainly previous antihypertensive treatment). Arterial hypertension was diagnosed according to the current guidelines.[13] Exclusion criteria were: antihypertensive treatment, symptoms or signs of heart failure, coronary artery disease, previous cerebrovascular events, atrial fibrillation, congenital heart disease, heart valve disease (more than mild), neoplastic disease, liver cirrhosis, kidney failure or endocrine diseases including type 2 diabetes mellitus. Additionally, all controls and untreated hypertensive patients were matched by age and gender with WCH subjects in order to avoid the impact of age and gender.

Anthropometric measures (height, weight) and laboratory analyses (level of fasting glucose, blood creatinine, total cholesterol and triglycerides) were obtained from all the subjects included in the study. Fasting venous blood samples were drawn between 08 and 09 o’clock in the morning. Laboratory analyses were performed from serum. Body mass index (BMI) and body surface area (BSA) were calculated for each patient.

The study was approved by the local Ethics Committee and informed consent was obtained from all the participants.

Clinic BP measurement and 24-h ambulatory BP monitoring

All the participants underwent a 24-h BP monitoring. Clinic arterial BP values were obtained by aneroid manometer in the morning hours by measuring the average value of the two consecutive measurements in the sitting position, taken within an interval of 5 min, after the subject had rested for at least five minutes in that position. BP was measured in at least two separate occasions: during clinical examination by a cardiologist and before the echocardiographic examination.

The noninvasive 24-h ambulatory BP monitoring was performed on the non-dominant arm, using Schiller BR-102 plus system (Schiller AG, Baar, Switzerland). The device was programmed to obtain BP readings at 20-min intervals during the day (07:00–23:00 h) and at 30-min intervals during the night (23:00–07:00 h). The patients were asked to attend to their usual daily activities, but to keep still at the times of measurement and to keep a journal of daily activities including the time of awakening and going to bed. Nighttime BP was defined as the average of BPs from the time when the patients went to bed until the time they got out of bed and daytime BP as the average of BPs recorded during the rest of the day. The recording was then analyzed to obtain a 24-h, daytime and nighttime average systolic BP, diastolic BP, mean BP and heart rates. When the readings exceeded at least 70% of the total readings programmed for the testing period, the recording was considered valid and satisfactory.

WCH was defined as clinic systolic BP ≥140 mmHg and/or diastolic BP ≥90 mmHg measured in at least two separate occasions associated with a 24-h ambulatory systolic BP <130 mmHg and diastolic BP <80 mmHg; whereas those with sustained hypertension had clinic systolic BP ≥140 mmHg and/or diastolic BP ≥90 mmHg, together with a 24-h ambulatory systolic BP ≥130 mmHg or diastolic BP ≥80 mmHg.

Echocardiography

Echocardiographic examinations were performed by using a commercially available Vivid 7 (GE Vingmed, Horten, Norway). Reported values of all 2DE parameters were obtained as the average value of three consecutive cardiac cycles. LV dimensions were measured according to the ASE guidelines.[14] Relative wall thickness (RWT) was calculated according to the formula: (2 × posterior wall thickness)/LV end-diastolic diameter. LV ejection fraction (EF) was calculated by using the biplane method. LVM was calculated by using the corrected ASE method and indexed for the BSA.[14]

Doppler assessment of transmitral flow was obtained in the apical four-chamber view according to the guidelines.[15] Tissue Doppler imaging was used to obtain LV myocardial velocities in the apical four-chamber view, with a sample volume placed at the septal and lateral segments of the mitral annulus during early diastole (e′). The average of the peak early diastolic relaxation velocity (e′) of the septal and lateral mitral annulus was calculated, and the E/e′ ratio was computed.

2DE assessment of left atrial volumes and function

LA volumes were measured in three different sequences of the cardiac cycle: maximal LA volume was measured just before the mitral valve opening, pre-A (pre atrial contraction) LA volume was determined at the onset of atrial systole (peak of P wave in ECG), whereas minimal LA volume was measured at the mitral valve closure. All the volumes were determined according to the biplane method in 4- and 2-chamber views, and all the values were indexed for BSA. The total emptying volume, which represents the LA reservoir function, was calculated as the difference between maximum and minimum LA volume; passive emptying volume, which represents the conduit function, was calculated as the difference between maximum and pre-A LA volume; and active emptying volume, which corresponds to LA booster function, was calculated as the difference between pre-A and minimum LA volume.[16] Accordingly, total emptying fraction (EF) was calculated as the ratio between total emptying volume and maximum LA volume; passive EF was computed as the ratio between passive and maximum; and active EF was calculated as the proportion between active and pre-A LA volume.

2DE strain imaging was performed in the apical 4- and 2-chamber views [16] and a commercially available software Echo PAC 201 (GE-Healthcare, Horten, Norway) was used for the 2DE strain analysis. LA strain was calculated from the peak of the P wave to the peak of the P wave in the next cardiac cycle. The LA endocardium was manually traced. An average longitudinal strain curve was automatically generated, and it included a negative deflection (LA negative longitudinal strain), representing LA active contraction, followed by a positive one during LA filling (LA positive longitudinal strain). Their summation represented total LA longitudinal strain. LA strain (positive, negative and total) was calculated by averaging the values obtained in 4- and 2-chamber apical views.

LA stiffness index was evaluated as the ratio between mitral E/e′ (e′ is the average between septal and lateral e′ values) and LA total longitudinal strain.

Arterial compliance assessment

Pulse pressure calculated from clinic BP measurements, as well as from 24-h BP monitoring (mean 24-h BP values), was used as a surrogate marker of arterial compliance evaluation of the large arteries’ wall properties.

Statistical analysis

Continuous variables were presented as mean ± standard deviation and were compared by the analysis of equal variance (ANOVA), as they showed normal distribution. Bonferroni’s post hoc analysis was used for the comparison between different groups. Differences in proportions were compared by the χ² test. The multivariate regression analysis was used to determine the association between different echocardiographic parameters and systolic BP (clinic and 24-h) without regard to age, BMI, LVMI and E/e′. The p value <0.05 was considered statistically significant.

Results

There is no difference in age and gender distribution between the different observed groups (Table 1). BMI and BSA are significantly higher in hypertensive patients than in normotensive controls (Table 1). Heart rates are similar among all three groups. Clinic BP and pulse pressure obtained from clinic BP values are significantly higher in WCH and sustained hypertensive patients than in controls (Table 1). The difference is not noticeable considering plasma glucose level, creatinine level and cholesterol level. Triglycerides level is higher in sustained hypertensive patients than in the other two groups (Table 1).

Table 1. Demographic characteristics and clinical parameters of study population.

	Normal BP(n= 52)	WCH(n= 49)	HTN(n= 56)	p
Age (years)	48 ± 7	50 ± 7	51 ± 7	0.080
Female (%)	25 (48)	22 (45)	25 (45)	0.556
BMI (kg/m^2)	24.6 ± 2.4	25.2 ± 2.2	26.0 ± 2.6^a	0.012
BSA (m^2)	1.88 ± 0.11	1.93 ± 0.12	1.96 ± 0.12^a	0.002
Heart rate (beats/min)	69 ± 6	71 ± 7	72 ± 8	0.086
Clinic systolic BP (mmHg)	120 ± 9	148 ± 8^a	150 ± 10^a	<0.001
Clinic diastolic BP (mmHg)	71 ± 7	93 ± 7^a	95 ± 7^a	<0.001
Pulse pressure (mmHg)	39 ± 4	54 ± 6^a	55 ± 7^a	<0.001
Plasma glucose (mmol/l)	4.9 ± 0.6	4.9 ± 0.7	5.1 ± 0.8	0.240
Triglycerides (mmol/l)	1.6 ± 0.3	1.6 ± 0.3	1.9 ± 0.4^a^,^b	<0.001
Total cholesterol (mmol/l)	5.0 ± 0.5	5.1 ± 0.5	5.2 ± 0.6	0.159
Serum creatinine (μmol/l)	79 ± 9	78 ± 8	79 ± 8	0.784

BMI: body mass index; BP: blood pressure; HTN: hypertension; WCH: white-coat hypertension.

^ap < 0.01 versus normal BP.

^bp < 0.01 versus WCH.

Twenty-four hour BP monitoring

Twenty-four hour, daytime and nighttime BPs are significantly higher in patients with sustained hypertension than in the other two groups (Table 2). Importantly, BP values obtained by 24-h BP monitoring are similar between normotensive and WCH subjects. Pulse pressure obtained from 24-h BP values is significantly higher among WCH and sustained hypertensive participants than in normotensive controls (Table 2).

Table 2. Twenty-four hour blood pressure monitoring parameters of study population.

	Normal BP(n= 52)	WCH(n= 49)	HTN(n= 56)	p
24-h systolic BP (mmHg)	117 ± 7	118 ± 6	138 ± 8^a^,^b	<0.001
24-h diastolic BP (mmHg)	68 ± 6	67 ± 5	86 ± 7^a^,^b	<0.001
24-h mean BP (mmHg)	84 ± 7	84 ± 7	103 ± 8^a^,^b	<0.001
Pulse pressure (mmHg)	48 ± 5	51 ± 5^c	53 ± 6^a	<0.001
Daytime systolic BP (mmHg)	120 ± 8	121 ± 7	142 ± 9^a^,^b	<0.001
Daytime diastolic BP (mmHg)	70 ± 7	69 ± 7	90 ± 8^a^,^b	<0.001
Daytime mean BP (mmHg)	87 ± 8	86 ± 8	107 ± 8^a^,^b	<0.001
Nighttime systolic BP (mmHg)	108 ± 7	109 ± 6	126 ± 7^a^,^b	<0.001
Nighttime diastolic BP (mmHg)	62 ± 6	61 ± 5	74 ± 6^a^,^b	<0.001
Nighttime mean BP (mmHg)	77 ± 7	77 ± 6	91 ± 7^a^,^b	<0.001

BP: blood pressure.

^ap < 0.01 versus normal BP.

^bp < 0.01 versus WCH.

^cp < 0.05 versus normal BP.

Conventional echocardiographic measurements

LV diameters are similar among the groups, while LV interventricular and posterior wall thicknesses are significantly higher in sustained hypertensive subjects than in controls and WCH subjects (Table 3). LVM index and relative wall thickness gradually increased from normotensive throughout WCH to hypertensive patients (Table 3). LV 2DE EF is similar among all three groups. Mitral E/A ratio decreased, while E/e′ increased, progressively from normotensive to sustained hypertensive individuals (Table 3).

Table 3. Echocardiographic parameters of left ventricular structure and function in the study population (adjusted for BMI).

	Normal BP(n= 52)	WCH(n= 49)	HTN(n= 56)	p
LV EDD (mm)	48.4 ± 4.3	48.8 ± 4.5	49.4 ± 4.7	0.508
LV ESD (mm)	30.2 ± 3.3	30.4 ± 3.4	31.6 ± 3.8	0.085
IVS (mm)	9.2 ± 1	9.7 ± 1.2	10.6 ± 1.3^a^,^b	<0.001
PWT (mm)	9.0 ± 1	9.4 ± 1.1	10.5 ± 1.2^a^,^b	<0.001
RWT	0.37 ± 0.02	0.39 ± 0.03	0.43 ± 0.03	<0.001^c
LVMI (g/m^2)	81 ± 7.4	86 ± 8.6	98 ± 11	<0.001^d
LV EF (%)	64 ± 3	64 ± 3	63 ± 4	0.216
E/A ratio	1.20 ± 0.25	1.07 ± 0.21	0.92 ± 0.22	<0.001^d
E/e′ ratio	6.5 ± 2.0	8.0 ± 2.1	9.4 ± 2.3	<0.001^c

A: late diastolic mitral flow (pulse Doppler); DT: deceleration time; E: early diastolic mitral flow (pulsed Doppler); e′: average of the peak early diastolic relaxation velocity of the septal and lateral mitral annulus (tissue Doppler); EF: ejection fraction; IVS: interventricular septum; LVMI: left ventricular mass index; LVEDD: left ventricle end-diastolic dimension; PWT: posterior wall thickness; RWT: relative wall thickness; WCH: white-coat hypertension.

^ap < 0.01 versus normal BP.

^bp < 0.01 versus WCH.

^cp < 0.01 for all comparisons.

^dp < 0.05 for all comparisons.

LA phasic function

Maximum, minimum and pre-A LAVs gradually and significantly increased from normotensive controls to sustained hypertensive patients (Table 4). The same changes were observed for corresponding LAVs indexes.

Table 4. Left atrial phasic function assessed by volumetric and strain methods in the study population (strain parameters were adjusted for BMI).

	Normal BP(n= 52)	WCH(n= 49)	HTN(n= 56)	p
LA volume analysis
LAVmax (ml)	53.0 ± 6.0	59.4 ± 7.0	64.5 ± 8.2	<0.001^c
LAVmax/BSA (ml/m^2)	28.2 ± 3.2	30.8 ± 3.6	32.9 ± 4.2	<0.001^d
LAVmin (ml)	21.2 ± 3.7	24.9 ± 3.9	28.4 ± 4.4	<0.001^c
LAVmin/BSA (ml/m^2)	11.3 ± 2.3	12.9 ± 2.5	14.5 ± 3.1	<0.001^c
LAVpre-a (ml)	30.7 ± 5.1	38.3 ± 5.9	45.1 ± 7.0	<0.001^c
LAVpre-a/BSA (ml/m^2)	16.3 ± 2.8	19.8 ± 3.1	23.0 ± 3.7	<0.001^c
LA TotEV (ml)	31.8 ± 5.7	34.5 ± 5.9	36.1 ± 6.5^a	0.001
LA PassEV (ml)	22.3 ± 4.2	21.1 ± 4.0	19.4 ± 4.1^a	0.001
LA ActEV (ml)	9.5 ± 2.7	13.4 ± 3.3	16.7 ± 4.3	<0.001^c
LA TotEF (%)	60 ± 6	58 ± 5	56 ± 4^b	<0.001
LA PassEF (%)	42 ± 5	36 ± 5	30 ± 4	<0.001^c
LA ActEF (%)	31 ± 4	35 ± 5^a	37 ± 5^a	<0.001
LA mechanics
Total longitudinal strain (%)	43 ± 6	40 ± 5	36 ± 4	<0.001^c
Positive longitudinal strain (%)	23 ± 5	18 ± 4	12 ± 3	<0.001^c
Negative longitudinal strain (%)	−20 ± 4	−22 ± 5	−24 ± 6^a	<0.001
LA stiffness index	0.15 ± 0.06	0.20 ± 0.07	0.26 ± 0.1	<0.001^c

ActEF: active emptying fraction; ActEV: active emptying volume; BP: blood pressure; HTA: hypertension; LAV_max: maximal left atrial volume; LAV_min: minimal left atrial volume; LAV_pre-a: left atrial volume before atrial contraction; LV: left ventricle; PassEF: passive emptying fraction; PassEV: passive emptying volume; TotEF: total emptying fraction; TotEV: total emptying volume; WCH: white: coat hypertension.

^ap < 0.01 versus normal BP.

^bp < 0.01 versus WCH.

^cp < 0.01 for all comparisons.

^dp < 0.05 for all comparisons.

Total emptying LAV is higher in sustained hypertensive patients than in normotensive controls. Total LA EF that corresponds to LA reservoir function is lower in sustained hypertensives than in controls (Table 4). Passive LAV is lower in hypertensive patients than in controls. Passive LA EF, a parameter of LA conduit function, gradually decreased from normotensive controls, throughout WCH, to sustained hypertensive subjects (Table 4). Active LAV and LA EF progressively increased from normotensive subjects to sustained hypertensive patients (Table 4).

Total LA longitudinal strain, as well as LA positive longitudinal strain, gradually reduced from controls to sustained hypertensive patients, whereas negative LA longitudinal strain was higher in sustained hypertensive individuals than in normotensive controls (Table 4).

LA stiffness index gradually and significantly increased from normotensive controls to sustained hypertensive patients (Table 4).

Regression analysis

Clinic systolic BP was associated with LA passive EF (β= −0.283, p = 0.001), LA active EF (β = 0.342, p < 0.001), LA total longitudinal strain (β= −0.356, p < 0.001), LA positive longitudinal strain (β= −0.264, p = 0.009) and LA stiffness index (β = 0.398, p < 0.001) without regard to age, BMI, LV structure and diastolic function in the whole study population.

Twenty-four hour systolic BP was associated with LA passive EF (β= −0.231, p = 0.032), LA total longitudinal strain (β= −0.298, p < 0.001), LA positive longitudinal strain (β= −0.214, p = 0.044) and LA stiffness index (β = 0.356, p < 0.001) without regard to clinical and main echocardiographic characteristics in the whole study population.

Pulse pressure measured from clinic BP was associated with LA total longitudinal strain (β= −0.198, p = 0.047) and LA stiffness index (β = 0.243, p = 0.028) independently of clinic systolic BP, age, BMI, LV structure and diastolic function in the whole study population.

Pulse pressure measured by 24-h BP monitoring was associated with LA passive EF (β= −0.212, p = 0.041), LA total longitudinal strain (β= −0.223, p = 0.043) and LA stiffness index (β = 0.31, p < 0.001) independently of 24-h systolic BP, age, BMI, LV structure and diastolic function in the whole study population.

Discussion

The present investigation revealed several new findings. First, maximum, minimum and pre-A LA volumes progressively increase from normotensive, throughout WCH, to sustained hypertensive subjects. Second, passive LA EF that represents LA conduit function gradually reduces from normotensive controls to sustained hypertensive patients, while active LA EF and the parameter of the LA booster pump function increase in the same direction. Results that were obtained by 2DE strain analysis are similar. Third, LA stiffness index gradually increases from normotensives to sustained hypertensives. Fourth, clinic and 24-h systolic BPs are associated with parameters of functional and mechanical LA remodeling in the whole study population.

Investigators have recently shown an association between LA reservoir function, estimated by strain analysis and LV diastolic function in asymptomatic hypertensive patients.[17] The latest trial revealed that LA reservoir and conduit function was markedly reduced before symptoms, LA enlargement and elevations of noninvasively estimated LV filling pressures occurred.[18] Previous research demonstrated that LA minimum volume and reservoir function are better predictors of LV diastolic function than LA maximal volume.[19] Moreover, a recent investigation has shown that LA minimum volume and reservoir function are independent predictors of paroxysmal atrial fibrillation in individuals without overt heart disease.[20] The Dallas Heart Study indicated a significant risk of atrial fibrillation occurrence in WCH subjects [21] and LA remodeling would partially explain this finding.

Our study indicates significant and progressive deterioration of LA reservoir function, assessed by speckle tracking imaging, from normotensive controls, throughout WCH subjects, to sustained hypertensive subjects. The same was obtained for LA conductive function, estimated by both, volumetric and strain methods. Interestingly, using three-dimensional volumetric method Ermiş et al. showed no difference in LA total and passive EFs between normotensive controls and WCH individuals.[12] The main reason for this conclusion is due to the limited number of participants and the inability to reach statistical significance. Our findings regarding LA remodeling in WCH subjects can partly explain the worsening in LV diastolic function, as well as higher cardiovascular morbidity and mortality in this population.

In this study, LA booster pump function is reduced in WCH and sustained hypertensive patients compared with normotensive controls. Ermiş et al. did not succeed to show any significant difference between WCH and hypertensives in LA active EFs, although the absolute difference is similar to the results in our study.[12] The reason probably lies in the small sample size.[12] This finding is significant and could be interpreted in a circumstance of decreased LA reservoir and conduit function. Namely, the compensatory elevation of the LA pump function is valuable for the maintenance of normal LV diastolic filling and atrioventricular coupling. LA booster pump function is dynamically changed in arterial hypertension. At the beginning it is elevated, while in the later course of hypertensive disease LA pump function reduces, which further elevates the risk of atrial fibrillation,[22,23] and global cardiovascular risk in WCH subjects. LA pump function is also related with heart failure symptoms,[24] which could contribute to the worse prognosis in WCH individuals.

A new parameter of LA function and mechanics – LA stiffness index, derived from LV diastolic function parameter E/e′ and LA global longitudinal strain, progressively increased from controls to sustained hypertensives. This could be related with the simultaneous increase in pulse pressure that could be used as a surrogate of large arteries’ compliance. In our study pulse pressure was significantly higher in WCH and hypertensive patients than in normotensive subjects, which suggests significantly lower aortic compliance in WCH and hypertensive participants. A recent study has shown the association between aortic stiffness and LV structural, functional and mechanical changes,[25] whereas Oishi et al. reported a significant relationship between LA function and aortic stiffness.[26] Our study supports these results because they show that aortic stiffness, assessed by pulse pressure, is independently associated with LA phasic function and LA stiffness in WCH and sustained hypertensive participants. Previous investigations showed a significant association between LA stiffness index and atrial fibrillation.[27,28] Therefore, it is reasonable to hypothesize that LA remodeling has an important role in atrial fibrillation development in WCH population.

The comprehensive volumetric evaluation of LA function is time demanding and probably not feasible in everyday clinical practice. However, strain assessment of LA remodeling is rapid and easier, which makes this technique very attractive for daily clinical usage. LA dysfunction and remodeling significantly contributes to the development of atrial fibrillation and diastolic heart failure, two conditions that are very prevalent among hypertensives and in the same time associated with significantly increased cardiovascular morbidity and mortality. Therefore, it should be carefully considered, from a clinical point of view, the recommendation to perform strain evaluation of LA function in WCH and hypertensive subjects, but especially in those individuals with additional risk factors such as obesity, metabolic syndrome, hyperglycemia or dyslipidemia. This is particularly important because of the existing necessity to determine the need and time for the introduction of antihypertensives in WCH patients.

Limitations

This investigation has several limitations. The echocardiographic assessment of LA remodeling could be significantly influenced by the quality of ultrasound images. Additionally, there are several definitions of WCH that could partly interfere with the comparison of our results and the other studies. Finally, we could not determine the causal relationship between WCH and LA phasic function due to the cross-sectional nature of this study.

Conclusion

The present study revealed that there is a negative influence of WCH and sustained hypertension on LA phasic function. Volumetric and strain parameters of LA conduit function gradually and significantly decrease, whereas LA pump function increases, from normotensive controls to sustained hypertensive patients. LA reservoir function is reduced in sustained hypertensive patients, but there is no difference between normotensives and WCH. LA stiffness, as well as aortic stiffness, gradually increases from controls to sustained hypertensives. Further investigations are necessary to evaluate the potential predictive value of LA remodeling in WCH and hypertensive patients.

Disclosure statement

None.