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ORIGINAL ARTICLE
Year : 2014  |  Volume : 27  |  Issue : 2  |  Page : 322-328

Comparison between strain and strain rate in hypertensive patients with and without left ventricular hypertrophy: a speckle-tracking study


Department of Cardiovascular Disease, Menoufia University Hospitals, Menoufia University, Shebin El Kom, Egypt

Date of Submission09-Jun-2013
Date of Acceptance18-Aug-2013
Date of Web Publication26-Sep-2014

Correspondence Address:
Ahmad Gabr Braik
MBBCh, Department of Cardiovascular Disease, Menoufia University Hospitals, Menoufia University, Shebin El Kom
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-2098.141691

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  Abstract 

Objective
The aim of the study was to compare strain and strain rate (SR) values, measured by speckle tracking, in hypertensive patients with left ventricular hypertrophy (LVH) and in those without LVH.
Background
Echocardiographic evaluation of the left ventricular (LV) strain and SR by two-dimensional speckle tracking may be a useful tool to assess the substantial impairment of systolic or diastolic function both in hypertensive patients with and without LVH.
Patients and methods
We compared 50 patients with hypertension, 25 with LVH and 25 without LVH, with age-matched and sex-matched control group (25 patients) using two-dimensional speckle tracking measurements of LV longitudinal strain and SR in the apical two-chamber, three-chamber, and four-chamber views.
Results
Significant reduction of global longitudinal LV systolic strain was observed in hypertensive patients with LVH (group 1) when compared with hypertensive patients without LVH (group 2) (P = 0.04). Significantly reduced global LV longitudinal SR values were found in group 1 when compared with controls at peak systole (peak S) (P = 0.02) and when compared with group 2 (P = 0.02) in early diastolic phase (at peak E). In contrast, no significant reduction of SR values was found between the studied groups in late diastolic phase (at peak A) (P = 0.13).
Conclusion
Substantial impairment of LV systolic function assessed by longitudinal strain was found in both the hypertensive groups as evidenced by the highly significant reduction of LV global strain values. The SR values were significantly reduced in both the hypertensive group in early diastole and the hypertensive group with LVH at peak systole.


How to cite this article:
Monaster SS, Ahmad MK, Braik AG. Comparison between strain and strain rate in hypertensive patients with and without left ventricular hypertrophy: a speckle-tracking study. Menoufia Med J 2014;27:322-8

How to cite this URL:
Monaster SS, Ahmad MK, Braik AG. Comparison between strain and strain rate in hypertensive patients with and without left ventricular hypertrophy: a speckle-tracking study. Menoufia Med J [serial online] 2014 [cited 2019 Nov 14];27:322-8. Available from: http://www.mmj.eg.net/text.asp?2014/27/2/322/141691


  Introduction Top


Hypertension is a health concern because it is a major risk factor for a number of cardiovascular diseases including stroke, atherosclerosis, type II diabetes, coronary heart disease, and renal disease. It affects 26% of adults worldwide, and its prevalence is predicted to increase to 29% by 2025 [1].

Left ventricular hypertrophy (LVH) is a common consequence of hypertension and an independent risk factor for cardiovascular morbidity and mortality [2].

Tissue deformation imaging is a recently introduced technique, which enables the objective assessment of regional myocardial deformation assessed by ultrasound-based strain and strain rate (SR) using myocardial Doppler data or B-mode images. This is a promising new technique to quantify regional left and right ventricular function and appears of added value in unmasking or unraveling cardiac pathology [3].

Strain is a measure of tissue deformation. As the ventricle contracts, muscle shortens in the longitudinal and circumferential dimensions (a negative strain) and thickens or lengthens in the radial direction (a positive strain) [4].

SR measures the time course of deformation. SR is the local rate of deformation or strain per unit time [5].

In contrast to TDI, speckle-tracking echocardiography (STE) is an angle-independent technique that may allow an accurate assessment of segmental myocardial deformation by grey-scale-based imaging analysis frame by frame. Moreover, the lack of angle dependency is of great advantage because myocardial strain (e) could be tracked in two-dimensional echo imaging, along the direction of the wall and not along the ultrasound beam [6].


  Patients and methods Top


Study group

This study was conducted on 50 patients, who were referred to Menoufia University Hospital for clinical evaluation of hypertension. Patients were categorized into two groups:

Group 1 included 25 hypertensive patients with LVH. Their mean age was 52.20 ± 6.0 years, including 12 (48%) men and 13 (52%) women.

Group 2 included 25 hypertensive patients without LVH. Their mean age was 51.6 ± 5.1 years; this group included 13 (52%) men and 12 (48%) women.

The study also included age-matched and sex-matched control group (20 patients). Their mean age was 50.5 ± 6.0 years, and this group included 10 (50%) men and 10 (50%) women.

Inclusion criteria were any patient with chronic hypertension with or without ECG criteria of LVH in sinus rhythm and normal ejection fraction (EF). Exclusion criteria were any rhythm other than sinus rhythm, depressed left ventricular (LV) systolic function, significant valvular heart disease (more than mild), ischemic heart disease (proven by an ECG, coronary angiography, or thallium study), cardiomyopathies, congenital heart disease, pericardial disease, and significant renal and hepatic disease.

Methods

Every patient was subjected to the following:

Resting 12-lead surface electrocardiogram

It was performed with special attention for the ECG voltage criteria of LVH, according to the Sokolow-Lyon voltage criteria: SV1 + RV5 or RV6 ≥ 3.5 mV (35 mm) or RaVL ≥ 1.1 mV (11 mm) [7].

Full echocardiographic study

Transthoracic echocardiographic examination was performed with Vivid 9 GE with measurements of chamber dimensions taken from two-dimensional-guided M-mode, mitral inflow, and calculation of left ventricular mass (LVM) and relative wall thickness (RWT).

RWT was defined as:

RWT = 2 × LVPWd/LVDd.

where LVPWd is the left ventricular posterior wall diastolic thickness and LVDd is the left ventricular diastolic diameter [8].

LV RWT and LVM defined LV geometric patterns: normal geometry, concentric remodeling, eccentric hypertrophy, and concentric hypertrophy. Concentric left ventricular hypertrophy (C-LVH) was defined as RWT of at least 0.42 with an increased LVM. Eccentric left ventricular hypertrophy (E-LVH) was defined as increased LVM with an RWT of less than 0.42. Concentric remodeling was defined as RWT of at least 0.42 with a normal LVM [9].

LVM was calculated according to the formula of American Society of Echocardiography Conventions:

LVM(g) = 0.8 [1.05 [(LVID + IVST + PWT) 3 − (LVID) 3 ]].

where LVID is the left ventricular internal dimension, IVST is the intraventricular septum thickness, and PWT is the posterior wall thickness [10].

LVH was defined by LVM higher than the reference values for LVM: 88-224 g in male individuals and 67-162 g in female individuals [9].

Diastolic function was assessed by recording mitral flow with standard pulsed Doppler technique and by measurements of early diastolic peak flow velocity (E), late diastolic peak flow velocity (A), and the ratio of early-to-late flow velocity peaks (E/A ratio).

E/A ratio less than 1 is an indicator of delayed relaxation profile; E/A of greater than 2 is typical for restriction; and values of E/A between 1 and 2 is either normal or pseudonormal pattern.

Measurement of two-dimensional-based strain and strain rate using speckle-tracking method

Measurements were obtained in apical four-chamber, three-chamber, and two-chamber views on axis nonforeshortened, with a narrow two-dimensional sector width to include entire LV myocardium, and base of left atrium (LA). The frame rate per second was adjusted between 40 and 90 or at least 40% of HR. Three cardiac cycles were acquired and averaged for conventional measurements [Figure 1] and [Figure 2].
Figure 1:

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Figure 2:

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  Results Top


Regarding demographics and risk factors of the study population, there were no significant differences between the studied groups.

Regarding ECG voltage criteria of LVH, there was highly statistically significant difference between group 1 (hypertension with LVH) and the control group (P = 0.000) and between group 1 and group 2. However, there was no significant difference between group 2 and controls.

Regarding conventional echocardiographic parameters, when group 1 (hypertension with LVH) was compared with controls, highly significant difference was present with respect to interventricular septum thickness (IVSD), LVPWd, E/A ratio, LVM, and RWT, in addition to significant difference with respect to peak E and A waves and LA dimension. In contrast, when it was compared with group 2 (hypertensive only), highly significant difference was present with respect to IVSD, LVPWd, and LVM and significant difference with respect to peak E wave, peak A wave, E/A ratio, and RWT [Table 1].
Table 1: Comparison between the three groups regarding conventional echocardiographic parameters

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When group 2 (hypertension only) was compared with controls, significant difference was present with respect to peak E wave and peak A wave and highly significant difference with respect to E/A ratio [Table 1].

Regarding longitudinal systolic strain, there was highly significant reduction in group 1 when compared with the control group in the apical four, three, and two chambers and global LV. Comparing group 2 and controls with respect to global systolic strain showed highly significant reduction of the strain values in the apical four and three chambers and global LV (P < 0.001) and significant difference between them in the apical two-chamber view (P = 0.02). Significant reduction in the global strain values was observed in group 1 when compared with group 2 in the apical four, three, and two chambers and global LV strain [Table 2].
Table 2: Comparison between the three groups regarding global strain

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Regarding global LV SR, in the apical four-chamber, three-chamber, and two-chamber views, (i) at peak systole (peak S), when group 1 was compared with controls, there was significant reduction in SR values. In contrast, despite reduction of SR values in group 2 when compared with controls and in group 1 when compared with group 2, they did not reach statistical significance. (ii) At peak E (early in diastole), highly significant reduction in the SR values was found when groups 1 and 2 were compared with controls, and significant reduction was found when group 1 was compared with group 2. (iii) At peak A (late diastole), no significant differences were present between the studied groups [Table 3].{Table 2}


  Discussion Top


We studied longitudinal strain and SR, measured by non-Doppler-two-dimensional-based speckle tracking, in 50 hypertensive patients and in age-matched and sex-matched control group (20 patients).

Regarding echocardiographic parameters

With respect to left ventricle conventional echocardiographic parameters, our study did not show any significant difference between the three groups with respect to LVEDD. Expectedly, IVSD and LVPWd) were significantly higher in hypertensive patients with LVH than in hypertensive patients without LVH and the controls. Meanwhile, our study clarified that the LVM and RWT in hypertensive patients with LVH (group 1) are significantly exceeded that of hypertensive patients without LVH (group 2) and of the control group, but no difference was present between group 2 and controls. In contrast, we have demonstrated that most hypertensive patients with LVH (group 1), in our study, have concentric LV geometry, whereas hypertensive patients without LVH (group 2) and the control group have normal LV geometry [Table 1].

Mozdzan et al. [11] found that hypertensive patients compared with controls presented larger dimensions of both ventricles and LA, thicker LV walls, and higher LVM and mass index. These findings occurred independently of sex, age, BMI, and diurnal blood pressure levels. There is some similarity between our findings and this study, and the difference in LV and LA dimensions may be attributed to the large number of patients who have eccentric LV geometry in Mozdzan and colleagues' study.

Przewlocka-Kosmala et al. [12] stated that, expectedly, LVMI, IVSD, and LV posterior wall thickness (PW) were significantly higher in hypertensive patients than in controls. These findings are in agreement with our study.

Our data are consistent with the results of Mizuguchi et al. [13], who studied 98 hypertensive patients; LVM was classified as normal geometry (N-LV) in 31 patients, C-LVH in 25 patients, and E-LVH in 42 patients with 22 age-matched normal controls. They concluded that the relative LV wall thickness was markedly increased in the C-LVH group than in the other three groups. The LV mass index was greater in both LVH groups, particularly in the C-LVH group, than in the control and N-LV groups.

With respect to LA dimension, the present study showed that LA dimension in hypertensive patients with LVH (group 1) is significantly larger than that of hypertensive patients without LVH (group 2) and of the control group. Meanwhile, there was no difference between hypertensive patients without LVH (group 2) and the control group [Table 1].

Our results are compatible with those of Tedesco et al. [14] who stated that left atrial enlargement was present in 36% of patients with and in 21% of patients without LVH.

There is some similarity between our results and those of Savage et al. [15], who observed LA enlargement in only 5% of hypertensive patients and no significant difference in the mean LA size between hypertensive and normotensive patients.

Regarding electrocardiography voltage criteria of left ventricular hypertrophy

In the present study, we have demonstrated that ECG voltage criteria of LVH are present in 72% of hypertensive patients with LVH (group 1), whereas these criteria were present in 12% of hypertensive patients without LVH (group 2).

Our results are compatible with those of Kansal et al. [16], who documented that the current electrocardiographic criteria for the diagnosis of LVH fail to diagnose 30-40% cases of increased LVM.

Devereux et al. [17] found that, in validation studies, the sensitivity of echocardiography to detect LVH has been reasonably high (85-100%), whereas that of ECG has ranged from as high as 50% in severely diseased necropsy populations to as low as 6-17% in recent studies Cornell and Framingham.

Regarding the left ventricular systolic function as assessed by systolic longitudinal strain, strain rate, and left ventricular ejection fraction

With respect to LV systolic function as assessed by EF, it has been found from the present study that there were no significant differences between the three studied groups [Table 1].

Our results are compatible with those of Narayanan et al. [18], who studied 52 hypertensive patients and 52 control individuals of similar age; they found that EF and endocardial shortening were similar in both groups.

The results of our study showed subtle or substantial reduction of LV systolic function in both hypertensive groups as evidenced by the highly significant reduction of LV strain in hypertensive patients with LVH (group 1) and in hypertensive patients without LVH (group 2). In contrast, significant reduction in strain was found in group 1 with respect to group 2 [Table 2].

This agreed with the finding recorded by Di Bello et al. [19], who demonstrated that longitudinal two-dimensional strain in prehypertensive (-18.9 ± 3.4%) and in hypertensive (-18.0 ± 3.3%) was significantly lower than in normotensive (-23.9 ± 3.0%) (P < 0.002). They concluded that early abnormalities of LV longitudinal systolic deformation were found both in prehypertensive and hypertensive, together with a mild LV diastolic dysfunction. In both groups, there is early cardiac systolic and diastolic dysfunction.

In addition, Imbalzano et al. [20] studied 51 patients (56.5 ± 14 years) and 51 controls (52 ± 12.6 years). According to the presence or absence of LVH, patients were classified as LVH+ and LVH-; STE revealed an impairment of systolic longitudinal strain in all patients, including those without hypertrophy (P = 0.02).

The latent regional LV longitudinal systolic dysfunction, despite the normal EF in hypertensive patients, may be explained by: (i) the compensatory augmentation of the LV circumferential shortening and twist. This was proven by Imbalzano et al. [20], who demonstrated that STE revealed an impairment of systolic longitudinal strain in all patients, including those without hypertrophy (P = 0.02). Furthermore, in the LVH+ group, STE showed reduced radial strain and increased circumferential strain and LV twist or torsion. (ii) The limited sensitivity of global EF as demonstrated by Edvardsen et al. [21], who stated that the apparently normal systolic function in heart failure with normal EF reflects limited sensitivity of global EF, and assessment of regional systolic function by STE may provide important diagnostic information, and further confirmed by Sjøli et al. [22], who compared LV global strain by speckle tracking and left ventricular ejection fraction (LVEF) by echocardiography in evaluating LV function and infarct size in patients with ST-elevation myocardial infarction treated with thrombolysis; they found that LVEF by echocardiography is limited by observer variability and suboptimal agreement with reference methods, and LV global strain seems to have several advantages over LVEF by echocardiography in the evaluation of LV function in patients with AMI. LV global strain does not rely on such geometric assumptions but rather measures regional myocardial function with precision. In addition, LV global strain may be more sensitive than LVEF to changes in long-axis shortening.

Regarding the left ventricular diastolic function as assessed by strain rate and pulsed wave Doppler

The findings of this research indicated that the LV diastolic impairment is common, as shown by inversion of the E/A ratio, in both hypertensive groups with and without LVH, although it was more evident in hypertensive patients with LVH (group 1). Meanwhile, both hypertensive groups have significant diastolic impairment when compared with the control group [Table 1].

The present observation is in agreement with the study by Dekleva et al. [23], who studied 30 patients with hypertension (19 men/11 women, aged 55 ± 8 years); they demonstrated that all patients had preserved systolic function (EF = 58 ± 15%) and impaired LV relaxation (E/A = 0.79 ± 0.15).

It was confirmed by Redfield et al. [24], who concluded that diastolic dysfunction is estimated to affect ~50% of hypertensive patients in the community.

The results of this study indicated that the SR values were significantly reduced in both hypertensive groups with and without LVH in early diastole (at peak E). However, there was no significant reduction in SR between the studied groups in late diastole (at peak A) [Table 3].

This is in agreement with the study by Goebel et al. [25], who found that, in the patient group with LVH, systolic SR and early diastolic SR, quantified in longitudinal and circumferential direction, were lower compared with the group without LVH. In addition, systolic twist rate and diastolic untwist rate were significantly lower in this patient group. They concluded that LVH in patients with arterial hypertension predominantly affected longitudinal and circumferential deformation rate.

Huang [26] studied 88 patients with essential hypertension in addition to age-matched and sex-matched 30 normotensive healthy volunteers serving as normal controls. His analysis showed that the essential hypertension group early diastolic longitudinal SR and circumferential SR were lower than normal controls.


  Acknowledgements Top


Conflicts of interest

None declared.

 
  References Top

1.Kearney PM, Whelton M, Reynolds K, et al. Global burden of hypertension: analysis of worldwide data. Lancet 2005; 365 :217-223.  Back to cited text no. 1
    
2. Okin PM, et al. Regression of electrocardiographic left ventricular hypertrophy during antihypertensive treatment and the prediction of major cardiovascular events. JAMA 2004; 292 :2343-2349.  Back to cited text no. 2
    
3. TeskeAJ, De BoeckBWL, Melman PG, et al. Assessment of regional right ventricular function. A head to head comparison between 2D-strain and tissue Doppler derived strain analysis. J Am Soc Echocardiogr 2008; 21 :275-283.  Back to cited text no. 3
    
4. Kowalski M, Kukulski T, Jamal F, et al. Can natural strain and strain rate quantify regional myocardial deformation? A study in healthy subjects. Ultrasound Med Biol 2001; 27 :1087-1097.  Back to cited text no. 4
    
5. Weidemann F, Mertens L, Gewillig M, et al. Quantitation of localized abnormal deformation in asymmetric nonobstructive hypertrophic cardiomyopathy: a velocity, strain rate, and strain Doppler myocardial imaging study, Pediatr Cardiol 2001; 22 :534-537.  Back to cited text no. 5
    
6. Dandel M, Lehmkuhl H, Knosalla C, et al. Strain and strain rate ýmaging by echocardiography - basic concepts and clinical applicability. Curr Cardiol Rev 2009; 5 :133-148.  Back to cited text no. 6
    
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8. Kumar D, Patel A, Lavie CJ, et al. Impact of relative wall thickness on left ventricular geometry and mortality in 47 865 patients with preserved systolic function: does the method matter? Circulation 2009; 120 :58-83.  Back to cited text no. 8
    
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12.Przewlocka-Kosmala M, Kosmala W, Mazurek W. Left ventricular circumferential function in patients with essential hypertension. J Hum Hypertens 2006; 20 :666-671.  Back to cited text no. 12
    
13.Mizuguchi Y, Oishi Y, Miyoshi H, et al. Concentric left ventricular hypertrophy brings deterioration of systolic longitudinal, circumferential and radial myocardial deformation in hypertensive patients with preserved left ventricular pump function. J Cardiol 2010; 55 :23-33.  Back to cited text no. 13
    
14.Tedesco M, IsalvomG, et al. Left atrial size in 164 hypertensive patients: an echocardiographic and ambulatory blood pressure study. Clin Cardiol 2001; 24 :603-607.  Back to cited text no. 14
    
15.Savage DD, Drayer JI, Henry WL. Echocardiographic assessment of cardiac anatomy and function in hypertensive subjects. Circulation 1979; 59 :623-632.  Back to cited text no. 15
    
16.Kansal S, Roitmanm I, Sheffield T. A quantitative relationship of electrocardiographic criteria of left ventricular hypertrophy with echocardiographic left ventricularmass: a multivariate approach. Clin Cardiol 1983; 6 :456-463.  Back to cited text no. 16
    
17.Devereux RB, Koren MJ, de Simone G, et al. Methods for detection of left ventricular hypertrophy: application to hypertensive heart disease. Eur Heart J 1993; 14 :8-15.  Back to cited text no. 17
    
18.Narayanan A, Aurigemma GP, Chinali M, et al. Cardiac mechanics in mild hypertensive heart disease: a speckle-strain ýmaging study. Circ Cardiovasc Imaging 2009; 2 :382-390.  Back to cited text no. 18
    
19.Di Bello V, Talini E, Dell′Omo G, et al. Early left ventricular mechanics abnormalities in prehypertension: a two-dimensional strain echocardiography study. Am J Hypertens 2010; 23 :405-412.  Back to cited text no. 19
    
20.Imbalzano E, Zito C, Carerj S, et al. Left ventricular function in hypertension: new ýnsight by speckle tracking echocardiography. Echocardiography 2011; 28 :649-657.  Back to cited text no. 20
    
21.Edvardsen T, Helle-Valle T, Smiseth OA. Systolic dysfunction in heart failure with normal ejection fraction: speckle-tracking echocardiography. Prog Cardiovasc Dis 2006; 49 :207-214.  Back to cited text no. 21
    
22.Sjøli B, Ørn S, Grenne S, et al. Comparison of left ventricular ejection fraction and left ventricular global strain as determinants of infarct size in patients with acute myocardial ýnfarction. J Am Soc Echocardiogr 2009; 22 :1232-1238.  Back to cited text no. 22
    
23.Dekleva M, Pencic B, Bakic-Celic V, et al. Impact of left ventricular diastolic dysfunction on maximal exercise capacity in hypertensive patients. Eur J Echocardiogr 2003; 4 :S57.  Back to cited text no. 23
    
24.Redfield MM, Jacobsen SJ, Burnett JC Jr, et al. Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JAMA 2003; 2 :194-202.  Back to cited text no. 24
    
25.Goebel B, Gjesdal O, Kottke D, et al. Detection of irregular patterns of myocardial contraction in patients with hypertensive heart disease: a two-dimensional ultrasound speckle tracking study. J Hypertens 2011; 29 :2255-2264.  Back to cited text no. 25
    
26.Huang CY. Investigation on left ventricular myocardial diastolic strain rate in hypertension using 2-dimensional strain echocardiography (dissertation). Fujian: Fujian Medical School; 2011.  Back to cited text no. 26
    


    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]


This article has been cited by
1 Myocardial Strain and Stiffness Parameters as a Novel Target of Antihypertensive Treatment
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Kardiologiia. 2018; 58(11): 72
[Pubmed] | [DOI]



 

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