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 Table of Contents  
ORIGINAL ARTICLE
Year : 2016  |  Volume : 13  |  Issue : 1  |  Page : 11-17

Right ventricle morphology and function in systemic hypertension


Department of Cardiology, Cairo University, Giza, Egypt

Date of Web Publication13-Jan-2016

Correspondence Address:
Noha H Hanboly
Department of Cardiovascular, Cairo University, Cairo
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0189-7969.173854

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  Abstract 

Background: Functional and structural consequences of hypertension on the right ventricle (RV) have received scarce attention due to the complex shape and orientation. The aim of the current study is to study the RV systolic and diastolic function in untreated hypertensive patients using two-dimensional speckle tracking analysis and correlating the findings with the morphological and functional changes of the left ventricle.
Methods: This cross-sectional study involved 80 patients with mild to moderate untreated systemic hypertension and 40 healthy controls. M-mode echocardiography measurements of the right ventricular wall (RVW) diastolic thickness, tricuspid annular plane systolic excursion, left ventricular (LV) dimensions, and systolic function were performed. Pulsed Doppler echocardiography was used to measure peak early (TE) and peak atrium (TA) right ventricular diastolic filling velocities. Similar parameters of the LV diastolic filling were recorded. Tissue Doppler imaging (TDI) was done to determine the left and right myocardial annular velocities. Mean pulmonary artery pressure (MPAP) was measured noninvasively by the estimation of pulmonary artery acceleration time (AT). Apical 4-chamber images were acquired at high frame rate to extract RV peak systolic strains.
Results: The current study revealed significantly thicker RVW in hypertensive group (5.3 vs. 2.8 mm in controls, P < 0.001). The RV diastolic dysfunction (RVDD) defined as tricuspid E/A ratio <0.8 was recorded in 60% of the hypertensive group. Significant positive correlation was found between tricuspid and mitral E/A ratio. Pulmonary AT was significantly reduced in hypertensive group (128.1 ± 5.4 vs. 143.6 ± 1.8 ms in healthy group, P < 0.001). Pulmonary artery systolic pressure (PASP) was significantly elevated in untreated hypertensive group 39.3 ± 7.8 mm Hg. The RV diameter was 2.2 and 2.1 cm in controls and hypertensive group (P = 0.011). Global RV systolic strain values were remarkably reduced in hypertensive group (−19.6 ± 1.4 vs. −24.1 ± 2.2% in controls, P < 0.001).
Conclusions: The RV diastolic and systolic dysfunction was found in 60% and 30%, respectively, in the hypertensive group. Body mass index is a predictor of RVDD while several variables were found to be significantly (P < 0.001) associated with RV systolic dysfunction. These variables were left atrium dimensions, systolic blood pressure, and PASP. Possible causes of these structural and functional changes in the RV are translation of the increased LV filling pressure in the pulmonary circulation and interaction of the right and left ventricle.

Keywords: Pulmonary artery systolic pressure, right ventricle dysfunction, speckle tracking echocardiography, systemic hypertensionAddress


How to cite this article:
Hanboly NH. Right ventricle morphology and function in systemic hypertension. Nig J Cardiol 2016;13:11-7

How to cite this URL:
Hanboly NH. Right ventricle morphology and function in systemic hypertension. Nig J Cardiol [serial online] 2016 [cited 2019 Dec 13];13:11-7. Available from: http://www.nigjcardiol.org/text.asp?2016/13/1/11/173854


  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] Systemic hypertension induces a progressive increase of left ventricular (LV) mass with consequent LV hypertrophy (LVH) with resulting derangement of LV function.[2] Left ventricle hypertrophy is associated with impaired LV myocardial contractility and LV diastolic dysfunction that predict heart failure in population-based studies.[3] Ventricular interdependence refers to the fact that the shape, size, and compliance of one ventricle may influence the shape, size, or pressures in the other ventricle; an essential concept for understanding the pathology of right ventricle (RV) dysfunction.[4] The previous studies reported that hypertension affects the diastolic function of the left ventricle and these changes are accompanied by similar changes in the RV. The changes are prominent in the diastolic wave velocities, right ventricular wall (RVW) dimensions, and internal chamber dimensions.[5]

Tissue deformation imaging enables the objective assessment of regional myocardial deformation assessed by ultrasound-based strain and strain rate using myocardial Doppler data or B-mode images. This is a promising technique to quantify the regional right ventricular function and appears of added value in unmasking or unraveling cardiac pathology.[6] On these grounds, this study was designed to study RV diastolic and systolic functions by different echocardiography and Doppler modalities.


  Methods Top


The study was carried out in the echocardiography laboratory of Cardiovascular Department at Cairo University Hospitals. The Research Ethics Committee of the hospital reviewed and approved the study protocol. Eighty adult hypertensive participants aged 54.8 ± 14 years old were compared with 40 age and gender matched control subjects. Patient written consent was given by all the participants. All the enrolled patients were hypertensive on treatment and in sinus rhythm. Patients with other causes of LVH, myocardial disease, ischemic heart disease, valvular heart disease, or cor pulmonale were excluded. Hypertension was defined as the use of antihypertensive therapy or the persistent elevation of blood pressure above 140/90 mm Hg on two or more occasions with the patient in a sitting position for at least 5 min.[7]

The patients were subjected to history taking and physical examination including body mass index (BMI) and waist circumferences.

Echocardiography

All subjects had echocardiography performed with the use of a Philips iE33 (Philips Healthcare, Massachusetts, USA) ultrasound according to the recommendations of the American Society of Echocardiography.[8]

Left ventricle structure, dimensions, and functions were studied. Left ventricle mass was calculated using the Devereux formula.[9] The LV mass index (LVMI, g/m 2) was defined as LV mass divided by body surface area (m 2). The reference ranges used to define LVH was LVMI above 115 and 95 g/m 2 for males and females, respectively.[10] According to the current ASE/European Association of Cardiovascular Imaging Guidelines, we tried refinements in image processing to measure the actual visualized thickness of the ventricular septum and other chamber dimensions as defined by the actual tissue–blood interface, rather than the distance between the leading edge echoes, which had previously been recommended.[11]

Right ventricle wall thickness was measured in diastole from the subcostal views wall and wall thickness ≥5 mm indicates RV hypertrophy.[10]

Tricuspid annular plane systolic excursion

TAPSE is a method to measure the distance of systolic excursion of the RV annular segment along its longitudinal plane from a standard apical 4-chamber window. The greater the descent of the base in systole is the better the RV systolic functions (RVSDs). Tricuspid annular plane systolic excursion (TAPSE) below 17 mm indicates RV systolic dysfunction.[10]

Diastolic function of both ventricles was assessed by recording mitral and tricuspid 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).[12]

Using tissue Doppler imaging, 2 mm sample volume was placed at the lateral corner of the mitral and tricuspid annuli. An average of 3–5 consecutive cardiac cycles was taken for the calculation of all echo-Doppler parameters systolic velocity (S'), early diastolic velocity (E'), and myocardial velocity associated with atrium contraction (A'). Pulsed Doppler S' wave below 9.5 cm/s indicates RV systolic dysfunction.[10]

Hemodynamic study

Mean pulmonary artery pressure was estimated using pulmonary acceleration time (AT) measured by pulsed Doppler of the pulmonary artery in systole, whereby mean pulmonary artery pressure = 79 − (0.45 × AT) [Figure 1].[13]
Figure 1: Calculation of the pulmonary acceleration time

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Continuous Doppler echocardiography

Pulmonary artery systolic pressure (PASP) (assumed to be equal to RV systolic pressure) can be estimated with the Bernoulli equation formula: 4 × TRv2 + RAP where v is the maximum velocity of the tricuspid valve regurgitant jet measured by continuous wave Doppler added to the estimated right atrium pressure RAP calculated on the basis of the inferior vena cava diameter and the extent of collapse with inspiration [Figure 2].
Figure 2: Calculation of pulmonary artery systolic pressure (a) right ventricle systolic pressure with the Bernoulli equation formula (b) right atrium pressure calculated on the basis of inferior vena cava diameter

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Pulmonary vascular resistance was obtained using the equation: PVR = TRV/TVI RVOT × 10 + 0.16 where TRV is peak tricuspid regurgitant velocity and TVI RVOT is right ventricular outflow tract time-velocity integral [Figure 3].[14]
Figure 3: Echo-Doppler calculation of the pulmonary vascular resistance

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Speckle-tracking strain and displacement analysis

The speckle-tracking analysis was used to generate regional and global myocardial strain in the RV. Longitudinal RV strain was assessed in the apical 4-chamber view. Average frame rate for the analysis was 64 ± 9 Hz. Myocardial strain was expressed as the percent change from the original dimension at end diastole, and myocardial thickening or lengthening was represented as a positive value while myocardial thinning or shortening was represented as a negative value.

The software automatically divided the RV into six standard segments in the 4-chamber views. Peak systolic strain (PSS) obtained from time-strain curves were defined as the indices of myocardial systolic contraction. Global RV PSS in the six segments was assessed, and the free wall RV PSS was obtained by averaging 3-site strain signals simultaneously (basal, mid, and apical RV lateral wall [Figure 4].[15]
Figure 4: Apical 4-chamber view for the assessment of right ventricle longitudinal myocardial systolic function. Solid colored lines indicate corresponding segmental strain curves and the white dotted line indicates global strain curves

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Statistical analysis

All statistical calculations were done using computer program SPSS (Statistical Package for the Social Science; SPSS Inc., Chicago, IL, USA) release 15 for Microsoft Windows (2006). All data were statistically described in terms of mean ± standard deviation. Comparison of numerical variables between the study groups was done using Student's t-test for independent samples and one-way analysis of variance test when comparing three groups. P < 0.05 was considered statistically significant.


  Results Top


Age and heart rate were similar in both groups. Body mass index, mean systolic and diastolic blood pressures (DBPs) were significantly higher in the hypertensive group. General characteristics of the hypertensive and normotensive groups are listed in [Table 1].
Table 1: Baseline characteristics of the study groups

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M-Mode echocardiography examination

Septum wall thickness, left atrium diameter (LAD), and RVW thickness were increased in hypertensive group (1.1, 4.2, and 5.3 vs. 0.8 cm, 3.4 cm, and 2.8 mm in controls, P < 0.001 for all). Left ventricle hypertrophy was found in 57.5% of the hypertensive group (n = 46) while RV hypertrophy was found in 30% of hypertensive subjects (n = 24). Ejection fraction and LV diastolic dimensions were 62 ± 6.3 and 4.8 ± 0.6 in hypertensive group versus 66 ± 10.1% and 4.6 ± 0.4 cm in normotensive group.

Pulsed Doppler imaging

Mitral E/A ratio was 1.2 ± 0.1 and 0.9 ± 0.1 in controls and hypertensive groups, respectively (P < 0.001), while Tricuspid E/A was 1.3 ± 0.1 and 0.9 ± 0.2 in control and hypertensive participants. Positive significant correlation was found between mitral and tricuspid E/A ratio (P < 0.001, r = 0.842). Right ventricle diastolic dysfunction (RVDD) defined as E/A < 0.8[10] was found in 60% of hypertensive patients (n = 48). Tricuspid E/E′ was increased in hypertensive group (5.7 ± 1.7 vs. 3.8 ± 0.3 in the control group, P < 0.001). Tricuspid and mitral E'/A' ratio were decreased in hypertensive group (0.8 ± 0.1 and 0.9 ± 0.3 vs. 1.1 ± 0.1 and 1.3 ± 0.1 in the control groups, respectively, P < 0.001 for both). Univariate regression analysis revealed that BMI was found to be a significant predictor of RVDD (P = 0.023).

Right ventricle systolic function

Lateral tricuspid annulus peak S' annular velocity was 10.5 ± 1.6 and 15.7 ± 2 cm/s in hypertensive and control groups, respectively (P < 0.001). TAPSE was reduced in hypertensive patients 18.8 mm versus 22 mm in healthy group P < 0.001 [Figure 5].
Figure 5: Tricuspid annular plane systolic excursion in study groups

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Right ventricle speckle tracking imaging

Global RV systolic strain was significantly reduced in hypertensive group (−24.12 ± 2.2 and − 19.1 ± 1.5% in control and hypertensive subjects, respectively P < 0.001) [Figure 6].
Figure 6: (a) Peak systolic strain of right ventricle in healthy (b) and hypertensive patient

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Moreover, segmental RV systolic strain (RVSS) and strain rates were reduced in hypertensive patients [Figure 7] and [Figure 8].
Figure 7: Basal, mid, apical septum and free wall right ventricle systolic strain in study groups

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Figure 8: Basal, mid, apical, global right ventricle systolic strain rates of septum and free walls in the study groups

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Right ventricle systolic parameters including systolic strain were correlated negatively with PASP and LAD (P < 0.001) [Figure 9].
Figure 9: Right ventricle systolic strain and echo Doppler pulmonary artery systolic pressure

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Hemodynamic study

Echo derived systolic pulmonary artery pressure and pulmonary vascular resistance were significantly increased in hypertensive group (39.3 ± 7.8 and 1.3 ± 0.1 vs. 22 ± 6 mm Hg and 1.2 ± 0.1 wood units in controls P < 0.001 for both).


  Discussion Top


Both ventricles are structurally and functionally interdependent on each other. The study demonstrated that RVDD accompanies LV diastolic dysfunction that is due to hypertensive heart disease. The overall prevalence of RVDD was higher than that of RVSD, and the highest prevalence of the latter was recorded in subjects with elevated PASP and dilated left atrium. The current study revealed that tricuspid E/A and isovolumic relaxation time were 0.9 ± 0.2 and 83 ± 7.9 in hypertensive patients versus 1.3 and 75.7 ± 2.9 ms in controls (P < 0.001). Cicala et al.[16] reported that mitral annular E'/A' ratio and BMI were the only predictors of RVDD, while age, DBP, heart rate, and RV wall thickness were not associated with the RVDD. The current study found no relationship between RVDD and LVMI, but significant relationship was found between RVDD and mitral inflow velocities (P = 0.001, r = 0.842) [Figure 10]. However, the relationship between RVDD and mitral annular variables was not assessed in the present study.
Figure 10: Correlation between mitral and tricuspid inflow velocities in hypertensive patients

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Ventricular interdependence defined as the forces that are transmitted directly from one ventricle to the other through the myocardium and pericardium, independent of neural, humoral, or circulatory effects. It is a consequence of the close anatomical association between the ventricles. The ventricles are encircled by common muscle fibers, share a septum wall, and are enclosed within the pericardium.[17] The present study found the highest prevalence of RVSD among hypertensive patients who had the lowest mean left ventricle ejection fraction (LVEF) and the worst LV systolic function, while the lowest prevalence of RVSD was recorded among those had the highest mean LVEF. The current study supported the use of multiple echocardiography modalities to assess RVSD. According to recent guidelines, RVSD was found if RV free wall two-dimensional strain (<20 in magnitude with the negative sign, TAPSE <17 mm and tricuspid pulsed Doppler S' wave <9.5 cm/s.[10] According to these criteria, RVSD was found in 30% of hypertensive patients. These results were concordant with studies [18] but discordant with others [19] which showed higher prevalence using reduced TAPSE (<15 mm) perhaps because 51% of the patients in their series had coronary artery disease and 32.5% had cardiomyopathies.

The current study assessed RVSD using speckle tracking that revealed impaired RVSS in 30% of the hypertensive patients concordant with other studies [20],[21],[22] that revealed early sub-clinical RV dysfunction even in the absence of overt diastolic heart failure.

Nunez et al.[23] demonstrated that RV wall hypertrophy occurs in hypertensive subjects. Combination of increased interventricular septum and RV wall thickness will ultimately lead to progressive reduction in the RV end-diastolic dimensions before progressive dilatation may occur in the right heart. RV hypertrophy was found in 30% of the study group and was associated with LVH (i.e., biventricular hypertrophy) in 57.5% of the patients discordant with others [24] who found one-fifth of patients had biventricular hypertrophy the explanation was that most of our study groups are naive hypertensive patients not on medical treatment.

A recent study showed an increase in pulmonary resistance and right-sided pressures by echo-Doppler study in hypertensive patients.[25] The present study was able to show the relation between PASP and RV systolic strain in hypertensive patients. Concordant with previous study

that used complete hemodynamic and RV cineangiographic evaluation to assess right sided pressures in hypertensive patients,[26] the current study demonstrated increased pulmonary artery systolic and mean pressure, as well as pulmonary vascular resistance, by echo-Doppler study in hypertensive patients this may reflect enhanced activity of catecholamine, angiotensin, or some other humoral substance that is capable of producing pulmonary vasoconstriction.[27],[28]


  Conclusion Top


The concept that RV is immune from the effects of systemic hypertension is no longer tenable. Possible causes are a translation of the increased LV filling pressure in the pulmonary circulation and interaction of the right and left ventricles.

Since RV function is a crucial determinant of short-term prognosis in several heart diseases, the current study recommended more emphasis on the assessment of the RV functions using different echocardiography modalities in the follow-up of hypertensive patients.

Acknowledgments

The assistance of staff members at echocardiography laboratory Cardiovascular Department Cairo University is greatly appreciated. No external source of funding.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10]
 
 
    Tables

  [Table 1]


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