Nigerian Journal of Cardiology

: 2013  |  Volume : 10  |  Issue : 1  |  Page : 9--13

Clinical and echocardiographic determinants of diastolic dysfunction among Nigerian hypertensive subjects

Adeseye A Akintunde1, Adebayo T Oyedeji2, Oladimeji G Opadijo1,  
1 Department of Medicine, Ladoke Akintola University of Technology Teaching Hospital, Ogbomoso, Nigeria
2 Department of Medicine, Ladoke Akintola University of Technology Teaching Hospital, Osogbo, Nigeria

Correspondence Address:
Adeseye A Akintunde
P. O. Box 3238, Osogbo


Background: Diastolic dysfunction can occur either as an early marker or in late stages of hypertensive heart disease. Knowledge about its determinants is crucial to its management. Reports about clinical and echocardiographic determinants of diastolic dysfunction among Nigerian hypertensive subjects are few. This study aimed at describing the main clinical and echocardiographic determinants of diastolic dysfunction among Nigerian hypertensive subjects. Methods: Two hundred and forty-five hypertensive subjects and 68 age and sex-matched normotensives that had echocardiography were used for this study. Diastolic function was assessed by a combination using the ratio of early and late mitral flow velocity E/A ratio, isovolumic relaxation time (IVRT) and deceleration time (DT). Statistical analysis was carried out with the SPSS 16.0. Correlation and stepwise regression analysis were used for univariate and multivariate analysis respectively. Results: Mean age of the hypertensive subjects was similar with that of the controls (56.8±12.2 vs. 55.0±7.9 respectively, P>0.05). Diastolic dysfunction was commoner among hypertensive subjects than controls. Age, systolic and diastolic blood pressure (BP), and left ventricular chamber dimensions generally showed the greatest correlation with indices of diastolic function among the study population. Using the multivariate analysis, age was the strongest determinant of DT and IVRT followed by left ventricular chamber dimension for DT and systolic BP for IVRT. Left ventricular internal chamber dimension was the strongest determinant of mitral E/A ratio followed by diastolic BP. Conclusion: Age, systolic BP, and left ventricular volume and dimension are the major determinants of the diastolic dysfunction among hypertensive Nigerians. They affect different aspect of the diastolic parameters.

How to cite this article:
Akintunde AA, Oyedeji AT, Opadijo OG. Clinical and echocardiographic determinants of diastolic dysfunction among Nigerian hypertensive subjects.Nig J Cardiol 2013;10:9-13

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Akintunde AA, Oyedeji AT, Opadijo OG. Clinical and echocardiographic determinants of diastolic dysfunction among Nigerian hypertensive subjects. Nig J Cardiol [serial online] 2013 [cited 2022 Sep 25 ];10:9-13
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Diastolic dysfunction is extremely common in hypertension and left ventricular hypertrophy (LVH) occurring due to impairment of relaxation and/or compliance. [1],[2],[3] Diastolic and systolic dysfunctions are interrelated. Up to half of subjects with heart failure have been shown to have preserved ejection fraction (EF) (otherwise called diastolic heart failure or heart failure with preserved EF), while most subject with systolic heart failure often have associated diastolic dysfunction. [4],[5]

It is thought that diastolic dysfunction begin early in hypertensive heart disease. [6] It is associated with considerable morbidity and mortality although less than what obtains for systolic dysfunction. Despite use of antihypertensive therapy, diastolic dysfunction still persists among treated hypertensive subjects. Whether this is as a result of pressure changes, wall hypertrophy, increase left ventricular mass (LVM) or other factors is not well described. LVH is an independent risk factor for cardiovascular event. [7] Hypertension and LVH are often associated with diastolic dysfunction. [7],[8] The complex interplay of pressure and volume changes lead to various changes in wall dimension and geometric adaptations. [9] Diastolic function parameters can be influenced by several factors such as age, left ventricular inflow, heart rate, left ventricular wall and chamber dimensions, systolic, and diastolic blood pressure (BP). [3],[10],[11] Achieving good BP control and enhancement in systolic function has been shown to correlate with improvement in diastolic function in early hypertensive subjects. [12],[13] Persistence of diastolic dysfunction in hypertensive subjects despite antihypertensive therapy may suggest additional factors responsible for it which may further require definite attention. The determinants of diastolic dysfunction in treated hypertensive subjects among Africans are not well described. This study aimed to determine the clinical and echocardiographic determinants of diastolic dysfunction among treated hypertensive subjects.

 Materials and Methods

Two hundred and forty five hypertensive subjects and 68 controls were used for this study. It was a cross-sectional study among adult hypertensive subjects at a tertiary health facility, LAUTECH Teaching Hospital, Osogbo, Nigeria. Hypertension was diagnosed by the standard protocols when BP was ≥140/90 mmHg on at least two occassions and/or the use of antihypertensive therapy. [14] Clinical history and physical examination were performed on each participant. The following informations were obtained: gender, age, weight, height, duration of hypertension, and BP, the weight was taken with the patient in light clothing to the nearest 0.5 kg. Body mass index (BMI) was calculated as weight in kg/height 2 (kg/m 2 ).

Echocardiography was performed on all the subjects using a SUIS APOGEE ultrasound with 3.5MHz probe. 2-D, color and pulse wave Doppler were done. Echocardiography was carried out according to the recommendation of the American Society of Echocardiography guidelines. [15] Basic measurements of left ventricle (LV) systolic and diastolic dimension including, posterior wall thickness, inter-ventricular septum dimension, and chamber dimensions were measured using M-mode echocardiography. Average of three measurements was taken. LVM was calculated from the measurements of the LV using the equation:

LVM (g)=0.81 (1.04 [inter-ventricular septal thickness + posterior wall thickness + LV end diastolic internal dimension] 3 − [LV end diastolic internal dimension] 3 ) + 0.6. [16]

LVM index (LVMI) was calculated as LVM/height in m 2.7 Correcting LVM for height [2.7] has been shown to minimize the effect of gender, race, age, and obesity on the validity of various parameters for the diagnosis of LVH for which many parameters exist. [17],[18] One adult criterion for LVH is LVMI>51 g/m [2.7] LV geometry was determined after calculation of the relative wall thickness (RWT) by using the formula the formula (2 × posterior wall thickness)/LV end diastolic internal dimension. [19]

RWT was considered abnormal if it was <0.45. [19] Four left ventricular geometric patterns were described: Normal geometry, concentric remodeling, eccentric hypertrophy, and concentric hypertrophy. LV geometry was defined as concentric hypertrophy (elevated LVMI and RWT), concentric remodeling (normal LVMI and elevated RWT), eccentric hypertrophy (increased LVMI and normal RWT) and normal geometry (normal LVMI and RWT). LV EF was calculated using Teichholz's et al. [20] formula.

Diastolic filling was assessed by Doppler mitral inflow velocities in the apical four chamber view with the sample volume placed at the tip of the mitral valve leaflet. The peak early diastolic flow (E wave), late atrial contraction (A wave) were determined and the E/A ratio was calculated. With the sample placed between the LV inflow and outflow tract in the apical five chamber view, isovolumic relaxation time (IVRT) was measured as the time interval between the end of systolic output flow and the beginning of transmitral E wave onset. Deceleration time (DT) was calculated as the time from the peak of E wave to the time it reaches the minimum point.

Statistical analysis was carried out using the Statistical Package for Social Sciences, SPSS 16.0 (Chicago Ill.) Quantitative data were summarized using means± standard deviation while qualitative data were summarized using percentages and proportions. Student t-test and Chi-square were used as appropriate for intergroup comparisons. Correlation analysis was used for univariate association between the numerical variables. Multiple regression analysis was also used. Values with P<0.05 were taken as statistically significant. Ethical approval was obtained for the study.


[Table 1] shows the clinical characteristics of the study participants. The hypertensive subjects and the controls were well matched for age and gender distribution. Hypertensive subjects had significantly higher systolic BP, diastolic blood pressure (DBP), BMI, left ventricular posterior wall dimension, inter-ventricular septal wall dimension, DT, RWT and LVM than normal controls. The mean mitral E/A ratio was higher among the controls than the hypertensive subjects. Mean EF was similar among the two groups.{Table 1}

Univariate association of diastolic parameters (namely: Mitral E/A ratio, DT and IVRT) and clinical and relevant echocardiographic parameters are as shown in [Table 2] (only significant variables are shown). Age was inversely related to the mitral E/A ratio (r=0−0.116, P<0.05), directly related to IVRT (r=0.281, P<0.05) and DT (r=0.208, P<0.05). Left ventricular chamber internal diastolic and systolic dimension were directly related to mitral E/A ratio (r=0.192 and 0.228, P<0.05) and inversely related to DT (−0.171 and −0.155, P<0.05) respectively. DBP was inversely related to mitral E/A ratio (r=−0.120, P<0.05) and directly related to IVRT (0.159, P<0.05) but not to DT. Systolic blood pressure (SBP) was directly related to IVRT alone (r=0.233, P<0.05) but not to DT or mitral E/A ratio.{Table 2}

The clinical and echocardiographic determinants of the parameters of diastolic function were determined in a stepwise regression model. Variables with significant univariate associations were considered. Age was the strongest determinant for the isovolumic relaxation and DT while left ventricular internal dimension was the strongest determinant of the mitral E/A ratio. SBP was the next in line among the determinants of IVRT while DBP was next in line for the mitral E/A ratio and left ventricular internal dimension for the DT as shown in [Table 3].{Table 3}


The determinants of diastolic function parameters/indices among treated hypertensive Nigerians in this study included age, left ventricular dimension and/or volume, and BP. This is similar to what other authors have reported showing the significance of age, left ventricular dimensions, left ventricular geometry and BP as major determinants of diastolic dysfunction among hypertensive subjects. [21],[22]

Diastole is an important part of the cardiac cycle and it is divided into four phases; isovolumic relaxation, rapid filling, slow filling (diastasis), and atrial contraction. Abnormality of diastolic function is a reflection of impairment in any of the four phases. Two major determinants of diastolic filling are ventricular relaxation and compliance. Relaxation is typified by the rate and duration of left ventricular post-systolic pressure while compliance is indicated by volume changes, which occur as a result of pressure change during the diastolic filling. [23]

The association shown in this study with regard to diastolic function and left ventricular chamber dimension suggest that progressive cardiac chamber enlargement is associated with an increasing diastolic dysfunction. [24] The pattern of involvement of the left ventricular internal dimension is reflective of the left ventricular end diastolic volume. This means that the higher the end diastolic volume, the more severe the degree of diastolic dysfunction. This agrees with other studies among subjects with acute myocardial infarction that have reported that progressive LV dilatation is associated with impaired relaxation and restrictive filling pattern following myocardial infarction. [24],[25] In such patients, increased deposition of collagen fibers, which occur in the in the myocardium due to the LV remodeling processes is associated with the restrictive pattern of diastolic dysfunction. [25] This was suggested to be due to increasing LV volume and increasing myocardial stiffness. Similarly, treated hypertensive subjects have significant LV remodeling pattern, which modify the pressure and volume changes that are associated with hypertensive heart disease. [9] In the early phase, diastolic dysfunction may be as a result of increased wall tension consequent upon pressure changes. [6] However, as LV volume progressively increases, persistent of diastolic dysfunction may be mainly due to increasing LV volume and myocardial stiffness.

This study also showed that age is an important predictor of diastolic dysfunction among treated hypertensive subjects. Age has been shown to have an independent association with the increasing diastolic dysfunction in several studies. [22],[23] It has been reported that mitral E/A ratio decreases with the age. [26] Other authors however, suggests that the decrease of mitral E/A ratio with age is a reflection of the impact of cardiovascular risk factors, which tend to cluster among the elderly. Slotwiner et al. [27] showed in a group of normal adults that cardiac index and total peripheral resistance index did not change significantly with age. He further reported that the increase in BP associated with the age is offset by increasingly concentric ventricular geometry in women and an enhanced ventricular systolic function in men. However, in that study, pulse pressure to stroke volume ratio, which is a measure of arterial stiffness increased strongly with age in that study. Therefore, the association of age with diastolic dysfunction can be explained by the age-associated increase in BP, increasing arterial and vascular stiffness and associated compensatory remodeling mechanisms, which were initially compensatory. Arterial and vascular stiffness resulting from progressive atherosclerosis and arterial wall hypertrophy has also been shown to be related to LV geometry in normotensive and hypertensive adults. [28],[29]

The progression from mild to moderate to severe hypertension has been reported to be associated with emergence of significant hemodynamic profile changes from increased cardiac index with normal peripheral vascular resistance to normal cardiac index with increased peripheral resistance to reduced cardiac index with markedly increased peripheral resistance respectively. [27],[30] Therefore, the presence of diastolic dysfunction may be as a result of interplay between left ventricular volume and pressure changes among treated hypertensive subjects.

It is worthy of note that diastolic dysfunction still depend to a significant extent on the BP among treated hypertensive subjects. Elevated BP will increase wall tension, a major determinant of myocardial hypertrophy, left ventricular remodeling and consequent diastolic dysfunction. [1],[3],[6] Pressure overload, high heart rate, reduced myocardial perfusion are associated with elevated BP and also contribute to diastolic dysfunction. Though, this hypertensive is already on treatment, a large percentage of them had suboptimal control. Achieving target BP have been associated with normalization and reversal of diastolic dysfunction among newly diagnosed hypertensive subjects. [12],[13] Therefore, treated hypertensive especially, those who do not achieve target BP are at risk of increasing diastolic dysfunction due to changes associated with increasing wall tension and pressure hemodynamics. This has also been reported among similar hypertensive subjects in Sweden. [21]

In conclusion, this study showed that age, left ventricular volume, and BP contribute to the persistence of diastolic dysfunction among treated hypertensive subjects. Interplay of these factors is likely to be more responsible for the diastolic dysfunction rather than any of them in isolation. Consequently, aggressive BP reduction to target values and also prevention of progressive LV dilatation may further reduce the burden of diastolic dysfunction among hypertensive Nigerian subjects.


1Shepherd RF, Zachariah PK, Shub C. Hypertension and left ventricular diastolic function. Mayo Clin Proc 1989;64:1521-32.
2Akintunde A, Akinwusi P, Opadijo O, Adebayo R, Ogunyemi S. Prevalence of echocardiographic indices of diastolic dysfunction in patients with hypertension at a tertiary health facility in Nigeria. Internet J Cardiol 2009;6:2.
3De Mora Martín M, Aranda Lara P, Aranda Lara FJ, Barakat S, Zafra Sánchez J, Rubio Alcaide A, et al. Diastolic dysfunction, left ventricular hypertrophy, and microalbuminuria in mild to moderate essential arterial hypertension. Rev Esp Cardiol 1997;50:233-8.
4Oyati IA, Danbauchi SS, Alhassan MA, Isa MS. Diastolic dysfunction in persons with hypertensive heart failure. J Natl Med Assoc 2004;96:968-73.
5Paulus WJ, Tschöpe C, Sanderson JE, Rusconi C, Flachskampf FA, Rademakers FE, et al. How to diagnose diastolic heart failure: A consensus statement on the diagnosis of heart failure with normal left ventricular ejection fraction by the Heart Failure and Echocardiography Associations of the European Society of Cardiology. Eur Heart J 2007;28:2539-50.
6Pavlopoulos H, Grapsa J, Stefanadi E, Kamperidis V, Philippou E, Dawson D, et al. The evolution of diastolic dysfunction in the hypertensive disease. Eur J Echocardiogr 2008;9:772-8.
7Kahan T. The importance of left ventricular hypertrophy in human hypertension. J Hypertens Suppl 1998;16 suppl 7:S23-9.
8Messerli FH, Ketelhut R. Left ventricular hypertrophy: an independent risk factor. J Cardiovasc Pharmacol 1991;17 suppl 4:S59-67.
9Gerdts E, Cramariuc D, de Simone G, Wachtell K, Dahlöf B, Devereux RB. Impact of left ventricular geometry on prognosis in hypertensive patients with left ventricular hypertrophy (the LIFE study). Eur J Echocardiogr 2008;9:809-15.
10Verdecchia P, Schillaci G, Guerrieri M, Boldrini F, Gatteschi C, Benemio G, et al. Prevalence and determinants of left ventricular diastolic filling abnormalities in an unselected hypertensive population. Eur Heart J 1990;11:679-91.
11Balci B, Yilmaz O. Influence of left ventricular geometry on regional systolic and diastolic function in patients with essential hypertension. Scand Cardiovasc J 2002;36:292-6.
12Almuntaser I, Mahmud A, Brown A, Murphy R, King G, Crean P, et al. Blood pressure control determines improvement in diastolic dysfunction in early hypertension. Am J Hypertens 2009;22:1227-31.
13Onose Y, Oki T, Yamada H, Manabe K, Kageji Y, Matsuoka M, et al. Effect of cilnidipine on left ventricular diastolic function in hypertensive patients as assessed by pulsed Doppler echocardiography and pulsed tissue Doppler imaging. Jpn Circ J 2001;65:305-9.
14Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003;42:1206-52
15Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, et al. Recommendations for chamber quantification. Eur J Echocardiogr 2006;7:79-108.
16Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E, Sachs I, et al. Echocardiographic assessment of left ventricular hypertrophy: Comparison to necropsy findings. Am J Cardiol 1986;57:450-8.
17De Simone G, Daniels SR, Devereux RB, Meyer RA, Roman MJ, de Divitiis O, et al. Left ventricular mass and body size in normotensive children and adults: Assessment of allometric relations and impact of overweight. J Am Coll Cardiol 1992;20:1251-60.
18Daniels SR, Kimball TR, Morrison JA, Khoury P, Meyer RA. Indexing left ventricular mass to account for differences in body size in children and adolescents without cardiovascular disease. Am J Cardiol 1995;76:699-701.
19Savage DD, Garrison RJ, Kannel WB, Levy D, Anderson SJ, Stokes J 3 rd , et al. The spectrum of left ventricular hypertrophy in a general population sample: The Framingham Study. Circulation 1987;75:I26-33.
20Teichholz LE, Kreulen T, Herman MV, Gorlin R. Problems in echocardiographic volume determinations: Echocardiographic-angiographic correlations in the presence of absence of asynergy. Am J Cardiol 1976;37:7-11.
21Müller-Brunotte R, Kahan T, Malmqvist K, Edner M, Swedish ibesartan left ventricular hypertrophy investigation vs atenolol (SILVHIA). Blood pressure and left ventricular geometric pattern determine diastolic function in hypertensive myocardial hypertrophy. J Hum Hypertens 2003;17:841-9.
22Rosa EC, Moysés VA, Rivera I, da Cintra Sesso R, Kohlmann N, Zanella MT, et al. Left ventricular diastolic function in essential hypertensive patients: Influence of age and left ventricular geometry. Arq Bras Cardiol 2002;78:466-77.
23Brogan WC 3 rd , Hillis LD, Flores ED, Lange RA. The natural history of isolated left ventricular diastolic dysfunction. Am J Med 1992;92:627-30.
24Poulsen SH. Clinical aspects of left ventricular diastolic function assessed by Doppler echocardiography following acute myocardial infarction. Dan Med Bull 2001;48:199-210.
25Poulsen SH, Jensen SE, Egstrup K. Longitudinal changes and prognostic implications of left ventricular diastolic function in first acute myocardial infarction. Am Heart J 1999;137:910-8.
26Masugata H, Senda S, Goda F, Yoshihara Y, Yoshikawa K, Fujita N, et al. Cardiac function as assessed by echocardiography in the oldest old>or=90 years of age. Int Heart J 2007;48:497-504.
27Slotwiner DJ, Devereux RB, Schwartz JE, Pickering TG, de Simone G, Ganau A, et al. Relation of age to left ventricular function in clinically normal adults. Am J Cardiol 1998;82:621-6.
28Saba PS, Roman MJ, Pini R, Spitzer M, Ganau A, Devereux RB. Relation of arterial pressure waveform to left ventricular and carotid anatomy in normotensive subjects. J Am Coll Cardiol 1993;22:1873-80.
29Roman MJ, Pickering TG, Schwartz JE, Pini R, Devereux RB. Relation of arterial structure and function to left ventricular geometric patterns in hypertensive adults. J Am Coll Cardiol 1996;28:751-6.
30Lund-Johansen P. Central haemodynamics in essential hypertension at rest and during exercise: A 20-year follow-up study. J Hypertens Suppl 1989;7 suppl 6:S52-5.