CAPITULO IV: Análisis de resultados
4.1. Resultados método cuántico
4.1.2. Encuestas aplicadas al personal administrativo y docentes de la UTPL
The criteria for depressed LV function was based upon FS < 29%, and EF < 50%68
The patients being investigated are hypertensive patients therefore M- Mode is appropriate29.
The grading for systolic function will be classified as follows68. Systolic function EF (%)
Normal LV systolic function ≥ 50%
Mild LV systolic dysfunction 40 - 49% , Moderate LV systolic dysfunction 30 - 39%
Severe LV systolic dysfunction <30%
The above mentioned parameters were defined as follows:
True positives are cases with elevated BNP values and echo confirmed parameter of left ventricular dysfunction. True negatives are cases with normal BNP values and echo confirmed parameter of normal left ventricular function. False negatives are cases with normal BNP values, but presence of left ventricular dysfunction on echocardiography. False positives are cases with elevated BNP values, but finding of normal left ventricular function on echocardiography.
These parameters were presented in 2x2 contigency table as shown below:
Screening Test (NT-proBNP) Standard Test Echo ) Total
+VE -VE
+VE TP FP TP+FP
-VE FN TN FN+TN
Total TP+FN FP+TN TP+FP+FN+TN
Also positive predictive value- PV (+ve) and negative predictive value- PV (-ve) of NT-proBNP as a screening test will be determined as follows.
PV(+ve)= TP/ (TP+FP) X 100
PV(-ve)= TN/(TN+FN) X 100
The NT-proBNP values and indices of ALVD were correlated using the Pearson correlation coefficient. A multiple logistic regression analysis was performed to evaluate the determinants of
(
ALVD with correction for the possible contributions of co-founding factors like advancing age in the population studied. P- value of < 0.05 was taken as significant.
CHAPTER 4- RESULTS.
DEMOGRAPHIC AND ANTHROPOMETRIC INDICES OF PATIENTS AND CONTROLS
A total of 229 participants were recruited for the study: 140 hypertensive patients and 89 age and sex matched controls. Six hypertensive patients were excluded from the study because of elevated creatinine level (2 patients) and finding of ischemic changes on their electrocardiographic tracings (4 patients). Of the 134 hypertensives used in the research, 56
(41.8%) were males while 78 (58.2%) were females, whereas 37(41.6%) were males and 52 (58.4%) were females in the controls group. The age distribution is as shown in figure 1.
0 5 10 15 20 25 30 35 40 45
21 yrs
< 21-30 yrs 31-40 yrs 41-50 yrs 51-60 yrs 61-70 yrs
0 1
15
35
40
43
0 2
12
22
26 27
AGE DISTRBUTION OF SUBJECTS AND CONTROLS
SUBJECTS CONTROLS
FIGURE 2 - AGE DISTRIBUTION OF SUBJECTS AND CONTROLS.
The mean duration of hypertension amongst the hypertensive subjects was 7.7 ±8.5years, (range :
< one month- 48years). More than half of the hypertensive population (53.2%) had hypertension duration of ≤5years, 16.7% had a duration of 6- 10years. The mean duration of hypertension was noted to differ significantly between the two hypertensive subgroups (p=0.003). Hypertensive subjects with no dysfunction recorded a lower mean duration of hypertension (3.07± 3.32 years) compared with a duration of 9.21 ± 8.89 years recorded amongst hypertensives with LV dysfunction (P= 0.003).
TABLE II: BASELINE CHARACTERISTICS AND BIOCHEMICAL PARAMETERS OF HYPERTENSIVE PATIENTS AND CONTROLS
Parameters Hypertensive patients n=131
Controls n=79 p-values
Mean (SD)/% Mean (SD)/% student’s t test/X
2
AGE (years) 53.64 (10.32) 53.01 (11.17) 0.679 GENDER M (42.0); F (58.0) M (38.0); F (62.0) 0.566 BMI (Kg/m2) 28.73 (4.12) 26.65 (5.52) 0.004 * BSA (m2) 1.86 (0.17) 1.79 (0.18) 0.004 * SBP (mmHg) 140.89 (20.91) 123.00 (10.58) <0.001 * DBP (mmHg) 86.81 (12.90) 78.58 (8.30) <0.001 * PR (bpm) 78.80 (12.09) 71.63 (9.95) <0.001 * NT-proBNP (pg/ml) 390.33 (464.68) 55.58 (40.09) <0.001 *
ALT (u/l) 6.24 (6.35) 6.61 (2.90) 0.637
AST (u/l) 17.69 (23.10) 17.63 (4.50) 0.984 ALB (g/l) 50.66 (7.35) 48.69 (25.70) 0.456 UREA (mmol/l) 5.16 (2.11) 3.61 (1.16) <0.001* CR (μmol/l) 96.95 (29.46) 76.20 (17.77) 0.001*
*P is significant at <0.05. NT-proBNP - N-terminal pro-brain natriuretic peptide, FBS-fasting blood sugar, ALT- alanine transaminase, AST-aspartate transaminase, TP -total protein, ALB- albumin, CR-creatinine, BMI-body mass index, BSA-body surface area, SBP-systolic blood pressure, DBP-diastolic blood pressure, PR-pulse rate.
The mean age of both hypertensive patients and controls were similar (53.64 ±10.32 vs 53.01
±11.17 years, p=0.679). The mean age of hypertensive patients with ALVD was found to be significantly higher than those without dysfunction (43.17 ± 8.47 vs 55.90 ± 9.28, p<0.001). The mean BMI was significantly higher in hypertensive patients compared to controls (28.73 ± 4.12 vs 26.65 ±5.52, p=0.004). Mean systolic and diastolic blood pressures; and pulse rate were
significantly lower in control subjects when compared with hypertensive subjects (123.00 ±10.58 vs 140.89 ±20.91, p<0.001; 78.58 ± 8.30 vs 86.81 ± 12.90, p<0.001 and 71.63 ± 9.95 vs 71.63 ± 9.95, p<0.001, respectively).
NT-proBNP level in hypertensive patients was much higher than in controls (390.33 ± 464.68 vs 55.58 ± 40.09, p<0.001). Mean urea and creatinine were much higher in hypertensive patients when compared with their values in the control group ( 5.16 ± 2.11 vs 3.61±1.16, p<0.001 and
96.95 ± 29.46 vs 76.20 ±17.77, p=0.001, respectively).
TABLE III: ECHOCARDIOGRAPHIC DIMENSION OF PATIENTS AND CONTROLS.
Parameters Subjects n=131
Controls n=79
p-values
Mean (SD)
Mean (SD) student’s t test
IVSD (cm) 1.08 (0.24) 0.89 (0.13) <0.001 * IVSS (cm) 1.59 (0.33) 1.43 (0.31) 0.002* LVDD (cm) 4.56 (0.56) 4.56 (0.49) 0.990 LVDS (cm) 2.93 (0.51) 2.73 (0.49) 0.007* LVPWD (cm) 1.07 (0.21) 0.88 (0.10) <0.001* LVPWS (cm) 1.57 (0.25) 1.46 (0.21) 0.001* LA (cm) 3.47 (0.44) 3.21 (0.44) 0.002* AO (cm) 2.99 (0.35) 2.95 (0.32) 0.369 RWT 0.48 (0.11) 0.39 (0.49) <0.001* LVM (gm) 175.72 (54.11) 134.34 (33.21) <0.001* LVMI (gm/m2) 94.43 (25.98) 74.08 (16.11) <0.001*
*P is significant at <0.05. IVSD = Interventricular septum thickness in diastole, IVSS = Interventricular septum thickness in systole, LVDD = Left ventricular internal diameter in diastole, LVDS = Left ventricular internal diameter in systole, LVPWD = Left ventricular posterior wall thickness in diastole, LVPWS = Left ventricular posterior wall thickness in systole, LA-Left atrium, AO- Aortic root diameter. RWT = Relative wall Thickness, LVM = Left ventricular mass, LVMI = Left ventricular mass index.
FIGURE 3- DISTRIBUTION OF LEFT VENTRICULAR GEOMETRY IN SUBJECTS.
Hypertensive patients had higher interventricular septum thickness in diastole and systole compared to controls (1.08±0.24 vs 0.89±0.13, p<0.001 and 1.59±0.34 vs 1.43±0.31, p<0.001, respectively).
Left ventricular internal diameter in diastole in hypertensive patients was comparable to that in controls (4.56±0.55 vs 4.57±0.47, p=0.874), but it was higher in systole with a difference that was statistically significant (2.92±0.50 vs 2.76±0.49, p=0.015). Left ventricular posterior wall thickness in diastole and systole were also higher in hypertensive patients compared to controls (1.07±0.21 vs 0.89±0.11 and 1.57±0.25 vs 1.46±0.22 respectively).
The difference was statistically significant with p values of <0.001 and < 0.001 respectively.
Relative wall thickness in hypertensive patients was higher compared to controls and was statistically significant (0.47±0.11; 0.39±0.05, p <0.001). Left atrium, left ventricular mass and left ventricular mass index were higher in the hypertensive patients compared to controls (3.46±0.44
vs 3.21±0.48; 176.20±53.99 vs 136.18±32.65 and 94.54 ±25.83 vs 75.06±16.01 respectively) and showed statistically significant difference with corresponding p values of <0.001, <0.001 and
<0.001. Although, the aortic root diameter was higher in hypertensive patients compared to controls, there was no statistically significant difference (3.00±0.35 vs 2.93±0.39, p=0.182).
Of the 134 hypertensive subjects, 31% had normal left ventricular geometry, 40% had concentric remodeling, 24% had concentric left ventricular hypertrophy while the remaining 5% had eccentric left ventricular hypertrophy. This shows that 69% of the hypertensive patients had one form of remodeling or the other (Fig 3).
TABLE IV: PARAMETERS OF LEFT VENTRICULAR FUNCTION IN PATIENTS AND CONTROLS.
Parameters Subjects n=131
Controls n=79
p-values
Mean (SD) Mean (SD)
student’s t test
SYSTOLIC FUNCTION FS (%)
EF (%)
DIASTOLIC FUNCTION
E/A DT (ms) IVRT (ms)
35.41 (7.13) 64.85 (8.46)
1.01 (0.39) 190.81 (46.71) 95.35 (20.55)
39.94 (6.48) 69.27 (8.85)
1.11 (0.32) 197.19 (40.56) 95.96 (17.68)
<0.001* <0.001*
0.070 0.323 0.832
*P is significant at <0.05. FS = Fractional shortening, EF = Ejection fraction, E-WAVE=mitral inflow early rapid peak velocity; A= late atrial peak velocity; E/A = ratio of mitral inflow early rapid peak velocity to late atrial peak velocity; DT = deceleration time; IVRT = isovolumic relaxation time.
The mean ejection fraction and fractional shortening were significantly lower in hypertensive subjects than in the control group (69.25± 8.85 vs 65.04±8.48 and 39.81±6.65 vs 35.57 ±7.15, p=0.001 in both instances). The parameters of diastolic function were also lower among
hypertensives than the controls, but the difference is not statistically significant.
TABLE V: PREVALENCE OF ASYMPTOMATIC LEFT VENTRICULAR DYSFUNCTION AMONG HYPERTENSIVE SUBJECTS.
PARAMETERS FREQUENCY (n)
PERCENTAGE (%)
ALVD 107 81.7
Mild LVDD 77 58.8
Moderate LVDD 24 18.3
Severe LVDD 1 0.8
Combined LVDD & LVSD 5 3.8
Normal LVF 24 18.3
LVSD- left ventricular systolic dysfunction; LVDD- left ventricular diastolic dysfunction.
A total of 107 (81.7%) hypertensive subjects had asymptomatic left ventricular dysfunction whilst the remaining 24 (18.3%) had normal LV function (Table V). Majority (102) 95.3% of the hypertensive subjects with asymptomatic left ventricular dysfunction had isolated LVDD, while only 5 (4.7%) patients had both asymptomatic LVSD and LVDD. Mild (Grade 1) diastolic dysfunction was found in 58.8%, moderate (Grade 2) diastolic dysfunction in 22.1% and only one subject with severe (Grade 3) diastolic dysfunction constituting 0.8%.
TABLE VI: NT- proBNP LEVELS IN HYPERTENSIVE PATIENTS WITH ASYMPTOMATIC LEFT VENTRICULAR DYSFUNCTION.
PARAMETERS
TYPE OF LV FUNCTION Normal Dysfunction
p-values
(A) OVERALL LV FUNCTION n = 24 n = 105 0.017 *
NT-ProBNP LEVEL (pg/ml) 175.21 (227.75) 430.13 (491.88)
(B) SYSTOLIC FUNCTION
n = 24
n = 5
<0.001* NT-ProBNP LEVEL (pg/ml) 175.21 (227.75) **850.90 (583.93)
(C) DIASTOLIC FUNCTION
n = 24
n = 100
0.025* NT-ProBNP LEVEL (pg/ml) 175.21 (227.75) 409.09 (480.63)
*P is significant at <0.05. NT-proBNP - N-terminal pro-brain natriuretic peptide, LV= Left ventricular. **
- NT-proBNP in patients with combined Asymptomatic LVDD and LVSD
The mean plasma levels of NT-proBNP were significantly higher in hypertensive patients with ALVD compared to hypertensives without LV dysfunction (430.13 ± 491.88 vs 175.21 ± 227.75, p=0.017). Hypertensive subjects with LV systolic dysfunction had the highest level of NTproBNP and the difference was statistically significant compared to hypertensive patients with normal LV function. The findings also showed that hypertensive patients with isolated LV diastolic dysfunction also had NT-proBNP level that was significantly higher than in hypertensive subjects with normal LV function (409.09 ± 480.63 vs 430.13 ± 491.88). Amongst patients with ALVD, the highest mean value of NT-proBNP was found in hypertensive patients with combined
asymptomatic systolic and diastolic dysfunction, whilst those with isolated asymptomatic LV diastolic dysfunction had a lower NT-proBNP levels, but the difference was not statistically sigificant (850.90 ± 583.93 vs 409.09 ± 480.63, p= 0.050).
All different types of asymptomatic LV dysfunction was noted to have significantly higher NT- proBNP compared to hypertensives without dysfunction. (see Fig 4 below).
FIGURE 4: NT- PROBNP LEVELS INCREASE WITH SEVERITY OF LV DYSFUNCTION.
Normal LV Function Isolated DD Combined Systolic and
Diastolic Dysfunction
175.20
409.09
850.90
NT - proBNP Level (pg/ml) in Different Patterns of
LV Function
FIGURE 5: NT- PROBNP LEVELS IN DIFFERENT GRADES OF ASYMPTOMATIC LEFT VENTRICULAR DIASTOLIC DYSFUNCTION.
TABLE VII: CORRELATIONS BETWEEN NT-proBNP LEVELS AND LV 0
100 200 300 400 500 600
ALVDD Mild ALVDD Moderate-Severe ALVDD
409.09
347.96
551.72
BNP Levels (pg/ml) in Different Grades of
Diastolic Dysfunction
DIMENSIONS AND FUNCTIONS
PARAMETERS MEAN (SD) OF PARAMETERS
PEARSON
CORRELATION
P-VALUE
AGE (years) 53.64 (10.32) 0.073 0.406 HTN t0 (years) 8.06 (8.56) 0.288 0.004* IVSD (cm) 1.08 (0.24) 0.224 0.011* IVSS (cm) 1.59 (0.33) 0.241 0.007* LVDD (cm) 4.56 (0.56) -0.068 0.439 LVDS (cm) 2.93 (0.51) 0.030 0.736 LVPWD (cm) 1.07 (0.21) 0.236 0.007* LVPWS (cm) 1.57 (0.25) -0.011 0.904 LA (cm) 3.47 (0.44) -0.015 0.861 AO (cm) 2.99 (0.35) -0.206 0.019
RWT 0.48 (0.11) 0.215 0.014*
LVM (gm) 176.30 (53.91) 0.174 0.048* LVMI (gm/m2) 94.75 (25.85) 0.203 0.026* EF (%) 64.85 (8.46) -0.165 0.060 FS (%) 35.41 (7.13) -0.073 0.408
E/A 1.01 (0.39) -0.031 0.726
DT (ms) 190.81 (46.65) -0.162 0.073 IVRT (ms) 95.35 (20.55) -0.135 0.139
*P is significant at <0.05. HTN t0 = Duration of hypertension. IVSD = Interventricular septum thickness in diastole, IVSS = Interventricular septum thickness in systole, LVDD = Left ventricular internal diameter in diastole, LVDS = Left ventricular internal diameter in systole, LVPWD = Left ventricular posterior wall thickness in diastole, LVPWS = Left ventricular posterior wall thickness in systole, EF = Ejection fraction, FS = Fractional shortening, E/A: ratio of mitral inflow early rapid peak velocity to late atrial peak velocity; DT = deceleration time; IVRT = isovolumic relaxation time.
There were significant positive correlations between the mean NT-proBNP levels and IVS in diastole, IVS in systole and LVPW thickness in diastole (r=0.224, 0.244 and 0.236, p=0.011,
0.007 and 0.007 respectively. RWT, LVM and LVMI were also significantly positively correlated with NT- proBNP levels (see Table VII).
Interestingly, a significant positive correlation was found between the level of NT- proBNP and duration of hypertension. This parameter appears to be better correlated positively than the aforementioned parameters (r= 0.288, p=0.004).
A significant negative correlation was noted between aortic root diameter and NT-proBNP levels (r= -0.206, p= 0.019). Parameters of LV systolic function such as ejection fraction and fraction shortening were negatively correlated with NT-proBNP levels. The correlation was however noted to be non- significant. Non-significant negative correlation was also noted between NT- proBNP levels and LVDD, LVPWS, LA, and parameters of diastolic function such as ratio of mitral inflow velocity, deceleration time and isovolumic relaxation time.
TABLE VIII: SENSITIVITY AND SPECIFICITY OF NT-proBNP IN DETECTING ALVD IN HYPERTENSIVE PATIENTS
PARAMETERS STANDARD TE ST (ECHO) TOTAL Screening Test (NT-proBNP):
Cut-off value: 56.0pg/ml
ALVD NO ALVD
+VE TP (66) FP (9) TP + FP (75)
-VE FN (39) TN (14) FN +TN (53)
TOTAL TP+FN (105) FP+TN (23) TP + FP+ FN +TN (128)
NT-proBNP- N-terminal pro-brain natriuretic peptide; ALVD- asymptomatic left ventricular dysfunction; +ve = positive; -ve = negative; TP = True positives; TN= True negatives; FN= False negatives; FP = False positives
Echocardiography is taken as the gold standard.
Using Cut-off Value of 56.0pg/ml obtained amongst control subjects as normal NT-proBNP level:
Sensitivity = TP (TP+FN) x 100 =66/ (66+39) x 100 = 6600/105 = 62.8%
Specificity = TN/(TN+FP) x 100 = 14/ (14+9) x 100 =1400/23 = 60.9%
The obtained echocardiographic parameters of LV functions were taken as true positives.
The calculation showed that NT-proBNP is moderately sensitive and specific for detection of asymptomatic left ventricular dysfunction in hypertensives.
Positive and Negative Predictive Values of NT- proBNP in detecting ALVD in hypertensive patients who are asymptomatic for heart failure using Cut-off value of 56.0pg/ml:
PV(+ve) = TP/ (TP+FP) x 100 = 66/66+9 x 100 = 88.0%
PV(-ve) = TN/(TN+FN) x 100 = 14/14+39 x 100 = 26.4%
The calculation showed that NT-proBNP has a strong positive predictive value, but low negative predictive value.
Positive and Negative Predictive Values of NT- proBNP in detecting ALVD in hypertensive patients who are asymptomatic for heart failure using Cut-off value of 56.0pg/ml:
CHAPTER FIVE
DISCUSSION
This study aimed at determining the prevalence of asymptomatic left ventricular dysfunction in patients with systemic hypertension and diagnostic usefulness of NT-proBNP in its early detection.
The mean age of hypertensive and control subject in the study were 54 years and 53years, respectively. This is comparable to an earlier finding in Abuja by Ojji et al, where the mean age of hypertensive subjects was 53.8 ± 13.2years,103 and the data from Abeokuta by Ogah et al with a mean age of 56.9 ± 13.3years amongst the male hypertensive subjects and 55.0 ± 12.0years amongst their female counterparts68. A study on BNP in congestive heart failure patients done at Lagos University Teaching Hospital by Ajuluchukwu et al29 also had an average age of 54years amongst the subjects. Although that study was conducted amongst heart failure patients, it is important to note that hypertension was the main cause of heart failure amongst the subjects. The age recorded in this study is lower than that recorded in studies done in California and Italy with mean ages of 68.8 ± 11.7 and 66.4 ± 7.8years respectively30, 42. The lower age in the current study population might point to higher risk of developing hypertension amongst blacks at an earlier age compared to Caucasians.
Prevalence of Asymptomatic Left Ventricular Dysfunction.
The present study revealed a high burden of asymptomatic left ventricular dysfunction among hypertensive patients in LASUTH with a prevalence of 81.7%. Isolated asymptomatic left ventricular diastolic dysfunction accounted for most of the dysfunction- 102 (77.9%). Combined asymptomatic systolic and diastolic dysfunction contributed only (5) 3.8%. Isolated systolic dysfunction was not found in any of the hypertensive subjects studied. Prevalence of asymptomatic left ventricular dysfunction obtained in the current study is much higher than that obtained in a previous study conducted by Betti et al42 amongst Caucasians in a population at high risk for heart failure. That study recorded a prevalence of 37.5% as against 81.7% documented in the present study. Diabetic patients were included in the study by Betti et al, but this category of patients were excluded in the present study. Despite this, the prevalence recorded in this study more than doubled that obtained amongst the caucasians. The majority of asymptomatic left ventricular dysfunction reported amongst the caucasians was also due to asymptomatic left ventricular diastolic dysfunction (36.4%). Only 1.1% of the study population had asymptomatic left ventricular systolic dysfunction.
As in the current study, low prevalence of asymptomatic left ventricular dysfunction was found in a German study on natriuretic peptides in the detection of preclinical LV dysfunction amongst primary care patients with risk factors for LV dysfunction such as hypertension, diabetes and coronary artery disease77. In the German study, LV dysfuction was recorded in a total of 69%.
Majority (65%) of the subjects in the German demonstrated echographic sign of diastolic dysfunction and only a small percentage of them (4%) had systolic dysfunction. This suggests that the prevalence of Asymptomatic Left Ventricular Dysfunction is very high in our environment compared with caucasians. This established the fact that the course of hypertension is worse amongst blacks compared to their white counterparts.
Several reasons have been documented for this peculiarity amongst black hypertensives. Increased salt sensitivity is an important contributor to the higher risk of hypertension in black people compared to whites. Salt sensitivity has been associated with ventricular hypertrophy and hypertensive nephropathy106. It could also be due to lack of awareness, hence late presentation, and consequently earlier onset of target organ damage among black hypertensives69.
Furthermore, black hypertensives suffer disproportionately from a given blood pressure when compared to whites70.
The implication of Asymptomatic Left Ventricular Dysfunction amongst the middle age individuals is that, it could lead to increase in mortality, morbidity and disability- adjusted life years of the working class age by being more proned to developing heart failure.
The finding of high prevalence of diastolic dysfunction in this study is similar to earlier reported prevalence of 82.86% at University of Nigeria Teaching Hospital, Enugu by Ike and Ikeh61 and a prevalence of 85.0% at LAUTECH, Osogbo by Akintunde et al63. A much lower prevalence of 62% was obtained by Adamu64 et al at University of Ilorin Teaching Hospital. The lower prevalence obtained by Adamu64 et al may be due to the fact that only newly diagnosed hypertensive subjects were recruited for his study. Balogun et al in a preliminary audit of twodimensional and doppler echocardiographic service amongst hypertensive patients in a Nigerian tertiary private hospital also reported a lower prevalence of 58%107. Impaired relaxation pattern was the most common form of diastolic dysfunction- 77subjects (58.8%) in this study, followed by pseudonormalisation pattern- 29 (22.1%). Restrictive pattern diastolic dysfunction was found to be rare- only 1 subject (0.8%).
This is similar to findings in other studies, where majority of patients with diastolic dysfunction showed impaired relaxation pattern42,63-64.
The relatively low prevalence of asymptomatic left ventricular systolic dysfunction (3.8%) in current study is at variance with a much higher prevalence of 18.1% obtained by Ogah68 et al in a hospital based study on prevalence of this entity in hypertensive Nigerians conducted at Abeokuta.
The present study found only mild grade of systolic dysfunction amongst the 5 hypertensive subjects that had combined dysfunction. This is at variance with Ogah study that recorded all the 3 different grades of systolic dysfunction in the hypertensive cohorts studied. Over 50% of ALVSD recorded by Ogah et al however had mild systolic dysfunction. The much higher prevalence reported by Ogah68 et al could be due to the fact that a larger study population of 832 hypertensives were enrolled in that study. Secondly, the study was conducted over a three-year period and a much older age group of up to 88years were recruited for the study. Diabetic hypertensives were also not excluded from the study as metabolic profiles were not carried out in the study subjects. The present study showed a higher prevalence of Asymptomatic Left Ventricular Systolic Dysfunction in women who represented a total of 60%. This is contrary to the findings by Ogah et al that recorded a prevalence that was twice as common in men compared to women. The reason for this is not certain.
LV systolic and diastolic dysfunction coexist to varying degrees. This is due to the fact that both systole and diastole are active and complementary components of the cardiac cycle and they both contribute to overall myocardial performance. In the present study, patients with Asymptomatic Left Ventricular Systolic Dysfunction were also found to have mild degree of diastolic dysfunction.
This is similar to the finding by Betti at al42., where all the 11 patients with asymptomatic left ventricular systolic dysfunction also had Grade 1 diastolic dysfunction.
The prevalence of asymptomatic left ventricular dysfunction increased significantly with age and the duration of hypertension. The highest mean age (55.90 ± 9.28 years) and mean duration of hypertension (12.20 ± 6.98 years) was noted amongst patients with combined diastolic and systolic dysfunction. This is similar to the finding by the Strong Heart Study65. Majority of the hypertensive subjects with left ventricular hypertrophy (96.4%) were noted to have
Asymptomatic Left Ventricular Dysfunction. Amongst the hypertensive subjects with LV dysfunction, 32.3% had left ventricular hypertrophy. This finding is similar to other studies
63-64,103.
The heart typically responds to increased vascular loading by hypertrophy and LV stiffening108. Hypertension has been identified as a chief precursor of Left ventricular hypertrophy. The latter is a determinant of LV dysfunction. Patients with left ventricular hypertrophy have increased myocardial fibrosis, particularly in the subendocardium. This leads to abnormal relaxation and increased filling pressures. The presence of Asymptomatic Left Ventricular Dysfunction and left ventricular hypertrophy may imply a higher mortality64, 103. It is also important to note that left ventricular hypertrophy was absent in quite a number (67.7%) of hypertensive subjects with Asymptomatic Left Ventricular Dysfunction in the current study; despite echocardiographically documented evidence of the dysfunction. This finding is in keeping with that of Adamu et al that found 39.8% of patients with diastolic dysfunction did not have LVH64. The presence of Asymptomatic Left Ventricular Dysfunction in the absence of LVH may be due to increased tension on the myocardium from elevated blood pressure.
Diagnostic usefulness of NT- proBNP in detection of ALVD.
The present study showed that the plasma level of NT-proBNP was significantly higher in hypertensive subjects than control (390.33.± 464.68 vs 55.58 ± 40.09 pg/ml, p<0.001).
It is well known that plasma levels of BNP are markedly elevated in heart failure patients38-39. Ajuluchukwu et al demonstrated NT-proBNP values were significantly higher in heart failure patients and has significant negative association with LV function29. Similar results were reported by Gbadamosi et al at the University of Ilorin Teaching Hospital112. The present study demonstrates that NT-proBNP levels were also significantly higher in hypertensive subjects than control (390.33.± 464.68 vs 55.58 ± 40.09 pg/ml, p<0.001). This is in agreement with a study on BNP in essential hypertension113. The current study further showed that NT-proBNP level in hypertensive patients with LV dysfunction was significantly higher than in hypertensive patients with normal LV function. This finding is similar to that reported by Vikas Bhalla30 in California and Betti42 in Italy amongst patients at risk for heart failure. They recorded a higher level of NTproBNP in high risk hypertensive patients with LV dysfunction. This is also in keeping with the finding by Ajuluchukwu29 et al in a study on NT-proBNP in heart failure, where they showed that NT-proBNP rises significantly in both systolic and diastolic heart failure. Results from the
Dallas Heart Study111 also revealed a better performance of NT-proBNP in detecting LVH or LVSD in subjects at high-risk for heart failure compared to BNP.
This finding raises the probability that NT-proBNP may be useful in differentiating those hypertensives with asymptomatic LV dysfunction from those without LV dysfunction. The usefulness of NT-proBNP in detecting asymptomatic LV dysfunction has been well established amongst Caucasians30,35,40,77,83.
The study further demonstrated that NT-proBNP level increases significantly with increasing severity of diastolic dysfunction. The highest value was recorded amongst patients with moderate-to-severe diastolic dysfunction. This finding is in keeping with that recorded by Lang et al. They first showed that BNP was raised in patients with isolated diastolic dysfunction, however the level of rise was not related to the severity of diastolic dysfunction114. Troughton et al in their study found that plasma BNP levels increase significantly according to severity of overall LV diastolic dysfunction as it progresses from abnormal relaxation to pseudonormal and restrictive filling pattern115. Similar finding was reported by the PROBE-HF study42. However, the PROBE-HF study was only able to establish a significant relationship between NT-proBNP and moderate-severe-diastolic dysfunction, but not with mild moderate-severe-diastolic dysfunction.
This is at variance with the finding by Ojji et al103, in which no relationship was found between diastolic dysfunction and NT- proBNP levels in hypertensives. Romano et al in a similar study amongst diabetic patients found BNP to correlate with diastolic dysfunction only amongst uncontrolled diabetic patients116. He was unable to demonstrate any difference between those with normal function and the general diabetic cohort with diastolic dysfunction irrespective of blood sugar control. The reason could probably be due to the fact that all patients with diastolic dysfunction in the above mentioned study only had impaired relaxation pattern. Furthermore, the present study also demonstrated a posible prognostic role of BNP measurement in identifying patients with mild diastolic dysfunction. This is in agreement with some studies on BNP in heart failure117. This is however at variance with that obtained by Betti et al in the PROBE-HF study42.
NT- proBNP is a fragment of brain natriuretic peptide prohormone that is released from cardiac myocytes in response to multiple pathologic stimuli. Such stimuli include LV hypertrophy,