Nephrol Dial Transplant (2002) 17: 1795-1801
© 2002 European Renal Association-European Dialysis and Transplant Association
Aortic valve calcification is an independent factor of left ventricular hypertrophy in patients on maintenance haemodialysis
1 Servicio de Asistencia Renal Integral (SARI) and 2 Departamento de Cardiología, Hospital de Clínicas, Universidad de la República, Uruguay
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Abstract |
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Background. Calcification and dysfunction of aortic and mitral valves are frequently found in chronic dialysis patients, but their influence on the development of left ventricular hypertrophy (LVH) is not well defined.
Methods. Conventional echocardiography and Doppler measurement of trans-aortic flow velocity were performed in 135 chronic haemodialysis patients, and left ventricular mass index (LVMI) and trans-valve pressure gradients were calculated. Average values of systolic, diastolic and pulse pressure (PP), interdialytic weight gain, chronic overhydration (difference between mean post-dialysis and dry weights), plasma calcium, phosphate, haemoglobin, and urea reduction ratio over the year preceding this study were obtained in every patient.
Results. Aortic valve calcification was present in 105 patients (78%), associated with stenosis in eight (6%); 39 patients (29%) had aortic regurgitation. Mitral annular calcification occurred in 35 (26%) cases and mitral regurgitation in 45 (33%). LVH was observed in 104 patients (77%). Logistic analysis revealed that only aortic valve calcification predicted LVH. LVMI was higher in patients with aortic valve calcification than in those without calcification: (mean±SD) 241±52 vs 154±64 g/m2, P=0.001. LVMI was not different between patients with normal, calcified, or regurgitating mitral valves. Patients with aortic valve calcification had higher trans-valve peak flow velocities and pressure gradients than those with non-calcified valves: 1.65±0.53 vs 1.37±0.33 m/s, P=0.01, and 12.1±8.9 vs 7.9±3.6 mmHg, P=0.01, respectively. The LVMI correlated directly with both variables (r=0.27 and r=0.24, P<0.005). Stepwise linear regression on nine covariates potentially influencing LVMI (age, body mass index, time on dialysis, systolic blood pressure, PP, chronic overhydration, haemoglobin concentration, trans-aortic flow velocity, and urea reduction ratio) showed that LVMI was independently associated with (i) PP, (ii) haemoglobin (inverse correlation), (iii) peak aortic flow velocity, and (iv) chronic overhydration (r=0.502, R2=0.252, ANOVA F-ratio=10.19, P<0.0005).
Conclusion. Our findings show that aortic valve calcification is associated with LVH in chronic haemodialysis patients, probably because valve resistance to ventricular outflow is increased as shown by trans-aortic flow velocities and pressure gradients. The effect on LVMI is independent of PP, anaemia, and overhydration.
Keywords: aortic valve calcification; haemodialysis; left ventricular hypertrophy
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Introduction |
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Left ventricular hypertrophy (LVH) is present in about 60–80% of patients with chronic renal failure at the start of dialysis treatment [1] and is a strong predictor of mortality in this population [2]. High blood pressure, overhydration, anaemia, and the arterio-venous shunt are main factors of LVH development through the mechanisms of pressure and flow/volume overload [3]. Heart valve disease is frequent in uraemic patients [4,5], but although aortic and mitral valve alterations are potential factors of cardiac hypertrophy, its influence on LVH has not been properly defined.
The aim of this study was to examine the structural and functional alterations of mitral and aortic valves in haemodialysis patients, assessing their putative effects on LVH development. The second goal was to compare the influence of these valve alterations with other risk factors promoting cardiac hypertrophy.
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Subjects and methods |
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Non-selected 135 patients (75 men and 60 women) from three dialysis centres, undergoing chronic haemodialysis treatment (12–15 h/week) for >1 year were included in the protocol. Clinical and laboratory data were obtained from dialysis records over the year preceding this study. Average values of pre-dialysis systolic and diastolic blood pressure (SBP, DBP), brachial pulse pressure (PP), body weight before and after dialysis sessions, interdialytic weight gain (IDWG), blood urea, haematocrit, and haemoglobin concentration were calculated in every patient. Dry body weights had been set by the unit nephrologist according to established criteria [6], briefly, the lowest weight reached after dialysis when volume removal corrected clinical fluid overload and optimized blood pressure without symptomatic orthostatic hypotension. Dry weight was taken as the body weight on normal hydration status. The difference between mean post-dialysis weight and dry weight was used for assessing the water excess not removed by dialysis, and was referred as chronic overhydration. The urea reduction ratio was calculated: URR=1-(post-dialysis/pre-dialysis plasma urea). Blood pressure was recorded with sphygmomanometer on patients in seating position; phase V of Korotkoff sounds was used for DBP definition. Brachial PP was calculated by the difference between SBP and DBP. Hypertension was accepted when pre-dialysis blood pressures reached SBP
140 mmHg and/or DBP 90 mmHg. Forty-nine patients (36%) received antihypertensive drugs: angiotensin-converting enzyme (ACE) inhibitors in 20% cases, calcium channel blockers in 15%, ß-blockers in 5%, and others in 2%. All patients received oral calcium regularly as a supplement and/or phosphate binder, aluminium-containing phosphate binders were used in a few cases over a week period. Forty-one patients (30%) were treated with 1-25 (OH)2 vitamin D3, associated with calcium supplements. Dialysis fluid had 1.75 mmol/l calcium and 0.75 mmol/l magnesium concentrations in all three dialysis centres. Buffer bicarbonate was used in all cases.
The echocardiographic study was performed at the dialysis unit between 5 and 20 min after dialysis sessions in order to avoid acute cardiac modifications induced by the interdialytic volume gain. All studies included two-dimensional (2D), M-mode, Doppler colour flow imaging and pulsed and continuous wave Doppler modalities. Images were obtained from paraesternal long- and short-axis and two- and five-chamber apical and subcostal views. M-mode, 2D, and Doppler echocardiography was performed according to conventions proposed by the American Society of Echocardiography. 2D and 2D-directed M-mode echography was done for assessment of aortic and mitral valves structural alterations and calculation of left ventricular mass. Continuous and pulsed wave and colour Doppler were used for the study of valve functional changes. The highest pressure gradient across the aortic valve was calculated upon measurements of peak blood flow velocity.
Aortic calcification was defined upon increased thickness and bright echoes of the valve leaflets. Aortic stenosis was defined when the reduction of the mobility of the valve cusps reduced the systolic valve opening and increased the anterograde peak flow velocity 2.5 m/s across the valve [7]. Aortic regurgitation was diagnosed when a diastolic jet was observed at the left ventricle outlet tract by colour Doppler echography, and was classified as mild, moderate, or severe. With similar criteria, mitral annulus calcification and mitral regurgitation were diagnosed. Left ventricular mass was calculated using the formula described by Devereux [8]:
left ventricular mass (g)=1.04 (DIVS+LVDD+DPW)3 -LVDD3-13.6
where DIVS is the end-diastolic ventricular septum thickness, LVDD is the left ventricular (internal) end-diastolic dimension, and DPW is the end-diastolic posterior wall thickness, expressed in centimeters. The left ventricular mass index (LVMI) was calculated by correcting cardiac mass to body surface. Normal LVMI values were lower than 137 g/m2 in men and lower than 112 g/m2 in women [8]. Hypertrophy was defined as concentric when the septum or posterior wall thickness were >11 mm, and eccentric when septum and posterior wall thickness were 
11 mm.
Doppler echocardiography was performed by two cardiologists unaware of clinical data, recorded on super-VHS tape and revised by a third cardiologist (C.R.) without knowledge of the original results. Studies were made with an ATL HDI 3000 echocardiography instrument equipped with 2.5 MHz transducer probe.
Statistical analysis
Means and standard deviations were used as descriptive figures. Means were compared using Student's t-test for independent samples. 
2 test and OR were used for cross tabulation analysis of variables. The degree of association between variables was assessed by the first-degree Pearson's correlation. Logistic regression was used to predict the presence of LVH based on categories of valve alterations. Independent associations of LVMI with different variables were evaluated by stepwise multiple linear regression analysis. A 5% significance level was used in all cases. Data were processed using SPSS software for Windows, version No. 10.
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Results |
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Table 1
provides descriptive data of the clinical and biochemical status of patients over 1 year and the left ventricular mass echographic measurements. This was a middle-aged population with >6 years on dialysis treatment (mean). Sixteen per cent of patients were diabetics. High blood pressure was found in 60 (44%) patients, and isolated systolic hypertension in 47 (35%). Isolated systolic hypertension was highly prevalent (78%) among patients with high blood pressure. Blood pressure was higher in patients receiving antihypertensive drugs than in those without such treatment (149±16/84±8 vs 131±18/75±10 mmHg, respectively, P<0.001). The mean arterial PP was 58±12 mm in the population.
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Calcification of aortic valve cusps was present in 105 (78%) patients, and mitral annular calcification in 35 (26%). Combined aortic and mitral calcification was found in 32 (24%) cases (Table 2
). Three patients presented isolated mitral calcification, and 27 (20%) had non-calcified valves. Aortic calcification was associated with calcified mitral annulus more frequently than cases without aortic valve calcification (32/105 vs 3/30, P=0.032). Patients with two calcified valves were older and had spent longer time in dialysis than those without valve calcifications (65±12 vs 39±16 years, P<0.0005 and 91±48 vs 63±40 months, P=0.045, respectively). Patients with aortic valve calcification had serum Ca, PO4, and CaxPO4 product values (2.2±0.3, 1.74±0.53 mmol/l and 3.83 mmol2/l2, respectively) not significantly different from those found in patients without calcified aortic valves (2.2±0.2, 1.73±0.57 mmol/l and 3.8 mmol2/l2, respectively). However, cases presenting aortic calcification and stenosis had higher serum Ca than those without aortic calcification: 2.4±0.3 vs 2.2±0.2 mmol/l, respectively, P=0.03. In 86 studied patients, intact parathyroid hormone (PTH) levels were similar in calcified and non-calcified aortic valve groups: 391±421 vs 561±472 ng/l, respectively, P=0,16. There was insufficient data regarding serum C-reactive protein or other inflammation markers in our population as to analyse the role of chronic inflammation in the pathogenesis of cardiac valve calcification.
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SBP was not elevated in patients with aortic valve calcification; only the group presenting two calcified valves had SBP higher than patients without valve calcification (143±17 vs 134±21 mmHg, P=0.01). On the other hand, arterial PP was higher in patients with aortic valve calcification than those without (59±12 vs 53±13 mmHg, P=0.03), and it was highest in the group presenting two calcified valves (64±10 mmHg, P=0.01).
Aortic stenosis, according to defined echo-Doppler criteria, was observed in eight patients (6%) with valve calcification; there was one case of non-rheumatic calcified mild mitral stenosis. Echographic aortic regurgitation was present in 39 (29%) cases: 35 in calcified and four in non-calcified valves. Patients with aortic valve calcification were more likely to have valve regurgitation than patients without calcified aortic valves (35/105 vs 4/30, P=0.04, odds ratio (OR) for aortic regurgitation 3.250, 95% CI 1.052–10.042). Aortic regurgitation was mild in 36 and moderate in three cases. Mitral valve regurgitation was present in 45 patients (33%); it was mild in 34 (25%), moderate in nine (7%) and severe in two (1.5%) cases. Mitral regurgitation was more likely to be associated with calcified than non-calcified mitral annulus (18/35 vs 27/100, P=0.012, OR 2.86, CI 1.29–6.35). In patients with mitral regurgitation chronic overhydration was higher than in those without regurgitation: 0.96±0.9 vs 0.60±0.9 kg, P=0.03.
Valve disease and LVH
One hundred and ten patients (81.5%) had LVH, which was concentric in 94 (69.5%) and eccentric in 16 (12%). Mean LVMI values were 208.7±73.2 g/m2 for male and 170.8±57.9 g/m2 for female patients. The LVMI was higher in patients with aortic valve calcification than in those without calcified aortic valves (203±68 and 154±60 g/m2, respectively, P=0.001). The LVMI was also higher in the group presenting aortic regurgitation compared with those without valve regurgitation (224±71 and 179±64 g/m2, respectively, P=0.001). Due to the significant coincidence of aortic calcification and regurgitation, a logistic regression analysis for the risk of LVH was performed using these two valve alterations. Aortic valve calcification was the only independent predictor of LVH (B=1.672 SE=0.524, Wald 10.173, R=0.275, P=0.001; aortic regurgitation had a score=2.1, R=0.03, P=0.14). On the other hand, LVMI was not significantly different between patients with mitral calcification or regurgitation and those without these mitral alterations: LVMI was 211±70 g/m2 in mitral annular calcification and 185±68 g/m2 in non-calcified valve cases, P=0.07; and 202±59 g/m2 in mitral regurgitation and 187±73 g/m2 in non-regurgitating valve cases, P=0.24.
Factors associated with LVMI
The magnitude of the resistance to left ventricular outflow imposed by the aortic valve calcification was assessed by measuring the systolic peak flow velocity across the valve and calculating the trans-aortic pressure gradient. Peak flow velocities and maximal pressure gradients were higher through calcified valves compared with non-calcified cases: 1.65±0.53 vs 1.37±0.33 m/s, P=0.01 and 12.1±8.9 vs 7.9±3.6 mmHg, P=0.005, respectively. Figure 1 shows the frequency distribution of trans-aortic peak flow velocities in patients with or without valve calcification. Excluding from analysis eight aortic stenosis cases, peak flow velocity was still higher in calcified valves than in non calcified cases: 1.56±0.39 m/s vs 1.37±0.33 m/s, P=0.01; by definition, aortic stenosis cases had maximal peak flow velocity: 2.83±0.65 m/s, P=0.001 compared with non-stenotic calcified valves. Accordingly, the maximal pressure gradient in non-stenotic calcified aortic valves was higher than in normal valves: 10.4±5.3 vs 7.9±3.6 mmHg, P=0.005, and it was highest in aortic stenosis: 33.1±15.6 mmHg (P=0.004 compared with non-stenotic calcified valves).
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In the whole population the LVMI was directly related to aortic peak flow velocity: r=0.27, P=0.002; in the subgroup of patients with aortic valve calcification LVMI maintained a direct association with aortic peak flow velocity: r=0.225, P=0.024 (Figure 2
). Accordingly, LVMI and maximal pressure gradients were directly correlated in the population: r=0.25, P=0.005, and in the subgroup of patients with calcified aortic valves: r=0.204, P=0.042.
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Other factors usually associated with LVMI in chronic haemodialysis patients, such as blood pressure, sodium/water retention, and anaemia, were analysed. LVMI correlated with SBP and DBP: r=0.37, P<0.001 and r=0.28, P=0.002, respectively, and with the brachial arterial PP: r=0.38, P<0.0005 (Figure 3
). From LVMI components, septum thickness had stronger association with PP (r=0.34, P<0.001) than with ventricular diastolic dimension (r=0.20, P=0.02). No significant differences in LVMI were observed between the group of patients receiving ACE inhibitors and the group without antihypertensive treatment.
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The LVMI was related to the degree of anaemia, presenting an inverse correlation between LVMI and haemoglobin concentration (r=–0.25, P=0.005). Septum thickness was the parameter inversely associated with haemoglobin concentration (P<0.05); ventricular diastolic dimension was not (P=0.13). Regarding the hydration status, the LVMI correlated directly with chronic overhydration, namely the body water excess not removed by dialysis, r=0.21, P=0.018. There was a direct association between septum thickness and chronic overhydration (r=0.20, P=0.02). On the other hand, the LVMI and septum thickness were not related to the IDWG (P=0.23 and P=0.91, respectively); but the diastolic dimension had a direct linear association with IDWG: r=0.33, P<0.001.
Patients older than 65 years were at higher risk for LVH than younger patients: 51/57 vs 53/78, P=0.004, OR 4.01 (1.52–10.58).
To analyse the simultaneous influences of these and other covariates on LVMI, we performed a stepwise multiple linear regression in a model constructed with nine risk factors potentially related to cardiac hypertrophy in chronic dialysis patients: age at study, time on dialysis, body mass index, SBP, PP, haemoglobin concentration, chronic overhydration, trans-aortic peak blood flow velocity, and urea reduction ratio. Analysis revealed that four variables were independently associated with LVMI, in decreasing order of significance: PP, haemoglobin concentration (inverse relationship), trans-aortic peak flow velocity, and chronic overhydration (multiple r=0.502, multiple R2=0.252, ANOVA F-ratio=10.19, P<0.0005) (Table 3); other variables had no significant independent correlation with LVMI and were removed from the model. The same result was obtained when substituting trans-aortic pressure gradient for peak blood flow velocity.
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Discussion |
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The frequency of aortic valve calcification in this chronic dialysis population (78%) was higher than that found in other studies (28–55%) [4,5,9], this could be influenced by total calcium intake, regularly received as supplement or phosphate binder by all patients. Aortic valve calcification was prevalent in older patients and in those with a longer time on dialysis treatment, in accordance with earlier studies demonstrating the influence of age and dialysis duration on this process [4,5]. On the other hand, an association between valve calcification and high serum Ca, PO4, and CaxPO4 product was not found in our population. Increased calcium-phosphate product in chronic haemodialysis patients is a condition favourable for development of valve calcification [4]. However, this role has not always been recognized [5], and Ribeiro et al. [9] found no association between calcium-phosphate or PTH levels and aortic valve calcification. The predominance of aortic over mitral valve calcification (78–26%, combined involvement in 24%) suggests an influence of local factors at aortic level, other than metabolic conditions involved in valve disease. According to others [4], blood pressure was not higher in patients with calcified aortic valves, making this mechanical stress unlikely as a pathogenic factor. The finding of elevated arterial PP in patients with calcified aortic valves could be representative of the frequent association between aortic atherosclerosis, which accounts for high PP, and aortic valve calcification. In non-uraemic subjects Fendley-Stewart et al. [7] found that standard risk factors for atherosclerosis were similar to the factors associated with primary aortic valve calcification.
Aortic regurgitation was associated with (or produced by) valve calcification in most patients, there were only four cases (out of 39) with regurgitation in non-calcified valves. The presence of higher LVMI in patients with valve calcification, including aortic stenosis, and also in patients with valve regurgitation, suggests that cardiac hypertrophy is influenced by increased afterload produced by these valve alterations. When both aortic regurgitation and calcification cases were analysed simultaneously, only calcification held statistical significance for predicting the risk of LVH development. The coincidence of valve calcification and regurgitation in most patients is a probable explanation for this result.
Mitral regurgitation was present in 33% of our patients, a proportion higher than calcified cases (26%). Another study has reported 24% mitral regurgitation in cases of calcified mitral annulus [5]. Mitral incompetence was mostly mild (34 out of 45 cases), and was associated with higher values of chronic overhydration and/or the presence of mitral calcification. The finding of valve incompetence not associated with calcification in cases with high volume expansion, is suggestive of a hypervolaemic effect. It has been stated that cardiac dilatation plays a major role in the occurrence of mitral regurgitation [4]. Both mitral calcification and regurgitation were unrelated to the presence of LVH, but thicker interventricular septa were found in patients with calcified mitral annulus.
The long mean time spent on haemodialysis treatment is probably a factor for the high prevalence of cardiac hypertrophy observed in this population, whose mean LVMI was 192 g/m2. Foley et al. reported a mean LVMI of 161g/m2 in 227 patients within 1 year of starting dialysis treatment [10]. Progressive left ventricular parietal thickness has been associated with the duration of haemodialysis treatment [11].
The presence of higher left ventricular mass in patients with calcified aortic valves suggests a pathogenic link between these two conditions. Variable degrees of resistance to left ventricular outflow are produced in calcified valve cusps, and are related to the magnitude of tissue calcification [12]. In our study the presence of valve calcification was associated with higher trans-aortic peak flow velocities, reaching values superior to 2.5 m/s in eight patients (aortic stenosis). This threshold of peak flow velocity makes an arbitrary separation between calcification with and without stenosis, and does not represent substantial haemodynamic differences between both conditions. In patients with aortic peak flow velocities <2.5 m/s, calcified valve cases were still associated with higher peak velocities and pressure gradients than those without valve calcification. Blood flow velocity across calcified valves can be increased by two factors: reduced mobility of cusps with narrowing of valve luminal area and the magnitude of cardiac output. When cardiac output is low, flow velocities underestimate the severity of valve stenosis. Haemodialysis patients usually have high-normal or elevated cardiac outputs because of anaemia and arterio-venous shunts. On these conditions the trans-valve flow velocities and pressure gradients are a reliable assessment of the resistance to systolic ejection. The direct association between LVMI and trans-aortic flow velocities or pressure gradients was also found within the group with calcified valves. High trans-aortic pressure gradients promote LVH by the mechanism of increasing cardiac afterload.
In multiple regression analysis of factors associated with LVMI, age did not provide additional information when analysed simultaneously with trans-aortic peak flow velocity; this result is consistent with the concept that calcified and obstructive aortic valve disease is an age-associated process [7]. Our study confirmed the direct association between LVMI and the average values of pre-dialysis blood pressure. The LVMI was more closely related to SBP than to SBP, as has been reported previously [13]. Isolated systolic hypertension was found in 35% patients, representing 78% of patients with high blood pressure. Systolic hypertension is commonly observed in most haemodialysis patients, and accounts for wide-range PP [14]. We observed an elevated average PP at the brachial artery level (58±12 mmHg). The main determinants of the rise in SBP and PP are the increase in large-artery stiffness and wave reflection amplitude [15]. In our study, both SBP and PP had a fair direct association with LVMI as separate variables, but multiple regression analysis revealed that PP was a stronger independent factor of LVMI, and SBP did not provide additional information concerning ventricular mass. This result is in agreement with the earlier observation that aortic pulse wave velocity (a marker of aortic stiffness), and not mean blood pressure, was the independent variable significantly associated with left ventricular mass in chronic haemodialysis patients [16]. Ventricular hypertrophy has been found to be directly associated with high PP or arterial stiffness in chronic haemodialysis patients [16,17]. High PP augments the stroke work index by increasing the peak SBP, thus contributing to progressive LVH [18]. Decreased arterial distensibility raises the pulse wave velocity, and wave reflections return earlier and impact on the incident wave during systole, increasing aortic pressures and the left ventricular systolic stress [19].
Our findings show that increased PP (a marker of aortic atherosclerosis), and aortic valve calcification contribute separately to left ventricular enlargement.
These two different processes related to the same cardiac consequence have been linked to a common pathogenic factor. In more than 5000 subjects enrolled in the Cardiovascular Health Study, Fendley-Stewart et al. [7] observed that standard risk factors for atherosclerosis were similar to factors associated with aortic valve calcification, supporting the hypothesis of common mechanisms for both conditions.
Together with these factors of pressure overload, anaemia, overhydration, and the arterio-venous shunt promote LVH by increasing flow overload [20]. In our population anaemia and overhydration were independently associated with the magnitude of LVMI. We did not analyse the effects of arterio-venous shunt in this study. Chronic anaemia in haemodialysis patients increases cardiac output and cardiac work. Low haemoglobin levels induce cardiac hypertrophy through an increased stroke volume and hyperkinetic high-output state (flow/volume overload). At first, internal dimensions of the left ventricle increase, retaining normal the wall thickness/diastolic dimension ratio; later, chronically elevated cardiac output determines ventricular hypertrophy.
The inter-dialytic weight gain, a measure of the cyclic changes in volume, was associated with left ventricular dilatation, as has been described [21], but was not related to LVMI. On the other hand, the magnitude of chronic overhydration or residual post-dialysis volume excess was correlated with the left ventricular mass. In a previous study we observed that chronic overhydration was directly associated with pre-dialysis blood pressure levels [22]. It is possible that chronic overhydration promotes ventricular hypertrophy by combined mechanisms of volume and pressure overload.
In conclusion, the association between LVMI and the magnitude of valve resistance to ventricular outflow, measured by trans-valve peak flow velocities and pressure gradients, provides support for the hypothesis that aortic valve calcification contribute to development of LVH in chronic haemodialysis patients. The effect on LVMI appears to be independent of blood pressure, anaemia, and overhydration.
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Notes |
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Correspondence and offprint requests to: Dr José E. Ventura, SARI-Ibirapita 2743, Casilla de Correo 16217, CP11600, Montevideo, Uruguay. Email: jevent{at}elsitio.net.uy
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Accepted in revised form: 24. 5.02
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