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Department of Medicine & Therapeutics, Center for Nutritional Studies, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong.
Correspondence to Dr. Angela Y. M. Wang, Department of Medicine & Therapeutics, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin N.T., Hong Kong. Phone: 852-2632-3129; Fax: 852-2637-5396; E-mail: awang{at}cuhk.edu.hk
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Abstract |
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Autopsy studies have consistently shown an association between coronary artery calcifications and atherosclerosis (16,17). These studies also noted an association between coronary artery calcification and cardiac VC. In addition, presence of coronary artery calcification was shown to be predictive of coronary artery disease in individuals both with and without renal failure (18), indicating that both atherosclerosis and calcification may be sharing similar pathogenetic mechanisms. Recent studies noted associations among inflammation, malnutrition, and atherosclerosis (19). Inflammation has been shown to increase risk of atherosclerosis in individuals both with (20,21,22) and without renal failure (23,24). One study also reported an association between hypoalbuminemia and vascular disease (25). Whether calcification of cardiac valves shares similar pathogenetic factors as atherosclerosis or should be considered as part of the atherosclerotic process remains unknown. We therefore undertook this study to determine the prevalence of cardiac VC in end-stage renal failure patients who were on continuous ambulatory peritoneal dialysis (CAPD) and to identify risk factors associated with the development of cardiac VC. In particular, we examined the possible role of inflammation and malnutrition in VC in dialysis patients.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Echocardiography
Echocardiography was performed using a Vingmed GE System V sonographic
machine and a 3.3-MHz probe. All echocardiographic images were analyzed by
cardiologists who were blinded to clinical details of patients. VC was defined
as bright echoes on one or more cusps of more than 1 mm in either mitral or
aortic valves or both. Sensitivity and specificity for echocardiographic
detection of calcium in both the mitral and the aortic valves have been
reported to be 76% and 89 to 94%, respectively
(26).
Data Collection
Demographic data including age at study, gender, duration on dialysis,
presence of underlying diabetes, underlying cause of renal failure, and
smoking history were collected. Study participants were classified as current
smoker (if they were still smoking), ex-smoker (if they had quitted smoking),
or non-smoker (if they had never smoked). Both current and ex-smokers were
considered to have positive smoking history. Systolic and diastolic BP was
measured on every follow-up visit. Serum biochemical parameters were collected
on every regular follow-up visit at 6- to 8-wk intervals preceding
echocardiography in each patient, and these results were averaged to obtain a
mean value for each measurement. They included measurements of hemoglobin,
hematocrit, plasma calcium, phosphate, alkaline phosphatase, parathyroid
hormone (PTH), and calculations of the calcium x phosphate product (Ca
x PO4). Other biochemical parameters, including PTH and lipid
profile (which include total cholesterol, HDL cholesterol, LDL cholesterol,
and triglyceride [TG]) were measured every 3 mo, and the results also were
averaged to obtain a mean value. PTH was determined by Immulite immunoassay
(Diagnostic Products Corporation, Los Angeles, CA). Total, HDL, and LDL
cholesterol and TG were measured after overnight fasting. Systolic and
diastolic BP and all other biochemical data also were collected for the 12 mo
preceding echocardiography or before parathyroidectomy if this had been
done.
Assessment of Inflammation
Degree of inflammation was assessed by levels of C-reactive protein (CRP)
and fibrinogen. CRP was measured using an immunoassay kit (Berkman, Fullerton,
CA). The detection limit of CRP is 0.1 mg/L. Levels below 0.1 mg/L are
expressed as 0.1 mg/L. Fibrinogen was measured by a prothrombin time-derived
and turbidimetric clot detection method using the ACL Futura (Instrumentation
Laboratory, Lexington, MA). Basal metabolic rate was performed in all patients
using indirect calorimetry after having an overnight fast for 12 h and was
expressed in kilocalories per kilogram of dry body weight. Dry body weight was
defined as the body weight measured after the abdomen was completely drained
of peritoneal fluid.
Assessment of Nutritional Status
Nutritional status was assessed on the basis of the following parameters:
body weight and height, body mass index (the weight in kilograms divided by
the square of the height in meters), serum albumin, handgrip strength (HGS),
and subjective global nutrition assessment (SGNA). Serum albumin was measured
using the bromcresol purple method. Bimonthly serum albumin was averaged for
the 12 mo preceding echocardiography or before parathyroidectomy if this had
been done. Nutritional status was assessed by experienced research staff using
SGNA (27), and patients were
graded to have normal, mild, moderate, or severe malnutrition status
accordingly. Research staff who performed SGNA were blinded to all clinical
and biochemical details of patients. HGS was assessed using a hand
dynamometer. HGS of the nondominant arm was measured three times, and the
average of the best two readings was taken to be the final HGS
(28).
Statistical Analyses
Statistical analysis was performed using SPSS 10.0 for Windows software
(SPSS, Inc., Chicago, IL). Results are presented as mean ± SD for
normally distributed data and as median (interquartile range) for data not
normally distributed. Categorical data were compared between groups by
2 test. Continuous data were compared between groups using
unpaired t test for normally distributed variables or using
Mann-Whitney U test for variables not normally distributed. Multiple
logistic regression analysis was performed to assess the relative importance
of the different risk factors associated with cardiac VC. Significance was
taken at the 5% level.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Clinical, biochemical, and nutritional parameters were compared between patients with no cardiac VC (No VC group; n = 93) and patients who had either mitral or aortic VC or both, grouped together as VC group (n = 44). The demographic data of patients with and without VC are shown in Table 1. No difference was noted in the gender distribution between patients with and without VC. Patients with cardiac VC were significantly older (60 ± 10 versus 54 ± 12 yr; P = 0.005). Indeed, the prevalence of VC was much higher in patients age 51 or older compared with those younger than 50 (Figure 1A). There also was a trend toward longer duration of dialysis (45 [25, 75] versus 36 [21, 57] mo; P = 0.177; Figure 1B) and higher incidence of diabetes (36 versus 26%; P = 0.230) among patients with VC, although it was statistically insignificant. Positive history of smoking was noted in a greater percentage of patients with VC compared with those with no VC (50 versus 33%; P = 0.090; Table 1).
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In terms of calcium-phosphate metabolism, patients with VC showed significantly higher mean plasma calcium (2.64 ± 0.19 versus 2.57 ± 0.17 mmol/L; P = 0.022), phosphate (1.89 ± 0.52 versus 1.64 ± 0.41 mmol/L; P = 0.003), and resulting higher Ca x PO4 product (5.01 ± 1.46 versus 4.24 ± 1.11; P = 0.003) compared with patients with no VC (Table 2). Indeed, the prevalence of calcification seemed to be especially increased with plasma calcium over 2.8 mmol/L or phosphate over 2.5 mmol/L or Ca x PO4 product over 4 (Figure 2, A through C). VC patients also had more severe hyperparathyroidism as indicated by higher ALP (149 [113, 274] versus 111 [83, 163] mmol/L; P = 0.001) and PTH (83 [40, 145] versus 38 [16, 71] pmol/L; P = 0.001) compared with patients with no VC (Table 2). The prevalence of VC was increased especially in patients with PTH over 100 pmol/L (Figure 2D). History of parathyroidectomy was noted in 14% patients with VC versus 3% patients with no VC (P = 0.031). No difference was noted in the percentage of patients who received vitamin D therapy (VC versus no VC group, 50 versus 39%, respectively; P = 0.096; Table 2).
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One-yr mean systolic and diastolic BP was not significantly different between patients with and without VC. However, patients with VC were using a slightly higher number of antihypertensives for BP control compared with patients with no VC (1.68 ± 1.09 versus 1.48 ± 1.07; P = 0.317), although it was statistically insignificant. No difference was noted in the mean total, HDL, and LDL cholesterol and TG between patients with and without VC. The percentage of patients who were treated with lipid-lowering drugs also was similar between patients with and without VC. There was a trend toward lower hemoglobin in the VC group (9.1 ± 1.3 versus 9.5 ± 1.6 g/dl; P = 0.123). However, no difference was noted in the frequency of erythropoietin (EPO) use for patients with and without VC (Table 2). Despite a tendency toward a lower hemoglobin, VC patients who were receiving EPO received a higher cumulated EPO dosage (192 [106, 192] versus 185 [96, 192] x 103 units; P = 0.174) compared with those with no VC.
Patients with VC were significantly more malnourished than patients with no VC. This was reflected by the more severe degree of hypoalbuminemia (26 ± 4 versus 29 ± 3 g/L; P = 0.004) and lower HGS in patients with VC (12 [8, 18] versus 16 [8, 23] kg; P = 0.051; Table 3). The prevalence of VC was particularly increased in patients with serum albumin below 28 g/L (Figure 3A) or HGS below 20 kg (Figure 3B). Twenty-three percent of patients with VC versus 17% of patients with no VC were graded to have moderate to severe malnutrition according to subjective global assessment (Table 3). Patients with VC also had a higher degree of inflammation as denoted by higher CRP (4.5 [0.1, 13.4] versus 0.2 [0.1, 4.4] mg/L; P = 0.004) and higher fibrinogen (6.6 ± 1.9 versus 5.7 ± 1.3 g/L; P = 0.002; Table 3). Indeed, the prevalence of calcification was especially increased when CRP was more than 5 mg/L (Figure 3C) or fibrinogen was more than 6 g/L (Figure 3D). There also was a trend toward a higher basal metabolic rate (22.3 ± 3.6 versus 21.2 ± 3.6 kcal/kg dry body weight; P = 0.109) for patients with VC, although it was statistically insignificant. No significant correlation, however, was noted between CRP and basal metabolic rate. Only very weak association was noted between fibrinogen and basal metabolic rate (R = 0.17, P = 0.007), which suggests that the presence of inflammation may not necessarily be associated with increase in resting energy expenditure.
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Even after adjustment for the effect of age, duration of dialysis and diabetes, Ca x PO4 product (odds ratio [OR], 2.17; 95% confidence interval [CI], 1.44 to 3.27; P = 0.0002), serum albumin (OR, 0.85; 95% CI, 0.75 to 0.96; P = 0.01), and CRP (OR, 1.05; 95% CI, 1.01 to 1.10; P = 0.026) remained strongly associated with cardiac VC in CAPD patients (Table 4).
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Indeed, the prevalence of VC was studied in relation to the total number of
risk factors present, namely high Ca x PO4 product 
5,
malnutrition (as denoted by serum albumin 
28 g/L), and inflammation (as
indicated by CRP 10 mg/L). A significant stepwise increase in the
prevalence of VC was noted with the presence of increasing number of
calcification risk factors (number of risk factors, 0 [21%] versus 1
[24%] versus 2 [52%] versus 3 [86%]; P < 0.001;
Figure 4).
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Interaction among CRP, albumin, and Ca x PO4 in
predisposing patients to VC is shown in
Figure 5. Calcification was at
its lowest prevalence (20.8%) when Ca x PO4 < 5 and there
was no evidence of malnutrition and inflammation (M-ve, I-ve: albumin >28
g/L; CRP <10 mg/L). Prevalence of VC increased in the presence of either
malnutrition (M+ve, I-ve: albumin 28 g/L; CRP <10 mg/L) or inflammation
(M-ve, I+ve: albumin 28 g/L; CRP 10 mg/L), indicating an independent
contribution of inflammation and malnutrition to this increased risk of
calcification. The prevalence of VC increased significantly to 57% in the
presence of both malnutrition and inflammation without an increased Ca x
PO4 product (M+ve, I+ve: albumin 28 g/L; CRP 10 mg/L),
indicating possible synergism of these two factors in predisposing to VC
(Figure 5A). However, among
patients with Ca x PO4 product 5
(Figure 5B), prevalence of VC
was only 25% without evidence of malnutrition and inflammation (M-ve, I-ve).
The prevalence increased in the presence of either inflammation (M-ve, I+ve)
or malnutrition (M+ve, I-ve), suggesting an independent contribution of
inflammation and malnutrition, other than high Ca x PO4
product, to this increased risk of VC. The prevalence of calcification was the
highest (85.7%) when both malnutrition and inflammation (M+ve, I+ve) coexisted
with a Ca x PO4 product 5. This indicated that
inflammation, malnutrition, and high Ca x PO4 all contributed
significantly and independently to an increased risk of VC. That the presence
of both inflammation and malnutrition substantially increased the risk of
calcification more than the presence of either factor alone, irrespective of
the Ca x PO4 product level, confirmed synergism of these two
factors in predisposing to VC.
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Consistent with previous studies (31,33,34,35), we noted that patients with VC were significantly older. The prevalence of VC was significantly higher in patients who were older than 50 yr (38%) compared with those who were younger than 50 yr (19%). With logistic regression analysis, age was one of the most important predictor for VC. We also noted a trend toward increased risk of VC with increasing duration on dialysis, although not as significant as that reported previously (33). However, because nearly 40% of the VC was already present within first 3 yr on dialysis (Figure 1B), a prospective study will be needed to determine whether calcification is already present at the time of initiation of dialysis or it develops subsequently during dialysis. This will provide further evidence regarding whether potential risk factors for VC should be modified as early as in the predialysis phase of chronic renal failure to prevent subsequent development of VC.
Our data are compatible with previous reports of VC in dialysis patients (33,35) in that elevated Ca x PO4 product was strongly associated with the development of VC. The risk of VC increased markedly with Ca x PO4 product above 4, and this risk increased further with increasing Ca x PO4 product. A Ca x PO4 product of 7 or above was invariably associated with the development of VC (Figure 2C). This increase in Ca x PO4 product was associated with an increase in both plasma calcium and phosphate, although more significantly so for phosphate. The risk of VC in our PD patients was particularly increased when plasma calcium was more than 2.8 mmol/L (Figure 2A) or phosphate was more than 2.5 mmol/L (Figure 2B). This degree of hyperphosphatemia was related partly to secondary hyperparathyroidism, which itself also strongly predisposed to VC. Significant positive correlation was noted between the level of PTH and the degree of hyperphosphatemia (R = 0.505, P < 0.001). This suggests that more effective treatment of secondary hyperparathyroidism may improve both calcium and phosphate control and hence reduce the development of VC in dialysis patients.
Valvular calcification also was observed in patients without hypercalcemia, hyperphosphatemia, and hyperparathyroidism, indicating that other factors may be responsible for the development of VC. Our study clearly demonstrated a novel association of inflammation and malnutrition with VC in dialysis patients. Previous studies suggested a strong association among malnutrition, inflammation, and atherosclerosis (MIA syndrome) in chronic renal failure patients (19). An association between hypoalbuminemia and vascular disease also has been reported in dialysis patients (25). In our study, we demonstrated an increase in the risk of valvular calcification with increasing inflammation as denoted by increased circulating CRP and fibrinogen. A strong association also was noted between the degree of hypoalbuminemia and valvular calcification. Likewise, other nutrition markers, including HGS and SGNA, showed similar association with VC. However, further prospective studies are needed to determine whether malnutrition triggers the inflammatory process or vice versa.
Our finding provides support for the concept that VC not only is a passive,
degenerative process but also involves active inflammation similar to that
seen with atherosclerosis of central and peripheral arteries. Indeed, recent
studies showed that using Salmonella typhi vaccine to generate an
acute systemic inflammatory response causes temporary but profound dysfunction
of vascular endothelium in humans, confirming the role of inflammation in
initiating atherosclerosis
(36). We hypothesized that
cardiac VC, like atherosclerosis, involves active inflammation with valvular
endothelial damage and macrophage activation, which further lay down
osteopontin and enhance VC
(37). Indeed, the role of
inflammation in VC is evidenced by the accumulation of macrophages and T
lymphocytes other than LDL and lipoprotein(a) in early aortic VC
(36,
38,
39). Within regions of
lipoprotein accumulation are areas of microscopic calcification, and
macrophages within the lesions produce osteopontin, a protein that further
modulates tissue calcification
(40). Osteopontin also
coexists similarly with intimal macrophages in calcific human mitral annulus,
indicating that cardiac VC is indeed an actively mediated phenomenon
(41). Recent findings of
increased circulating soluble adhesion molecules in patients with nonrheumatic
aortic stenosis also adds strength to the hypothesis that inflammation
underlies the VC process (42).
Indeed, increased circulating soluble adhesion molecules have been reported to
be associated with malnutrition, inflammation, cardiovascular disease, and
mortality in predialysis patients
(43). However, more recent
studies also noted that tumor necrosis factor-
, a proinflammatory
cytokine secreted mainly by macrophages, enhanced in vitro
calcification of vascular cells by increased expression and activity of
alkaline phosphatase, an enzyme important in matrix mineralization
(44). This finding, together
with previous reports of mice showing an association between tumor necrosis
factor- and calcified vascular lesions
(45), provides further
evidence that inflammation does play an active role in mediating the process
of calcification. The presence of increased CRP and fibrinogen, together with
hypoalbuminemia and lower HGS in CAPD patients with VC, is consistent with the
hypothesis that inflammation and malnutrition mediate the valvular
calcification process other than the presence of uncontrolled
hyperphosphatemia, hyperparathyroidism, and resulting high Ca x
PO4 product.
Previous autopsy studies showed an association between coronary artery calcification and atherosclerosis (16, 17). These studies also confirmed a link between coronary artery calcification and cardiac VC (16, 17). Moreover, significant correlation was noted between valvular calcification and aortic atheroma in nonuremic patients, indicating that valvular calcification may indeed be a marker for atherosclerosis of the aorta (46). Our current study demonstrated that certain risk factors for atherosclerosis, such as positive smoking history and presence of diabetes, also increased risk of VC. Although no significant difference was noted in the average systolic and diastolic BP between patients with and without VC, there was a trend toward a greater number of antihypertensive use among patients with VC. There also was higher preponderance of VC among patients with renal failure secondary to hypertensive nephrosclerosis. These findings indicate that both cardiac VC and coronary atherosclerosis may indeed be associated syndromes, with the severity of VC reflecting the extent of coronary atherosclerosis.
It is intriguing to note, however, that although both calcification and atherosclerosis shared similar association with inflammation and malnutrition, some other established risk factors for atherosclerosis, such as male gender and hyperlipidemia, were not shown to increase risk of VC. On the contrary, there was a trend toward lower total, HDL, and LDL cholesterol as well as TG in patients with VC, although it was statistically insignificant. There also was no difference in the use of lipid-lowering therapy between patients with and without VC. One possible explanation is that different risk factors act at different time points in the process of VC. As VC involves a very long-standing process and probably represents the end stage of an active disease process (36), the importance of lipid status as well as hemodynamic factors in the early development of VC may have been underestimated when only 1-yr data preceding echocardiography were used to predict the subsequent risk of calcification. Further prospective studies with baseline as well as serial echocardiographic and biochemical measurements will be needed to clarify the role of hyperlipidemia and hypertension in VC in dialysis patients.
In summary, apart from confirming the importance of aging, diabetes, uncontrolled hyperphosphatemia, and hyperparathyroidism in the development of VC, our study demonstrates a strong association of inflammation and malnutrition with cardiac VC, similar to that of atherosclerosis (MIA syndrome). This finding is in keeping with the concept that calcification and atherosclerosis are associated syndromes and that cardiac VC may be a marker for the presence of underlying coronary or generalized atherosclerosis. The presence of calcification of cardiac valves may be the tip of the iceberg, representing underlying generalized atherosclerosis and vascular calcification. Further prospective long-term studies with baseline echo-cardiographic measurements relating the presence of inflammation and malnutrition to the development of cardiac VC as well as coronary artery disease and mortality will be required to answer this important question.
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Acknowledgments |
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References |
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valve calcification (VC); 
, VC.
