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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4012_Библиотеки_им_академика_М_И_Перельмана
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Pulse Wave Velocity and Cardiovascular Morbidity …
127
Parameters
N =73
hypertension
28 (38.4)
Current smoking
19 (26)
Diabetes mellitus
7 (9.6)
Results are means±SD, n(%) or median (25
th
-75
th
percentiles).
Table 2. Cox-regression analysis for the impact of adjusted for
confounders carotid-femoral pulse wave velocity (c-f PWV) on overall
mortality in 73 patients on renal replacement therapy
p-value
Odds ratio
Confidence interval
c-f PWV
0.01
1.63
1.11-2.39
Kt/V for urea
0.01
46.01
2.4-863.05
LDL/HDL
0.5
0.8
0.4-1.5
hypertension
0.2
0.4
0.1-1.5
Dialysis vintage
0.08
0.9
0.8-1.01
Diabetes mellitus
0.2
0.23
0.02-2.24
Current smoking
0.38
1.8
0.46-7.44
age
0.1
1.04
0.98-1.11
sex
0.09
3.08
0.8-11.6
Figure 2. The impact of pulse wave velocity on death hazard function for 73 dialysis
patients during a median follow up time of 60 months(p=0.006, OR=1.5, 95%CI=1.12-
1.98).
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128
Table 3. Cox-regression analysis for the impact of adjusted for
confounders carotid-femoral pulse wave velocity (c-f PWV) on coronary
disease in 73 patients on renal replacement therapy
p-value
Odds ratio
Confidence interval
c-f PWV
0.03
1.4
1.02-1.98
Kt/V for urea
0.9
1.01
0.05-19.3
LDL/HDL
0.006
0.4
0.2-0.78
hypertension
0.8
1.1
0.4-3.1
Dialysis vintage
0.8
0.9
0.9-1.08
Diabetes mellitus
0.8
1.2
0.2-7.06
Current smoking
0.2
1.9
0.67-5.67
age
0.3
1.02
0.97-1.06
sex
0.1
1.9
0.7-5.07
Table 4. Differences between groups of patients according to the mean
value of carotid-femoral pulse wave velocity (c-f PWV) equal to
11.3 ± 1.83 m/s
Patients with
c-f PWV less than
11.3 m/s
(n = 39)
Patients with
c-f PWV more than
11.3 m/s
(n = 34)
Age (years)
57.6 ± 14.3
66.1± 14.6
*
Dialysis vintage (years)
7.2 ± 6.3
7.1± 5.9
Body mass index (BMI, Kg/m
2
)
24.2 ± 2.8
24.4 ± 3.1
Kt/V for urea
1.3 ± 0.2
1.3 ± 0.1
Normalized protein catabolic rate (nPCR,
g/Kg/day)
2.5 ± 0.4
2.2 ± 0.5
*
Serum bicarbonate concentrations (mEq/L)
21.3 ± 1.5
18.4 ± 2.03
*
LDL/HDL
2.3 ± 0.9
2.2 ± 0.7
HOMA-IR (mmol/L x μU/ml)
4.6 ± 3.5
6.1 ± 6.5
i-PTH(pg/ml)
132.8 ± 155.4
236.09 ± 218.2
*
hsCRP(mg/L)
6.08 ± 5.04
10.3 ± 5.9
*
oxLDL (ng/ml)
126.3 ± 152.8
140.8 ± 196.3
Albumin (gr/dl)
4.08 ± 0.27
3.8 ± 0.5
*
MBP (mmHg)
98.1 ± 11.9
98.4 ± 14.01
carotid-femoral pulse wave velocity
(c-f PWV, m/s)
9.9 ± 0.9
12.9 ± 1.1
*
carotid augmentation index (AIx, %)
23.2 ± 1.89
25.3 ± 1.96
*
Pulse pressure (mmHg)
55.3 ± 18.7
61.2 ± 20.4
Percent sodium removal (PSR, %)
1.7 ± 2.07
1.2 ± 2.5
Hemoglobin(gr/dl)
12.07 ± 1.1
11.6 ± 1.6
*
p < 0.05.
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Pulse Wave Velocity and Cardiovascular Morbidity …
129
In Table 4, the differences between the groups of patients with higher (n =
34) or lower (n = 39) than the mean value of c-fPWV (11.3 ± 1.83m/s) are
shown. We observed that the patients with c-fPWV> 11.3 had significantly
higher age, i-PTH and hsCRP, although they had significantly lower serum
albumin, nPCR and serum bicarbonate concentrations than the patients with c-
fPWV< 11.3. Additionally, the higher c-fPWV group of patients had increased
HOMA-IR values, pulse pressure, oxLDL and circulating monocytes, but
decreased urine volume excretion and sodium removal than the lower c-fPWV
group of patients.
Multivariable correlations showed that c-fPWV was positively associated
with i-PTH, hsCRP and PP, but inversely associated with serum bicarbonate
concentrations (Figure 3) (r = 0.261, p = 0.02, r = 0.400, p = 0.001, r = 0.346,
p = 0.003 and r = -0.719, p = 0.001 respectively).
DISCUSSION
It has been demonstrated that the renal replacement therapy significantly
improves the survival rate of end-stage renal disease patients, but the
underlying mechanism by which occurs such an improvement is not entirely
understood. Cardiovascular parameters are not completely corrected by
dialysis therapy. Cardiovascular disease is characterized by several cardiac and
arterial disorders in patients with end-stage renal disease. It has been already
reported that the arterial stiffness is a strong predictor of cardiovascular
mortality in general population and in dialyzed patients [19, 20]. Indeed, the
definition of arterial stiffness is increasingly used in the clinical assessment of
patients. Measurement of regional large arterial pulse wave velocity, such as
carotid-femoral pulse wave velocity (c-fPWV), is generally accepted to
determine the pathophysiological effects of arterial stiffness demonstrating a
predictive role on cardiovascular events [5, 6].
Pulse wave velocity is a major determinant of systolic hypertension,
increasing left ventricular afterload, left ventricular hypertrophy and left
ventricular oxygen consumption. Another consequence of arterial stiffening is
the decreased diastolic blood pressure, which is associated with altered timing
of wave reflection and decreased coronary perfusion contributing to ischaemic
heart disease [21].
Nevertheless, the relationship between arterial stiffness and renal
replacement therapy is still unclear, since the research results are inconsistent.
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Vaia D. Raikou
130
Figure 3. Correlation between c-fPWV and serum bicarbonate concentrations (r=-
0.719, p = 0.001).
In this study, c-fPWV was found as a significant independent predictor for
coronary disease manifestation, which is the main underlying cardiovascular
disorder in dialysis patients, adjusting for traditional and specific for these
patients confounders. Also, we notified that non-adjusted and adjusted for the
same confounding factors c-fPWV was a significant predictive factor for
overall mortality during our median follow up time of 60 months. However, in
our data Kaplan-Meier analysis did not demonstrate significant impact of
higher or lower c-fPWV on mortality rate.
Previous studies showed that c-fPWV is an excellent predictor of fatal
cardiovascular events and all-cause mortality in dialysis patients [4, 22] in
agreement with our findings. Additionally, recent study assessed the aortic-
brachial stiffness mismatch using the c-fPWV divided by carotid-radial pulse
wave velocity in 310 adults patients on dialysis and examined its effect on
mortality during a median follow up time of 29 months. The conclusion was
that aortic-brachial arterial stiffness mismatch was significantly associated
with increased mortality of the patients [23].
On the other hand, another recent study in a cohort of 391 adults (PACE
study) reported that PWV was not associated with left ventricular (LV) mass
after multivariable adjustment in incident hemodialysis patients, although
higher systolic, diastolic and pulse pressure were associated with higher LV
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Pulse Wave Velocity and Cardiovascular Morbidity …
131
mass and cardiovascular disorders regardless of timing with dialysis [24].
In the meantime, another study supported that hemodialysis patients with
intradialytic rise of systolic blood pressure had higher PWV and wave
reflections not affected by dialysis procedure [25].
These research results including our findings for non-significant impact of
higher or lower c-fPWV on mortality rate, despite the discovered significant
predictive value of non-adjusted and adjusted for confounders c-fPWV on
coronary disease and on overall mortality, may suggest that the relationship
between renal replacement therapy and arterial stiffness is not yet elucidated.
Moreover, in this chapter we observed that the patients with higher c-
fPWV were older and they had significantly higher i-PTH, hsCRP and
metabolic acidosis status, although significantly lower albumin and nPCR, in
comparison to the patients with lower c-fPWV. Also, they had elevated insulin
resistance, ox-LDL and pulse pressure values, but decreased sodium removal
comparatively to the lower c-fPWV group of patients. The sodium retention in
combination to increased pulse pressure in high c-fPWV group of patients
suggests that the arterial stiffness changes in our data could be originated
partly by volume overload. Indeed, it has been reported that PWV varies
during dialysis due to alterations in hydration status and also volume overload
plays an important role in the development of arterial stiffness in HD patients
[9, 26, 27]. In addition, our previous studies showed that pulse pressure
was influenced by both, hydration status alterations and arterial stiffness
defined by increased c-fPWV [28, 29]. The decreased diastolic blood pressure
due to increased PWV in combination to fluid overload depended systolic
hypertension result in increased pulse pressure [3].
Supportingly, in this chapter we observed that the correlation between c-
fPWV and PP, hsCRP and i-PTH was significantly positive. In agreement,
previous study reported significant correlation between CRP and PWV [30]
and it has been showed that i-PTH can promote vascular calcification and
arterial stiffness as a final consequence of a complicated function in dialysis
patients [31].
On the other hand, in this study we observed inverse correlation between
c-fPWV and serum bicarbonate concentrations and the group of patients with
higher c-fPWV had worse metabolic acidosis status, than the group of patients
with lower c-fPWV.
The worse acidosis state could be linked to lower albumin, lower nPCR,
higher insulin resistance and higher oxLDL values. Previously, we and other
authors have reported that acidosis promotes inflammation of the arterial wall,
releasing cytokines that may induce vascular calcification and arterial
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Vaia D. Raikou
132
stiffness, even whether the influence of acidosis on vascular function is
complicated [32, 33]. Also, the anti-anabolic and catabolic effect of acidosis is
known [34].
According to the findings of this chapter we could suggest that the good
regulation of liquids balance, the treatment of bone disease, the prevention
of inflammatory conditions and the correction of metabolic acidosis status,
affecting the arterial stiffening, are associated with the improvement of
mortality rate by renal replacement therapy in dialysis patients.
CONCLUSION
Carotid-femoral pulse wave velocity was found as a significant predictor
for coronary disease and overall mortality in dialysis patients.The hydration
status, bone disease, inflammation and uncorrected metabolic acidosis state
may be the main variables which impact on arterial stiffening and mortality of
these patients.
REFERENCES
[1] Guérin, Alain P., Pannier, Bruno, Marchais, Sylvain J., London, Gérard
M. Cardiovascular disease in the dialysis population: prognostic
significance of arterial disorders. Current Opinion in Nephrology &
Hypertension 2006; 15(2):105-110.
[2] Karras A., Haymann J. P., Bozec E., Metzger M., Jacquot C., Maruani
G. et al. Large Artery stiffening and remodeling are independently
associated with all-cause mortality and cardiovascular events in chronic
kidney disease. Hypertension. 2012;60:1451-7.
[3] Johnon R., Leopold J., Loscardo J. Vascular Calcification:
Pathobiological Mechanisms and clinical implications. Circulation
Research 2006; 99:1044-1059.
[4] Zoungas S., Cameron J. D., Kerr P. G., Wolfe R., Muske C., McNeil J. J.
et al. Association of carotid intima-medial thickness and indices of
arterial stiffness with cardiovascular disease outcomes in CKD. Am J
Kidney Dis. 2007;50:622-30.
[5] Rodriguez R. A., CroninV., RamsayT., ZimmermanD., RuzickaM.
and BurnsK. D. Reproducibility of carotid-femoral pulse wave velocity
https://t.me/med1917
Pulse Wave Velocity and Cardiovascular Morbidity …
133
in end-stage renal disease patients: methodological considerations.
Canadian Journal of Kidney Health and Disease. 2016; 3:20.
[6] Fischer E. C., Zócalo Y., Galli C., Wray S. and Bia D. Arterial Stiffness
and Renal Replacement Therapy: A Controversial Topic. International
Journal of Nephrology, 2015, Article ID 729609, 7 pages.
[7] Utescu M. S., Couture V., Mac-Way F. et al. “Determinants of
progression of aortic stiffness in hemodialysis patients: a prospective
longitudinal study,” Hypertension, 2013;62(1):154-160.
[8] CharitakiE. and DavenportA., “Do higher dialysate calcium
concentrations increase vascular stiffness in haemodialysis patients as
measured by aortic pulse wave velocity?” BMC Nephrology, 2013; 14
(1):189.
[9] HurE., UstaM., TozH. et al. “Effect of fluid management guided
by bioimpedance spectroscopy on cardiovascular parameters in
hemodialysis patients: a randomized controlled trial,”American Journal
of Kidney Diseases, 2013;61(6):957-965.
[10] KuraganoT., KidaA., FurutaM. et al. The Impact of β2-Microglobulin
Clearance on the Risk Factors of Cardiovascular Disease in
Hemodialysis Patients. ASAIO Journal 2010; 56:326-332.
[11] StenvinkelPeter, HeimbürgerOlof, PaultreFurcy et al. Strong association
between malnutrition, inflammation, and atherosclerosis in chronic renal
failure. Kidney International 1999; 55: 1899-1911.
[12] Chauveau P., Nguyen H., Combe C., Chêne G., Azar R., Cano N. et al.
French Study Group for Nutrition in Dialysis. Dialyzer membrane
permeability and survival in hemodialysis patients. Am J Kidney Dis.
2005;45(3):565-71.
[13] Daugirdas J. T. Second generation logarithmic estimates of single-pool
variable volume Kt/V: an analysis of error. J Am SocNephrol 1993; 4:
1205-1213.
[14] Silva E. A., Flexa F., Zanella. Impact of abdominal fat and insulin
resistance on arterial hypertension in non-obese women. MT Arq Bras
EndocrinolMetabol 2009;53(3):340-3.
[15] Kirschbaum B. Spurious metabolic acidosis in hemodialysis patients. Am
J Kidney Dis 2000;35:1068-1071.
[16] Daugirdas J. T. Simplified equations for monitoring Kt/V, PCRn, eKt/V,
and ePCRn. AdvRenReplace Ther 1995;2:295-304.
[17] Nitta K., Kawashima A., Yumura W. et al. Plasma concentration of
brain natriuretic peptide as an indicator of cardiac ventricular function in
patients on hemodialysis. Am J Nephrol 1998;18:411-415.
https://t.me/med1917
Vaia D. Raikou
134
[18] Asmar R., Benetos A., Topouchian J. et al. Assessment of arterial
distensibility by automatic pulse wave velocity measurement. Validation
and clinical application studies. Hypertension 1995; 26: 485-490.
[19] London Gérard M., BlacherJacques, Pannier Bruno et al. Arterial Wave
Reflections and Survival in End-Stage Renal Failure. Hypertension.
2001; 38:434-438.
[20] Shoji T., Emoto M., Shinohara K. et al. Diabetes mellitus, aortic
stiffness, and cardiovascular mortality in end-stage renal disease. J Am
SocNephrol. 2001; 12(10):2117-24.
[21] Mourad J. J., Pannier B., Blacher J. et al. Creatinine clearance, pulse
wave velocity, carotid compliance and essential hypertension. Kidney
Int. 2001; 59(5):1834-41.
[22] Blacher J, Safar ME, Guerin AP, Pannier B, et al. Aorticpulse wave
velocity index and mortality in end-stage renal disease. Kidney Int.
2003;63:1852-60.
[23] FortierC., Mac-WayF., DesmeulesS., MarquisK. et al. Aortic-Brachial
Stiffness Mismatch and Mortality in Dialysis Population. Hypertension.
2015;65:378-384.
[24] KimE. D., SozioS M., EstrellaM. M., JaarB. G. et al. Cross-sectional
association of volume, bloodpressures, and aortic stiffness with left
ventricularmass in incident hemodialysis patients: thePredictors of
Arrhythmic and Cardiovascular Riskin End-Stage Renal Disease
(PACE) study. BMC Nephrology, 2015; 16:131.
[25] Georgianos P. I., Mpoutsiouki F., Sabani E., Stamatiadis D. N. et al.
Hemodialysis patients with intradialytic rise in blood pressure display
higherbaseline aortic stiffness and negligible drop in augmentation index
withdialysis. IntUrolNephrol. 2016;48(4):601-8.
[26] Di Iorio, B., Nazzaro, P., Cucciniello, E., Bellizzi, V. Influence
of haemodialysis on variability ofpulse wave velocity in chronic
haemodialysis patients. Nephrol. Dial. Transplant. 2010;25:1579-1583.
[27] Zheng, D., Cheng, L. T., Zhuang, Z., Gu, Y., Tang, L. J., Wang, T.
Correlation between pulsewave velocity and fluid distribution in
hemodialysis patients. Blood Purif. 2009;27:248-252.
[28] RaikouV. D., TentolourisN., KyriakiD., EvaggelatouA., TzanatouH. B2-
microglobulin, pulse pressure and metabolic alterations in hemodialysis
patients. Nephron ClinPract 2011;117:c237-c245.
[29] RaikouV. D. Inflammation, arterial stiffness and cardiovascular
eventsin hemodialysis. Chapter in the Book“Hemodialysis, When,
https://t.me/med1917
Pulse Wave Velocity and Cardiovascular Morbidity …
135
How, Why.” Pub. Date: 2012 November. Section 7. Convective
Treatments,(29) pp. 413-426.
[30] Libby P., Ridker P. M., Maseri A. Inflammation and atherosclerosis.
Circulation. 2002; 105:1135-1143.
[31] Swarthout J. T., D’Alonzo R. C., Selvamurugan N., Partridge N. C.
Parathyroid hormone-dependent signaling pathways regulating genes in
bone cells. Gene. 2002; 282:1-17.
[32] Raikou V. D., Kyriaki D., BoletisJ. N. Arterial stiffness
and inflammation in patients on hemodialysisJournal of Molecular
Pathophysiology, 2012; 1(1): 21-28.
[33] London G. M., Drueke T. B. Atherosclerosis and arteriosclerosis in
chronic renal failure. Kidney Int. 1997; 51(6):1678-95.
[34] Mitch W. E., Bailey J. L., Wang X. et al. Evaluation of signals activating
ubiquitin-proteasome proteolysis in a model of muscle wasting. Am J
Physiol 1999;276:C1132-1138.
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