Scholarly article on topic 'Assessment of hypotension during dialysis as a manifestation of myocardial ischemia in patients with chronic renal failure'

Assessment of hypotension during dialysis as a manifestation of myocardial ischemia in patients with chronic renal failure Academic research paper on "Basic medicine"

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Abstract of research paper on Basic medicine, author of scientific article — Randa Aly Soliman, Mohamed Fawzy, Hussein Kandil, Alia Abd el Fattah

Abstract Introduction Intradialytic hypotension (IDH) remains to be a major complication of hemodialysis occurring in nearly 25% of dialysis sessions. It is a significant independent factor affecting mortality in hemodialysis patients. Autonomic nervous system dysfunction, blood sequestration in the setting of hypovolemia, cardiovascular diseases and increased plasma level of end products of nitric oxide metabolism are possible causes. In this controlled prospective study we examined patients with chronic renal failure and intradialytic hypotension to evaluate the relationship between this hypotension and myocardial ischemia after controlling other possible causes. Materials and methods Thirty patients with chronic renal failure who are on regular dialysis were enrolled. Before dialysis, patients were subjected to history taking and clinical examination. Echocardiography and several lab tests were done. Glomerular filtration rate (GFR) was calculated using Cockcroft’s and Gault formula. Autonomic dysfunction was also assessed. The dialysis session was standardized in all patients. Intradialytic blood pressure was monitored and hypotension was classified as mild (SBP>100mmHg), moderate (SBP 80–100) or severe (SBP<80). After dialysis, myocardial ischemia was assessed using stress myocardial perfusion imaging (MPI) (Pharmacologic stress testing using Dipyridamole) and is further classified as mild, moderate or severe ischemia. Patients with sepsis, hemoglobin level less than 9g/dL, diabetes mellitus, low cardiac output, coronary artery disease, significant valvular lesion or body weight below the dry weight of the patient were excluded from the study. Bronchial asthma, emphysema and severe COPD are contraindications to Dipyridamole and thus were also excluded from the study. Results Twenty patients had no or mild intradialytic hypotension whereas ten patients had moderate or severe hypotension. Among the first group, only two patients (10%) were found to have myocardial ischemia, while in the latter group, seven patients (70%) had myocardial ischemia that’s mostly moderate (p =0.002). Stress induced LV dysfunction was also significantly prevalent in patients with moderate or severe intradialytic hypotension as opposed to other group (p =0.002) LVED. Conclusions Patients with CKD and regular hemodialysis who experience moderate or severe intradialytic hypotension have significantly higher prevalence of myocardial ischemia and stress induced myocardial dysfunction, than those who experience no or mild intradialytic hypotension.

Academic research paper on topic "Assessment of hypotension during dialysis as a manifestation of myocardial ischemia in patients with chronic renal failure"

No. of Pages 6

The Egyptian Journal of Critical Care Medicine (2014) xxx, xxx-xxx

The Egyptian College of Critical Care Physicians The Egyptian Journal of Critical Care Medicine

http://ees.elsevier.com/ejccm www.sciencedirect.com

ORIGINAL ARTICLE

Assessment of hypotension during dialysis as a manifestation of myocardial ischemia in patients with chronic renal failure

Randa Aly Soliman a *, Mohamed Fawzy a, Hussein Kandil b, Alia Abd el Fattah a

a The Critical Care Department, Cairo university, Egypt b The Critical Department in the National Liver Institute, Egypt

Received 4 September 2013; revised 3 May 2014; accepted 15 May 2014

KEYWORDS

Intradialytic hypotension (IDH);

With chronic renal failure (CRF);

Myocardial perfusion; Imaging (MPI)

Abstract Introduction: Intradialytic hypotension (IDH) remains to be a major complication of hemodialysis occurring in nearly 25% of dialysis sessions. It is a significant independent factor affecting mortality in hemodialysis patients. Autonomic nervous system dysfunction, blood sequestration in the setting of hypovolemia, cardiovascular diseases and increased plasma level of end products of nitric oxide metabolism are possible causes. In this controlled prospective study we examined patients with chronic renal failure and intradialytic hypotension to evaluate the relationship between this hypotension and myocardial ischemia after controlling other possible causes.

Materials and methods: Thirty patients with chronic renal failure who are on regular dialysis were enrolled. Before dialysis, patients were subjected to history taking and clinical examination. Echocardiography and several lab tests were done. Glomerular filtration rate (GFR) was calculated using Cockcroft's and Gault formula. Autonomic dysfunction was also assessed. The dialysis session was standardized in all patients. Intradialytic blood pressure was monitored and hypotension was classified as mild (SBP > 100mmHg), moderate (SBP 80-100) or severe (SBP < 80). After dialysis, myocardial ischemia was assessed using stress myocardial perfusion imaging (MPI) (Phar-macologic stress testing using Dipyridamole) and is further classified as mild, moderate or severe ischemia. Patients with sepsis, hemoglobin level less than 9 g/dL, diabetes mellitus, low cardiac output, coronary artery disease, significant valvular lesion or body weight below the dry weight of the patient were excluded from the study. Bronchial asthma, emphysema and severe COPD are contraindications to Dipyridamole and thus were also excluded from the study.

Results: Twenty patients had no or mild intradialytic hypotension whereas ten patients had

* Corresponding author. Address: 20 Abou Hazem st., Madkour, Haram, Giza, Egypt. Tel.: +20 1222402018. E-mail address: randaalysoliman@hotmail.com (R.A. Soliman). Peer review under responsibility of The Egyptian College of Critical Care Physicians.

Elsevier I Production and hosting by Elsevier

2090-7303 © 2014 Production and hosting by Elsevier B.V. on behalf of The Egyptian College of Critical Care Physicians. http://dx.doi.org/10.1016/j.ejccm.2014.05.001

EJCCM 25 9 June 2014 ARTICLE IN PRESS No. of Pages 6

2 R.A. Soliman et al.

moderate or severe hypotension. Among the first group, only two patients (10%) were found to have myocardial ischemia, while in the latter group, seven patients (70%) had myocardial ischemia that is mostly moderate (p = 0.002). Stress induced LV dysfunction was also significantly prevalent in patients with moderate or severe intradialytic hypotension as opposed to the other group (p = 0.002) LVED.

Conclusions: Patients with CKD and regular hemodialysis who experience moderate or severe intradialytic hypotension have significantly higher prevalence of myocardial ischemia and stress induced myocardial dysfunction, than those who experience no or mild intradialytic hypotension.

© 2014 Production and hosting by Elsevier B.V. on behalf of The Egyptian College of Critical Care

Physicians.

1. Introduction

Intradialytic hypotension (IDH) remains to be a major complication of hemodialysis. It occurs in nearly 25% of dialysis sessions [1] and often requires aggressive resuscitative measures and sometimes premature termination of hemodialysis. It is also a significant independent factor affecting mortality in hemodialysis patients [2].

Despite the advances of machines with ultrafiltration control devices, modifying dialysate composition, temperature control, correction of nutritional deficiencies and treatment of anemia with erythropoietin therapy, many patients still have episodes of intradialytic hypotension. Among other factors, the major pathophysiology of these episodes is the removal of large volume of blood water and solutes over a short period of time, overwhelming normal compensatory mechanisms, which include plasma refilling and reduction of venous capacity (due to reduction of pressure transmission to veins).

In some patients, a seemingly paradoxical and inappropriate reduction of sympathetic tone may occur, causing reduction of arteriolar resistance, decreased transmission of pressure to veins with corresponding increase in venous capacity. Increased sequestration of blood in veins under conditions of hypovolemia reduces cardiac filling, cardiac output and ultimately blood pressure. Hypotensive episodes during hemodial-ysis in patients with end stage renal disease in the absence of inadequate maintenance of the plasma volume, pre-existence of cardiovascular disease, or autonomic nervous system dysfunction are accompanied by increased plasma concentrations of the end-products of nitric oxide metabolism (above the expected levels, based on the reduction of urea [3]).

In this controlled prospective study, patients with chronic renal failure and intradialytic hypotension episodes were thoroughly investigated, to evaluate the relationship between hypotension and myocardial ischemia after controlling other possible causes.

2. Patients and methods

This prospective study was conducted in King Fahd Hemodialysis unit in Kasr Al-Aini hospital, Hemodialysis Unit in Al-Zahraa hospital and Critical Care Medicine Department in Kasr Al-Aini hospital over the time period from February 2010 to June 2011. All patients included in the study provided informed written consent. The study includes 30 patients with chronic renal failure who receive regular hemodialysis sessions. Twenty patients developed hypotension during hemodialysis session, and the remaining 10 patients did not develop hypo-

Table 1 Baseline characteristics of the study group (n = 30).

Parameter Value [N (%) or mean ± SD]

Age (years) 44 ± 13

Weight (Kg) 66 ± 10

Male 12 (40)

Clinical

Smokers 7 (23)

Hypertension 12 (40)

History of chest pain 6 (20)

Family history of IHD 9 (30)

Autonomic neuropathy 9 (30)

AV fistula 23 (77)

Duration of hemodialysis (years) 3.7 ± 2.1

ECG and ECHO

Arrhythmia in ECG 4(13)

LVH in ECG 6 (20)

RWMA 5(17)

LVEDD (mm) 49.7 ± 5.4

LVESD (mm) 32.4 ± 4

EF (%) 62.3 ± 7.6

Grades of Albuminuria*

( + ) 6 (20)

(++) 7 (23)

(+ + +) 2(7)

Urine specific gravity 1009 ± 2.1

Hb (g/dL) 10.5 ± 0.73

Hct (%) 32.6 ± 2.9

TLC (103 cells/cmm) 6.1 ± 2.1

FBS (mg/dL) 70.2 ± 11.2

PPBS (mg/dL) 123.5 ± 15.2

HB A1C (mg/dL) 5 ± 0.59

Serum Triglycerides (mg/dL) 109.7 ± 43

Serum Cholesterol (mg/dL) 151 ± 60

Serum Urea (mg/dL) 129.8 ± 29.7

Serum Creatinine (mg/dL) 7.9 ± 2.1

GFR (ml/min/1.73 m2) 11 ± 4.2

Serum Sodium (mEq/L) 138 ± 5.8

Serum Potassium (mEq/L) 5.2 ± 0.63

IHD, ischemic heart disease; LVH, left ventricular hypertrophy;

RWMA, regional wall motion abnormalities; LVEDD, left ven-

tricle end-diastolic diameter; LVESD, left ventricle end-systolic

diameter; EF, ejection fraction Hb, hemoglobin; Hct, hematocrit;

TLC, total leukocytic count; FBS, fasting blood sugar; PPBS, post

prandial blood sugar; HB A1C, hemoglobin A1C; GFR, glomerular

filtration rate.

* Done only for the 15 patients who were not anuric.

EJCCM 25 9 June 2014 ARTICLE IN PRESS No. of Pages 6

Q1 Assessment of hypotension during dialysis as a manifestation of myocardial ischemia 3

Figure 1 Myocardial ischemia diagnosed by MPI in patients with moderate or severe intradialytic hypotension, in comparison to those with no or mild hypotension (p = 0.002).

78 tension during the sessions. Myocardial ischemia was assessed

79 in all patients using stress myocardial perfusion imaging (MPI)

80 (Pharmacologic stress testing using Dipyridamole).

81 Patients with sepsis, hemoglobin level less than 9 g/dL,

82 diabetes mellitus, low cardiac output, acute coronary

83 syndrome, significant valvular lesion or body weight below

84 the dry weight of the patient were excluded from the study.

85 Bronchial Asthma, emphysema and severe COPD are

86 contraindications to Dipyridamole and thus were also

87 excluded from the study.

88 2.1. Before dialysis

89 All eligible patients were subjected to full history taking and

90 clinical examination. Serum Urea and Creatinine were mea-

91 sured. Glomerular filtration rate (GFR) was calculated using

92 Cockcroft's and Gault equation. Autonomic dysfunction was

93 assessed using at least 2 of the following tests; blood pressure

94 (BP) response to standing, BP response to sustained handgrip,

95 Heart Rate (HR) response to standing, HR response to deep

96 breathing and HR response to valsalva. Positive result of

97 any test indicates autonomic dysfunction [4].

98 2.2. During dialysis

99 Dialysis was done via AV fistula (23 patients) or dialysis cath-

100 eter (7 patients), using Fresenius 4008B, Nipro machine with

101 ultrafiltration volume control and polysulfone, Fresenius F6

102 filters. Temperature of dialysate was kept at 36 0C. Blood

103 pump was kept between 250 and 350 ml/min except during

104 the hypotensive episodes during which the blood pump was

105 decreased to only 200 ml/min and not less to insure adequate

106 dialysis session. Dialysate flow was 500 ml/min. All dialysis

107 sessions lasted around 4 h.

108 BP is recorded using standard sphygmomanometer every

109 30 min in supine position. Each time the mean of 3 measure-

110 ments is recorded. Intradialytic hypotension is defined as a

111 symptomatic decrease of more than 30 mmHg in systolic blood

112 pressure or as an absolute systolic blood pressure under

113 90 mmHg [5]. Hypotension is further classified as mild (Sys-

114 tolic Blood Pressure (SBP) > 100 mmHg), moderate (SBP

115 80-100 mmHg) and Severe (SBP < 80 mmHg) [6].

Patients who required vasopressors were unstable and 116

accordingly were excluded from this study. 117

2.3. After dialysis 118

Within 2-5 h after dialysis, patients had both trans-thoracic 119

echocardiography and MPI. The echo was done using an 120

ATL machine HDI 5000 with the patient lying in the left lat- 121

eral decubitus using a 3.5 MHZ probe. MPI was done at the 122

nuclear laboratory of the critical care medicine department, 123

Kasr Al-Aini hospital, Cairo University utilizing the ''freeze 124

imaging protocol''. The set of SPECT images was acquired 125

using a triple head Siemens gamma camera with high resolu- 126

tion collimators (model Symbia E). Pharmacological stress 127

testing using Dipyridamole was done as most patients with 128

CKD could not achieve target HR during treadmill stress test- 129

ing due to marked physical limitations. 130

Patients were instructed to fast for at least 6-8 h, stop the- 131

ophylline medications for at least 24 h and not to have any caf- 132

feinated drinks or beverages for at least 24 h prior to the study. 133

Dipyridamole 0.56 mg/kg was diluted with 40 cc normal saline 134

and infused over 4 min. 2 min later, 20-25 mCi Tc-99 m Sestam- 135

ibi were injected intravenously through a wide bore cannula fol- 136

lowed by saline flush. Patients were monitored for at least 5 min 137

or till vital signs returned to baseline. Ambulant patients were 138

asked to walk for 4 min after Dipyridamole infusion. 139

Twenty projections were acquired (30 s for each frame) at 140

120 degree arc and total acquisition time of 12 min. SPECT 141

images were processed using the back-projection technique to 142

get trans-axial images then short axis, vertical long axis and 143

horizontal long axis cuts. The twenty-segment scoring system 144

was applied to estimate the Myocardium At Risk (MAR), 145

and the severity of perfusion defect was assessed for each seg- 146

ment using a ''0-4'' scoring system with ''0'' indicating normal 147

perfusion and ''4'' indicating no photon activity. The sum of 148

these scores is the Summed Stress Score (SSS). 149

Seventy two hours later, patients were re-injected with 20- 150

30 mCi Tc-99 m Sestamibi intravenously to acquire the second 151

set of SPECT images at rest, and to estimate the left ventricu- 152

lar ejection fraction (EF) utilizing the Gated SPECT tech- 153

nique. The severity of perfusion defects of MAR in this set 154

of SPECT images is assessed similarly and the sum of these 155

scores is the Summed Rest Score (SRS). 156

R.A. Soliman et al.

Table 2 Comparison of demographic, clinical, laboratory and MPI data between the 2 study groups.

Parameter Group A (n = 20) Group B (n = 10)

Age (years) 43.5 (33-54) 47.5 (28-58) 0.63

Weight (Kg) 65.5 (56-73) 67 (58-77) 0.81

Male 9(45) 3 (30) 0.69

Clinical

Smokers 5 (25) 2 (20) 1.0

Hypertension 7 (35) 5 (50) 0.69

Family history of IHD 5 (25) 4 (20) 0.43

Autonomic neuropathy 4 (20) 5 (50) 0.115

AV fistula 16 (80) 7 (70) 0.66

Duration of hemodialysis (years) 4 (3-6) 2.5 (1-4) 0.1

ECG and ECHO

Arrhythmia in ECG 1 (5) 3 (30) 0.095

LVH in ECG 3 (15) 3 (30) 0.37

RWMA 2(10) 3 (30) 0.30

LVEDD (mm) 52 (46.5-55) 44.5 (44-51) 0.046

LVESD (mm) 32 (30-35) 31.5 (28-34) 0.63

EF (%) 63 (56-70) 59.5 (56-62) 0.19

Grades of Albuminuria* n = 8 n = 7

( + ) 5/8 (62.5) 1/7 (14.3) 0.092

(++) 3/8 (37.5) 4/7 (57.1)

(+ + +) 0/8 2/7 (28.6)

Urine specific gravity 1010 (1008-1010) 1009 (1005-1010) 0.12

Hb (g/dL) 10.4 (9.8-10.9) 10.5 (10.3-11.3) 0.15

Hct (%) 31.9 (30.3-35) 33 (32.3-37) 0.098

TLC (103 cells/cmm) 5.4 (4.8-7.6) 5.2 (4-8) 0.74

FBS (mg/dL) 71 (60-80) 69 (62-76) 0.88

PPBS (mg/dL) 123 (116-131) 119 (108-134) 0.58

HB A1C (mg/dL) 4.9 (4.6-5.5) 4.8 (4.3-5.5) 0.42

Serum Triglycerides (mg/dL) 90.5 (80-117) 97 (75-170) 0.75

Serum Cholesterol (mg/dL) 135 (113-165) 117 (109-247) 0.55

Serum Urea (mg/dL) 138 (101-151) 121 (106-144) 0.4

Serum Creatinine (mg/dL) 8.4 (6.3-9.7) 7.7 (6.5-9) 0.63

GFR (ml/min/1.73 m2) 10.2 (7.9-12.4) 9.5 (8.9-12.6) 0.55

Serum Sodium (mEq/L) 138.5 (133-144) 138.5 (133-142) 1.0

Serum Potassium (mEq/L) 5.2 (4.7-5.5) 5.3 (5-6.1) 0.094

Ischemia (total count) 2(10) 7 (70) 0.002

Mild ischemia 1/1 (50) 1/7 (14.3) 0.417

Moderate ischemia 1/1 (50) 6/7 (85.7)

Scar 0 2 (20) 0.103

Stress induced LV dysfunction 2(10) 7 (70) 0.002

Data are displayed as n (%) or median (inter-quartile range).

IHD, ischemic heart disease; LVH, left ventricular hypertrophy; RWMA, regional wall motion abnormalities; LVEDD, left ventricle end-

diastolic diameter; LVESD, left ventricle end-systolic diameter; EF, ejection fraction; Hb, hemoglobin; Hct, hematocrit; TLC, total leukocytic

count; FBS, fasting blood sugar; PPBS, post prandial blood sugar; HB A1C, hemoglobin A1C; GFR, glomerular filtration rate.

* Done only for the 15 patients who were not anuric.

157 The difference between SSS and SRS is the Summed Differ-

158 ence Score (SDS). It is classified as follows; 0-4 indicates no

159 ischemia, 5-8 mild ischemia, 9-12 moderate ischemia and

160 more than 12 is severe ischemia.

161 2.4. Statistical methods

162 Statistical analysis was done using Statistical Package for

163 Social Sciences (SPSS) software, release 16.0.0 for Windows™

164 (SPSS Inc., Chicago, Illinois).

Categorical variables are described as frequency (n) and 165

percentage (%). Quantitative variables are described as 166

mean ± standard deviation (SD) whenever parametric. Non- 167

parametric quantitative variables are described as median 168

and interquartile range (IQR). Bivariate analysis of categorical 169

variables was done using Chi-square test with Yates Continu- 170

ity correction for 2 x 2 tables. Whenever cell frequency is <5, 171

Fisher's Exact test is used. 172

Comparison of two groups of quantitative variables was 173

done using Independent-Samples Student's t test for paramet- 174

ric data, and Mann-Whitney test for non-parametric data. 175

EJCCM 25 9 June 2014 ARTICLE IN PRESS No. of Pages 6

Q1 Assessment of hypotension during dialysis as a manifestation of myocardial ischemia 5

Figure 2 Stress induced LV dysfunction diagnosed by MPI in patients with moderate or severe intradialytic hypotension in comparison to those with no or mild hypotension (p = 0.002).

Figure 3 Left ventricular end-diastolic diameter in patients with moderate or severe intradialytic hypotension (44.5 mm [44—51]) in comparison to those with no or mild intradialytic hypotension (52 mm [46.5-55]) (p = 0.046).

176 In all cases, the 2-sided significance was always taken as p

177 value. p value <0.05 is considered statistically significant.

178 3. Results

179 Thirty patients were included in this study. Their baseline

180 characteristics are listed in Table 1.

181 We found that 70% (7/10) of patients who had moderate or

182 severe hypotension (Group B) had myocardial ischemia on

183 MPI, in comparison to 10% (2/20) of patients who experienced

184 no or mild intradialytic hypotension (Group A); a difference

185 that is statistically significant (p = 0.002) (Fig. 1).

186 Several other variables were compared across both study

187 groups (Table 2). It is to be noted that patients of Group B

188 were more likely to have stress induced LV dysfunction on

189 MPI (7/10, 70%) than patients of Group A (2/20, 10%)

190 (p = 0.002) (Fig. 2). LVED was wider in Group A (Median

52mm, IQR 46.5-55) than in Group B (44.5 mm, 44-50.75) 191

(p = 0.046) (Fig. 3). 192

4. Discussion 193

Intradialytic hypotension (IDH) is a major complication of 194

hemodialysis. Two to four liters of fluid needs to be removed 195

during a regular session, equivalent to 40-80% of the blood 196

volume. It is therefore not surprising that hypotension occurs 197

so often. Although many factors - patient or treatment related 198

- play a role, a reduction of blood volume is crucial in its path- 199

ogenesis [1]. 200

Hypotension is one of the clinical presentations of CVD in 201

patients with CKD [7]. There are a number of possible expla- 202

nations for the independent association of reduced GFR and 203

CVD outcomes. First, a reduced GFR may be associated with 204

an increased level of nontraditional CVD risk factors that fre- 205

6 R.A. Soliman et al.

206 quently are not assessed in many studies. Second, reduced

207 GFR may be a marker of undiagnosed vascular disease or

208 alternatively a marker of the severity of diagnosed vascular

209 disease, especially in high or highest risk populations. Third,

210 reduced GFR may have had more severe hypertension or dysl-

211 ipidemia and therefore have suffered more vascular damage

212 secondary to hypertension or dyslipidemia. Fourth, recent

213 studies have suggested that subjects with reduced GFR are less

214 likely to receive medications or therapies such as angiotensin

215 converting enzyme inhibitors, B-blockers, aspirin, platelet

216 inhibitors, thrombolytics, or percutaneous intervention than

217 patients with preserved GFR. Perhaps as important was the

218 fact that in the same studies, patients with reduced GFR

219 who did receive the above interventions obtained similar ben-

220 efit as patients with preserved GFR. Finally, decreased GFR

221 itself may be a risk factor for progression of ventricular remod-

222 eling and cardiac dysfunction [7].

223 Different studies stated that, during hemodialysis, patients

224 are particularly susceptible to myocardial ischemia for number

225 of reasons including: LV hypertrophy [8], intradialytic hypo-

226 tension and instability [9], high prevalence of decreased coro-

227 nary flow reserve even in the absence of coronary vessel

228 stenosis [10,11].

229 Hakeem et al. [12] reported that in patients with CKD 40%

230 of perfusion scans were abnormal (SSS P 4) with 20% mild

231 defects and 20% moderated to severe defects.

232 Q4 In line with Hakeem's result, we found that patients who

233 experience moderate or severe intradialytic hypotension have

234 significantly higher prevalence of myocardial ischemia (70%,

235 7/10), in comparison to those who have no or mild intradialyt-

236 ic hypotension (10%, 2/20) (p = 0.002).

237 Paoletti et al. [13] stated that there is growing evidence that

238 patients with CKD have unrecognized LV dysfunction, both

239 systolic and diastolic. They also pointed at the importance of

240 LV dysfunction (LV ejection fraction <40%) as a predictor

241 of cardiac death in patients with CKD.

242 We similarly found that CKD patients who develop moder-

243 ate or severe intradialytic hypotension, have significantly

244 higher prevalence of stress induced LV dysfunction (70%, 7/

245 10) than those who have no or mild hypotensive episodes

246 (10%, 2/20) (p = 0.002).

247 Deterioration of renal function in CKD may lead to dysli-

248 pidemia or accumulation of uremic toxins, which can stimulate

249 oxidative stress and inflammation, which in turn contributes to

250 endothelial dysfunction and progression of atherosclerosis

251 [14]. Renal failure causes changes in plasma components and

252 endothelial structure and function that favor vascular injury,

253 which may play a role as a trigger for inflammatory response.

254 Dyslipidemia associated with CKD contributes to the inflam-

255 matory response in renal failure [15]. However, in our study

256 we found that levels of serum cholesterol and triglycerides were

257 not significantly different between the two study groups, a

258 finding probably attributed to the small number of the study

259 group and the relatively low economic standard of those

260 patients.

261 Patients with CKD also have a high prevalence of arterio-

262 sclerosis and remodeling of large arteries. Remodeling may

263 be due to either pressure overload - which is distinguished

264 by wall hypertrophy and an increased wall-to-lumen ratio -

265 or flow overload, which is characterized by a proportional

266 increase in arterial diameter and wall thickness [16].

In conclusion, we found that patients with CKD and regu- 267

lar hemodialysis who experience moderate or severe intradia- 268

lytic hypotension have significantly higher prevalence of 269

myocardial ischemia and stress induced myocardial dysfunc- 270

tion, than those who experience no or mild intradialytic 271

hypotension. 272

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