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![Page 1: Chronic Kidney Disease In Acute Coronary Syndrome Prof. Dr. Alia Abd El-Fattah, MD Professor of Critical Care Medicine, Critical Care Department, Cairo.](https://reader033.fdocuments.net/reader033/viewer/2022051516/56649edd5503460f94bedfce/html5/thumbnails/1.jpg)
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Chronic Kidney DiseaseIn
Acute Coronary Syndrome
Prof. Dr. Alia Abd El-Fattah, MDProf. Dr. Alia Abd El-Fattah, MDProfessor of Critical Care Medicine,
Critical Care Department ,Cairo University
20102010
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ST-segment Elevation
No ST-segment Elevation
ST-Elevation MI Non-ST-Elevation Unstable Angina
Q-Wave MI Non-Q-Wave MI
Initial ECG
Cardiac Markers
ECG Evolution
Acute Coronary Syndrome
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Invasive Reperfusion Available Yes PCI
No
Rapid Transfer to Facility With PCI Capability Possible Yes Transfer Within 30 Minutes
No
Candidate for Thrombolysis
Yes
Thrombolytic Agent Given
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The higher the patient's mortality risk:
Large infarctions,
Heart failure or
Hemodynamic instability,
Previous infarctions, or
Acute LBBB,
The more primary PCI is preferred.
The higher the risk of thrombolysis, also the more primary PCI is preferred.
Choice of reperfusion strategy:Choice of reperfusion strategy:
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ACS
CKD
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Chronic Kidney Disease
www.usrds.org
Stages based on GFR (ml/min/1.73 m2 )
Stage 1: normal (proteinuria, abnormal markers)
Stage 2: 60-89
Stage 3: 30-59
Stage 4: 15-29
Stage 5: < 15 (dialysis or renal failure)
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Age-Standardized Rates of Death from Any Cause According to the Estimated GFR
0
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
Age
-Sta
ndar
dize
d R
ate
of D
eath
from
Any
Cau
se (p
er 1
00 p
erso
n-yr
)
Estimated GFR (ml/min/1.73 m2)
> 60 45 - 59 30 - 44 15 - 29 < 15
0.76 1.08
4.76
11.36
14.14
Go, A. et al., N Engl J Med 2004;351:1296-305.
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Age-Standardized Rates of Death from CV Events According to the Estimated GFR
0
5
10
15
20
25
30
35
40
Age
-Sta
ndar
dize
d R
ate
of C
ardi
o.Ev
ents
(per
100
per
son-
yr)
Estimated GFR (ml/min/1.73 m2)
> 60 45 - 59 30 - 44 15 - 29 < 15
2.113.65
11.29
21.80
36.60
Go, A. et al., N Engl J Med 2004;351:1296-305.
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Age-Standardized Rates of Hospitalization According to the Estimated GFR
0
10
20
30
40
50
60
70
80
90
100
110
120
130
140
150
Age
-Sta
ndar
dize
d R
ate
of
Hos
pita
lizat
ion
(per
100
per
son-
yr)
Estimated GFR (ml/min/1.73 m2)
> 60 45 - 59 30 - 44 15 - 29 < 15
13.54 17.22
45.26
86.75
144.61
Go, A. et al., N Engl J Med 2004;351:1296-305.
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Kidney Int 2008; 74: 1335-42J Am Coll Cardiol, 2003; 41:725-728
Coronary Heart Disease in CKD
CRP levels are increased (1/3-1/2 have high levels) esp. in stage 5 where it may be X10 as high
IL-6, produced in abdominal adipocytes, is elevated which stimulates the hepatocytes to produce CRP
CRP falls with treatment of risk factors and may not be pathogenic in itself
CRP is related to anemia, calcification and progression of CKD
Systemic inflammation:
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Coronary Heart Disease in CKD
• Structural and physiological changes in myocardium: LVH. LV/RV dilation. Fibrosis. Ischemia.
• Imaging: Nuclear 2DE. MRI: There is a small risk of nephrogenic systemic
fibrosis with use of gadolinium. CT/ EBCT.
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Circulation 2007; 116: 85-97
Endothelial dysfunction
Nitric oxide availability
Dyslipidemia
Inflammation
Oxidative stress
Renin-Angiotensin System
Vascular calcification
CKD: Mechanisms of CV Complications
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Risk of contrast nephrotoxicity due to contrast agents before stage 5
Rates of morbidity, mortality and in-stent stenosis are higher in CKD than non- CKD patients
DES is superior to BMS, though still not as good as in patients with no CKD
Based on non-randomized trials, there is evidence that PCI and CABG are superior to medical therapy
in select patients
Coronary Heart Disease in CKD:Coronary revascularization (based on review of
>80 published reports)
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after CABG 1998-2000 after PCI 1998-2000
Survival
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Foley RN et al Kidney Int 1995; 47(1): 186-92
Echo findings at onset dialysis (n=443)Echo finding (prevalence)
Systolic dysfunction 15%
LV Dilation
32%
LV Hypertrophy
74%
Clinical correlates
AgeCAD
Age MaleAnemiaLow CaHigh PO4
AgeFemaleWide Pulse PressureLow BUNLow albumin
Uremic CardiomyopathySt. John's, Newfoundland, Canada
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LVEF by MIBI
Normal(--> 50%)
1,598 / 63%
Decreased (< 40%)
402 / 16%
Borderline (40-49%)521 / 21%
Systolic Function
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0
0.5
1
1.5
2
2.5
<= 30% 31 - 40% 41 - 50% 51 - 60% => 71%
adj-RR for All-causes Mortality
Relative- risk
LVEF and Mortality on the Wait-List
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Survival on waitlist (months)
847260483624120
Pro
po
rtio
n S
urv
iva
l1.0
.8
.6
.4
.2
0.0
<=30%
31- 40%
41- 50%
51- 60%
> 60%
Adjusted Survival Curvesby Categories of LVEF
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J Am Coll Cardiol 2005;45:1051-1060
0
10
20
30
40
50
60
All No CAD CAD No CABG CABG No PTCA PTCA No DM DM
Pre LVEF Post LVEF
LVEF%
Pre-transplant (while on dialysis) & post-transplant LVEF
in different subgroups of patients
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Relation Between Perfusion Defect Size and Survival
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Circulation 2008;118:2540-2549
Annual CD stratified by presence of ischemia and scar
4.7%
2.2%
0.9%0.4%0%
5.5%
2.2%3.3%
9.6%
11%
3.8%3.4%
0
2
4
6
8
10
12
> 90 (N = 176) 60-89 (N=875) 59-30 (N=511) <30 (N=90)
Normal Scar Ischemia
Card
iac d
eath
/yea
r
Estimated GFR
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Outcome TotalAnnual
RateTotal
Annual Rate
P value
Cardiac Death 11(1.6%) 0.8% 16 (5.3%) 2.7% 0.001
All Cause Mortality 56 (8.1%) 4% 37 (12.3%) 6.2% 0.04
MI 15 (2.2%) 1% 11 (3.6%) 1.9% 0.15
Circulation 2008;118:2540-2549
GFR>60(n=684) GFR<60(n=304)
Unadjusted event rates for Patients With No Defects on MPI (n=664)
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Outcome Total Annual Rate Total Annual Rate P value
Cardiac Death 29(8%) 4% 58 (19.3%) 9.5% <0.001
All Cause Mortality
48 (13%) 6.5% 76 (25.3%) 12.5% <0.001
MI 24 (6.6%) 3.3% 23 (7.6%) 3.8% 0.59
Circulation 2008;118:2540-2549
GFR > 60 (n=364) GFR < 60 (n=300)
Unadjusted event rates for Patients With Defects on MPI (n=988)
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Autonomic Dysfunction
Renalase is excreted in an inactive form by the
kidneys
It is activated in the presence of catecholamine
surges and hypertension to inactivate the
excess catecholamines
It is deficient in CKD
Also, DM is common in CKD
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318 pts had dual imaging, None had prior MI, PCI or CABG, 50 died at 31/2 years, Age: >70 (HR 2.3), BMIPP > 12 (HR 21.8)
JACC 2008, 51: 139-145
BMIPP Imaging in ESRD
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Sasano, T. et al. J Am Coll Cardiol 2008;51:2266-2275
Perfusion-Innervation Mismatch in a Pig with Inducible VT after LAD Occlusion
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0. 00
0. 25
0. 50
0. 75
1. 00
sur v_ year s
0 1 2 3 4 5 6 7
STRATA: hr r at i o=0 Censor ed hr r at i o=0 hr r at i o=1 Censor ed hr r at i o=1Time after myocardial perfusion imaging (years)
Su
rviv
al
Pro
po
rtio
n
%ΔHR>15
%ΔHR≤15
Relationship between HR response and survival in ESRD
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Excludes patients whose cause of death was unknownSource: US Renal Data System: 1999 Annual Data Report
Total CVD45.7%
Malignancy, 13%
Other, 21%
Cerebral-vascular, 7.4%
Myocardial infarct, 13% Other
cardiovascular, 25.3%
Infection,20.4%
Cause of Death in Renal Transplant Recipients with functioning grafts (1995–97)
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Circulation 2008;118:2540-2549
Risk-adjusted Kaplan-Meier survival plot for CD combining SSS and GFR
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>20%5-20%
<5%
0
10
20
30
40
50
60
Total defect size
Mo
rtal
ity
%ΔHR>15
%ΔHR≤151
1
12
5
24
7
Interaction between perfusion defect size and HR response in ESRD
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Post Renal Transplant
Immuno-suppression
HT.
HL: Fluvastatin decreased the rates of death and MI but not the primary endpoint of death,
MI, revascularization, (Lancet 2003; 361: 2024-31).
DM
• Risk for death, MI and HF remains high:
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Post Renal Transplant
Smoking
Obesity
Pre-transplant dialysis duration
Chronic infection
Hypercoagulable state
Allograft rejection
Type of donor: living vs. deceased
Anemia
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J Am Coll Cardiol 2005;45:1051-1060
Kaplan-Meier analysis of survival plots for death in the post-transplant period
(after first six months after transplantation)
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Survivors (n=97) Non-Survivors (n=53)
Abnormal Perfusion 80% 94%*
PD size 20+16% 26+16%*
EF 40+12% 44+13%*
EDV (ml) 111+48 131+ 64*
LV mass (gm) 192+46 203+58
# diseased vessels 1.5+1.2 2.0+1.2*
PCI/CABG 47% 40%
Renal Transplant 44% 9%*
* P < 0.05
Comparison of survivors and non-survivors with ESRD
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Ref N Age men Technique Abnormal (%) End-point F/U (mons)Outcome
P-valueAbnormal Normal
Am J Surg 1983;146: 331-5
60 35 75 Ex-MPI 21 CV events 30 22% 4% P<0.05
Am J Kid Dis 1994; 24:65-71
95 40 NA Ex-MPI 56 Cardiac death 46 23% 5% P<0.05
AJC 1996; 77:175-9 53 36 64 DSE 38 Cardiac death 14 45% 6% P=0.003
J Inten Med 1998;244:155-61
193 63 62 DSE 37 Cardiac death 38 34% 16% P=0.006
Clin Transpl 2003;92:146-51
176 43 67 Dip MPI 43 Cardiac death 1.5 11% 0.9% P<0.05
AJC 2003; 92:146-151
174 48 61 Aden-MPI 31 Cardiac death 42 15% 3% P=0.006
Kid Intern 2004;66:1633-9
97 48± 66 Ex/Dip-MPI 10 CV events 4 years 25% 1.2% P<0.0001
Studies examining the outcome of ESRD patients in relation to non-invasive
assessment for myocardial ischemia
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MPI: Special Considerations in ESRD
The septum is often brightest area in LV, which may lead to downscaling of other regions esp. the lateral wall. This
may lead to over diagnosis of “scar” even when quantitative programs are used.
The severe and disproportionate LV hypertrophy, may affect endocardial edge detection and under-estimation
of EF by gated SPECT. Review of slices cine without outlines is helpful.
LV and RV dilatation is common even with normal perfusion and EF.
Study timing in relation to last dialysis is important in serial images as it may change LV/RV size and EF.
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Patient Management
Patient 1: ESRD, EF 25%, normal MIBI.
Does this patient move up or down on the waiting list for
renal transplant ?
Question
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Patient Management
Patient 2: Stage 3 CKD with atypical CP that warranted ED visit
what is the line of W/U?
Question
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Patient Management
Patient 3:
What is the risk in this patient and what is “best” treatment?
Stage 3 CKD, stable angina, ischemia on MIBI, normal EF
Question
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CKD & CV Events
CKD is a common problem.
CV events are higher than in patients without
CKD.
The causes of high CV events are more
complex than in any other group of patients
and mechanisms of death and esp. sudden
death remain to be defined.
Conclusions
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Roles of vascular stiffness, calcification, Ca, P,
inflammatory markers, homocysteine level and
the potential for their reversals need to be
better defined.
The role of coronary revascularization remains
to be determined
CKD & CV Events
Conclusions
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• Imaging plays an important role in patient management, but not necessarily in the traditional
way:
MBF, fibrosis, ischemia.
LV EF, mass, function, LV dyssynchrony.
Neuro-imaging.
Autonomic dysfunction.
Metabolic imaging.
CKD & CV Events
Conclusions
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