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CASE

PRESENTATION
Male BP 130/90 mmHG

53yo HR 90 bpm

Chest dyscomfort 8h prior RR 24 x/m


shortness of breath rales on basal both lung
Risk factors :
ECG
Diabetes Mellitus
Tobacco use
ECG

Sinus Rhythm 98 bpm Ischemia Anterolateral


CHEST X-RAY

CARDIOMEGALY + CEPHALIZATION
LABORATORY
FINDING

TROPONIN I (+)

0.1 ng/mL (cutt off 0.01 ng/mL)

0.2 ng/mL (6h later)

SK 2.1 mg/dL ~ eGFR 31

BUN 33

GDA 154
DIAGNOSE

NSTEMI
DKD 3
NSTEMI
RISK
1. IMMEDIATE INVASIVE
STRATIFICATION
2. EARLY INVASIVE
3. INVASIVE
RISK
STRATIFICATION
NSTEMI

DKD 3
NSTEMI

DKD 3
TREATMENT STRATEGY
HIGH RISK CRITERIA
EARLY INVASIVE <24H
sk 2.1 ?

what should we do?


BALANCING
THE RISK
CABG VS PCI
PCI VS CABG

PCI possessed lower short-term all-cause mortality,


but higher long-term revascularization risk, than CABG
Long-term all- cause mortality was not different
DIALYSIS PATIENTS
PCI VS CABG
SHORT -T ERM ALL-CAUSE MORT ALIT Y LONG-T ERM ALL-CAUSE MORT ALIT Y

did not show a significant difference


PCI was significantly lower vs CABG
(OR = 1.09; 95% CI 0.95 to 1.25)
(OR = 0.45; 95% CI 0.35 to 0.57)
DIALYSIS PATIENTS
PCI VS CABG
LONG-T ERM MI EVENT S LONG-T ERM REVASCULARIZAT ION

higher late revascularization risk after


The PCI group had higher long-term MI risk PCI
than those in the CABG group (OR = 1.70;
95% CI 1.50 to 1.93) (OR = 7.67; 95% CI 4.44 to 13.24)
MULTIVESSEL CORONARY DISEASE PATIENTS IN CKD
SHORT -T ERM ALL-CAUSE MORT ALIT Y LONG-T ERM ALL-CAUSE MORT ALIT Y

DONEC QUIS NUNC

No significant difference between the


Only one trial provided data for short-term all- two groups was shown after pooled
18

cause mortality (OR = 0.48; 95% CI 0.22 to analysis (OR = 0.98; 95% CI 0.89 to
1.05) 1.07)
MULTIVESSEL CORONARY DISEASE PATIENTS IN CKD
PCI VS CABG
LONG-T ERM MI EVENT S LONG-T ERM REVASCULARIZAT ION

The pooled outcome did not reveal significant After pooled analysis, PCI still
difference in long-term MI incidence between showed obviously higher long-term
PCI and CABG (OR = 1.54; 95% CI 0.94 to revascularization risk than CABG (OR
2.52) = 3.81; 95% CI 2.72 to 5.33)
PCI ON CKD
DES VERSUS CABG
SHORT -T ERM ALL-CAUSE MORT ALIT Y LONG-T ERM ALL-CAUSE MORT ALIT Y

DES group showed a remarkable benefit No significant difference in long- term


in short-term mortality over CABG all-cause mortality

(OR = 0.34; 95% CI 0.25 to 0.46) (OR = 1.16; 95% CI 0.95 to 1.42)
DES VERSUS CABG
LONG-T ERM MI EVENT S LONG-T ERM REVASCULARIZAT ION

DES group had higher incidence of late


no difference between the two procedures revascularization compared with CABG
(OR = 1.23; 95% CI 0.30 to 5.04) (OR = 2.84, 95% CI 1.92 to 4.20)
CONTRAST INDUCED
NEPROPATHY
CONTRAST INDUCED NEPROPATHY
(CIN)

acute kidney injury that begins soon after the contrast


administration
NO SPECIFIC TREATMENT
an increase in serum creatinine of at least 0.5 mg/dL within 48h
THE BEST TREATMENT IS PREVENTION
incremental predictor of cardiovascular events
HOW TO
PREVENT IT?
small doses of contrast and avoidance of repetitive studies

selected low- or iso-osmolal nonionic contrast agents

Avoidance of volume depletion or NSAIDs, both of which can


increase renal vasoconstriction

administration of intravenous saline or sodium bicarbonate

administration of the antioxidant acetylcysteine

Specialized techniques during coronary angiography, such IVUS,


OCT, FFR
PREPARATION

INTERNIST : DKD III

Avoid volume depletion

Use of iodixanol or nonionic low osmolal contrast agents

If there are no contraindications to volume expansion we recommend :

A suggested regimen is a bolus of 3 mL/kg of isotonic bicarbonate for one hour


prior to the procedure, and continued at a rate of 1 mL/kg per hour for six hours
after the procedure OR

Isotonic saline at a rate of 1 mL/kg per hour, begun at least two and preferably 6
to 12 hours prior to the procedure, and continuing for 6 to 12 hours after contrast
administration

Acetylcysteine 1200mg bid p.o day before and the day of the procedure
TYPE OF CONTRAST
HIDRATION
ACETYLSYSTEIN
HEMOFILTRATION/ HEMODIALYSIS
CONTRAST
AGENT
CONTRAST AGENT

(Reed et al., 2009)


LOW-OSMOLAL VS HYPER-OSMOLAL
RENAL INSUFFICIENCY

RCT 1200 px angiography

Among patients with a baseline serum creatinine above 1.4 mg/dL a


rise in the serum creatinine of at least 1.0 mg/dL (88 mol/L) was seen
less often after the use of iohexol (7.2 versus 15.8 percent with an ionic
agent).

The benefit was greater in diabetic patients (11.8 versus 27 percent)

low osmolal nonionic agent iohexol with the high osmolal agent
diatrizoate > benefit from iohexol was seen in patients with renal
insufficiency alone or with diabetes mellitus
NONIONIC ISO-OSMOLAL AGENTS
IODIXANOL, 290 MOSMOL/KG

lower risk of nephropathy than some low osmolal agents, particularly


iohexol, among diabetic patients with CKD

A meta-analysis of 16 randomized trials also suggested that


iodixanol was associated with a reduction in risk among patients with
chronic kidney disease who received contrast when compared to
iohexol (relative risk 0.19, 95% CI 0.07-0.56) but not when compared to
other nonionic low osmolal contrast agents (relative risk 0.79, 95% CI
0.56-1.12) (Reed et al., 2009)

ACC/AHA guidelines PCI 2009 were revised to suggest the use of either
an iso-osmolal contrast agent or a low molecular weight contrast agent
other than iohexol or the ionic low osmolal agent, ioxaglate
A META-ANALYSIS OF 16 RANDOMIZED TRIALS
IODIXANOL, NONIONIC ISO -OSMOLAL AGENTS

ACC/AHA GUIDELINES ON PCI :


USE OF EITHER AN ISO-OSMOLAL CONTRAST AGENT OR A LOW -MOLECULAR-WEIGHT CONTRAST
AGENT OTHER THAN IOHEXOL OR THE IONIC LOW -OSMOLAL AGENT, IOXAGLATE [24].

THE 2012 KDIGO GUIDELINES :


RECOMMENDED LOW-OSMOLAL OR ISO-OSMOLAL RATHER THAN HIGH-OSMOLAL CONTRAST AGENTS

iodixanol was associated with a reduction in risk among patients with


CKD who received contrast when compared with iohexol (relative risk
[RR] 0.19, 95% CI 0.07-0.56), but not when compared with other
nonionic low-osmolal contrast agents (RR 0.79, 95% CI 0.56-1.12

(Reed et al., 2009)


HIDRATION VS
DIURESIS
HIDRATION

Intravenous volume administration is beneficial

If no contraindications to volume expansion > isotonic


intravenous fluids hidration is recommended

Isotonic solutions provide superior benefit compared with hypotonic


solutions
INTRAVENOUS SALINE
ISOTONIC VS 1/2 ISOTONIC SALINE

prospective randomized trial of 1620 px

The overall incidence of CIN was significantly lower in patients


given isotonic saline (0.7 versus 2.0 percent).

The benefit with isotonic saline was more pronounced in diabetic


patients

HYDRATION WITH ISOTONIC SALINE SOLUTION IS


SUPERIOR TO ONE-HALF NORMAL SALINE,

(Mueller C et al., 2002).


INTRAVENOUS BICARBONATE

Alkalinization may protect against free radical injury

meta-analyses.

The results were conflicting as some showed a significantly lower


rate of contrast-induced nephropathy with sodium bicarbonate [44-
48]

ISOTONIC SODIUM BICARBONATE MAY BE SUPERIOR


TO ISOTONIC SALINE.
HIDRATION
TIMING AND RATE

OUTPATIENTS

3 mL/kg over one hour preprocedure

and 1 to 1.5 mL/kg/hour during procedure

6 mL/kg four to six hours postprocedure, regardless of fluid


type.

INPATIENTS

1 mL/kg/hour for 6 to 12 hours preprocedure,intraprocedure,


and for 6 to 12 hours postprocedure.
HYDRATION, MANNITOL, AND DIURETICS

In one trial (Solomon et al., 1994), 78 patients with stable CKD (mean
SK= 2.1 mg/dL) undergo coronary angiography were randomly
assigned to one of three regimens :

1. One-half isotonic (0.45 percent) saline at a rate of 1 mL/kg per hour for
12 hours beforeLOWEST
and 12 hours after the angiogram
RISK

2. One-half isotonic saline plus 25 g of mannitol infused intravenously


during the one hour before the procedure
NO BENEFIT

3. One-half isotonic saline plus 80 mg of furosemide infused


intravenously during
SLIGHTLY the 30
INCREASED THE minutes
RISK before angiography
MANNITOL + FUROSEMIDE
VS SALINE HYDRATION CONTROLS

92 px moderate renal
insufficiency (mean sk 2.8 mg/dL)

acute renal failure (defined as a mannitol and saline


25 percent increase in serum furosemide hydration
creatinine)


DIURETICS
occurred AGENTSamong
more frequently DO NOT APPEAR TO BE BENEFICIAL
DIURETICS
patients who MAY BE mannitol
received REQUIRED TO TREAT VOLUME OVERLOAD
and furosemide compared to
placebo
acute renal
There was no difference in net 23 of 46 13 of 46
failure
fluid balance between the groups

(Majumdar et al., 2009) OR 3.73, 95% CI 1.12-12.38


SALINE VS DOPAMIN, MANNITOL, ANP

study 50 px (24 diabetic) with CKD (mean sk 2.5 mg/dL) undergo coronary angiography

randomly assigned to :

1. Dopamine [2 g/kg per min],

2. Mannitol [15 g/dL in a one-half isotonic saline solution given at 100 mL/h]

3. Atrial natriuretic peptide

Saline hydration was associated with a 40 percent incidence of renal dysfunction in diabetic and
nondiabetic patients.

Dopamine, mannitol, and atrial natriuretic peptide were associated with a much higher incidence
of renal dysfunction (75 to 83 percent) in diabetic subjects. On the other hand, there were no
cases of contrast toxicity in the nondiabetic patients, suggesting a possible benefit.

(Weisberg et al., 1994)


ACETYLSYSTEIN
E
ACETYLCYSTEINE

direct scavenger of free radicals (antioxidant)

improves blood flow through nitric oxide-mediated pathways, which


results in vasodilatation protect against CIN
DONEC QUIS NUNC

THE GREATEST REDUCTION IN CIN :

N-ACETYLCYSTEINE + IV SALINE IN PATIENTS RECEIVING


LOCM

STATINS + N-ACETYLCYSTEINE + IV SALINE

(Subramaniam et al., 2016)


OTHER AGENT
INHIBITION OF RENAL VASOCONSTRICTION

Theophylline

meta-analysis that included 13 studies and 1222 patients (Dai et al., 2012)

reduction inreduction risknephropathy, but not for dialysis or in-house mortality


risk for contrast

The prostacyclin analog, iloprost

RCT 208 iloprost (1 ng/kg/min) vs placebo (Spargias et al., 2009)

increase sk = 8 vs 22 %, need a larger & definitive trial


increase sk
INHIBITION OF RENAL VASOCONSTRICTION

Fenoldopam

CONTRAST trial in 315px (1/2 DM) (Stone et al., 2003)

no reduction in the incidence of contrast nephropathy


no reduction in the incidence of CIN

Nonselective endothelin receptor antagonist

multicenter, double-blind RCT 158 px (Wang et al., 2000)

exacerbate
exacerbate radiocontrast
radiocontrast nephrotoxicity
nephrotoxicity compared with hydration alone
OTHER AGENT

Statins

meta-analysis n=5024 (Subramaniam et al., 2016)

did not show a conclusive benefit of statins plus intravenous saline


compared with saline alone

Oral sodium citrate

randomized trial 202px (Markota et al., 2013)

CIN lower among patients who received oral citrate compared with
placebo (4 versus 20%)
OTHER AGENT

Atrial natriuretic peptide

a multicenter, prospective, double-blind,RCT (Kurnik et al., 1998)

no benefit was observed

Ascorbic acid

Meta-analysis 6 studies (Subramaniam et al., 2016)

did not conclusively demonstrate a benefit of ascorbic acid


HEMOFILTRATIO
NHEMODIALYSIS
HEMOFILTRATION

Trial of 114 px hemofiltrati isotonic


on saline
who required a coronary
intervention lower rates of
a serum
creatinine
5 50
elevation >25

requirement
for dialysis
3 25
EFFECTIVE INPREVENTING CIN
IMPROVED IN-HOSPITAL AND LONG-TERM OUTCOMES
in-house
mortality
2 14

one-year
mortality
10 30

(Marenzi et al., 2003)


HEMODIALYSIS
2012 meta-analysis of 9 studies

9 randomized controlled and 2 nonrandomized trials were included (n = 1010


patients);

8 studies used hemodialysis (HD) and 3 used hemofiltration or hemodiafiltration.

Radiocontrast-induced nephropathy (RCIN) incidence was 23.3% in the RRT


group and 21.2% in standard medical therapy.
NOT DECREASE THE INCIDENCE OF CIN
INCREASE
RRT did not decrease RCIN CIN RISK
incidence compared with SMT (risk ratio [RR] 1.02;
95% confidence interval [CI], 0.54-1.93);

however, intertrial heterogeneity was high. In sensitivity analyses, limiting to only


HD studies significantly reduced heterogeneity. HD appeared to increase RCIN
risk (RR 1.61; 95% CI, 1.13-2.28) and had no effect on need for permanent RRT
or progression to end-stage renal disease (RR 1.47; 95% CI, 0.56-3.89).

(Cruz et al., 2012)


TX FOR PREVENTING CIN

iso osmolal non ionic contrast

use minimal volume contrast

acetylsystein 2x 1200mg

diuretic because of lung congestion

sk before pci 2.0 mg/dL


ANTITHROMBOTIC
THERAPY IN ACS PATIENTS
WITH CKD
ACS CKD
ANTITROMBOTIC DRUG

CKD have a higher risk of ACS

significantly higher mortality

increased bleeding complications


DONEC QUIS NUNC
DONEC QUIS NUNC
ANTIPLATELET- ANTITROMBOTIC
Strategy for Reversal in Patients
Drug Recommended Dose Route of Elimination Half-Life Effect of Renal Failure on Dose
With Bleeding

Discontinue; platelet transfusion,


Aspirin 81325 mg Renal (pH- dependent) 219h None
and desmopressin

Loading dose: 300600 mg Discontinue; platelet transfusions


Clopidogrel Renal (50%) feces (50% 6h None
Maintenance dose: 75 mg and desmopressin

Loading dose: 60 mg Maintenance Discontinue; platelet transfusions


Prasugrel Renal (6070% 215 h None
dose: 10 mg and desmopressin

Loading dose: 180 mg


Ticagrelor Biliary 613 h None Discontinue
Maintenance dose: 90 mg PO BID

250 g/kg bolus followed by Discontinue; platelet transfusions


Abciximab Spleen, RES 30 min None
0.125 g/kg/min for 12 and desmopressin

CrCl <30 ml/min/1.73 m2: 0.2


0.4 g/kg/min 30-min bolus
Tirofiban Renal (40%70%) 1.41.8 h g/kg/min 30-min bolus Discontinue; FFP
followed by 0.1 g/kg/min
followed by 0.05 g/kg/min

Unfractionated heparin PTT: 5070 s RES 11.5 h None Protamine

Enoxaparin 1 mg/kg SC every 12 Renal (40%) 47 h Decrease to mg/kg SC daily Partial reversibility (2/3) to

Recombinant factor VIIa (90


Fondaparinux 2.5 mg SC daily Renal 1721 Increases in renal failure Avoid if CrCl <30 ml/min/1.73 m2 g/kg) Based on laboratory
data only

0.75 mg/kg IV bolus followed by 25 min Increases if CrCl <30 No single antidote; may consider
Bivalirudin Renal Avoid if CrCl <30 ml/min/1.73 m2
1.75 mg/kg/during procedure ml/min/1.73 m2 hemodialysis
SAFETY AND EFFICACY OF ANTIPLATELET AND ANTITHROMBOTIC AGENTS STRATIFIED BY CATEGROY OF
CKD

Drug CKD 1 CKD 2 CKD 3 CKD 4 CKD 5 Comments RCT/RP/SC/R/MA/SA Evidence

Aspirin S, E S, E S, E S, E DONEC
S, E QUIS NUNC
RCT (12,16,17)RP (13) R(14)MA (18) Sufficient

Increased risk of
minor bleeding and
risk of blood
transfusions in CKD
35.Lack of efficacy
in CREDO (20) and
Further studies
CURE (22) trials in
Clopidogrel S, E S, E US, NE US, NE US, NE RCT (23)SA (20,22) of CKD 3
CKD 35. Further
patients needed
studies needed to
establish efficacy of
standard dose vs.
double dose
clopidogrel in
patients with CKD
No studies currently
available on safety
nd efficacy in
patients with CKD.
Further studies
Prasugrel S, E S, E UK UK UK No ifference based RCT (29)
of CKD
on pharmacokinetic
nd
pharmacodynamic
data.
May be considered

A = avoid; E = effective; GPI = glycoprotein inhibitor; LMWH = low molecular weight heparin; MA = meta
over standard dose
clopidogrel. Further
Ticagrelor S, E S, E S, E S, E S, E trials needed to RCT (33)SA (34) Sufficient
assess efficacy vs.
double dose
clopidogrel.
No interaction
observed between
MOHON ASUPAN DOKTER
PCINYA PAKAI STENT
ATAU YG TVD AKHIRNYA DI CABG?
TREATMENT

Aspirin 300mg

Clopidogrel 300mg

Atorvastatin 40mg

ISDN 5mg 1-0-1

acetylsystein 2x 1200mg
IF THERE IS CULPRIT LESION
WHAT WE CHOOSE?
DES/BMS?
TREATMENT

sk 2.3

tx :

Normal saline 1 mL/kg/hour for 6 to 12 hours postprocedure.

Aspirin 1x100 mg

Clopidogrel 1x75mg

Atorvastatin 1x40mg

ISDN 5mg SL

acetylsystein 2x 1200mg

fondaparinux 1x 2.5mg sc
SUMMARY
THANK YOU