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state of the art in ADVANCED HEART FAILURE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S SESION III: COMPLEX SURGERY AND SHORT-­‐TERM MECHANICAL CIRCULATORY SUPPORT (MCS) Cardiogenic shock in pa>ent suitable for MCS or HT. Protocol in Galicia Miguel A. Solla-­‐Buceta UCC Cardiológicos. XXI A Coruña A Coruña, June 26 – 27, 2015 sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S Table of contents: §  MoPvaPon §  Applicability §  Structure §  Early management §  Refractory cardiogenic shock (CS) management §  Outcome and desPnaPon therapy §  Conclusions SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S MoPvaPon: High mortality of Cardiogenic Shock: CS remains 157the most common cause of death in paPents with AMI or ADHF 39,7 – 41,3% ices in cardiogenic shock
Acute Decompensated Chronic HF 2,2 Decompensated HF 11,3 Pulmonary oedema 10,4 73 Cardiogenic shock Hypertensive HF CS mortality 39,5% Right HF Trends in Mortality of CS in Acute Myocardial Infarc>on igure 1 Time trends in hospital case fatality rates (CFR) in patients with acute myocardial infarction + cardiogenic shock in the Worcester (MA,
SA) metropolitan area. Despite the survival improvement resulting from more widespread use of acute interventional reperfusion strategies,
verall cardiogenic shock mortality rates remain high at over 40%. The additional columns (from left to right) represent mortality rates from (A)
Werdan t al. Eur Heart J. 2014;35:156-­‐167 he SHOCK study2 (dark grey column: IMS, Initial Medical Stabilisation Group; light grey column: ERV, Early Revascularisation
Group); (B)ethe
RIUMPH Study52 [all patients with ERV; with (dark grey column) or without (light grey column) the nitric oxide synthase (NOS)
inhibitor
TilargiNieminen et al. EurHeart J 2006;27:2725-­‐2736 ne]; and (C) the IABP SHOCK II Trial4 [all patients with ERV; with (dark grey column) or without (light grey column) intraaortic balloon counterulsation (IABP)]. Modified from Goldberg et al.80
D
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S MoPvaPon: Research Original Investigation
Percutaneous Ventricular Assist
pVADs are increasingly used in paPents with CS. Lack of clear guidelines on IndicaPons, device selecPon and cost-­‐efecPve care Cardiogenic shock
Cardiogenic shock
IABP
PCI, no AMI or cardiogenic shock
PCI, no AMI or car
B
C
A
PVAD
AMI, no cardiogenic shock
AMI, no cardiogen
25 000
1800
1600
1400
1200
1000
800
600
30 fold increase in the es>mated annual pVAD u>liza>on 400
200
0
138 4,6 2007
300 000
IABPs per Million Discharges
2000
PVADs per Million Discharges
Overall Procedures per Million Discharges
Figure 1. Calendar Year Trends in the Use of Percutaneous Ventricular Assist Devices (PVADs) and Intra-aortic Balloon Pumps (IABPs)
in the United States, 2007 Through 2012
20 000
15 000
2009
2010
2011
2012
200 000
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20with 000 CS pVAD recipients 150 000
15 000
mortality 47,5% 10 000
10 000
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0
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0
2007
2008
Year
2009
2010
2011
2012
2007
2008
2009
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2
Year
Khera et al. JAMA Intern Med 2015;175(6):941-­‐950 The figure shows estimated use of PVADs and IABPs per million discharges, and
the error bars represent standard errors. A, Use of PVADs increased from 4.6
per million in 2007 to 138 per million in 2012 (P for trend < .001). In contrast,
shock, acute myocardial infarction (AMI) without cardiogenic
percutaneous coronary intervention (PCI) without AMI or card
(P for trend < .001 for all). C, Use of IABPs decreased in patien
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S MoPvaPon: SERGAS Clinical OrganizaPonal Structure 1"Heart"Transplant"
and"VAD"center"
3"Cardiac"surgery"
centers"
Area"Hospital"
Heart Team: healthcare providers have to cooperate to improve survival of CS Local"Hospital"
3+2"PCI"center"
Pre>hospital"
assistance"
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S MoPvaPon: The goal of this document is to provide some recomendaPons on management of CS and ADHF for potenPal heart transplant or durable VADs recipients in Galician Region GY
CARDIOLO
LLEGE OF
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1093 rt Journal
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1787
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VOL. 65, N
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sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S Applicability: PaPents in Cardiogenic Shock: “a state of criPcal end-­‐
organ hypoperfusion due to reduced cardiac output” Systolic)BP)<90)mmHg)for)>)30)min)or)vasopressors)required)to)achieve)a)
BP)≥90)mmHg;))
Pulmonary)congestion)or)elevated))leftAventricular)filling)pressures;))
Signs)of)impaired)organ)perfusion):))
(a))altered)mental)status;))
(b))cold,)clammy)skin;))
(c))oliguria;))
(d))increased)serumAlactate.))
… a`er ruling a reversible cause of heart failure … SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S Applicability: … that meet the following criteria: §  Ventricular funcPon is deemed unrecoverable or unlikely to recover without long-­‐term device support. §  Deemed too ill to be weaned from temporary MCS devices or inotropic support. §  Capacity for meaningful recovery of end-­‐organ funcPon and quality of life. §  Without irreversible end-­‐organ damage.
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S Applicability: ... whithout contraindicaPons: AcPve infecPon Severe peripheral arterial or cerebrovascular disease Unhealed pepPc ulcer Recent thrombo-­‐embolism Significant renal failure (e.g. CCl < 50 mL/min) Systemic disease with mulPorgan involvement (e.g. Diabetes Mellitus) §  Other serious co-­‐morbidity with poor prognosis (e.g COPD) §  Treated cancer in previous 5 years §  High, fixed pulmonary vascular resistance ( >4-­‐5 WU and mean TG > 15 mmHg) § 
§ 
§ 
§ 
§ 
§ 
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S Structure: 1.-­‐ Early management R efractory CS 2.-­‐ management Cardiogenic+Shock
Clinical+presenta3on:
Acute+vs+Chronic+HF
Inotropes+/+vasopressors
Reperfusion
Intra:Aor3c+balloon+pump
Suppor3ve+therapy
Inotropes+/+vasodilators
Diure3cs
Refractory+
Cardiogenic+Shock
INTERMACS+profile
No
Yes
Intermacs+4:7
Intermacs+1:2
Intermacs+2:3
Short:term+MCS+
devices
Yes
3.-­‐ Outcome and DesPnaPon Therapy Acute+Descompensated+Chronic+HF
Myocardial+Infarc3on+/+Acute+myocardi3s
Cardiac+recovery
Wean+and+remove+
device
Short:term+MCS+
devices
No
MOD+and
Neurological+recovery
No
Farmacological+
treatment
Electrical+Devices
Surgical+management
Exercise+tes3ng:+peak+VO2
HF+Survival+Score
Yes
Heart+Transplant
or
Durable+VADs
VO +<+12+:14+ml/Kg/min
₂
Palia3ve+Care
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S Structure: 1.-­‐ Early management: Cardiogenic+Shock
Acute+Descompensated+Chronic+HF
Myocardial+Infarc3on+/+Acute+myocardi3s
Clinical+presenta3on:
Acute+vs+Chronic+HF
Inotropes+/+vasopressors
Reperfusion
IntraBAor3c+balloon+pump
Suppor3ve+therapy
Inotropes+/+vasodilators
Diure3cs
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 1.-­‐ Early management: Clinical evaluaPon and diagnosPc invesPgaPons Clinical presentaPon: AHF (“de novo”) Vs ADCHF Age 622
Table 1 Underlying diseases and precipitating factors of ALARM-HF patients
Characteristics
Yes
Underlying diseases PrecipitaPng factors Hemodynamics profile Total De novo AHF
Patients, n (%)
4,953 1,792 (36.2)
Age (years)
\50
9.5
15.4
51–60
16.5 18.0 623
61–70
29.3 28.4
71–80
29.8 26.1
[80
14.9 12.1
Male gender (%)
62.4 63.6
Table 2 Hemodynamics and initial findings by de novo or pre-existing episode(s) of AHF
and by ICU
versus CCU versus ward
Underlying
diseases
Chronic systolic heart
36.4
2.6
Variable
De novo AHF
p value Patients hospitalized
in (%)
p valueb
failure
Coronary artery disease (%) 30.7 25.4
Yes,
No,
ICU,
CCU,
Hypertension
(%)a Ward, 70.2 66.3
n = 1,792
n = 3,161
n = 2,247
n = 1,475
n = 1,23145.3 38.8
Diabetes
(%)
Atrial fibrillation/flutter (%) 24.4 13.4
Median SBP (mmHg) (IQR) 130 (95–160) 130 (103–160) \0.0001 120 (95–160) Chronic
130 (100–160)
\0.0001
renal disease140 (110–160)
21.4 11.0
(as
SBP \ 100 (mmHg),
466 (26.3)
549 (17.5)
\0.0001 617 (27.7)
298reported)
(20.3) (%) 100 (8.3)
\0.0001
Anaemia
(%)
14.4
8.9
no. (%)
COPD/asthma
24.8 15.8
Median DBP (mmHg) (IQR) 75 (60–90)
80 (60–95)
\0.0001 78 (58–95)
80 (60–94) (%) 80 (70–95)
\0.0001
(%)
5.5 \0.0001
2.2
Heart rate, median (IQR)
110 (90–122) 107 (90–120)
0.002 110 (90–125) Pacemaker
110 (90–120)
100 (86–118)
Cardiomyopathy
(%) 2.9
12.6 \0.0001
6.2
Cardiogenic shock (%)
19.1
7.5
\0.0001 16.2
12.3
Precipitating
factors (on
admission) \0.0001
Pulmonary edema (%)
39.8
35.0
0.0008 38.1
42.8
27.0
Acute
36.9 48.6
Cold extremities (%)
29.3
24.3
0.0001 33.1
26.2coronary
13.2
\0.0001
syndrome
(%)
Normal diuresis at baseline 55.2
52.6
0.093 47.2
54.3
65.5
\0.0001
Arrhythmia
(%)
26.9
19.1
(%)
Infection (%)
16.3 12.1
Median BNP (IQR)a
908
1,040
0.020 1108
1045
700
0.009
Poor compliance with
13.4
2.2
(415–1,572)
(576–2,212)
(552–1,995) medications
(642–2,136)
(313–1,640)
(%)
SBP systolic blood pressure, DBP diastolic blood pressure
a
b
BNP recorded in 307 patients
p among ICU versus CCU versus ward
3,161 (63.8)
6.2
15.7
29.8
31.8
16.5
61.7
p value
de novo
AHF, yes
versus no
\0.0001
Patients
ICU
2,247 (45
0.19
10.3
18.0
30.6
28.4
12.7
62.4
55.4
\0.0001
35.8
33.7
72.4
49.0
30.6
27.1
\0.0001
\0.0001
\0.0001
\0.0001
\0.0001
29.4
73.2
47.9
22.2
21.2
17.4
29.7
7.4
16.3
\0.0001
\0.0001
\0.0001
\0.0001
15.7
25.9
3.9
11.3
30.2
\0.0001
40.9
31.3
18.7
19.7
\0.0001
\0.0001
\0.0001
27.9
18.9
10.9
ICU intensive care unit, CCU cardiac care unit, AHF acute heart patients admitted to ICU
Follath efailure,
t al. COPD
Intensive Care Med 2011;37:619-­‐626 chronic obstructive
pulmonary
disease,
ICU/CCU at had median age between
Table 3 Treatment during hospitalization ICU versus CCU versus ward
Treatment performed
Nob
least 1 day hospital stay in ICU or CCU, ward no stay in ICU or a Systolic blood pressur
CCU
C90 mmHg or recei
Exact age was not recorded, but only 5-year age categories. Median medication
b
age was between 66 and 70 years for the whole cohort, and for
Pre-existing episode(s
SESION III: Cardiogenic shock Protocol Patients hospitalized in
p value
sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 1.-­‐ Early management: Clinical evaluaPon and diagnosPc invesPgaPons Clinical profiles: CS forms a spectrum that ranges from mild hypo-­‐perfusion to profound shock Refractory Cardiogenic Shock: Pharmacological criteria INTERMACS profiles Yancy et al
Table 25.
Profile*
2013 ACCF/AHA Heart Failure Guideline
e281
INTERMACS Profiles
Profile Description
Features
1
Critical cardiogenic shock
(“Crash and burn”)
Life-threatening hypotension and rapidly escalating inotropic/pressor support, with critical organ hypoperfusion often
confirmed by worsening acidosis and lactate levels.
2
Progressive decline
(“Sliding fast” on inotropes)
“Dependent” on inotropic support but nonetheless shows signs of continuing deterioration in nutrition, renal function,
fluid retention, or other major status indicator. Can also apply to a patient with refractory volume overload, perhaps
with evidence of impaired perfusion, in whom inotropic infusions cannot be maintained due to tachyarrhythmias,
clinical ischemia, or other intolerance.
3
Stable but inotrope dependent
Clinically stable on mild-moderate doses of intravenous inotropes (or has a temporary circulatory support device) after
repeated documentation of failure to wean without symptomatic hypotension, worsening symptoms, or progressive
organ dysfunction (usually renal).
4
Resting symptoms on oral therapy Patient who is at home on oral therapy but frequently has symptoms of congestion at rest or with activities of daily living
at home
(dressing or bathing). He or she may have orthopnea, shortness of breath during dressing or bathing, gastrointestinal
symptoms (abdominal discomfort, nausea, poor appetite), disabling ascites, or severe lower-extremity edema.
5
Exertion intolerant (“housebound”) Patient who is comfortable at rest but unable to engage in any activity, living predominantly within the house or housebound.
6
Exertion limited
(“walking wounded”)
Patient who is comfortable at rest without evidence of fluid overload but who is able to do some mild activity. Activities of
daily living are comfortable and minor activities outside the home such as visiting friends or going to a restaurant can
be performed, but fatigue results within a few minutes or with any meaningful physical exertion.
7
Advanced NYHA class III
Patient who is clinically stable with a reasonable level of comfortable activity, despite a history of previous decompensation
that is not recent. This patient is usually able to walk more than a block. Any decompensation requiring intravenous
diuretics or hospitalization within the previous month should make this person a Patient Profile 6 or lower.
*Modifier options: Profiles 3–6 can be modified with the designation frequent flyer for patients with recurrent decompensations leading to frequent (generally at
least 2 in last 3 mo or 3 in last 6 mo) emergency department visits or hospitalizations for intravenous diuretics, ultrafiltration, or brief inotropic therapy. Profile 3 can be
modified in this fashion if the patient is usually at home. If a Profile 7 patient meets the definition of frequent flyer, the patient should be moved to Profile 6 or worse.
Other modifier options include arrhythmia, which should be used in the presence of recurrent ventricular tachyarrhythmias contributing to the overall clinical course
(eg, frequent implantable cardioverter-defibrillator shocks or requirement of external defibrillation, usually more than twice weekly); or temporary circulatory support
for hospitalized patients profiles 1–3.635
INTERMACS indicates Interagency Registry for Mechanically Assisted Circulatory Support; and NYHA, New York Heart Association.
Adapted from Stevenson et al.643
Samuels et al. J Card Surg 1999;14:288-­‐293 Beurtheret S et al. Eur Heart J 2013;34:112-­‐120 SESION III: Cardiogenic shock Protocol patients with HF regardless of symptoms or other considerations
does not appear to result in significant benefit.644 Limiting fluid
support to maintain systemic perfusion and preserve
end-organ performance. (Level of Evidence: C)
sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 1.-­‐ Early management: Clinical evaluaPon and diagnosPc invesPgaPons Yancy et al
Table 25.
Clinical profiles: INTERMACS INTERMACS Profiles
Profile*
Profile Description
2013 ACCF/AHA Heart Failure Guideline
e281
Features
1
Critical cardiogenic shock
(“Crash and burn”)
Life-threatening hypotension and rapidly escalating inotropic/pressor support, with critical organ hypoperfusion often
confirmed by worsening acidosis and lactate levels.
2
Progressive decline
(“Sliding fast” on inotropes)
“Dependent” on inotropic support but nonetheless shows signs of continuing deterioration in nutrition, renal function,
fluid retention, or other major status indicator. Can also apply to a patient with refractory volume overload, perhaps
with evidence of impaired perfusion, in whom inotropic infusions cannot be maintained due to tachyarrhythmias,
clinical ischemia, or other intolerance.
3
Stable but inotrope dependent
Clinically stable on mild-moderate doses of intravenous inotropes (or has a temporary circulatory support device) after
repeated documentation of failure to wean without symptomatic hypotension, worsening symptoms, or progressive
organ dysfunction (usually renal).
4
Resting symptoms on oral therapy Patient who is at home on oral therapy but frequently has symptoms of congestion at rest or with activities of daily living
at home
(dressing or bathing). He or she may have orthopnea, shortness of breath during dressing or bathing, gastrointestinal
symptoms (abdominal discomfort, nausea, poor appetite), disabling ascites, or severe lower-extremity edema.
5
Exertion intolerant (“housebound”) Patient who is comfortable at rest but unable to engage in any activity, living predominantly within the house or housebound.
6
Exertion limited
(“walking wounded”)
Patient who is comfortable at rest without evidence of fluid overload but who is able to do some mild activity. Activities of
daily living are comfortable and minor activities outside the home such as visiting friends or going to a restaurant can
be performed, but fatigue results within a few minutes or with any meaningful physical exertion.
7
Advanced NYHA class III
Patient who is clinically stable with a reasonable level of comfortable activity, despite a history of previous decompensation
that is not recent. This patient is usually able to walk more than a block. Any decompensation requiring intravenous
diuretics or hospitalization within the previous month should make this person a Patient Profile 6 or lower.
*Modifier options: Profiles 3–6 can be modified with the designation frequent flyer for patients with recurrent decompensations leading to frequent (generally at
least 2 in last 3 mo or 3 in last 6 mo) emergency department visits or hospitalizations for intravenous diuretics, ultrafiltration, or brief inotropic therapy. Profile 3 can be
modified in this fashion if the patient is usually at home. If a Profile 7 patient meets the definition of frequent flyer, the patient should be moved to Profile 6 or worse.
Other modifier options include arrhythmia, which should be used in the presence of recurrent ventricular tachyarrhythmias contributing to the overall clinical course
(eg, frequent implantable cardioverter-defibrillator shocks or requirement of external defibrillation, usually more than twice weekly); or temporary circulatory support
for hospitalized patients profiles 1–3.635
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 1.-­‐ Early management: IniPal stabilizaPon: Fluids to obtain euvolaemia (pathophysiological considera>ons) Vasopressors: Norepinephrine T h e n e w e ng l a nfi
drst j o ucrhoice na l o f v
masopressor e dic i n e
Dopamine vs Norepinephrine: SOAP II study were roughly equipotent with respect to
Hazard Ratio (95% CI)
arterial pressure, and there were only m
Type of shock
ferences in is theassociated use of open-label
Dopamine with norepin
Hypovolemic
most of which were related to early ter
more arrhythmic events and 28-­‐d Cardiogenic
of the study drug and a shift to open-labe
Septic
m o r t a l i t y i n p a > e n t s w i t h nephrine because of the occurrence of
All patients
cardiogenic shock. mias
that
were
difficult to control. Doses
0.5
1.0
1.5
label norepinephrine and the use of op
Norepinephrine Dopamine
epinephrine and vasopressin were similar
Better
Better
the two groups. Second, we used a sequ
sign, which potentially allowed us to
Figure 3. Forest Plot for Predefined Subgroup
Analysis
RETAKE:
1st
AUTHOR: De Backer
De Backer D et al. N Engl J Med 2010;362:779-­‐89 study early if an effect larger than that
According to Type of Shock.
2nd
of 3 patients were in septic shock (542 in3rd
from observational trials occurred; how
AFIGURE:
total of 31044
III: Cardiogenic shock Protocol the dopamine group and 502 in theSESION norepinephrine
Revised
sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 1.-­‐ Early management: IniPal stabilizaPon: Inotropes: Norepinephrine-­‐dobutamine vs epinephrine Systemic and regional hemodynamics in CS tients in whom
output
marktientscardiac
in whom
cardiac
output markedly increased,
increasethe
in the
PCO2in the PCO
edlythe
increased,
increase
2
gap under epinephrine
is likely related
gap under epinephrine
is likely related
to the thermogenic
effects of epinephto the thermogenic
effects of epinephrine. Furthermore,
despite a marked
rine. Furthermore,
despiteina marked increase in epinephrine-treated
patients, patients,
crease in epinephrine-treated
the PCO2 gap
hrs
of
treatment
theafter
PCO24
gap
after
24
hrs
of
treatment
2
was no longer
when
compared
wasdifferent
no longer
different
when compared
to norepinephrine-dobutamine
pato norepinephrine-dobutamine
patients. This time-response
profile, identients. This time-response
profile, identicalkinetics,
to lactate
is highly evoctical to lactate
is kinetics,
highly evocative of aeffect.
metabolic effect.
ative of a metabolic
regard
to renal
function,
In regard to In
renal
function,
both
reg- both regimens
improved
diuresis
in these oliguric
imens improved diuresis in these
oliguric
patients,
thenorepieffects of norepipatients, although
thealthough
effects of
nephrine-dobutamine
were
greater. Crenephrine-dobutamine
were greater.
Crelevels alsowithout
improved
atinine levelsatinine
also improved
anywithout any
differences
between
regimens.
differences between regimens.
Altogether, norepinephrine-dobutamine
Altogether, norepinephrine-dobutamine
both the
adequacy
of gastric muimproves bothimproves
the adequacy
of gastric
mucosa perfusion, used as a surrogate for
cosa perfusion, used as a surrogate for
splanchnic perfusion, and indices of renal
splanchnic perfusion, and indices of renal
function. By contrast, epinephrine appears
function. By contrast, epinephrine appears
to be associated with potential deleterious
to be associated
with potential deleterious
effects on the adequacy of splanchnic pereffects on thefusion
adequacy
splanchnic per(17).ofNevertheless,
the clinical imfusion (17). Nevertheless,
the clinical
pact of this transient
gastricimhypoperfusion
pact of this transient
gastric hypoperfusion
is not established.
is not established.
Limitations of the Study. The main
Limitations
of the isStudy.
Thenumber
main of patients
limitation
the small
limitation is the
smallinnumber
of patients
enrolled
the study
that may limit the
enrolled in the
study that
may limit
conclusions
concerning
thethe
outcome. Nevconclusions concerning
the
outcome.
ertheless, the
data
obtainedNevwill be useful to
Figure 2. Evolution of mean arterial pressure
ertheless, the data obtained will be useful to
(MAP)
(top), arterial
cardiac pressure
index (CI) (middle), and Figure 3. Evolution of lactate (top), PCO2 gap plan an outcome-based prospective ranFigure 2. Evolution
of mean
plan anepi-outcome-based
prospective
domized study.
We choseranto restrict our
heart
rate (CI)
(HR) (middle),
(bottom). Squares,
epinephrine(middle),
and diuresis
(bottom).
Squares,
(MAP) (top), cardiac
index
and Figure
3. Evolution
of lactate
(top), PCO
2 gap
study
to nonischemic
cardiodomized study.
Wepopulation
chose to restrict
our
treated
patients;
triangles,
norepinephrinenephrine-treated
heart rate (HR) (bottom). Squares, epinephrine- (middle), and diuresis
(bottom). patients;
Squares,triangles,
epi- norepinephshock,
since hemodynamics
in carpatients. *p !
.05 vs. H0; rine-dobutamine-treated
nonischemic
cardiopatients. †p study
! .05 vs.population
H0 genic to
treated patients; dobutamine-treated
triangles, norepinephrinenephrine-treated
patients; triangles, norepineph†
p
!
.05
vs.
H
and
p
!
.05
epinephrine
vs.
†
shock associated
and *p patients.
! .05 epinephrine
genic shock, diogenic
since hemodynamics
in with
car- myocardial
0 .05 vs. H0;
dobutamine-treated patients. *p !
rine-dobutamine-treated
p ! .05 vs.vs.H0norepinephrine†
norepinephrine-dobutamine.
dobutamine.vs. norepinephrineinfarction
is highly
dependent on the sucp ! .05 vs. H0 and
p ! .05 epinephrine vs. and *p ! .05 epinephrine
diogenic shock
associated
with myocardial
cess rate
and the timing
myocardial repnorepinephrine-dobutamine.
dobutamine.
infarction is highly
dependent
on theofsuc(18).
on these
results, we are
cess rate and erfusion
the timing
ofBased
myocardial
reptio (14). During sepsis, but also in shock oxygen delivery/consumptionerfusion
in both
conducting
a
prospective
randomized
dou(18). Based on these results, we are
of various etiologies including cardio- groups, the PCO2 gap increased in epineph- ble-blind study in cardiogenic shock sec-
Epinephrine is associated with: §  transient lac>c acidosis, §  elevated HR, §  more arrhythmia, §  inadequacy of gastric mu-­‐
cosa perfusion No difference 28 d mortality Levy B et al. Crit Care Med 2011;39:450-­‐455 SESION III: Cardiogenic shock Protocol 1910
sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S Table 2 Major clinical studies using intravenous levosimendan in different clinical settings
Study
Patients
Levosimendan dosage
Comparator
Aim
Outcomes
HF
Nieminem et al.31
151 with NYHA II–IV
3–36 mg/kg þ
0.05–0.6 mg/kg/min
Dobutamine (6 mg/kg
/min) and placebo
Effects on haemodynamics
Levosimendan treatment was
associated with dose-dependent
favourable haemodynamic
responses
Levosimendan provided favourable
haemodynamic benefit and
symptomatic relief
The haemodynamic effects of
levosimendan were maintained
during a 48-h continuous infusion
and for at least 24 h after
discontinuation of a 24-h infusion
The combined treatment improved
haemodynamics and symptoms
for 24 h
Slawsky et al.32
146 with advanced HF
6 mg/kg þ 0.1–0.4 mg/
kg/min
Placebo
Effects on haemodynamics and
symptoms
Kivikko et al.26
146 with
decompensated HF
6 mg/kg þ 0.1–0.4 mg/
kg/min
Placebo
Determine whether the
haemodynamic effects of levosimendan are sustained after the
discontinuation of drug infusion
Nanas et al.34
18 refractory to
dobutamine and
furosemide
6 mg/kg þ 0.2 mg/kg/
min as adjunctive
therapy
Dobutamine (10 mg/kg/
min)
Parissis et al.36
27 with decompensated
advanced HF
6 mg/kg þ 0.1–0.4 mg/
kg/min
Placebo
Magnitude and duration of
haemodynamic effects of a combined infusion of dobutamine and
levosimendan in end-stage HF
Effects on circulating
pro-inflammatory cytokines and
apoptosis mediators
Effects on haemodynamics and
outcomes
L. De Luca et al.
1
Downloaded from by guest on February 1, 2015
SESION III: Cardiogenic shock Protocol L.Evidence-based
De Luca et al. use of levosimendan
Levosimendan improved
haemodynamics and survival at
180 days
51
CASINO Trial
227
with
16
mg/kg þ 0.2dosage
mg/kg/
Dobutamine
Effects
on death and
Clear
mortality benefit in favor of
Study
Patients
Levosimendan
Comparator (10 mg/kg/
Aim
Outcomes
decompensated
min
min)
and
placebo
rehospitalization
due
to
HF
levosimendan
Labriola et al.57
11 with severe LV
12 mg/kg þ 0.1 mg/
—
Efficacy in low-output syndrome
In eight patients, cardiac index was
low-output HF
deterioration
HF
dysfunction after CS
kg/min
following CS
increased by .30% and PCWP
51,52
REVIVE Trial
700
andII–IV
0.1–0.2
mg/kg/min
(I)
Placebo
Effects on composite
clinical
Levosimendan produced
early
Nieminem
et al.31
151 with HF
NYHA
3–36 mg/kg
þ
Dobutamine (6 mg/kg
haemodynamics
treatmentan
was
reduced to ,18 mmHg within 3 h
symptoms at rest
endpoints
greater
symptom
response and
0.05–0.6 mg/kg/min
/min) and placebo
associated
with dose-dependent
Nijhawan et al.58
18 after CABG
0.2–0.3 mg/kg/min (I)
Placebo
Efficacy after cardio-pulmonary
Increased cardiac output and reduced
decreased
creatinine
and BNP
favourable
haemodynamic
bypass
systemic vascular resistance
levels
responses
Barisin et al.59
31 after CS
12–24 mg/kg (B)
Placebo
Effects on ischaemic myocardial
Increase
in cardiac output, EF, and
54
SURVIVE et
Trial
1327
withadvanced HF
12mg/kg
þ0.1–0.4
0.1–0.2mg/
mg/
Dobutamine
(5–40 mg/
Effects on mortality
at 180 and
days
No
differences provided
in terms of
mortality
Slawsky
al.32
146 with
6 mg/kg þ
Placebo
haemodynamics
Levosimendan
favourable
impairment
during and after
decrease in systemic
vascular
decompensated HF
kg/min
kg/min)
between
levosimendan
symptoms
haemodynamic
benefit and
off-pump CABG
resistances
requiring
inotropes
dobutamine
symptomaticincreased
relief
56
Plochl and Rajek
10 after CS
0.1–0.2 mg/kg/min (I) as
—
Effects on haemodynamics in
Levosimendan
cardiac
CS
Kivikko
et al.26
146 with
6 mg/kg
þ 0.1–0.4
mg/
Placebo
Determine
the
The
haemodynamic
adjunctive
therapy
critically whether
ill post-operative
patients
output
and stroke effects
volumeof
with
Lilleberg et al.55
23decompensated
after CABG
8 or
24 mg/kg (B)
Placebo
Effects
on systemic
and coronary
Levosimendan
improved
systemic
HF
kg/min
haemodynamic
effects
of levosilevosimendan
were maintained
decreases
in systemic
vascular
haemodynamics
and myocardial
and
coronary
flow and
did
mendan are sustained
after the
during
a 48-h blood
continuous
infusion
resistance
substrate
utilization
not
myocardial
oxygen
discontinuation
of drug infusion
and increase
for at least
24 h after
Ischaemic heart disease
consumption
or change
substrate
70
discontinuation
of a 24-h
Sonntag et al.
24 with ACS
24 mg/kg (B)
Placebo
Effects LV function after coronary
Levosimendan
improved
the infusion
function
utilization treatment improved
Nanas et al.34
18 refractory to
6 mg/kg þ 0.2 mg/kg/
Dobutamine (10 mg/kg/
Magnitude
and duration of
The
angioplasty
of combined
stunned myocardium
57
72
dobutamine
and
min
as
adjunctive
min)
haemodynamic
effects
of
a
comhaemodynamics
and
symptoms
Labriola
et
al.
11
with
severe
LV
12
mg/kg
þ
0.1
mg/
—
Efficacy
in
low-output
syndrome
In
eight
patients,
cardiac
index
was
De Luca et al.
26
AMI
(B)
Placebo
Effects on haemodynamics and
Levosimendan improved
furosemide after CS
therapy
bined infusion
of dobutamine
for 24 h by .30%
dysfunction
kg/min
following
CS velocities
increased
PCWP
coronary
flow
after and
haemodynamics
andand
coronary
levosimendan
in end-stage HF
reduced
to ,18 mmHg within 3 h
primary
angioplasty
flow
reserve
36 58
Parissis etet
al.al.
27 with
with CAD
decompensated
6 mg/kg
þ(B)
0.1–0.4 mg/
Effects on
on
circulating
Levosimendan
reduced
the
of
Nijhawan
et
al.73
18
after
CABG
0.2–0.3
(I)
Placebo
Efficacy
after
cardio-pulmonary
Increased
cardiac
output
andlevels
reduced
Michaelis
10
24
mg/kgmg/kg/min
—
Effects
coronary
vasculature,
Levosimendan
exerted
vasodilator
advanced HF
kg/min
pro-inflammatory
cytokines
and
IL-6, soluble
Fas and
Fas-ligand
bypass
systemic
resistance
myocardial
wall stress
and oxygen
effects
onvascular
coronary
conductance
59
apoptosis
mediators
Barisin et al.
31 after CS
12–24 mg/kg (B)
Placebo
Effects
on ischaemic myocardial
Increase
in cardiac
output,decreasing
EF, and
uptake
and resistance
arteries,
LIDO Trial49
103 with severe HF
24 mg/kg þ 0.1 mg/kg/
Dobutamine (5 mg/kg/
Effects
on haemodynamics
and
Levosimendan
improved
impairment
during and after
decrease inoxygen
systemic
vascular
myocardial
extraction
min mg/kg/min (I)
min)
outcomes
haemodynamics
and survival
off-pump
CABG
resistances
RUSSLAN Trial74
504 LV failure
0.1–0.4
Placebo
Effects
on composite
clinical
Incidence
of ischaemia
and/or at
180 days
Plochl and Rajek56
10complicating
after CS
0.1–0.2 mg/kg/min (I) as
—
Effects
on haemodynamics in
Levosimendan
increased
AMI
end-points
hypotension
was
similarcardiac
in all
CASINO Trial51
227 with
16adjunctive
mg/kg þ 0.2
mg/kg/
Dobutamine (10 mg/kg/
Effects
on death
and
Clear
mortality
benefit
in favor
of
therapy
critically
ill post-operative
patients
output
andgroups.
stroke
volume
with
treatment
Mortality
was
decompensated
min
min) and placebo
rehospitalization due to HF
levosimendan
decreases
systemic vascular
lower
within
levosimendan
at 14 and
low-output HF
deterioration
resistance
180 days
51,52
REVIVE Trial
700 with HF and
0.1–0.2 mg/kg/min (I)
Placebo
Effects on composite clinical
Levosimendan produced an early
Ischaemic
heart
disease
Shock
70
endpoints
greater symptom
response
and in
Sonntag
et al.
24symptoms
ACS at rest
24 mg/kg
(B) (I)
Placebo
Effects
LV
after
coronary
Levosimendan
improved
the
function
Delle
Karth
et al.80
10
with cardiogenic
0.1
mg/kg/min
—
Efficacy
in function
cardiogenic
shock
Levosimendan
treatment
resulted
decreased
and
BNP
angioplasty
stunned creatinine
myocardium
shock
following
acute ischaemia or
aof
significant
increase in
cardiac
De Luca et al.72
26 with AMI
12 mg/kg (B)
Placebo
Effects
on surgery
haemodynamics and
Levosimendan
improved
levels together
cardiac
output
with a decrease in
coronary
flow velocities
haemodynamics
and
coronary
SURVIVE Trial54
1327 with
12mg/kg þ 0.1–0.2 mg/
Dobutamine (5–40 mg/
Effects
on mortality
at 180after
days
Nosystemic
differences
in terms
of mortality
vascular
resistance
primary
flow
reserve
kg/min
between
levosimendan
Lehmann et al.81
10 decompensated
with cardiogenicHF
6 mg/kg
þ 0.2 mg/
— kg/min)
Efficacy
in angioplasty
high risk patients, with
8 patients
survived
withoutand
any
Michaelis et al.73
10shock
with CAD
24kg/min
mg/kg (B)
—
Effects
on coronary
Levosimendan
exerted vasodilator
requiring
inotropes
dobutaminefailure
undergoing
cardiogenic
shock vasculature,
and acute
multiorgan
myocardial wall stress and oxygen
effects on coronary conductance
CS
emergency surgery
ischaemia
88 55
uptake
and resistance
arteries,
decreasing
Lilleberg
23 with
afterseptic
CABG shock
8 ormg/kg/min
24 mg/kg (B)
Placebo
Effects
on
systemic and coronary
Levosimendan
improved
systemic
Morelli
etet
al.al.
28
0.2
(I)
Dobutamine
(5 mg/kg/
Efficacy
in sepsis-induced
Levosimendan
improvef
systemic
myocardial
oxygen
haemodynamics and myocardial
and coronary
blood
flow
and did
min)
dysfunction
haemodynamics
andextraction
regional
RUSSLAN Trial74
504 LV failure
0.1–0.4 mg/kg/min (I)
Placebo
Effects
on
composite
clinical
Incidence
of
ischaemia
and/or
substrate utilization
not increase myocardial oxygen
perfusion
complicating AMI
end-points
hypotension
similar substrate
in all
consumptionwas
or change
(B), bolus only; (I), infusion only.
treatment
utilization groups. Mortality was
ACS, acute coronary syndrome; AMI, acute myocardial infarction; CABG, coronary artery bypass grafting; CAD, coronary artery disease; CS, cardiac surgery; EF, ejection fraction;
HF,with
heartlevosimendan
failure; LV, leftat
ventricle.
lower
14 and
180 days
Shock
Delle Karth et al.80
10 with cardiogenic
0.1 mg/kg/min (I)
—
Efficacy in cardiogenic shock
Levosimendan treatment resulted in
shock
following acute ischaemia or
a significant increase in cardiac
cardiac surgery
output together with a decrease in
Evidence-based use of levosimendan
LIDO Trial49
103 with severe HF
24 mg/kg þ 0.1 mg/kg/
Dobutamine (5 mg/kg/
min
min)
Table 2 Major clinical studies using intravenous levosimendan in different clinical settings
Levosimendan reduced the levels of
IL-6, soluble Fas and Fas-ligand
1910
1.-­‐ Early management: IniPal stabilizaPon: Inotropes: Levosimendan sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 1.-­‐ Early management: Treatment precipitaPng factors PaPents who present to hospitals without PCI capability are usually emergently transported to a PCI center, because mortality without 1"Heart"Transplant"
and"VAD"center"
3"Cardiac"surgery"
centers"
Area"Hospital"
Local"Hospital"
transfer is markedly elevated. 3+2"PCI"center"
Pre>hospital"
assistance"
2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Interven>on. Circula>on 2011;124:574-­‐651 SESION III: Cardiogenic shock Protocol Figure 2 Trend in use of intra-aortic balloon pump among
patients with cardiogenic shock managed invasively vs
conservatively.
revascularization (percutaneous coronary intervention or
coronary artery bypass graft surgery) in the invasive group
with the corresponding matched pair from the conservative
group, significantly lower odds of mortality were observed
(odds ratio [OR] 0.37; 95% confidence interval [CI],
0.34-0.39; P < .0001) with revascularization. This lower
mortality was consistently seen across all tested subgroups,
although the test for interaction was significant for most
of the subgroups (except sex) driven by a difference in
magnitude rather than the direction (Figure 3). Specifically,
this lower mortality was seen in the elderly (!75 years)
(44.0% vs 63.6%; OR 0.45; 95% CI, 0.42-0.49;
pump used in either of the patient groups (64% reduction
[35.0% vs 59.8%] vs 54% reduction [39.6% vs 58.8%] in
those where intra-aortic balloon pump was used;
Pinteraction ¼ .02), in patients without chronic kidney disease (61% reduction [37.2% vs 60.5%] vs 51% reduction
[39.2% vs 57.0%] in those with
C L Ichronic
N I C kidney
A L Pdisease;
R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S
Pinteraction ¼ .001), and in those presenting with STEMI
(63% reduction [40.7% vs 65.1%] vs 53% reduction [33.1%
vs 51.4%] in those with non-ST-segment elevation myocardial infarction [NSTEMI]; Pinteraction < .0001) (Figure 3).
There was significantly lower in-hospital mortality over
time both in those managed invasively (43.1% in 2002 to
33.4% in 2011) and those managed conservatively (63.2%
in 2002 to 55.8% in 2011) (Figure 4).
sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE 1.-­‐ Early management: Treatment precipitaPng factors RevascularizaPon: Class I (B) recomendaPon (AHA/ESC) SHOCK Trial and Shock Registry: 13% reduc>on 6m and 1y mortality Real world prac>ce: lower in-­‐
hospital mortality in pa>ents managed invasively ( N a > o n a l I n p a > e n t S a m p l e . U S hospitals. Propensity score matching) Sensitivity Analysis
The results were largely similar using the logistic regression
analysis on the overall cohort. In the propensity score-adjusted
regression analysis, invasive management was associated with
lower odds of mortality (adjusted OR 0.72; 95% CI, 0.64-0.81)
after adjustment for baseline characteristics, mode of revascularization, type of myocardial infarction, and intra-aortic
Figure 3 In-hospital mortality among patients with cardiogenic shock managed invasively vs
conservatively in the propensity score-matched cohort.
Hochman J et al. N Engl J Med 1999;341:625-­‐634 Bangalore et al. The American Journal of Medicine. 2015:128(6):601-­‐608 SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 1.-­‐ Early management: Treatment precipitaPng factors RevascularizaPon: Class I (B) recomendaPon (AHA/ESC) §  SHOCK Trial and Shock Registry: 13% reduc>on 6m and 1y mortality Surgical management: §  Prompt repair (with or without CABG) myocardial infarc>on mechanical complica>ons §  Valvular replacement (balloon dila>on) Arrhythmias threatment SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 1.-­‐ Early management: Intra-­‐aorPc balloon pump 466
K.D. Sjauw et al.
SystemaPc review and meta-­‐analysis Thrombolysis studies Vs Primary PCI studies the hypothesis that IABP increases the efficacy of thrombolytic
therapy in STEMI patients with cardiogenic shock by increasing
coronary perfusion.32 However, there are at least three other
explanations for the observed lower mortality in the IABP group
in this setting. First, the IABP-treated patients were on average 7
years younger and the frequency of men was 10% higher. As
known from the current literature, the odds for mortality increase
33,34
Decrease in for30 day ortality 8% by 49–60%
every
10m
years
increaseof in 1age.
Also, men have
a
lower
clinical
risk
profile
than
women,
particularly
in the setting
(95% CI, 16–20%;
P , 0.0001) 35
of cardiogenic shock. Second, in the thrombolysis studies,
co-treatment with coronary revascularization was substantially
more frequent in patients who received IABP therapy than in
patients who
IABP o
therapy.
Increase in 3did
0 dnot
ay receive
mortality f 6% The SHOCK trial
clearly showed that revascularization effectively reduced mortality
(95% CI, 3–10%; P = 0.0008) in cardiogenic shock patients.36 The revascularization rates in the
SHOCK trial in the emergent revascularization arm and the conservative medical treatment arm, respectively, were 87 and 25% (relative risk 3.4), whereas the rate of IABP therapy was 86% in both
groups. In comparison, the overall revascularization rates in the
t al. Ethe
ur H
eart J 2009;30:459-­‐468 thrombolysisSjauw studiesefrom
meta-analysis
in the IABP and no
IABP group were 39 and 9% (relative risk 4.0), respectively. Third,
in the thrombolysis studies, the sicker patients may have been con-
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 1.-­‐ Early management: Intra-­‐aorPc balloon pump SystemaPc review and meta-­‐analysis Thrombolysis studies Vs Primary PCI studies Sjauw et al. Eur Heart J 2009;30:459-­‐468 IABP SHOCK Trial No significant reduc>on in MODS and SIRS. Significant LV unloading IABP SHOCK Trial II Figure 2. Comparison of Acute Physiology and Chronic Health Evaluation (APACHE) II score (A),
cardiac index (B), plasma brain natriuretic peptide (BNP) (C), and serum interleukin (IL)-6 levels (D)
over 4 days between patients treated with intra-aortic balloon pump counterpulsation (IABP) and
patients not treated by IABP with cardiogenic shock as a complication of acute myocardial infarction.
Plasma BNP levels measured on days 2 and 3 were the only significant differences between treatment
groups (p " .05). For confidence intervals, see Table 3.
over time or between the two treatment
groups (Fig. 2D).
Confidence intervals for patients with
and without IABP are shown in Table 3.
n = 45 (IABP group 23) APACHE II Score, CI, IL-6,
Plasma BNP, and Survival
Data for initial and serial APACHE II
scores are shown in Figure 3A. Among
survivors, the initial APACHE II score
was 18.1 ! 1.7, falling to 13.9 ! 1.6 over
the 4-day observation period, i.e., a fall of
4.2 points (# $4.2). The initial APACHE
II score was significantly higher in nonsurvivors (29.9 ! 2.9) and rose still further to 30.6 ! 3.9 at day 4, i.e., an increase of 0.7 points (# %0.7). The fall in
APACHE II score of &4 points reflects a
considerable improvement in MODS severity in survivors.
CI and IL-6 levels were also found to
differ between survivors and nonsurvivors (Figs. 3B–D). CI on day 1 was significantly different among these groups,
while IL-6 levels were significantly lower
at the initial time point, day 1, and day 3
in survivors than in nonsurvivors. BNP
levels showed a poor relationship to survival. Confidence intervals for surviviors
Prondzinsky et al. Crit Care Med 2010;38:152-­‐160 SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 1.-­‐ Early management: Intra-­‐aorPc balloon pump SystemaPc review and meta-­‐analysis Thrombolysis studies Vs Primary PCI studies Sjauw et al. Eur Heart J 2009;30:459-­‐468 IABP SHOCK Trial No significant reduc>on in MODS and SIRS. Significant LV unloading IABP SHOCK Trial II The
n e w e ng l a n d j o u r na l
of
Prondzinsky et al. Crit Care Med 2010;38:152-­‐160 m e dic i n e
Intr a aortic Balloon Support in Cardiogenic Shock
Table 3. Clinical Outcomes.
Outcome
IABP
(N = 300)
included in the analysis of the primary end point.
Relativewas
Risksimilar among patients
At 30 days, mortality
Control in the IABP group
with
IABP
and
those in the control group
(N = 298)
P Value
(95% CI)
(39.7% and 41.3%, respectively; relative risk with
IABP, 0.96; 95% confidence interval [CI], 0.79 to
P = 0.69)0.96
(Table
3 and Fig. 1). Only minor
Primary end point: all-cause mortality at 30 days
119 (39.7)
123 (41.3) 1.17;0.69
(0.79–1.17)
in2.24
the (0.70–7.18)
relative risk estimates were obReinfarction in hospital
9 (3.0)
4 (1.3) differences
0.16
served in an analysis restricted to the per-protocol
Stent thrombosis in hospital
4 (1.3)
3 (1.0)
0.71
1.32 (0.30–5.87)
population (mortality, 37.5% in the IABP group
Stroke in hospital
2 (0.7)
5 (1.7) and 0.28
(0.08–2.03)
41.4% in 0.40
the control
group; relative risk, 0.91;
Ischemic
2 (0.7)
4 (1.3) 95%0.45
(0.09–2.71)
CI, 0.74 0.49
to 1.11;
P = 0.35) or in multivariate
for variables including
Hemorrhagic
0
1 (0.3) modeling
0.50 with adjustment
—
myocardial infarction,
Peripheral ischemic complications requiring intervention
13 (4.3)
10 (3.4) non–ST-segment
0.53
1.29elevation
(0.58–2.90)
anterior myocardial infarction, resuscitation bein hospital
fore
randomization,
and
clinical
site (relative risk,
Bleeding in hospital*
0.95; 95% CI, 0.68 to 1.32; P = 0.75).
Life-threatening or severe
10 (3.3)
13 (4.4)
0.51
0.76 (0.34–1.72)
Results with respect to the primary end points
Moderate
52 (17.3)
49 (16.4) were0.77
1.05in(0.74–1.50)
consistent
all prespecified and post hoc
Sepsis in hospital
47 (15.7)
61 (20.5) subgroups
0.15
0.772).
(0.54–1.08)
(Fig.
Among the 277 patients in
whom an intraaortic balloon pump was inserted
* Bleeding during the hospital stay was assessed according to the Global Use of Strategies
Openunderwent
Occluded Coronary
andtowho
revascularization, there was
Arteries (GUSTO) criteria.
no significant difference in mortality between the
37 patients (13.4%) in whom the balloon pump
was inserted before revascularization and the
end points and a Mann–Whitney U test for quan- intraaortic balloon pump,
most within the first
240 patients (86.6%) in whom the balloon pump
50
Control
40
number (percent)
titative end points.
P=0.92 by log-rank test
Mortality (%)
IABP
30
20
10
0
0
5
10
15
20
25
30
Days since Randomization
Figure 1. Time-to-Event Curves for the Primary End Point.
Time-to-event curves are shown through 30 days after randomization for
the primary end point of all-cause mortality. Event rates represent Kaplan–
Meier estimates.
Thiele et al. N Engl J Med 2012;367(14):1287-­‐96 Safety
The results with respect to safety end points are
shown in Table 3. There were no significant differences between the IABP group and the control
SESION III: Cardiogenic shock Protocol 24 hours after randomization; in the case of 26 of
sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 1.-­‐ Early management: Intra-­‐aorPc balloon pump. RecommendaPon for use: 1.-­‐ CS a`er STEMI who do not quickly stabilize with pharmacological therapy (Class IIa/IIb B). Rou>ne use of IABP in pa>ents with CS is not recommended (Class III A) 2.-­‐ IABP inser>on should be considered in pa>ents with haemodynamic instability/cardiogenic shock due to mechanical complicaPons (Class IIa C) 3.-­‐ Acute ICP failure: … When severe haemodynamic instability is present, IABP or mechanical circulatory assistance may be desirable before emergency surgery. 4.-­‐ Hospitals Without On-­‐Site Cardiac Surgery: Transfer emergently for coronary bypass surgery pa>ents with High-­‐grade len main or 3-­‐vessel coronary disease with clinical or hemodynamic instability, failed or unstable PCI result and ongoing ischemia; preferably with IABP support SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S Structure: 1.-­‐ Early management R efractory CS 2.-­‐ management Cardiogenic+Shock
Clinical+presenta3on:
Acute+vs+Chronic+HF
Inotropes+/+vasopressors
Reperfusion
Intra:Aor3c+balloon+pump
Suppor3ve+therapy
Inotropes+/+vasodilators
Diure3cs
Refractory+
Cardiogenic+Shock
INTERMACS+profile
No
Yes
Intermacs+4:7
Intermacs+1:2
Intermacs+2:3
Short:term+MCS+
devices
Yes
3.-­‐ Outcome and DesPnaPon Therapy Acute+Descompensated+Chronic+HF
Myocardial+Infarc3on+/+Acute+myocardi3s
Cardiac+recovery
Wean+and+remove+
device
Short:term+MCS+
devices
No
MOD+and
Neurological+recovery
No
Farmacological+
treatment
Electrical+Devices
Surgical+management
Exercise+tes3ng:+peak+VO2
HF+Survival+Score
Yes
Heart+Transplant
or
Durable+VADs
VO +<+12+:14+ml/Kg/min
₂
Palia3ve+Care
SESION III: Cardiogenic shock Protocol fit or higher mortality rates. There are no data comparing
the choice of BMS versus DES in cardiogenic shock; howsta t e o f t h e a r t i n ever, BMS are often used because compliance with long-term ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S DAPT is often unclear in the emergency setting.
In patients with multivessel disease, revascularization of
the noninfarct artery may be necessary to maximize myocardial perfusion.
Alternatively,
with multivessel
2.-­‐ Refractory CS inmpatients
anagement: Refractory)
disease and particularly left main disease, emergency CABG
Cardiogenic)Shock
as a primary reperfusion strategy may be preferred.50,441
Refractory
cardiogenic shock unresponsive to revascularizaYes
tion may necessitate institution of more intensive cardiac
Intermacs)1&2
Short&term)MCS)
support with a ventricular assist device or other hemodynamdevices
ic support devices to allow for myocardial recovery or
subsequent cardiac transplantation in suitable patients.
5.2.4. Revascularization Before Noncardiac
Surgery: Recommendations
Yes
Cardiac)recovery
No
Short&term)MCS)
devices
Class IIa
1. For patients who require PCI and are scheduledWean)and)remove)
for
MOD)and
Yes
Neurological)recovery
device
elective noncardiac surgery in the subsequent 12
months, a strategy of balloon angioplasty, or BMS
Heart)Transplant
No
or
implantation followed by 4 to 6 weeks of DAPT, is
Durable)VADs
PaliaIve)Care
reasonable.442– 448 (Level of Evidence: B)
2. For patients with DES who must undergo urgent
surgical procedures that mandate the discontinuation of
DAPT,
it is reasonable
tofor continue
aspirin
if Interven>on. Circula>on 2011;124:574-­‐651 2011 ACCF/AHA/SCAI Guideline Percutaneous Coronary possible and restart the P2Y12 inhibitor as soon as
444
possible in the immediate postoperative
period.
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 2.-­‐ Refractory CS management: Short-­‐Term MCS. Ideal MCS: Reduc>on wall stress and oxygen consump>on (Myocardial recovery), normaliza>on of hemodynamics (MODS preven>on/Therapy) and low adverse effects Effects of pVADs: §  Rapid reversed hemodynamic compromise §  Reduce LV wall stress and Neurohormonal axis ac>va>on, but increased systemic inflamma>on §  LV unloading may result in infarct size reduc>on and increased LV recovery Biswaijit Kar et al. J Am Coll Cardiol 2011;57:688-­‐696 Shah NR et al. J Am Coll Cardiol HF 2013;1:200-­‐206 Meyns et al. J Am Coll Cardiol 2003;41:1087-­‐95 SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 2.-­‐ Refractory CS management: Short-­‐Term MCS. Key ArPcles on MCS for Refractory Cardiogenic Shock: SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 2.-­‐ Refractory CS management: Short-­‐Term MCS. RecommendaPon for short-­‐term MCS LV assist devices for circulatory support may be considered in pa>ents with refractory cardiogenic shock. (Class IIb C)1 Non-­‐durable MCS (pVADs and extracorporeal VADs), is reasonable as a “bridge to recovery” or “bridge to decision” for selected pa>ents with HFrEF with acute, profound hemodynamic compromise. (Class IIa B)2 The use of temporary MCS should be strongly considered in pa>ents with MOF, sepsis, or on mechanical ven>la>on to allow successful opPmizaPon of clinical status and neurologic assessment prior to placement of a long term MCSD. (Class I C)3 1AHA and ESC Guidelines for the Management of STEMI 22013 ACCF/AHA Guideline for the Management of Heart Failure 32013 ISHLT MCS Guidelines. Feldman et al. J Heart Lung Transplant 2013:32:157-­‐187 SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 2.-­‐ Refractory CS management: Short-­‐Term MCS. Device selecPon: e10
Rihal et al.
JACC VOL. 65, NO. 19, 2015
Percutaneous MCS Devices in Cardiovascular Care
MAY 19, 2015:e7–26
Cardiac effects of Mechanical Support F I G U R E 2 Cardiac Effects of Mechanical Support
Illustrations of PV loops after activation of device therapy (gray loops). (A) Intra-aortic balloon pump (IABP) counterpulsation reduces both peak LV systolic
and diastolic pressures and increases LV stroke volume. The net effect is a reduced slope of arterial elastance (Ea2), (B) Percutaneous LV assist devices
Rihal et al. J Am Coll Cardiol 2015;65(19:7-­‐26 (pLVAD: Impella and TandemHeart) significantly reduce LV pressures, LV volumes, and LV stroke volume. The net effect is a significant reduction in cardiac
workload. (C) Veno-arterial extra-corporeal membrane oxygenation (VA-ECMO) without a LV venting strategy increases LV systolic and diastolic pressure, while
reducing LV stroke volume. The net effect is an increase in arterial elastance (Ea).
SESION III: Cardiogenic shock Protocol diotomy CS and as a bridge
AMI and CS undergoing percutaneous coronary intervention
a lo
(PCI) demonstrated that the addition of IABPs did not result stademonstrated
t e o f t h eto ahave
r t i n
complications
in a multicent
in a significant improvement in multiorganADVAN
dysfunction CED synHEA
RT F
AILU
RE 11
beOan
drome, cardiac index, or systemic
C L I Ninflammatory
I C A L P R A C Tactivation.
I C E A N D O R G Ademonstrated
N I Z A T I O N A to
L M
D Eeffect
L S patients with severe graft rej
Furthermore, a recent meta-analysis suggested that although
(1-year survival of 32%).19 A
IABPs may have a beneficial effect on hemodynamic paramdevice can be inserted pe
eters in infarct-related CS, the existing data do not support a
VAD currently has 510k a
mortality benefit.12 Finally, another recent meta-analysis
circulatory support and has h
evaluating the use of IABPs in patients with STEMI complito 30 days of circulatory sup
cated by CS suggested no improvement in 30-day survival or
failure. Finally, the Impella
LV ejection fraction and an increased risk of stroke and
13
Inc), a catheter-mounted mic
bleeding complications. Given these data, the role of IABPs
the LV in a retrograde fashio
in patients with CS is unclear, and further randomized trials
surgical cut-down that is c
are needed. Despite this ambiguity, the most current Ameri14
Cardiac effects of Mofechanical Support Association and
output by 5.0 L/min, has be
can College
Cardiology/American
Heart
1
effective as a bridge-to-t
European Society of Cardiology guidelines for the managebridge,22 and a bridge-to-rec
ment of STEMI state that initiation of IABP counterpulsation
Hemodynamic condiPon of the paPent and Device support Despite advances in surg
technology and improvemen
attributable to these device
remain, including the need
inflammation associated with
the often prolonged delay a
activation. To address these i
ability to provide adequate c
developed.
2.-­‐ Refractory CS management: Short-­‐Term MCS. Device selecPon: PVADs: Princ
An ideal PVAD should have
ability to be implanted rapid
Kar et al. Circula>on 2012;125:1809-­‐1817 approach;
effective and relia
Figure 1. Clinical spectrum of cardiogenic shock. IABP indiadequately unload the imp
cates intra-aortic balloon pressure; ECMO, extracorporeal
systemic perfusion pressure,
5
SESION III: Cardiogenic shock Protocol membrane oxygenation. Adapted from Samuels et al with
sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 2.-­‐ Refractory CS management: Short-­‐Term MCS. Device selecPon: Cardiac effects of Mechanical Support Hemodynamic condiPon of the paPent and Device support Technical consideraPons (ease and rapidity of inserPon) Cost EffecPveness SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 2.-­‐ Refractory CS management: Short-­‐Term MCS. Device selecPon: RV#failure#
LV#failure#
BiV#failure#
VA#ECMO#
Impella#5.0#
VA#ECMO#
VA#ECMO##
CentriMag'RVAD'
Tandem'Heart'
RVAD'
CentriMag##
Tandem'Heart'
LVAD'
or'a''combina3on'
of'LV'support'
devices'plus'RV'
support'devices'
Coexist#ALI#or#
ARDS#
VA#ECMO#
Lamarche et al. J Thorac Cardiovasc Surg 2011;142:60-­‐5 Sayer et al. Curr Opin Crit Care 2012;18:409-­‐416 SESION III: Cardiogenic shock Protocol and the high flow (Table 2). There is limited experience in CS for
sta t e o f t h e a r t i n percutaneous use for venoarterial ECLS with one single-centre, nonADVAN
randomized retrospective analysis showing improved survival
rates CED HEA RT F AILU RE C55L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S with ECLS in comparison to historical control. In a more recent prospective report, in-hospital mortality of ECLS patients was as high as
63.2%. The elderly patient group of .62 years and those with cardiopulmonary resuscitation were even characterized by a mortality of
100% questioning the unselective use of ECLS.56
HeartTM (Cardiac
Impellaw 2.5, 5.0,
any). Furthermore,
e device iVAC 2Lw
ed percutaneously
ulsatile support of
pump via a 17 F
blood is aspirated
en into the memp ejects the blood
the catheter valve
through the side
at’. The device dirnd simultaneously
aorta.
een described prend Table 2 provides
nd left-ventricular
ince the publishing
of the only three
VADs (two trials
additional randoreated with active
her mean arterial
pressure. On the
guest on May 26, 2015
P use in mechanical
2.-­‐ Refractory CS management: Short-­‐Term MCS. OpPmal management: §  Early when fluid resuscita>on and pharmacologic support fail to maintain a SBP > 90 mmHg and physiological evidence of visceral hypoperfusion (Serum lactate Level: risk factor for poor survival) §  Preven>on MODs §  Subjec>ve criteria. Thiele et al. Eur Heart J 2015;36:1223-­‐1230 Device-­‐efficacy Vs Device-­‐related complica>ons Figure
3 Considerations
on use of mechanical
support for
multiorgan system dysfunction prevention and therapy.
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S Structure: 1.-­‐ Early management R efractory CS 2.-­‐ management Cardiogenic+Shock
Clinical+presenta3on:
Acute+vs+Chronic+HF
Inotropes+/+vasopressors
Reperfusion
Intra:Aor3c+balloon+pump
Suppor3ve+therapy
Inotropes+/+vasodilators
Diure3cs
Refractory+
Cardiogenic+Shock
INTERMACS+profile
No
Yes
Intermacs+4:7
Intermacs+1:2
Intermacs+2:3
Short:term+MCS+
devices
Yes
3.-­‐ Outcome and DesPnaPon Therapy Acute+Descompensated+Chronic+HF
Myocardial+Infarc3on+/+Acute+myocardi3s
Cardiac+recovery
Wean+and+remove+
device
Short:term+MCS+
devices
No
MOD+and
Neurological+recovery
No
Farmacological+
treatment
Electrical+Devices
Surgical+management
Exercise+tes3ng:+peak+VO2
HF+Survival+Score
Yes
Heart+Transplant
or
Durable+VADs
VO +<+12+:14+ml/Kg/min
₂
Palia3ve+Care
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 3.-­‐ Outcome and DesPnaPon Therapy: Short&term)
MCS)devices
Yes
Wean)and)
remove)device
Cardiac)
Recovery
No
MOD)and)
Neurological)
recovery
No
Palia=ve)Care
Yes
Heart)transplant)
or)
Durable)VADs
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 3.-­‐ Outcome and DesPnaPon Therapy: 1"Heart"Transplant"
and"VAD"center"
3"Cardiac"surgery"
centers"
Area"Hospital"
PaPents stable on Short-­‐Term MCS and whithout cardiac recovery should be transfer to Heart-­‐
transplant /Durable VAD center. Local"Hospital"

3+2"PCI"center"





Pre>hospital"
assistance"







       
        
            




        
          


SESION III: Cardiogenic shock Protocol 
sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 3.-­‐ Outcome and DesPnaPon Therapy: MODS and neurology disfuncPon : Risk factors for 1006
The Journal of Heart and Lung Transplantation, Vol 33, No 10, October 2014
mortality Table 5
Risk Factors for Mortality for Adult Heart Transplants
Model
Variable
1 year mortality, n ¼ 10,739
(Jan 2007–June 2012)a
RVAD
No.
* Temporary circulatory supportb
Ventilator
Chronic pulsatile flow BiVAD
Recipient history of dialysis
Total artificial heart
Diagnosis: congenital vs CM
Previous transplant
Chronic continuous-flow LVAD
Transplant year: 2007 vs 2011/2012
Previous transfusion
Male recipient/female donor vs male
recipient/male donor
Transplant year: 2008 vs 2011/2012
IV drug therapy for recipient infection
Diagnosis: CAD vs CM
Not hospitalized just before transplant
ECMO at time of transplant
* * 10 year mortality, n ¼ 11,641
(Jan 1998–June 2003)c
HR
95% CI
p-value
22
3.26
1.60–6.65
0.0012
173
322
254
278
113
276
336
2,351
1,911
2,476
1,598
2.31
2.03
1.99
1.90
1.77
1.66
1.57
1.44
1.28
1.27
1.27
1.70–3.15
1.59–2.61
1.45–2.73
1.49–2.44
1.14–2.74
1.18–2.32
1.19–2.08
1.21–1.73
1.07–1.53
1.10–1.47
1.08–1.50
o.0001
o.0001
o.0001
o.0001
0.0104
0.0034
0.0016
o.0001
0.0081
0.0010
0.0039
1,829
1,093
4,206
5,914
28
1.26
1.24
1.17
0.80
1.74
1.05–1.51
1.04–1.47
1.02–1.34
0.70–0.91
1.09–2.79
0.0136
0.0162
0.0278
0.0010
0.0212
*Spanish Heart Transplanta>on Registry Ventilator at time of transplant
1.40–1.87 o.0001
2014 ISHLT Adult Heart Transplanta>on Report. J H374
eart 1.62
Lung Transplant 2014;33(10):996-­‐1008 Diagnosis: not CMd vs CM
86 1.61 1.16–2.24
0.0044
Recipient history of dialysis
Previous transplant
Prior pregnancy
308
302
1,648
1.46
1.34
1.30
1.25–1.71
1.12–1.59
1.18–1.43
o.0001
0.0010
o.0001
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 3.-­‐ Outcome and DesPnaPon Therapy: MODS and neurology disfuncPon : Risk factors for mortality 560
Table 6
The Journal of Heart and Lung Transplantation, Vol 33, No 6, June 2014
Adult Primary Continuous-flow LVAD and BiVAD Implants: June 2006 to December 2013 (N ¼ 9,372)
Early hazard
Risk factors for death
Demographics
Age (older)
Female
BMI (higher)
Clinical status
History of stroke
INTERMACS Level 1
INTERMACS Level 2
Destination therapy
Non-cardiac systems
Albumin (lower)
Creatinine (higher)
Dialysis
BUN (higher)
Right heart dysfunction
Right atrial pressure (higher)
RVAD in same operation
Bilirubin (higher)
Ascites
Surgical complexities
History of cardiac surgery
Concomitant cardiac surgery
Late hazard
Hazard ratio
p-value
1.36
1.20
1.13
o0.0001
0.007
o0.0001
1.30
1.69
1.44
1.24
0.03
o0.0001
o0.0001
0.0005
0.90
0.02
2.37
1.06
o0.0001
o0.0001
1.11
2.45
1.21
1.27
0.02
o0.0001
o0.0001
0.01
1.43
o0.0001
Hazard ratio
p-value
1.05
0.0003
1.06
0.01
1.21
0.0008
BiVAD, biventricular assist device; BMI, body mass index; BTT, bridge to transplant; BUN, blood urea nitrogen; DT, destination therapy; LVAD, left
ventricular assist device; RVAD, right ventricular assist device.
Sixth INTERMACS annual report. J Heart Lung Transplant 2014;33:555-­‐564 The overall freedom from pump exchange for thrombosis
and other device malfunction or infection was 96% at
12 months in the first era (Figure 16), compared with 91% in
Analog Scale (Figure 17), self-care (Figure 18) and usual
activities (Figure 19) dimensions. The quality-of-life improvements at 12 and 24 months have remained consistent
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 3.-­‐ Outcome and DesPnaPon Therapy: MODS and neurology disfuncPon : Risk factors for mortality End-­‐organ recovery is key to success for ECMO as a bridge to Heart transplantaPon or implantable LVAD 4
J. Riebandt et al. / European Journal of Cardio-Thoracic Surgery
Table 2: Clinical parameters before extracorporeal life support and before ventricular assist device
Creatinine (mg/dl)
MDRD-GFR (ml/min/1.78 m2)
Bilirubin (mg/dl)
Aspartate aminotransferase (U/l)
Alanine aminotransferase (U/l)
MELD-XI score (pts)
FiO2 (%)
Positive end-expiratory pressure (mbar)
Peak inspired pressure (mbar)
Noradrenaline (μg/kg/min)
Levosimendan (μg/kg/min)
Dobutamine (μg/kg/min)
Haemoglobin (mg/dl)
Platelets (×109)
C-reactive protein (mg/dl)
Leucocytes (×109)
Before ECLS
Before VAD
1.86 ± 0.91
48.73 ± 26.64
2.03 ± 1.30
1426 ± 2176
982 ± 1466
18.43 ± 7.72
52 ± 18
7±3
21 ± 4
0.408 ± 0.355
0.056 ± 0.085
4.362 ± 5.268
11.1 ± 2.0
166 ± 111
11.29 ± 9.45
14.0 ± 7.9
1.32 ± 0.52
66.26 ± 28.33
3.08 ± 2.13
277 ± 259
357 ± 447
16.08 ± 8.59
26 ± 23
5±4
17 ± 4
0.056 ± 0.097
0.010 ± 0.032
0.056 ± 0.097
9.6 ± 0.9
69 ± 47
13.21 ± 6.80
11.1 ± 3.5
P-value
0.02
0.01
0.05
0.04
0.04
0.05
<0.01
0.02
0.01
<0.01
0.06
0.06
<0.01
<0.01
0.80
0.21
Durinka et al. ASAIO J 2014;60(2):189-­‐92 Unless otherwise indicated, data expressed as mean ± SD.
MDRD-GFR: Modification of Diet in Renal Disease—Glomerular Filtration Rate; MELD-XI: Model for End-stage Liver Disease—excluding INR; FiO2: fraction of
inspired oxygen; ECLS: extracorporeal life support; VAD: ventricular assist device.
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 770
Circ Heart Fail
July 2013
3.-­‐ Outcome and DesPnaPon Therapy: INTERMACS profile and postoperaPve outcome: Heart Tx Postopera>ve mortality: INTERMACS 1 43%, INTERMACS 2 26,8% & INTERMACS 3-­‐4 18% INTERMACS 1 vs 3-­‐4: OR 4,38 (2,51-­‐7,66) INTERMACS 1 vs 2: OR 2,49 (1,56-­‐3,97) Circ
Heart
Fail
July
2013
INTERMACS 2 vs 3-­‐4: OR 1,76 (1,02-­‐3,03) 770
Figure 4. Long-term survival after heart transplantation. A, Entire cohort. B, Patients discharged alive
from hospital after heart transplantation. INTERMACS indicates Interagency Registry for Mechanically Assisted Circulatory Support.
Long-­‐term survival was not influenced by INTERMACS profile Figure 4. Long-term survival after heart transplantation. A, Entire cohort. B, Patients discharged alive
from hospital after heart transplantation. INTERMACS
indicates MCS
Interagency
for Mechanipreoperative
may Registry
adversely
impact post-transplant
cally Assisted Circulatory Support.
12,19,20
(ONT status 0) is reserved only for HT candidates supported
Barge-­‐Caballero et al. Circ eart MCS
Fail 2013:6:763-­‐772 on a H
temporary
device
or for those experiencing severe
Notwithstanding
outcomes, with controversial results.
this, outcomes of patients with profiles 1 and 2 who underwent emergency HT in our cohort were inferior to those of
patients undergoing VAD implantation as a bridge to HT in
the INTERMACS registry.17 Moreover, in a recent single-
complications of a long-term implantable VAD, such as infection, embolism, or mechanical dysfunction. In recent years,
Spanish multicenter registries have shown a steady increase
in the number of temporary MCS devices implanted3 and HT
SESION III: Cardiogenic shock Protocol 22
over the past 6 years.
sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S Survival impact of multiple pump replacements
The unusual need for pump exchange has a clearly
detrimental
on patientand survival
(Figure 20). T
One3.-­‐ effect
Outcome DesPnaPon herapy: year survival after the original continuous-flow implant
is now about 80%, but about 65% after a second implant
INTERMACS profile and postoperaPve outcome: VADs Continuous Flow LVAD/BiVAD Implants: 2008 – 2013, n = 9372
Levels 4-7, n=1789
Deaths=405
Kirklin et al.
Table 7
Level 1: n=1391
Deaths=381
Sixth INTERMACS Report
CF-LVAD/BiVAD Implants: January 2008 to December 2013 (N ¼ 9,372)
% Surviva
al
Implant date era
Level 3: n=2591
Deaths=544
Level 2: n=3601
Deaths=942
Deaths
942
P < .0001
Event: Death (censored at transplant and recovery)
2008–2010
2011–2013
Patient profile at time of implant
n
%
n
%
1 Critical cardiogenic shock
2 Progressive decline
3 Stable but inotrope-dependent
4 Resting symptoms
5 Exertion-intolerant
6 Exertion-limited
7 Advanced NYHA Class 3
Total
464
1,250
659
370
84
49
30
2,906
16.0%
43.0%
22.7%
12.7%
2.9%
1.7%
1.0%
100.0%
927
2,351
1,932
941
192
79
43
6,465
14.3%
36.4%
29.9%
14.6%
3.0%
1.4%
1.0%
100.0%
CF, continuous flow; NYHA, New York Heart Association.
Months post implant
and 50% after a third implant. Thus, solutions to prevent
Time-related causes of mo
malfunction and pump thrombosis are of great
Figure 12
Actuarial survival for primary continuous-flow pump
The time-related risks for the m
importance.
depicted in Figure 21. During t
devices, stratified by INTERMACS level atSixth implant.
Depiction
is
multi-system organ failure mort
INTERMACS annual report. J Heart Lung Transplant 2014;33:555-­‐564 4 months before it merges with a
as shown in Figure 9.
first 3 months, neurologic causes
Continuous Flow LVAD/BiVAD Implants: 2008 – 2013 n = 9372
SESION III: Cardiogenic shock Protocol BTR, n= 46
Deaths= 4
risk during the remainder of the
out to 4 to 5 years, the gradually
sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S 3.-­‐ Outcome and DesPnaPon Therapy: Short&term)
MCS)devices
Advanced Heart-­‐Failure and Heart Transplant Team: Yes
Wean)and)
remove)device
Cardiac)
Recovery
Mul>disciplinary evalua>on and lis>ng pa>ent or durable VAD inser>on No
MOD)and)
Neurological)
recovery
No
Palia=ve)Care
Yes
Heart)transplant)
or)
Durable)VADs
SESION III: Cardiogenic shock Protocol sta t e o f t h e a r t i n ADVAN CED HEA RT F AILU RE C L I N I C A L P R A C T I C E A N D O R G A N I Z A T I O N A L M O D E L S Conclusions: §  Cardiogenic shock mortality remain very high §  Short-­‐term MCS devices are useful in Refractory CS, but opPmal Pming and device selecPon are under invesPgaPon §  End-­‐organ recovery and improve in clinical profile is associated with berer prognosis §  Heart Team: healthcare providers have to cooperate to improve survival of CS SESION III: Cardiogenic shock Protocol