Causes of death in patients with STEMI
treated with fibrinolysis
(Kashani et al ,JACC,2004)
Variable
Inhospital Death
(N=913)
30 Days Death
(N=1006)
31-180 Days
Death (N=303)
CHF
30.0
29.6
17.5
Recurrent M
20.2
20.2
19.8
Rupture
18.5
16.9
.3
Intracranial
Hemorrhage
10
9
.7
Other
Cardiovascular
8.8
8.7
8.3
Dysrhythmia
6.6
6.9
8.6
Other Non-Cardiac
3.5
3.9
19.8
Unobserved
1.3
3.1
9.9
Unknown
1.2
1.7
15.2
Numbers in table represent percentages of death
Improve myocardial salvage &more aggressive treatment of post- MI CHF
• Cardiogenic Shock
• The impaired ability of the heart to
pump blood
• Pump failure of the right
• or left ventricle
• Most common cause is
• LV MI (Anterior)
• Occurs when > 40% of ventricular
mass damage
• Mortality rate of 80 % or >
• Cardiogenic Shock
• Etiologies
• Mechanical: complications of MI:
• Papillary Muscle Rupture!!!!
• Ventricular aneurysm
• Ventricular septal rupture
•
•
•
•
•
• Other causes:
Cardiomyopathies
tamponade
tension pneumothorax
arrhythmias
valve disease
• Cardiogenic Shock
• Pathophysiology
• Impaired pumping ability of LV leads to…
Decreased stroke volume leads to…..
Decreased CO leads to …..
Decreased BP leads to…..
Compensatory mechanism which may
lead to …
Decreased tissue perfusion !!!!
CRITERIA of C.S.
(1)Hypotension(SBP < 90 mm Hg >
30 minutes
(2) Hypoperfusion
(3) Hemodynamic confirmation
( PCWP > 15 mmHg + C.I. <
2
2.2 L /min./m )
(Hochmman J.S .etal , Am H.J.,1999)
Mortality :Major shock categories
Mortality %
100
80
60
40
20
0
Incidence
78.5%
3.9%
6.9%
2.8%
1.4%
(Hochman et al,JACC,2000)
6.7%
Clinical profile of C.S. with L.V.F.
Hypopercongestion
fusion
P.
N%
Mortality
Gp.A
-
-
14(3%)
21%
Gp. B
+
-
32(6%)
22%
Gp. C
-
+
158(28%)
70%
Gp.D
+
+
367(64%)
60%
(Hochmman et al , JACC , 2000)
In –hospital event rates by angiographic
findings in patients with LV or RV failure
(Wong et al,JACC, 2000)
Implications of the timing of onset of C.S.
after AMI
(John& Webb et al ,JACC ,2000)
Clinical correlates,management and outcome in M.T.
complicated by C.S. at hospital admission :
A report from the shock trial and registry.
C.S. admission
C.S. delayed
In hospital
mortality
75%
56%
Early
revascularization
60%
46%
Initial medical
stabilization
82%
62%
P< 0.001
C.S.A. have a more severe haemodynamic
derangement and higher mortality , benefit equally
from E.R.V.
(Raban V. Teger ,JACC, 2005)
C.S. with NSTEMI
Percent
100
50
0
Vessel disease
(Jacobs et al , JACC ,2000)
Percent
C.S. with NSTEMI
Rates of in-hospital coronary angiography
and revascularization after diagnosis of CS
caused by LV failure.
(Jacobs et al,JACC, 2000)
Cardiogenic shock complicating NSTEMI
Data from Rico survey
1945 AMI 148 (7.6 % had C.S.)
NSTEMI
STEMI
P
No:
35(23%)
113 (76%)
Age
78
73
P <0.001
D.M.
49%
27%
P=0.025
PVD
29%
3%
P<0.01
LVEF
45%
34%
P=0.048
IN hospital
mortality
46%
58%
P=0.032
C.S. + NSTEMI have higher risk profile than STEMI
,more recurrent angina IMJ, higher
revascularization ,mortality equally higher.
(Marianne Zeller etal ,JACC ,2005)
In-Hospital survival(%)
D.M. in CS complicating AMI
Shindler et al ,JACC, 2000
Survival benefit in diabetes (black bars) and
non diabetics (white bars)
CS due to acute severe MR
Valve surgery
(n=43)
No valve surgery
(n=51)
P value
Left heart
cathterization
93
61
<0.001
Intra-aortic
ballon pump
98
43
<0.001
Angioplasty
attempted
16
18
1.000
Bypass surgery
86
8
,0.001
Angioplasty or
by pass surgery
88
26
<0.001
Transfusion
93
40
<0.001
In-hospital
mortality
40
71
0.003
(Thompson et al ,JACC, 2000)
Patient characteristics :VSR vs.
acute severe MR in shock trial
registery patients
characteristics
VSR
Severe MR
n
54
97
History of MI
15.1
33
0.020
Diabetes
17
37
0.035
LV ejection
fraction
40.6+11
38.7+17.2
0.281
In-hospital
survival
13
45.4
<0.001
(Menon et al ,JACC , 2000)
P value
C.S. due to free – wall rupture or
tamponade
(Slater etal , JACC ,2000)
Intervention in subacute possible
Incidence : 2.7% of all C.S.
Less P . Edema ,D.M. prior MJ.
Pericardial effusion in 75%
27/28 had surgery or pericardiocetesis
Survival rate 39.3% as the overall group
Mortality by revascularization status
No LH CATH
N=334(38%)
88.6% Mortality
No revascularization attempt
N=146(17%)
59.6% Mortality
LH CATH
N=550(62%)
44.9% Mortality
PTCA
N=268(30%)
45.5% Mortality
CABG
N=136(15%)
27.9% Mortality
PTCA< 18 hours post-CS
N=199
47.2% Mortality
CABG < 18 hours post –CS
N=48
39.6% Mortality
(Hochman et al ,JACC,2000)
Thrompolysis , Ballon counter pulsation in the
shock trial registry
(Sanborn et al ,JACC, 2000)
Thrombolysis and JABPC in C.S.
(Sanborn etal ,JACC ,2000)
Mortality
No. T.T. no IABP
N=285 33%
IABP only
N=279 33%
TT only
N=132 15%
+ TT + JABP
N= 160 19%
77%
52%
63%
47%
• Intra-Aortic Balloon Pump
• Inflatable 32-40 cc balloon
• Triggered to inflate with helium
immediately after aortic valve closure
• Triggered to deflate with opening of the
aortic valve
• Intra-Aortic Balloon Pump
100
VAD
Cumulative survival %
90
80
70
60
IABO
50
40
30
20
10
Log –rank P=0.80
0
Days from randomization
VAD reverse C.s. more effectively than IABP
With more complications
(Thiele etal EHJ,2005)
Pharmacological support
Dopamine 89.35
Norepinphrine 31.6%
Epinephrine 41.9%
Dobutamine in 70.1%
Shock trial &registry
(Hochman etal ,JACC, 2000)
A comparison of continous I.V. arginine
Vasopressin to dopamine in the treatment
Of cardiogenic shock
AVP(N=16)
DOA(N=16)
P
Dose
13 + 10 IU/HR
12 +
7mcg/Kg/min.
H.R.
84 + 4 BPM
110 + 6 BPM
0.0024
TIMI 3
94%
81%
0.285
Meaning time
142 + 110 hrs
505 + 45 hrs
0.0092
3 month survival
81.2%13/16
62.5% 10/16
0.27
AVP is safe and might have some clinical and
haemodynamic advantages over DOA in the
treatment of C.S.
(Masehisa Janane etal ,JACC ,2005)
L- NAME :N-Monomethyl Larginine:anitric oxide synthesis
inhibitor
1 mg/kg bolus than 1mg/kg/hr for 5
hs versus placebo in 30 patients
with refractory C.S.
1 month survival 73% versus 33% in
placebo
(Cotlar etal ,EHJ,2003)
1 No treatment
2 L-Name
1.00
1 No
treatment
2 L-Name
Survival(%)
Survival (%)
0.75
0.50
0.25
1
0.00
1
0
6
12
18
24
Survival time (Days)
30
One –month survival in the two
treatment arms
Survival time (Days)
One-week survival in the two
treatment arms
One month survival in the two treatment
groups
( after Cotler etal ,EHJ,2003)
Levosimendan is safe and effective in patients with
severe LCOP failure and critical hypotension
(Franco etal ,JACC ,2004)
Clinical parameter*/ Outcome
Baseline
Group 1 Levo, Dob/Dop
(n=15)
Baseline
48 h.
Systolic BP (mmHg)
75 + 9
91 + 8 †
Heart Rate (beats/min)
106 + 16
100 + 12 †
Diuresis (mL/hr)
22 + 20
242 + 159 †
Creatinine (mg/dL)
3.3 + 1.7
In-hospital mortality (%)
Group 2 Dob/Dop (n=11
Baseline
77 + 6
103 + 20
30 + 27
2.3 + 1.6†
27
* Mean + SD; †P < 0.05
1.5 + 0.7
48 h.
93 + 7.8
107 + 16
114 + 112 †
2.8 + 2.4
64
COMMIT: Effects of METOPROLOL on Death
by attributed cause(s)
Cause(s)
Metoprolol Placebo
(22,927)
(22,922)
Odds ratio & 95% CI
Metop. better
Placebo better
Arrhythmia
388 (1.7%)
498 (2.2%)
22% SE 6
Shock
496 (2.2%)
384 (1.7%)
-29% SE 8
Other causes
892 (3.9%)
916 (4.0%)
3% SE 5
ANY DEATH
1776 (7.7%)
1798 (7.8%)
1% SE 3
(2P > 0.1; NS)
0.4
0.7
1.0
1.3
1.6
1.9
COMMIT: Absolute effects of
METOPROLOL on Re-MI, VF, Shock
and Death by KILLIP class
Killip
at entry
I
II
III
Any
Absolute differences per
1000
Re-MI
VF
Shock Death
4
3
-7
3
10
11
-14
3
-5
11
-58
-36
5
5
-11
1
COMMIT: Effects of METOPROLOL on
Cardiogenic Shock by day of event
Day of event
Metoprolol Placebo
(22,927)
(22,922)
0
475 (2.1%)
317 (1.4%)
1
282 (1.2%)
210 (0.9%)
2+
384 (1.7%)
361 (1.6%)
ALL
1141 (5.0%)
Odds ratio & 95% CI
Metop. better Placebo better
-29% SE 5
(2P < 0.00001)
888 (3.9%)
0.4
0.7 1.0 1.3
1.6 1.9
COMMIT: Effects of METOPROLOL on
Cardiogenic Shock by Killip class
Baseline
Killip class
Metoprolol Placebo
(22,927)
(22,922)
I
611 (3.5%)
487 (2.8%)
II
362 (7.9%)
296 (6.5%)
III
155 (16.2%)
100 (10.4%)
ALL
1141 (5.0%)
Odds ratio & 95% CI
Metop. better Placebo better
-29% SE 5
(2P < 0.00001)
888 (3.9%)
0.4
0.7 1.0 1.3
1.6 1.9
The CAPTIM
Had a lower incidince of cardiogenic
shock in the pre-hospital
thrombolysis arm than in the
primary PCI arm
(Bonnefoy E et al , Lancet , 2002)
C.S. death predictors
(1) Previous MI
(2) Age > 70 Y.
(3) Failed thrombolysis
(Suttor et al , BMJ ,2005)
B-Tpe Natriuretic Peptide Strongly Predicts Mortality in
Intensive Care Unit Shock
(Tung et al ,JACC ,2004)
(Hassan Kafri et al ,JACC, 2005)
C.S. with preserved L.V. systolic function
(Nayar etal ,JACC ,2004)
Shock trial : 24 patient had EF > 37%
Had non-dilated L.V. + abnormal vascular
tone C.S.
Long term outcome of patients with CS complicating
AMI
(Holmes et al ,JACC ,2004)
GUSTOI 9 years F.U.
47% 30d survival , 53% 9 Y. survival
N
Alive 457
Dead 402
P
Male
66.5%
65.7%
.793
Age (yrs)
60.6 +/- 10.56
66.5 +/- 11.02
<.001
Diabetes
9.9%
20.6%
<.001
Prior MI
10.8%
26.8%
<.001
Anterior MI
37.7%
50.3%
<.001
Inferior M
60.1%
47.8%
<.001
42.7%
28.9%
<.001
21.9%
21.1%
.763
58.3%
46.3%
<.001
Revasc within 30
days
PTCA
CABG
PTCA or CABG
Low output cardiogenic shock
Check blood pressure
Systolic BP
Greater than 100 mm HG
Nitroglycerine
10 to20 mcg/min IV
Systolic BP
70 to 100 mmHg
No signs/symptoms
Of shock
Dobutamine
2 to 20 mcg/kg
Per min. IV
Systolic BP
70 to 100 mmHg
signs/symptoms
Of shock
Systolic BP
Less than 70 mmHg
signs/symptoms
Of shock
Dopamine
5 to 15 mcg/kg
Per min. IV
Norepinephrine
0.5 to 30 mcg/min. IV
Further diagnostic /therapeutic considerations (should be considered in nonhypovolemic shock)
Dignostic
Therapeutic
Pulmonary artery catheter
intra-aortic ballon pump
Echocardiography
reperfusion
Angiography for MI/ischemia
revascularization
Additional diagnostic studies
ACC/AHA Guidelines further management of STEMI
Antman et al ,JACC, 2004
Conclusion
(1) Invasive strategy with early
revascularization is associated with a
better long term outcome than
continued medical treatment.
(2) Intensive medical treatment
(ventilation ,JABP ,late
revascularization action) is
associated with a better outcome
than previously experienced with a
conservative medical approach.