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Management of Cardiogenic Shock Complicating Acute Myocardial Infarction.

Pankaj Jariwala, Pravir Lathi, G. Ramesh, K. Sarat Chandra

INTRODUCTION

Cardiogenic shock is an important cause of
in-hospital mortality after AMI. Though
Cardiogenic shock commonly occurs
following AMI or ischemia, there are
multiple other causes producing this final
common pathway leading to death.
Cardiogenic shock may present on
admission or may develop after admission.
The timing of presentation depends upon
the pathophysiology behind the disease
involved.
1

Cardiogenic shock occurs approximately
in 5-8 % of patients admitted with
diagnosis of AMI. The incidence of
cardiogenic shock has not decreased over
period of time despite decrease in the
mortality after AMI with increasing use of
early revascularization. Several trials in
the recent past have shown that early
revascularization strategies are useful and
improve 6 and 12 month mortality among
those who survived.
2


INCIDENCE

The incidence of CS remained
approximately 7-8% between 1975 and
1988 in a community in Worcester,
Massachusetts, USA, where 14% of
patients received thrombolytics
3
. The
incidence of CS in the Global Utilization
of Streptokinase and TPA for Occluded
Coronary Arteries (Gusto 1) trial, in which
all patients received thrombolysis was 7.3
%
4
.


The extent of myocardial salvage from
reperfusion treatment decreases
exponentially with time to re-establishing
coronary flow. Unfortunately, there has
been little progress in reducing time to
hospital presentation over the past decade
5

and this perhaps accounts for the stagnant
incidence of cardiogenic shock in
community studies (7.1%).
6
Cardiogenic
shock also complicates non-ST elevation
acute coronary syndromes. The incidence
of shock in the PURSUIT trial was 2.9%
(which excluded ST-elevation MI)
7
similar
to the 2.5% incidence reported in the non-
ST elevation arm of the GUSTO II-B trial
(199495).
8

CS continues to complicate approximately
5% to 8% of STEMI and 2.5% of non-
STEMI cases
7,9,10
.
PROGNOSIS
The 7.2% of patients developing shock in
the GUSTO-I trial accounted for 58% of
the overall deaths at 30 days.
11
Similarly,
the 30 day death rates with non-ST
elevation MI cardiogenic shock in the
PURSUIT and GUSTO-II b databases
were 66% and 73%, respectively. Even
with early revascularization, almost 50%
die at 30 days.
The historic control mortality for CS
complicating AMI is 80%
12,13
. From 1975
to 1988, which antedates the widespread
use of reperfusion therapy, mortality rate
has been consistently high at 78%
3
.


PATHOPHYSIOLOGY

Cardiogenic shock complicating acute MI
is caused by predominant left ventricular
failure in 80% of cases
14,15
. In the
remaining 20%, shock results from right
ventricular infarction or mechanical
complications of MI, including ventricular
septal rupture, acute mitral regurgitation,
and free wall rupture. In patients who have
predominantly left ventricular failure,
extensive necrosis is evident and involves
more than 40% of the left ventricle on
autopsy
16
.
1
In many patients, acute occlusion of
the left anterior descending artery is the
culprit lesion and, in two thirds of all
patients, multi-vessel disease is present
17
.
The precipitating event leading to CS may
not necessarily be a massive MI secondary
to a single arterial occlusion, but the result
of multiple small MIs with the final
myocardial insult leading to a sudden loss
of critical functioning myocardial
mass
17,18
.
Infarct expansion and re-infarction
have been identified as important risk
factors for development of shock in
STEMI and non-STEMI. In settings of low
coronary blood flow, thrombus may
propagate to involve side branches and
increase infarct size.
MI is a hyper-coagulable clinical
state, and re-occlusion of re-canalized
arteries leading to re-infarction can occur
in upto 20% of patients undergoing
thrombolytic therapy and 2% of patients
post-PCI. Patients who experience
reinfarction have significantly increased
chance of developing cardiogenic
shock
19,20
.

The progressively downward course
that describes the clinical deterioration of
patients who have cardiogenic shock is
shown in Fig.1
21,15
The leading event of
ischemia and infarction leads to systolic
and diastolic heart failure which involves
the entire circulatory system with
compensatory mechanisms setting in
which leads to classical paradigm of
circulatory shock. The systemic
inflammatory response syndrome involves
many inflammatory markers part of
neurohormonal and cytokine system in
perpetuation of shock.
22
This leads to
hypoperfusion of all organs, particularly
vital organs including heart, brain and
kidneys. The coronary perfusion pressure
decreases further and adds to the already
existing state.
The initial insult of ischemia leads
to stunned myocardium. Most of the
patients having multivessel disease already
had hibernating myocardium which also
contributes to the functional loss of
myocardium. The ability of the unaffected
myocardium to be recruited to preserve
left ventricular function is impaired.
23

To increase cardiac output, the heart
rate increases, thereby increasing
myocardial oxygen consumption directly
and affecting coronary perfusion. As heart
rate increases, the time spent in diastole
decreases. The time for tissue perfusion
decreases resulting in further ischemia of
the subendocardium. The wave front of
ischemia results in eventual global
dysfunction and the spiral deterioration
continues. The resulting stuttering
ischemia and infarction eventually results
in left ventricular failure and death.
23


CLINICAL RECOGNITION
Early recognition of left ventricular (LV)
failure and low output state, the preshock
phase, is crucial for the success of
treatment and outcome. The pre-shock
phase is not easily recognizable. Although
CS is routinely diagnosed when
hypotension develops, high systemic
vascular resistance can maintain
reasonable systemic arterial pressure even
when severe depression of stroke volume
and end organ hypoperfusion are present.
A useful clue is tachycardia, which is often
due to a low stroke volume. Confirmation
of the diagnosis is the most important step
in the management of these patients.
24
In
the SHOCK trial registry, 64% of patients
presented with hypotension, evidence of
ineffective cardiac output (resting
tachycardia, altered mental status, oliguria,
cool peripheries), and pulmonary
congestion.
25
A substantial minority (28%)
presented with evidence of hypoperfusion
in the absence of pulmonary congestion
the silent lung syndrome. These latter
patients have an equal distribution of
anterior (50%) and non-anterior index
infarctions (50%) with pulmonary
capillary wedge pressure in the range of
21.56.7 mm Hg.
2



DIAGNOSTIC CRITERIA OF
CARDIOGENIC SHOCK
Cardiogenic shock is clinically defined as
a state of end-organ dysfunction caused by
hypoperfusion secondary to low cardiac
output with associated hypotension,
classically defined as a systolic blood
pressure less than 90 mm Hg.
26
Hochman
et al proposed criteria for diagnosis of
cardiogenic shock as shown in box 1.

The presence of clinically cardiogenic
pulmonary edema itself is evidence of
increased left ventricular end diastolic
pressure.
26
CS should be diagnosed in all
patients exhibiting signs of inadequate
tissue perfusion irrespective of blood
pressure.

OTHER CAUSES OF CARDIOGENIC
SHOCK
There are several possible causes of
cardiogenic shock in the setting of MIleft
ventricular dysfunction, right ventricular
dysfunction, and mechanical
complications. Ventricular septal rupture,
contained free wall rupture, and papillary
muscle rupture. Mechanical complications
must be strongly suspected in patients with
CS complicating nonanterior MI,
particularly a first MI. Hemorrhage,
infection, and/or bowel ischemia may
contribute to shock in the setting of MI. As
with mechanical complications, a high
index of suspicion is required to make
these diagnoses in MI patients.


MANAGEMENT OF CARDIOGENIC
SHOCK FOLLOWING AMI
The treatment of cardiogenic shock
patients consists of medical therapy,
percutaneous revascularization procedures,
cardiac surgery, and the implantation of
devices.

Right Heart Catheterization
Right heart catheterization is often not
necessary for diagnosis and need only be
performed when there is continued doubt
or to guide management when shock does
not rapidly resolve. There is retrospective
data on increased mortality hazard
associated with this procedure
27
. On the
other hand, data from the Global Use of
Strategies to Open Occluded Coronary
Arteries (GUSTO-I) trial
28
and the Should
We Emergently Revascularize Occluded
Coronaries in Cardiogenic Shock ?
(SHOCK) registry
29
suggest that it is not
harmful, and possibly beneficial, in terms
of outcome. The current American and
European guidelines recommend right
heart catheterization for patients who have
ST-elevation acute coronary syndromes
(ACS) and who have progressive heart
failure, cardiogenic shock or mechanical
complications, despite the paucity of
evidence proving its efficacy
30,31

Echocardiography
Doppler echocardiography is of paramount
importance for hemodynamic assessment
and for the evaluation of cardiac function,
valvular status, and mechanical
complications of ACS.
32
Perhaps this
noninvasive, readily available method has
supplanted right heart catheterization use
in most situations.
Echocardiography in cardiogenic shock
can help to
Evaluate left ventricular function
and myocardium at risk
Evaluate remote myocardial
segments
Screen for ventricular septal
rupture
Screen for severe mitral
regurgitation and proceed to
transoesophageal echocardiography
as needed
Look for tamponade/rupture
Assess right ventricular function

TREATMENT
In the early 80s, individual or single
centre observational data on early
3
revascularization strategy benefiting
patients with cardiogenic shock after AMI
were published, but large scale trials were
needed to prove the point. Hence, the
National Heart, Lung, and Blood Institute
funded the SHOCK trial in the USA, while
the SMASH trial in Switzerland evaluated
the same issue.
33,34
While SMASH failed
to recruit an adequate number of patients,
SHOCK reported an increase in 30 day
survival from 46.7% to 56.0% by the
adoption of an early revascularisation
strategy, but this absolute 9% difference
did not reach significance (p =0.11). On
follow up, the survival difference in favour
of the early revascularisation strategy
became larger and significant at six
months (36.9% v 49.7%, p =0.027) and
one year (33.6% v 46.7%) for an absolute
reduction of 13.2% (95% CI 2.2% to
24.1%, p <0.03) Fig.2 The benefit of early
revascularisation was large for those <75
years at 30 days.
Kaplan-Meier curve showing 12 month
survival in the early revascularization and
initial medical stabilization arms of the
SHOCK trial.
82

General Care and Resuscitation
These include correction of hypovolemia,
hypoxemia, acidosis, Aspirin and
intravenous Heparin. The most important
step is maintenance of mean arterial
pressure to prevent further damage to the
vital organs and halt the perpetuation of
circulatory shock. A mean arterial pressure
of 60 mm Hg is generally necessary for
tissue perfusion.
35
Intra-arterial
measurement of blood pressure is
advisable. Large-scale controlled studies
have not been performed to compare
different combinations of inotropes in
patients who have cardiogenic shock.



Inotropes
Dopamine and Dobutamine are the most
commonly used inotropic agents.
Dopamines myocardial inotropic and
chronotropic effects are mediated through
myocardial beta-1 adrenergic receptors,
and are most evident with doses above 5
micrograms/kg/minute. The theoretical
advantage of nephroprotective effect has
been not been proved in one of the recent
trials.
36
Dobutamine has both alpha and
beta-adrenergic agonistic activities. It
increases myocardial contractility through
beta adrenergic receptor stimulation, with
only a minute peripheral vasodilatory
effect. The drug is usually initiated at 2
micrograms/kg/minute and titrated
upwards according to the patients
response, usually to a maximum of 20
micrograms/kg/minute. Dobutamine is
often used together with low-dose
dopamine for the inotropic effect of the
former and suggested renal vasodilator
effect of the latter.
Norepinephrine is a potent alpha
adrenergic agonist with less marked beta-1
adrenergic agonistic properties and a short
half-life of 2 to 4 minutes.
Vasoconstriction is dose-related, and the
drug infusion is titrated upwards from an
initial low dose of 0.02 to 0.04
microgram/kg/minute to a dose that
maintains adequate systemic blood
pressure. Norepinephrine may be used in
conjunction with dopamine and
dobutamine; however, the cardiac effects
of these agents include worsening
ischemia and serious arrhythmias, and the
vasoconstriction induced by
norepinephrine can lead to end-organ
ischemia. Thus, one should avoid
prolonged triple or double inotropic
treatment.

Milrinone, a second-generation
phosphodiesterase inhibitor, can be used in
cardiogenic shock patients. Milrinone
prevents the breakdown of cyclic
adenosine monophosphate (cAMP), the
final common pathway for raising
intracellular calcium, thus increasing
inotropy. The significant vasodilatory
effect and relatively long plasma half-life
make Milrinone difficult to use as
4
monotherapy in patients who have
cardiogenic shock. Milrinone can be used
synergistically with other inotropic drugs
to enhance myocardial contractility
37
.
Levosimendan represents a new class of
positive inotropic agents. Levosimendan
causes conformational changes in cardiac
Troponin C during systole, leading to
sensitization of the contractile apparatus to
calcium ions
38,39
. In addition to its
positive inotropic action, Levosimendan
possesses vasodilating properties that
reduce cardiac preload and afterload.
Moreover, coronary blood flow is
enhanced and myocardial oxygen supply is
increased
40,41
. At present, however, use of
levosimendan is not recommended by the
manufacturer for the sole treatment of
cardiogenic shock, because of its
vasodilatory properties.
Based on effects of vasopressin in septic
shock
42
, J olly and colleagues
43

hypothesized that vasopressin would
increase mean arterial pressure without
altering pulmonary capillary wedge
pressure or cardiac index. In a cohort of
patients who developed refractory
cardiogenic shock after myocardial
infarction, vasopressin was associated with
increased mean arterial pressure and no
adverse effect on other hemodynamic
parameters
43
.

Randomized prospective trials are
warranted to confirm the utility and safety
of vasopressin in the setting of cardiogenic
shock after myocardial infarction.
Other measures including fluids and
diuretic therapy need intensive
measurement of pulmonary wedge
pressure with the help of right heart
catheterization and hourly measurement of
urine output. Arterial blood gas and
oxygen saturation should be monitored
with early institution of continuous
positive airway pressure or mechanical
ventilation as needed. The ECG should be
monitored continuously, and defibrillating
equipment, intravenous Amiodarone, and
Lidocaine should be readily available.
Thirty three per cent of patients in the
early revascularization arm of the SHOCK
trial had cardiopulmonary resuscitation,
sustained ventricular tachycardia or
ventricular fibrillation before
randomization.
33
Mechanical Circulatory Support
Mechanical circulatory devices play an
important role in providing temporary
support for patients in CS. Mechanical
devices are superior to pharmacological
therapy in CS in that perfusion is
supported without increasing myocardial
work and oxygen consumption.
Intra-Aortic Balloon Counterpulsation
Intraaortic balloon counter pulsation
(IABP) is the most commonly used
circulatory support device. A large,
nonrandomized cooperative study in the
prethrombolytic era showed that IABP
counterpulsation alone, without adjunctive
percutaneous coronary angioplasty
(PTCA) or coronary artery bypass graft
surgery (CABG) did not reduce mortality
rates, which remained disappointingly high
at 83%
44
. IABP therapy was, however,
highly effective in initial clinical
stabilization of patients, reversing end-
organ hypoperfusion in patients with AMI
and CS who proved refractory to
vasopressor therapy
44
. Recent reports have
suggested that IABP may be combined
with thrombolytic therapy to improve
reperfusion rates when CS is present, with
improvement of overall outcome
45-47
. In
one nonrandomized study, where more
than 40% of patients received thrombolytic
therapy, there was improved survival rate
of 46% in those who received IABP versus
38% in those who did not [P =0.001]
46
.
IABP is extremely useful especially in
patients in whom support of the circulation
is required for the performance of cardiac
catheterization and/or other interventional
revascularization procedures such as
PTCA or CABG. It is mandatory in
patients with mechanical complications of
AMI such as ventricular septal defect or
papillary muscle rupture as a temporary
support before surgical correction. Patients
5
treated with IABP in conjunction with
thrombolytic therapy had the lowest in-
hospital mortality rate (47%) in the
SHOCK registry.
48
The SHOCK registry
data suggest that initial stabilization of
cardiogenic shock patients using an IABP
may be associated with a 20% absolute
risk reduction in mortality.
48
Similarly,
retrospective analysis from the United
States National Registry of Myocardial
Infarction
5
has shown a 6% absolute
reduction in hospital mortality associated
with IABP use among cardiogenic shock
patients. IABP was recommended in the
SHOCK Trial protocol and used in 87% of
patients, for a median duration of
approximately 3 days. Overall, IABP
usage was not an independent predictor of
mortality at 12 months; however, in
patients who had systemic hypoperfusion
and whose hemodynamics and end-organ
perfusion were improved by IABP, the
mortality rates were lower at 12 months in
both the initial medical stabilization and
the ERV treatment groups
49
. According to
accumulated data and accepted guidelines,
all patients having cardiogenic shock
without contraindications should receive
IABP for at least 3 days or longer if
clinically indicated, for recovery from
myocardial stunning.
30,31


Other types of mechanical devices that are
currently used to provide circulatory
support: Ventricular assist device
50
,
percutaneous cardiopulmonary by-pass
with extracorporeal membrane
oxygenation (ECMO)
51
and hemopump
52
.
All have been successfully used in a
limited number of patients as temporary
support before interventions or as a bridge
to heart transplantation
53
. Left ventricular
assist devices were described in a few
retrospective single-center based studies as
a promising modality in the post-
myocardial infarction setting
54,55
.
Anecdotal case reports and case series
were published recently confirming the
emerging role of urgent cardiac
resynchronization therapy (CRT) in
inotropes-dependent patients
56-58
.



Thrombolysis
There are few randomized trials providing
data for assessment of the efficacy of
thrombolysis in patients presenting with
CS. Intracoronary streptokinase results in
low patency rates of only 43% for patients
in CS
59
. When reperfusion is established,
the mortality rate is significantly lower
than when intracoronary streptokinase fails
to establish reperfusion, 42% vs 84%,
respectively
60
. GISSI I is the only placebo-
controlled thrombolytic trial that assessed
mortality rates for patients who presented
in CS. Streptokinase alone without
adjunctive aspirin or anticoagulation
administered up to 12 hours after onset
(regardless of ECG findings) resulted in
the same mortality rate as the placebo
(70%).
61
The FTT group emphasized that
the possibility of saving seven lives in
every 100 patients treated represents a
large absolute benefit.
62
The more recent
GUSTO I and TIMI II trials, which
utilized more adjunctive anti-coagulation
reported mortality rates of 58% and 51% at
30 days and 6 weeks, respectively.
63,64
The
lack of apparent benefit of thrombolytic
agents in the treatment of cardiogenic
shock may be the result of reduced lysis of
thrombi in patients who have low
perfusion pressures
59
. Data from small
nonrandomized retrospective studies of
patients with shock complicating AMI
support the use of IABP in conjunction
with thrombolysis
45-47
.




Glycoprotein IIb/IIIa Receptor
Antagonists
The available data favor
administration of platelet IIb/IIIa
antagonists, particularly Abciximab, in
patients who have cardiogenic shock who
6
are undergoing percutaneous intervention,
unless the risk of bleeding is considered to
be excessive. In the recently published trial
65
, 40 patients who had ST-segment
elevation myocardial infarction and
cardiogenic shock were treated with
primary revascularization, abciximab,
heparin, and aspirin. The reported
mortality rate at 30 days was 42.5%.
Abciximab seemed to improve outcomes
of the younger population [<75 years)
versus elderly (>75 years), with mortality
rates of 24% versus 91%, respectively
(P<001)
65
. Also in those patients
presenting with NSTEMI with shock GP
IIb/IIIa inhibitors should be administered
before revascularization.
Other experimental agents like N-
Monomethyl-L-Arginine
66
, Tilarginine
Acetate Injection
67
Complement blocking
agents like Pexelizumab
68-70
, adenosine
71
,
Sodium/hydrogen-exchange
inhibitors.
72,73
, Antioxidants like
Recombinant human superoxide dismutase
(h-SOD)
74,75
, Glucose-insulin-potassium
infusion
76,77
did not demonstrate any
benefit in terms of reduction in serious
adverse outcomes.




Revascularization
Bypass surgery
Early studies of revascularization for
patients with cardiogenic shock focused on
surgical revascularization. Several small
surgical series reported relatively good
outcomes in patients who had cardiogenic
shock
78,79
. According to SHOCK trial data,
surgically revascularized patients benefited
mostly among 57 patients who underwent
bypass surgery, 30-m day mortality was
42.1%, versus 45.3% for those treated with
PCI. The trial was not designed to
compare percutaneous and surgical
revascularization strategies
26
. There are
several surgical techniques designed to
optimize outcomes for patients in
cardiogenic shock: the use of warm blood
cardioplegia enriched with glutamate and
aspartate, grafting of large areas of viable
myocardium first followed by treatment of
infarct-related artery last, and preference
of saphenous vein grafts for their high
initial flow rates and because they can be
rapidly harvested
14
. Pooled data from 25
non-randomized studies involving 391
patients in cardiogenic shock who
underwent CABG revealed a 35% in-
hospital mortality rate
80
, and is the lowest
mortality rate reported for CS in AMI. It is
possible that complete revascularization
achieved by CABG in this population is
the best therapy. Hence it is reasonable to
consider urgent CABG with IABP support
for CS patients if logistics permit in a
given setup.

Percutaneous Transluminal Coronary
Angioplasty
An important advance in the management
of CS complicating AMI is the use of
PTCA, which is a highly effective method
of restoring perfusion in the infarct related
artery. There are currently 22 published
studies with an aggregate of 646 patients
who underwent PTCA at some time during
their hospitalization for CS and AMI. The
pooled in-hospital mortality is 45%
80
,
which is lower than the historic control
mortality rate of 80%. When PTCA is
successful the mortality rates are
significantly lower than when it is not (33
vs 81%). In the GUSTO 1 trial, patients in
cardiogenic shock who were subjected to
angiography and PTCA performed within
the first 24 hours had a mortality rate of
38%, while the remaining patients had a
62% mortality rate at 30 days
81
. Two
prospective randomized trials evaluated
the role of revascularization among
patients who had cardiogenic shock. The
SMASH trial (Swiss Multicenter trial of
Angioplasty for Shock) involved 55
patients who had AMI complicated by
cardiogenic shock. They were randomized
to undergo revascularization (surgical or
percutaneous) versus medical therapy
alone
34
. SMASH was discontinued
7
prematurely due to low enrolment and
physician perception that revascularization
was beneficial. In this small study, a 9%
absolute reduction in 30-day mortality was
seen among patients treated with
revascularization (69% versus 78%). This,
however, did not achieve statistical
significance. The most important
randomized study in this context is the
SHOCK trial. In this study patients who
developed cardiogenic shock within the
first 36 hours of AMI (either ST-segment
elevation, or new left bundle-branch
block) were eligible for enrolment;
patients who had mechanical causes for
shock or predominantly right-ventricular
infarction were excluded
26,82
. In this study
an aggressive, invasive approach
(angioplasty or coronary artery bypass
surgery: emergency revascularization
[ERV], generally with IABP) was
compared with medical treatment, initial
medical stabilization (IMS), including
thrombolytic therapy and IABP.
Randomization was required within 12
hours of shock onset. Most patients
randomized to the ERV (n = 152)
underwent coronary angiography (97%),
and 87% underwent revascularization
(surgical or percutaneous). The primary
end point of the study was 30-day
mortality. In the ERV arm, the mortality
was 46.7%, as compared with 56.0% in the
conservative arm. The mortality difference
at 6 months achieved statistical
significance, and was lower in the ERV
group (50.3% versus 63.1%) . The survival
curves continued to diverge at 12 months
of follow-up
82
. In a prespecified subgroup
analysis, the benefits of ERV were seen
only in patients younger than 75 years of
age, in whom the 30-day mortality was
56.8% for the conservative arm versus
41.4% for the ERV arm, however, 30-day
survival among medically treated patients
older than 75 years tended to be better than
that of older patients in the ERV arm
(53.1% versus 75.0%).
14
The 13% absolute
reduction in mortality at 6 months
associated with the aggressive
revascularization strategy (50.3% versus
63.1%) was both statistically and clinically
significant. On the basis of the SHOCK
trial, the American College of
Cardiology/American Heart Association
(ACC/ AHA) guidelines for the treatment
of patients who have myocardial infarction
have included early revascularization for
shock as a Class I indication, particularly
for those less than 75 years of age
30
In the
Global Registry of Acute Coronary Events
(GRACE) study, percutaneous
revascularization with coronary stenting
was the most powerful predictor of
hospital survival among shock patients.
83


CONCLUSION
Cardiogenic shock continues to remain a
challenge for the cardiologist taking care
of patients of acute myocardial infarction.
Based on the data presented above, one
should adopt an aggressive approach with
emergency PCI with IABP for these
critically sick patients. Stenting supported
by IIb/IIIa blockers has to be part of the
interventional approach.

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Fig 1

Fig 1. Current concept of CS pathophysiology. The classic description of CS pathogenesis is
shown in black. Myocardial injury causes systolic and diastolic dysfunction. A decrease in
CO leads to a decrease in systemic and coronary perfusion.This exacerbates ischemia and
causes cell death in the infarct border zone and the remote zone of myocardium. Inadequate
systemic perfusion triggers reflex vasoconstriction, which is usually insufficient. Systemic
inflammation may play a role in limiting the peripheral vascular compensatory response and
may contribute to myocardial dysfunction.Whether inflammation plays a causal role or is
only an epiphenomenon remains unclear. Revascularization leads to relief of ischemia. It has
not been possible to demonstrate an increase in CO or LVEF as the mechanism of benefit of
12
revascularization; however, revascularization does significantly increase the likelihood of
survival with good quality of life. IL-6 indicates interleukin-6; TNF-, tumor necrosis factor-;
and LVEDP, LV end-diastolic pressure. Adapted from Hochman 21 and Hollenberg et al 15
with permission of the publishers. Copyright 2003, the American Heart Association, and
copyright 1999, the American College of Physicians.



Fig 2: Kaplan-Meier curve showing 12 month survival in the early revascularization and
initial medical stabilization arms of the SHOCK trial.
82




Box 1
Hochman et al proposed criteria for diagnosis of cardiogenic shock as shown in box 1.


Address for correspondence: Dr. K. Sarat Chandra, Additional Professor, Department of
Cardiology Nizams Institute of Medical Sciences, Hyderabad 500 082
13