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The lack of utilization of CABG in appropriate patients may account in part for a plateau inthe mortality rate.Long-term survival in patients with myocardial infarction complicated by ca

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Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction

Authors: Judith S Hochman, MD, Alex Reyentovich, MD

Section Editors: Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC, Stephan Windecker, MD

Deputy Editor: Gordon M Saperia, MD, FACC

All topics are updated as new evidence becomes available and our peer review process is complete

Literature review current through: Aug 2018. | This topic last updated: Nov 20, 2017.

INTRODUCTION — Cardiogenic shock (CS) is a clinical condition of inadequate tissue (end-organ) perfusion due

to cardiac dysfunction The definition includes the following hemodynamic parameters: persistent hypotension(systolic blood pressure <80 to 90 mmHg or mean arterial pressure 30 mmHg lower than baseline) with severereduction in the cardiac index (<1.8 L/min per m without support or <2 to 2.2 L/min per m with support) andadequate or elevated filling pressures [1] Short-term prognosis is directly related to the severity of the

hemodynamic disorder and patients most commonly succumb to multiorgan dysfunction due to ongoing organhypoperfusion

The most common etiology of CS is an acute myocardial infarction (usually ST elevation myocardial infarction)with left ventricular failure, but it can also be caused by mechanical complications, such as acute mitral

regurgitation or rupture of either the ventricular septal or free walls However, any cause of acute, severe left orright ventricular dysfunction may lead to CS

The prognosis and therapy of CS complicating acute myocardial infarction (MI) will be reviewed here The largerdiscussion of the causes of CS, other presentations that mimic CS secondary to MI, as well as the clinical

manifestations and diagnosis of this disorder are discussed separately (See "Clinical manifestations and

diagnosis of cardiogenic shock in acute myocardial infarction".)

PROGNOSIS

Temporal trends — The incidence of cardiogenic shock (CS) appears to be falling since the mid-1970s In a

report from one United States metropolitan area (Worcester, Massachusetts), the incidence of CS was around 7percent between 1975 and 1990 and has decreased to between 5.5 to 6.0 percent since then [2

The historic mortality rate for CS complicating an acute myocardial infarction (MI) was 80 to 90 percent [3

However, lower values for in-hospital mortality have been noted in more studies, ranging from 48 to 74 percent[4-9] Studies have suggested short-term mortality rates between 42 and 48 percent [2,9,10]

Two reports from the National Registry of Myocardial Infarction showed evidence of continued improvement inmortality from CS between 1994 and 2004 [5] Similar findings were noted in an analysis of over 23,000 acutecoronary syndrome patients in a Swiss registry (1997 to 2006) [11] Data published from the large CathPCIRegistry reported an increase in in-hospital mortality in patients treated with PCI from 27.6 percent (2005 to2006) to 30.6 percent in 2011 to 2013 [12]

The decrease in the incidence of shock and the associated improvement in overall mortality in part reflect

increased use of coronary reperfusion strategies, particularly primary percutaneous coronary intervention, which,

®

by restoring patency to the infarct-related artery, can limit infarct size and improves survival [5-7,13] In contrast,rates of performance of coronary artery bypass (CABG) have not increased despite the high rate of multivesseldisease in patients who develop cardiogenic shock and the potential of CABG surgery to provide completerevascularization [12] The lack of utilization of CABG in appropriate patients may account in part for a plateau inthe mortality rate.

Long-term survival in patients with myocardial infarction complicated by cardiogenic shock is improved withtimely revascularization in the acute setting, and functional status and quality of life in survivors are excellent[14,15]

Predictors of mortality — A number of studies have attempted to identify risk factors for mortality in CS An

analysis from the GUSTO-I database identified the following predictors of 30-day survival for patients with CScomplicating an ST elevation myocardial infarction (STEMI) who receive initial fibrinolysis [16]:

Hemodynamic parameters (including basic vital signs and measurements obtained from pulmonary arterycatheterization) also correlate with mortality in patients with CS These parameters include mean arterial

pressure (MAP), systolic and diastolic blood pressure, cardiac output (CO), and cardiac index, with cardiac powerindex (MAP x CO/451 x body surface area in m ) being the strongest hemodynamic predictor on multivariateanalysis [17]

The observational CardShock study, conducted between 2010 and 2015, and which included patients with either

MI and non-MI etiologies of cardiogenic shock, demonstrated that advanced age, a history of MI or CABG

surgery, altered mental status, low LV ejection fraction, low estimated glomerular filtration rate, and high bloodlactate levels were independently associated with increased in-hospital mortality [18]

STEMI versus NSTEMI — The mortality rate in patients in CS in GUSTO-IIb was similar in those with STEMI or

non-ST elevation acute coronary syndrome (ACS) [8] Although CS was significantly less common with non-STelevation infarcts (2.5 versus 4.2 percent, odds ratio 0.58), patients with non-ST elevation acute coronary

syndromes were older and more likely to have three vessel disease and diabetes mellitus

Coronary anatomy — Most patients with CS complicating an acute MI have severe and extensive coronary

disease In the SHOCK trial registry, for example, 16 percent of those who underwent angiography had significantleft main disease and 53 percent had three vessel disease [19] Mortality varied significantly with the location ofthe culprit lesion and was noted to be higher in patients with a left main or saphenous vein graft lesion than inthose with circumflex, left anterior descending, or right coronary artery lesions (79 and 70 percent versus 37 to

42 percent) Right coronary culprit lesions were associated with the best prognosis [20]

Echocardiographic predictors — In a substudy from the SHOCK trial, 169 patients had echocardiograms [21].The only independent echocardiographic predictors of outcome were left ventricular ejection fraction (LVEF) andseverity of mitral regurgitation (MR) For those with an LVEF <28 percent, survival at one year was 24 percent(versus 56 percent for those with a higher LVEF) For those with moderate or severe MR, survival at one year was

31 percent (versus 58 percent for those with mild or no MR) However, there was benefit of early

revascularization at all levels of LVEF and MR grade (See 'PCI' below.)

Increasing age (odds ratio 1.49 for each 10 year increase)

Symptom onset to reperfusion time — The time from symptom onset to reperfusion is an important

determinant of mortality in patients with STEMI who undergo primary PCI An analysis of 80 such patients whowere in CS showed that in-hospital mortality was only 6.2 percent in patients reperfused within two hours ofsymptom onset; this was more likely to occur in patients diagnosed with MI in the prehospital arena [22] (See

"Primary percutaneous coronary intervention in acute ST elevation myocardial infarction: Determinants of

outcome".)

Reversal of systemic hypoperfusion — Lack of a prompt improvement in systemic perfusion following intraaortic

balloon pump (IABP) placement in patients with cardiogenic shock after myocardial infarction identifies a group

of patients with worse survival regardless of application of early revascularization [23,24] Four hundred andninety-nine patients with record of systemic hypoperfusion status from the SHOCK trial [23] were evaluated forrelationship between rapid reversal (<30 minutes) of hypoperfusion and 30-day and one-year mortality Afteradjusting for important predictors of outcome, there remained a significant association between completereversal of hypoperfusion and 30-day mortality (odds ratio 0.18, CI 0.08-0.42) and one-year mortality (odds ratio0.28, CI 0.12-0.67) Of note, 85 percent of patients in the SHOCK trial were supported with IABP  

After successful reperfusion therapy — Early successful reperfusion therapy, particularly with percutaneous

coronary intervention, improves outcomes compared with conservative (medical) therapy The magnitude of thisbenefit is discussed below (See 'Reperfusion/revascularization' below.)

GENERAL MEASURES — Severe systemic hypoperfusion leads to hypoxemia and lactic acidosis, which can

cause further myocardial depression both directly and by decreasing the responsiveness to vasopressors such

as dopamine and norepinephrine Thus, if possible, correction of these metabolic disturbances is important(table 1) In addition, shock in the setting of myocardial infarction (MI) may be caused by factors not directlyrelated to the MI These include hypovolemia, use of blood pressure lowering drugs, rate slowing drugs, and othertypes of cardiovascular disease; they are discussed in greater detail elsewhere (See "Clinical manifestations anddiagnosis of cardiogenic shock in acute myocardial infarction", section on 'Contributing factors'.)

The following discussion is generally in accord with recommendations made in the 2013 American College ofCardiology/American Heart Association (ACC/AHA) guidelines on the management of patients with ST elevationmyocardial infarction (STEMI) [25] Similar principles apply to patients with non-ST elevation myocardial

infarction (NSTEMI) (table 2)

Medications — Aspirin, heparin, vasopressors, and inotropes are frequently given in cardiogenic shock (CS), whilecertain other medications should be avoided or used in reduced dose Medications that have hepatic or renalclearance should be used in reduced doses because of hypoperfusion of these organs One important example

is use of a lower dose of lidocaine, which is rarely given to treat ventricular arrhythmias

Oral antiplatelet therapy — Both Aspirin and clopidogrel reduce mortality from acute MI [26] (See "Antiplateletagents in acute ST elevation myocardial infarction" and "Antiplatelet agents in acute non-ST elevation acutecoronary syndromes".)

We recommend that all patients with CS complicating an acute MI receive aspirin even though its efficacy hasnot been specifically studied in this setting Alternative routes of administration for patients who are intubatedwithout a nasogastric tube include crushing a tablet for absorption through the buccal mucosa or administration

of a rectal suppository

Clopidogrel should be deferred until after angiography, as many with MI and CS will require urgent coronaryartery bypass surgery When clopidogrel is deferred, we suggest the use of glycoprotein (GP) IIb/IIIa inhibitors assoon as possible after the decision has been made to proceed to angiography (See 'GP IIb/IIIa inhibitors' below.)

Heparin — Intravenous heparin infusion, especially in conjunction with reperfusion therapy, reduces mortality

in acute MI [26] Even though heparin has not been evaluated in CS, there are compelling reasons that full-doseintravenous heparin therapy should be given Patients in shock are in a low flow state with high fibrinogen

concentrations As a result, they are at risk for left ventricular and deep vein thrombosis Heparin may alsomaintain coronary artery patency (See "Anticoagulant therapy in acute ST elevation myocardial infarction" and

"Anticoagulant therapy in non-ST elevation acute coronary syndromes".)

GP IIb/IIIa inhibitors — GP IIb/IIIa inhibitors improve the outcome of patients with non-ST elevation acute

coronary syndrome (ACS) (See "Antiplatelet agents in acute non-ST elevation acute coronary syndromes".)The impact of eptifibatide on patients with CS was evaluated in a post-hoc subgroup analysis from the PURSUITtrial [27] Randomization to eptifibatide did not affect the incidence of shock However, in patients who weretreated with eptifibatide and developed shock, compared to those receiving placebo, a significantly reducedincidence of death at 30 days was noted (48 versus 58 percent in patients without an MI and 69 versus 85

percent in patients with an MI) A possible mechanism of benefit is relief of microvascular obstruction

Another possible mechanism for benefit is the possible therapeutic effect of GP IIb/IIIa inhibitors in patients with

an STEMI and CS who undergo primary percutaneous coronary intervention (PCI) (See "Primary percutaneouscoronary intervention in acute ST elevation myocardial infarction: Determinants of outcome".)

Bivalirudin — Patients with CS have been excluded from pivotal trials that have examined the role of

bivalirudin In a small single center experience, outcomes were similar in patients who received bivalirudin andprovisional GP IIb/IIIa inhibitor (n = 37) compared to patients (n = 49) treated with heparin and GP IIb/IIIa

inhibitors [28]

Beta blockers and other negative inotropes — Drugs that have negative inotropic activity should be avoided in

patients with CS or "pre-shock" in which the cardiac output is severely diminished but hypotension has not yetdeveloped Included in this group are beta blockers and calcium channel blockers [26] Evidence for this

recommendation comes from the COMMIT trial in which randomization to early beta blockade was associatedwith a 30 percent higher occurrence of cardiogenic shock in patients over the age of 70, those with systolic bloodpressure (BP) <120 mm Hg or presenting heart rate greater than 110 beats per minute, and those with KillipClass >1 In addition, antiarrhythmic drugs with negative inotropic or vasodilating properties, such as lidocaine,

procainamide, bretylium, and quinidine, should be used with caution Amiodarone, although it has beta blockingproperties, is the preferred antiarrhythmic agent when one is required for sustained ventricular or atrial

tachyarrhythmias

Vasopressors and inotropes — Prompt treatment of hypotension and hypoperfusion is essential to the

management of CS Both pharmacologic and nonpharmacologic methods of circulatory support are employed toreverse hypotension, maintain vital organ perfusion, and maintain coronary perfusion pressures as high aspossible (See 'Mechanical support' below.)

Sympathomimetic inotropic and vasopressor agents (table 3) remain the mainstay of first-line therapy [26] (see

"Use of vasopressors and inotropes"):

Norepinephrine is a potent vasopressor with some positive inotropic properties that may be used for rapidinitial circulatory support for CS The minimum required dose should be used

●

Dopamine is a vasopressor; its effect varies based upon the dose range administered At low doses, it hasprimarily positive inotropic effects but at higher doses it stimulates alpha adrenergic receptors, resulting invasoconstriction and increased systemic vascular resistance This may produce an undesirable elevation inpulmonary capillary wedge pressure (PCWP) The minimum required dose should be used

●

While dopamine has often been chosen/recommended before norepinephrine, and the latter used when theresponse to dopamine is inadequate, some evidence suggests that outcomes may be better with norepinephrine.

In a trial of 1679 patients with circulatory shock due to varying etiologies (septic, hypovolemic, and CS) who wererandomly assigned to initial therapy with either dopamine or norepinephrine, there was a trend toward higher rate

of death at 28 days with dopamine and there were significantly more arrhythmias, predominantly atrial

fibrillation There was no difference in the treatment effect based on shock type, including in the subset of 280patients with cardiogenic shock [29]

There is insufficient evidence upon which a firm recommendation for the choice of the first vasopressor orinotrope in patients with cardiogenic shock can be made Our experts suggest starting with norepinephrine butemphasize that efforts should be made to minimize both the number of agents and their dose In some patients,measurement of hemodynamic parameters such as cardiac output and arterial pressure (as well as the

calculation of systemic vascular resistance) may guide the choice of vasopressors and inotropes However, there

is no evidence that titrating medications based on hemodynamics improves outcomes

Unfortunately, increasing systemic vascular resistance (SVR) with vasopressors in patients who already have anelevated SVR induced by endogenous norepinephrine and angiotensin II limits the improvement in cardiac

output, increases cardiac work, and raises the PCWP As a result, mechanical support devices are preferred assoon as they can be instituted

A possible alternative is the administration of dobutamine or a phosphodiesterase inhibitor, such as milrinone,which are inotropic agents that also produce vasodilation These drugs do not reverse the hypotension in post-MIshock, which, as noted above, is sometimes accompanied by vasodilation rather than vasoconstriction

Dobutamine may be used in less sick patients with a low cardiac index and high PCWP but without severe

hypotension (eg, systolic blood pressure <80 mmHg) Milder cases (ie, nonhypotensive patients in low outputstate) can also be treated with dobutamine in combination with vasodilators (such as intravenous nitroglycerin),which will further reduce both afterload and preload

Phosphodiesterase inhibitors are potent inodilators that have not been studied in patients with an acute MI and

CS The possible role of intravenous L-NMMA (tilarginine acetate), an inhibitor of nitric oxide synthase thatproduces vasoconstriction, was evaluated in the TRIUMPH trial [10] Enrollment was stopped prematurely basedupon a prespecified futility analysis There was no statistically significant difference in all-cause mortality at 30days between treatment and placebo (48 and 42 percent, respectively) [10]

We generally begin therapy with a vasopressor (norepinephrine) in patients with severe hypotension (eg, SBP <80mmHg) The administration of dobutamine is limited to less sick patients with a low cardiac index, high PCWP,and borderline blood pressure without severe hypotension Non-hypotensive patients in a low output state canalso be treated with dobutamine plus a vasodilator (intravenous nitroglycerin or nitroprusside) This combinationwill further reduce both afterload and preload Some clinicians advocate use of a pulmonary artery (Swan-Ganz)catheter to help guide management in patients not responding to initial attempts at stabilization

A table that includes dosing regimens for some of these agents is available (table 3)

Differences compared to patients without shock — Based upon the discussion above, the following summarizes

potential differences in care compared to patients without CS:

In most cases, clopidogrel should be held until after angiography

●

If used, lidocaine should be used in lower doses

●

Hemodynamic monitoring — The insertion of a balloon-tipped pulmonary artery (Swan-Ganz) catheter and an

intraarterial blood pressure monitoring catheter are in general useful as part of the diagnostic evaluation of thepatient with CS (See "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction",section on 'Hemodynamic monitoring'.)

Reperfusion therapy should not be delayed for the placement of a pulmonary artery catheter Hemodynamicmonitoring is useful in patients with refractory shock despite revascularization

Repeated determination of hemodynamics is in general useful to guide therapeutic intervention [26,30,31]:

Volume management — Hypovolemia may be present, particularly in the setting of diuretic use or vomiting.

Intravenous fluid replacement should be guided by measurement of the PCWP, arterial oxygen saturation (SaO2),systemic arterial pressure, and cardiac output (See 'Hemodynamic monitoring' above.) Each patient's optimalPCWP is the lowest value that results in the highest cardiac output as long as the SaO2 is above 90 percent Theusual value in CS is between 18 and 25 mmHg [32]

An empiric intravenous volume challenge of 250 mL of isotonic saline can be given prior to right heart

catheterization in patients with suspected CS when there is no evidence of pulmonary congestion on physicalexamination or chest radiograph and the patient is not in respiratory distress [26] Overly vigorous fluid

challenges in patients with extensive left ventricular infarction, particularly older adults, will result in pulmonaryedema and should be avoided

On the other hand, there are two settings in which more volume support is indicated: right ventricular (RV) shockdue to a right ventricular MI, in which increased filling pressures are required to maximize flow to the left

ventricle; and the venodilation and hypotension that are common with inferior MI, but do not constitute a shockstate The diagnosis of right ventricular MI is suspected in patients with inferior MI, clear lung fields, and shock Itcan also be confirmed by the use of right sided electrocardiogram (ECG) leads In patients with presumed rightventricular shock intravenous (IV) fluid replacement is indicated if jugular (central) venous pressure is not

elevated Excess fluid administration (for example, to central venous pressure >15 mmHg) generally should beavoided, as it may lead to marked RV dilatation with septal shift into the left ventricle, which diminishes LV filling[33] An early echocardiogram can be performed in this setting to guide clinical management (See "Right

ventricular myocardial infarction".)

Patients with volume overload and cardiogenic pulmonary edema without hypotension may require therapy withdiuretics, morphine, supplemental oxygen, and vasodilators The management of this complication is discussedseparately (See "Treatment of acute decompensated heart failure: General considerations".)

Drugs with negative inotropic properties such as beta blockers and calcium channel blockers should beavoided during the period of shock

Detection and quantification of intracardiac shunting in ventricular septal defect complicating acute MI (See

"Mechanical complications of acute myocardial infarction", section on 'Rupture of the interventricular

Ventilatory support — Ventilatory support may be required for several reasons in patients with CS (see "Overview

of mechanical ventilation"):

The use of mechanical ventilation may increase the likelihood of successful weaning from intraaortic balloonpump (IABP) support This was suggested by a report of 28 patients with strictly defined CS receiving inotropicmedication and IABP counterpulsation; 10 patients were also supported with mechanical ventilation [34] Asignificantly larger proportion of ventilated patients were weaned from IABP (90 versus 44 percent) and

discharged from the hospital (80 versus 28 percent)

In selected patients who require mechanical ventilation, endotracheal intubation may not be necessary and a trial

of noninvasive positive pressure ventilation is warranted (table 4) This issue is discussed separately (See

"Noninvasive ventilation in acute respiratory failure in adults".)

Glucose control — The optimal blood glucose target in patients with MI, including those who are critically ill, is

unknown The data addressing the issue of glucose targets during the acute phase of myocardial infarction,including very ill patients, are presented separately (See "Glycemic control for acute myocardial infarction inpatients with and without diabetes mellitus" and "Glycemic control and intensive insulin therapy in critical

illness".)

MECHANICAL SUPPORT

Intraaortic balloon pump — The available evidence does not support the routine use of an intraaortic balloon

pump (IABP) in most patients with acute myocardial infarction (MI) complicated by cardiogenic shock (CS) inwhom primary percutaneous coronary intervention (PCI) is attempted or performed or in whom fibrinolytictherapy is administered However, benefit may exist in patients with mechanical defects (such as mitral

regurgitation or a ventricular septal defect) and selected other patients who are rapidly deteriorating (See

"Intraaortic balloon pump counterpulsation" and "Mechanical complications of acute myocardial infarction",section on 'Rupture of the interventricular septum' and "Mechanical complications of acute myocardial

infarction", section on 'Acute mitral regurgitation'.)

The best evidence against the routine use of IABP for patient with MI comes from the IABP-SHOCK II trial inwhich 600 patients with CS complicating acute MI (ST elevation myocardial infarction [STEMI] and non-ST

elevation myocardial infarction [NSTEMI]) were randomly assigned to the device or no device [35] All patientswere expected to undergo early revascularization (predominantly with PCI) and to receive best available medicalcare At 30 days, there was no difference in the rate of all-cause mortality (39.7 versus 41.3 percent, respectively;relative risk 0.96, 95% CI 0.79-1.17) There were no significant differences in secondary end points such as length

of stay in the intensive care unit, renal function, or the rates of major bleeding, peripheral ischemic complications,sepsis, or stroke These outcomes were similar at 12-month follow-up; for example, there was no difference inthe rate of all-cause death (52 versus 51 percent, respectively) [36] A 2015 meta-analysis of seven studies (n =790), including IABP-SHOCK, came to similar conclusions [37]

One weakness of the study was a high rate of crossover of patients in the control group to IABP for reasonsother than the development of a mechanical complication (26 of 30 insertions were thought to be protocolviolations) However, a per protocol adjusted analysis that excluded patients who crossed over came to the same

To protect the airway and maintain oxygen supply in patients with a deterioration in consciousness or

conclusions It is possible that rapidly deteriorating patients may not have been enrolled and if enrolled, crossedover; the study cohort may represent those who stabilized on vasopressor/inotropic support Thus, the trialresults may not apply to severe shock with rapid deterioration Further data and longer follow-up is needed tobetter understand subsets that may benefit from IABP.

Two earlier observational studies support the findings in IABP-SHOCK II

For those patients with CS undergoing PCI in whom an IABP is chosen, the optimal timing of placement is

unknown as the observational evidence is conflicting In IABP SHOCK II, there was no difference in outcomesbetween those who received an IABP before or after PCI In a study of 48 patients with MI and CS, a significantlylower in-hospital mortality at 30 days (19 versus 69 percent) was found in those who received the IABP before asopposed to after PCI [41] However, an earlier analysis from the SHOCK trial registry suggested that the mortalitywas similar whether IABP was placed before or after PCI [42]

Use with fibrinolysis — The role of IABP in MI patients treated with fibrinolytic therapy who will be transferred

for possible revascularization is not well established, as there is little evidence that can be used to guide theformation of recommendations (See "Management of failed fibrinolysis (thrombolysis) or threatened

reocclusion in acute ST elevation myocardial infarction", section on 'Primary failure'.)

Animal studies have suggested that the rate of clot dissolution with fibrinolysis in CS can be restored to normallevels if the blood pressure is raised by aggressive use of vasopressors [43] or insertion of an IABP (figure 1)[44] There are no randomized clinical data demonstrating the efficacy and safety of combined IABP and

fibrinolysis in CS complicating MI However, there is some evidence suggesting efficacy

The National Registry of Myocardial Infarction 2 evaluated 23,180 patients who had CS during hospitalization; anIABP, which was used in 31 percent of patients, was associated with a significantly lower in-hospital mortality inthose who received fibrinolytic therapy (49 versus 67 percent without IABP) [38] A similar benefit from IABPcombined with fibrinolytic therapy was noted in the SHOCK trial registry [42] and the GUSTO-1 trial [45] Thepotential for bias in these studies is great

Few MI patients with CS will present to hospitals where fibrinolysis will be administered instead of

revascularization but where an IABP is available For these uncommon patients whose hemodynamic

parameters and clinical status are rapidly deteriorating while on vasopressor and inotropic support and who will

be transferred for cardiac catheterization, our authors and reviewers have differing approaches, with somerecommending placement of an IABP and others not The decision to place an IABP or not should be made inconsultation with physicians at the receiving cardiac catheterization laboratory The decision should be included

by the expertise of the team placing the IABP, potential delays in transfer, and patient-related factors such as risk

of bleeding and quality of vascular access

Other mechanical devices — Though outcome evidence is lacking, mechanical circulatory support devices are

sometimes used or are being investigated in patients with CS (See "Short-term mechanical circulatory assistdevices", section on 'Non-IABP percutaneous circulatory devices'.)

The National Registry of Myocardial Infarction (NRMI) 2 found no reduction in in-hospital mortality

associated with the use of an IABP in patients undergoing primary percutaneous coronary intervention (PCI)for CS (47 versus 42 percent without IABP) [38], although some benefit was found in hospitals with a higherrate of IABP use [39] (See "Intraaortic balloon pump counterpulsation".)

●

A 2009 meta-analysis of nine observational studies including over 10,000 patients with CS found no

significant benefit with IABP in the entire cohort, but a significant decrease in 30-day mortality in patientstreated with fibrinolysis [40] However, this meta-analysis is limited due to selection bias and the lack ofrandomization of IABP in this setting (See 'Use with fibrinolysis' below.)

●

Recommendations of others — The 2013 American College of Cardiology/American Heart Association

(ACC/AHA) guidelines on STEMI, which state that the use of intraaortic balloon pump (IABP) counterpulsationcan be useful for patients with cardiogenic shock after STEMI who do not quickly stabilize with pharmacologicaltherapy (table 5) [25] The European Society of Cardiology makes a more conservative recommendation for IABP

in STEMI complicated by cardiogenic shock [50] and found it potentially harmful with routine use in patients withnon-STEMI [47] Based on the lack of improved mortality with IABP in a population that directly went to thecardiac catheterization laboratory, with most undergoing primary PCI, we do not recommend routine use of IABPfor these patients

Left ventricular and biventricular assist devices In the setting of CS, these surgically placed devices areusually placed as a bridge to recovery in patients who had rapid reperfusion but with persistent

hypoperfusion, or as a bridge to transplantation in eligible patients in whom ventricular function is not

Percutaneous transvalvular left ventricular assist device (LVAD) This device (Impella LP 2.5 or Impella CP)

is placed via the femoral artery, retrograde across the aortic valve into the left ventricle It has a microaxialpump that decompresses the left ventricle and delivers a maximum flow of 2.5 to 4.0 L/min into the

ascending aorta In a multicenter observational registry of 120 patients with CS after acute myocardialinfarction who received the Impella-2.5 device following initial IABP support, 30-day mortality was 64.2percent [46] Without a comparison group, we do not know how this would compare to no device or to otherdevices

●

The Impella RP System (Abiomed, United States) is a right ventricular assist device (RVAD) that providesperipherally-placed circulatory support in patients with refractory RV shock The pump is inserted via thefemoral vein, into the right atrium, and through to the pulmonary artery, and can provide flow of up to 5 L/min[47]

●

The first study compared the LVAD (Tandem Heart) in 41 patients [48] Although hemodynamic and

metabolic parameters were more effectively reversed with the LVAD, complications such as severe bleedingand limb ischemia were more common The mortality rates were similar, but this study was not powered toassess mortality

●

In the second study, 25 patients were randomly assigned to LVAD (Impella LP 2.5) or an IABP [49] The LVADwas placed safely in all assigned patients and significantly improved hemodynamic parameters, such ascardiac index at 30 minutes to a greater extent than IABP (0.5 versus 0.1 L/min/m ) Important outcomessuch as death could not be meaningfully assessed due to the small sample size, but as noted above for theTandem Heart study, mortality rates were similar for the two groups

●

2

REPERFUSION/REVASCULARIZATION — There is evidence that the high mortality associated with cardiogenic

shock (CS) has improved over time [5,7,9,51] This benefit is thought to be predominantly due to increased use ofcoronary reperfusion strategies, which, by restoring patency to the infarct-related artery, can limit infarct size, aswell as interrupt the vicious spiral that characterizes CS [5-7,13] Outcomes are better when successful

reperfusion can be delivered early in the course of myocardial infarction (MI) However, benefit is derived as late

as 24 hours after CS onset, and shock onset can occur quite late following MI onset (See "Clinical

manifestations and diagnosis of cardiogenic shock in acute myocardial infarction", section on 'Pathophysiology'.)Observational data suggest that an open infarct-related artery in patients with CS complicating an acute MIcorrelates strongly with in-hospital survival In a report of 200 patients from Duke, for example, the in-hospitalmortality was much lower in patients with a patent compared to a closed infarct-related artery (33 versus 75percent); this relationship was independent of how patency was achieved (eg, spontaneous or pharmacologicfibrinolysis or mechanical intervention) [52] Similar findings were noted in the SHOCK trial registry [19] In-hospital mortality was lower in patients with TIMI grade 3 (normal) flow (26 versus 47 percent with TIMI grade0/1 [no or faint flow])

Fibrinolysis — Although reperfusion can be established with fibrinolysis in patients with ST elevation MI (STEMI),

we prefer direct revascularization with either percutaneous coronary intervention (PCI) or coronary artery bypassgraft surgery (CABG) There are limited randomized data assessing the efficacy of fibrinolysis compared to eitherplacebo or PCI in patients who have CS at presentation The available studies have demonstrated some benefit

of fibrinolysis compared to placebo, but superiority of PCI or CABG compared to fibrinolysis Fibrinolysis isrecommended if PCI is not possible or if it is significantly delayed (See "Fibrinolysis for acute ST elevationmyocardial infarction: Initiation of therapy".)

The 1994 meta-analysis from the Fibrinolytic Therapy Trialists' (FTT) Collaborative Group found that, amongpatients with a systolic blood pressure <100 mmHg and a heart rate >100 beats per minute, fibrinolysis wasassociated with a 7 percent absolute reduction in mortality at one month compared to control (54 versus 61percent) [53] The apparently limited efficacy of fibrinolysis may have reflected failure to augment coronaryperfusion pressure during administration of the fibrinolytic agent In animal studies, the rate of dissolution of acoronary artery thrombus by fibrinolytic therapy is markedly depressed when hypotension is present [43,44]

In a post-hoc analysis of the SHOCK trial, the use of fibrinolytic therapy was associated with a significant

reduction in mortality at 12 months (60 versus 78 percent without fibrinolysis) in the group assigned to medicaltherapy [54]

Based upon the apparent benefit in those who did not receive immediate revascularization and the absence ofadverse effects in those who underwent invasive procedures, fibrinolytic therapy should be given to patients whopresent to a facility without primary PCI or timely transfer for primary PCI capability, particularly those whopresent within three hours of symptoms However, all patients should be transferred to a PCI-capable facility assoon as possible (See "Acute ST elevation myocardial infarction: Selecting a reperfusion strategy" and 'Use withfibrinolysis' above.)  

There are limited data, derived only from subset analyses of major fibrinolytic therapy trials, evaluating the

comparative efficacy of different fibrinolytic agents There is no evidence to suggest greater benefit of one agentcompared with another [6,55] Thus, the choice of agent should probably not be different from patients without

CS (table 6) (See "Characteristics of fibrinolytic (thrombolytic) agents and clinical trials in acute ST elevationmyocardial infarction".)

Late shock — The preceding observations on fibrinolysis were primarily made in patients who had CS at or

soon after presentation However, the majority of patients develop shock after initial emergency departmentpresentation [6,8,27,56,57] Such patients have a somewhat lower in-hospital mortality than those in CS on

admission [56,57] (See "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial

infarction", section on 'Time of onset'.)

The only role for fibrinolysis administered more than 12 to 24 hours after onset of an MI is if the development oflate shock is thought to be due to recurrent coronary artery occlusion and if urgent angiography and

revascularization cannot be performed; prompt transfer to a tertiary center with revascularization facilitiesshould be arranged for patients in whom late shock is thought to be due to recurrent coronary artery occlusion,unless impossible

PCI — PCI is preferred to no reperfusion or to fibrinolysis for patients with CS complicating acute STEMI and

non-ST elevation MI (Nnon-STEMI) [23,58-62] Immediate PCI should be performed on the culprit lesion(s) of the related artery, and PCI of severe disease in other vessels should be deferred

infarct-Initial experience with coronary intervention in CS was obtained in studies of the benefits of early angiographyfollowing fibrinolysis Nonrandomized [61] and randomized trials [23] have shown benefit The benefits of earlyrevascularization in patients with CS were confirmed in the 1999 SHOCK trial, a randomized comparison ofemergency revascularization versus a strategy of initial medical stabilization including fibrinolysis and intraaorticballoon pump (IABP) in patients with an STEMI (or new left bundle branch block) and CS

The trial included 302 patients with confirmed CS developing within 36 hours of an acute MI [23] The patientswere randomly assigned within 12 hours of the diagnosis of shock to emergency revascularization (CABG in 40percent and PCI in 60 percent) within six hours of randomization or to initial medical stabilization Almost half ofthe patients assigned to emergency revascularization had had prior fibrinolysis, and therefore underwent rescuePCI or CABG; 63 percent of patients in the medical arm also received fibrinolytic therapy Late revascularizationwas performed in 25 percent of patients in the medical stabilization arm at a minimum of 54 hours after

randomization at the discretion of the local physician Intraaortic balloon counterpulsation was utilized in 86percent of patients in both groups

At 30 days, there was an insignificant 9 percent absolute difference in total mortality (primary end point) betweenthe two treatment groups (47 versus 56 percent with initial medical therapy with fibrinolysis); the lack of

significance could represent beta error since the trial was underpowered to detect such a difference The benefitincreased over time and became significant at six months (See 'Long-term outcome' below.)

Patients in CS on admission have a higher in-hospital mortality than the majority of patients who develop shockafter hospitalization [56,57] However, in the SHOCK trial and registry, patients in shock on admission derived thesame in-hospital mortality benefit from emergency revascularization (60 versus 82 percent) as those who

developed shock later (46 versus 62 percent) [56] (See 'Late shock' above.)

For CS patients who undergo PCI, the target of revascularization is the culprit lesion(s) in the infarct-relatedartery The issue of whether nonculprit stenoses should be treated has been debated Revascularization of thesenonculprit lesions is recommended for MI patients without CS, and the timing of PCI of these lesions is

discussed elsewhere (See "Primary percutaneous coronary intervention in acute ST-elevation myocardial

infarction: Non-culprit lesions", section on 'Our approach'.)

With regard to the issue of whether nonculprit lesions in patients with CS should undergo PCI, a 2017 analysis of 10 cohort studies that included over 6000 patients with CS showed a higher mortality with

meta-multivessel PCI than with culprit-lesion-only PCI (37.5 versus 28.8 percent; p = 0.001) [63] The CULPRIT-SHOCKtrial, published after the meta-analysis, randomly assigned 706 patients with both STEMI and NSTEMI with CS toPCI of the culprit lesion only, with the option of stage revascularization of nonculprit lesions or immediate

multivessel PCI [64] At 30 days, the primary end point (a composite of death or renal failure leading to replacement therapy) occurred less often in the culprit-lesion-only group (45.9 versus 55.4 percent; relative risk

renal-0.83, 95% CI 0.71-0.96) The secondary end point of the relative risk of death was also lower (0.84, 95% CI 0.98) Staged revascularization was performed in 17.7 percent of the culprit-lesion-only group There were nosignificant differences in the rates of other adverse outcomes.

0.72-Determinants of outcome — The clinical response to primary PCI is highly variable While some patients

improve rapidly after PCI, others show no immediate hemodynamic improvement, and a few transiently

deteriorate after reperfusion is established, particularly if there is late reperfusion This is also true for latereperfusion with fibrinolysis Concurrent use of an IABP protects against sudden hemodynamic deterioration.(See 'Intraaortic balloon pump' above.)

Data from the nonrandomized SHOCK trial registry suggest that the in-hospital mortality after PCI is related tothe degree of reperfusion achieved in the infarct related artery [65] Among 276 patients undergoing PCI, themortality for TIMI grade 3 (normal), grade 2, or grade 0/1 flow was 33, 50, and 86 percent, respectively A similarrelationship to TIMI flow grade was noted in a report from the ALKK primary PCI registry in Germany (37, 66, and

78 percent in-hospital mortality, respectively) [51] (See "Fibrinolytic (thrombolytic) agents in acute ST elevationmyocardial infarction: Markers of efficacy", section on 'TIMI flow grade'.)

The time from symptom onset to PCI may be another determinant of outcome In the ALKK report, the in-hospitalmortality was 44 percent in patients receiving primary and rescue PCI as well as urgent CABG within three hoursfrom symptom onset, 45 percent from three to six hours, 54 percent from 6 to 12 hours, and 58 percent from 12

to 24 hours [51] However, the benefits of primary PCI were seen in both early and late presenters in the SHOCKtrial [23] As a result, late presenters should not be denied emergency revascularization based upon timing alone.(See 'PCI' above.)

In a prespecified subset analysis of the SHOCK trial, the benefit of revascularization on survival was limited topatients <75 years old, but there were too few elderly patients in this subgroup to be confident of the observation[62] Subsequent studies, including the SHOCK registry, have found the same magnitude of benefit in patients

≥75 years old [66,67] At present, no firm conclusion regarding the magnitude of benefit (or harm) can be made inolder patients

Use in left main stenosis — In the SHOCK trial registry, 16 percent of patients with CS had significant left main

disease (although not necessarily left main occlusion) [19] Although emergent CABG is a revascularizationoption, it appears to be seldom utilized in contemporary clinical practice [9

Potential efficacy of PCI in patients with CS and left main disease was suggested in an observational registry ofunprotected left main stenosis; 40 patients with an acute MI (37 of whom had CS) underwent emergency PCI (17with stenting) [68] The rate of in-hospital death (35 versus 70 percent) was lower in those who received a stentcompared to primary balloon angioplasty alone Stenting was also associated with a higher survival rate at 12months (53 versus 35 percent) A much higher in-hospital mortality rate of 81 percent was noted after primaryPCI among 80 patients with a left main stem infarct-related artery in the ALKK primary PCI registry in Germany[51] (See "Management of left main coronary artery disease".)

Coronary artery bypass surgery — The majority of patients with CS after MI have significant left main or three

vessel disease (16 and 53 percent, respectively, in the SHOCK trial registry) [19] In such patients, the ability toachieve complete revascularization makes CABG a potentially critical therapeutic strategy A surgical approachalso permits the correction of concomitant severe mitral regurgitation, which is often present Pooled data on

370 patients in 22 studies revealed an in-hospital mortality rate of 36 percent when CABG was performed duringthe hospitalization for acute MI with CS [59] (See "Coronary artery bypass graft surgery in patients with acute STelevation myocardial infarction", section on 'Cardiogenic shock'.)

The relatively low mortality rate in these nonrandomized series may reflect a true benefit or selection bias, inwhich patients at lowest risk are selected for CABG However, similar findings (41 percent overall mortality) werenoted in the patients who underwent emergency CABG in the SHOCK trial within six hours of randomization [23].Despite this benefit, CABG is underutilized in the community setting In a review from the National Registry ofMyocardial Infarction of 25,311 patients with CS seen from 1995 to 2004 in the United States, the overall rate ofimmediate CABG was stable at about 3 percent [9

PCI versus CABG — The relative efficacy of PCI and CABG was evaluated in the 128 patients with predominant

left ventricular failure who underwent emergency revascularization in the SHOCK trial [69] Not surprisingly, the

47 patients (37 percent) who underwent CABG were significantly more likely to have diabetes and three-vessel orleft main disease; 85 percent of these patients received two or more grafts and 52 percent received three ormore grafts Despite the more extensive disease in the CABG group, overall survival was similar to PCI at 30 days(57 versus 56 percent with PCI) and one year (47 versus 52 percent) The similar outcomes, despite the worsedisease in patients undergoing CABG, may reflect in part the higher rate of complete revascularization (87 versus

23 percent with PCI)

In clinical practice, a combination of these two revascularization strategies is often indicated This may involveemergent percutaneous recanalization of the infarct related artery in the catheterization laboratory followed byemergent/urgent revascularization with CABG

Population-based studies — Observations from population-based studies suggest that the results of the SHOCK

trial itself can be applied to clinical practice As an example, similar 30-day survival benefits with early

revascularization were noted in the larger nonrandomized SHOCK trial registry [67,70] The outcome with

revascularization was the same in men and women [71] (See "Management of coronary heart disease in

women".)

Observations were comparable in the review cited above from the National Registry of Myocardial Infarction(NRMI) of 25,311 patients with CS seen between 1995 and 2004 [9

Long-term outcome — In addition to the short-term benefits, follow-up reports from the SHOCK trial

demonstrated that the benefit of revascularization persists for many years At one year, early revascularizationwas associated with a lower mortality rate (eg, 53 versus 66 percent) [62] In addition, the patients who wereassigned to emergency revascularization were significantly more likely to remain stable after discharge (71versus 44 percent at one year) and less likely to worsen or die after 30 days (15 versus 34 percent) [14]

The mortality benefit persisted at six years (67 versus 80 percent with medical stabilization) (figure 2) [15] Thepreviously observed significant interaction between age and treatment effect was no longer evident on long-termfollow-up

Evidence of long-term benefit was also suggested in a subset analysis from the GUSTO-I trial of over 39,000patients who were alive at 30 days after an acute MI, 1306 of whom had been in CS [72] Revascularization within

30 days was performed in 44 percent of the patients with CS; the one-year mortality in these patients was

significantly lower than in those who were not revascularized (8 versus 15 percent, odds ratio 0.6 after adjustingfor differences in baseline characteristics) Not surprisingly, the survivors of CS had higher one-year mortalitythan those without shock (12 versus 3 percent)

Major society guidelines — The American College of Cardiology Foundation/American Heart Association

guidelines for the management of patients with STEMI recommend primary PCI or emergent CABG with anSTEMI or MI with new or presumably new left bundle branch block who develop shock irrespective of the timedelay from the onset of MI [73,74] Advanced age alone should not be considered a contraindication to

revascularization In older patients, physicians should individualize the approach and consider comorbidities,baseline functional status, and patient’s prior advanced directives

Revascularization summary — The optimal strategy for the management of CS is characterized by an early

revascularization strategy with adjunctive IABP support Our approach is as follows:

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries

and regions around the world are provided separately (See "Society guideline links: Non-ST elevation acutecoronary syndromes (non-ST elevation myocardial infarction)" and "Society guideline links: ST elevation

myocardial infarction (STEMI)".)

SUMMARY AND RECOMMENDATIONS — Mortality in patients with cardiogenic shock (CS) complicating

myocardial infarction (MI) approaches 50 percent, despite advances in therapeutic interventions such as theearly use of percutaneous coronary intervention and improvements in medical care, particularly aggressiveantithrombotic therapy (See 'Prognosis' above.)

This high mortality can be lowered with further improvements in the speed with which reperfusion is delivered,and vigilant observation of those hospitalized patients with MI at risk (See "Clinical manifestations and

diagnosis of cardiogenic shock in acute myocardial infarction", section on 'Risk factors'.)

In patients with STEMI, revascularization with either PCI or CABG is preferred to fibrinolytic therapy, if it can

be performed in a timely manner (within 90 minutes from initial hospital presentation for PCI) (See "Acute

ST elevation myocardial infarction: Selecting a reperfusion strategy", section on 'Summary and

recommendations'.)

●

PCI is preferred to CABG for MI (either STEMI or NSTEMI) patients with one- or two-vessel coronary diseaseand technically suitable lesions [75] Immediate CABG may be considered for left main or severe three-vessel disease If CABG cannot be performed, single-vessel or multivessel PCI may be attempted CABG isthe treatment of choice if there are associated mechanical complications

●

For those STEMI patients treated with fibrinolytic therapy who appear to have been successfully reperfusedwith fibrinolytic therapy and who no longer manifest CS, we suggest not taking the patient to the

catheterization laboratory urgently, based on the evidence of harm with PCI soon after fibrinolysis (See

"Percutaneous coronary intervention after fibrinolysis for acute ST elevation myocardial infarction", section

●

The following is a summary of our approach to the treatment of patients with CS.

Diagnostic testing — An emergency echocardiogram should be performed to determine the etiology of shock in

the absence of a large MI [26] Echocardiography can be useful to estimate left atrial pressure as well as toidentify the etiology of shock (See "Clinical manifestations and diagnosis of cardiogenic shock in acute

myocardial infarction", section on 'Echocardiography'.)

Hemodynamic monitoring, including pulmonary artery catheterization, may be useful to guide optimal medicalmanagement, particularly when the diagnosis is in doubt Monitoring is also useful in distinguishing

vasoconstrictive from vasodilatory shock However, placement of a pulmonary artery catheter should not delaytransferring the patient to the catheterization laboratory (See 'Hemodynamic monitoring' above and "Clinicalmanifestations and diagnosis of cardiogenic shock in acute myocardial infarction".)

Medical management — Initial therapy of CS consists of early identification, optimally before frank hypotension

is present, and rapid stabilization with correction of metabolic abnormalities

Antiplatelet agents — The recommendations for the use of antiplatelet agents in patients with MI are given

separately (See "Antiplatelet agents in acute ST elevation myocardial infarction", section on 'Summary andrecommendations' and "Antiplatelet agents in acute non-ST elevation acute coronary syndromes", section on

In patients with CS in whom revascularization is planned, we recommend not giving a thienopyridine until afterdiagnostic coronary angiography (and percutaneous coronary intervention [PCI] is to be performed) and adding aglycoprotein (GP) IIb/IIIa inhibitor to heparin as early as possible after diagnosis (Grade 1B) This

recommendation is based upon the fact that a higher percentage of patients with CS complicating MI will requirecoronary artery bypass graft surgery (CABG) compared to those without and the potential benefits for GP IIb/IIIaagents with PCI in the highest risk subsets (See 'Oral antiplatelet therapy' above.)

Beta blockers — We recommend withholding beta blockers and calcium channel blockers in patients with CS

(Grade 1B) (See 'Beta blockers and other negative inotropes' above.)

Vasopressors and inotropes — We recommend vasopressors for initial management of patients with

cardiogenic shock and severe hypotension (systolic blood pressure <80 mmHg) (Grade 1B) Although there is nodefinitive evidence of the superiority of one vasopressor over another, we suggest beginning with norepinephrine

(Grade 2B) (See 'Vasopressors and inotropes' above.) Pulmonary artery (Swan-Ganz) catheter placement may

be useful to guide further use of vasopressors/inotropes if there is ongoing hypoperfusion after revascularizationand initial attempts at resuscitation

IABP — Our recommendations for the use of an intraaortic balloon pump (IABP) in patients with acute MI and

cardiogenic shock are as follows (see 'Intraaortic balloon pump' above):

For patients in whom mechanical complications (eg, acute mitral regurgitation or rupture of the ventricularseptum) are not present and for whom revascularization is planned, we suggest not placing an IABP as aroutine strategy (Grade 2B)

However, for such patients whose hemodynamic parameters and clinical status are rapidly deterioratingwhile on vasopressor and inotropic support, we suggest placement of an IABP (Grade 2C) Deterioration isconsidered present when the systolic blood pressure is persistently below 80 mmHg, there is a fall urineoutput or a worsening of mentation, the arterial oxygen saturation is falling, or cardiac arrhythmias

(including heart block or ventricular tachycardia or fibrillation) develop or worsen

●

Reperfusion — All patients with CS complicating MI should undergo an attempt at reperfusion (See

'Reperfusion/revascularization' above.)

Our recommendations for the use of reperfusion therapy in patients with MI complicated by CS are similar tothose for most patients with MI and differ principally in the level of evidence (see "Acute ST elevation myocardialinfarction: Selecting a reperfusion strategy", section on 'Summary and recommendations'):

ACKNOWLEDGMENT — The UpToDate editorial staff would like to thank Dr Venu Menon for his contributions as

an author to previous versions of this topic review

Use of UpToDate is subject to the Subscription and License Agreement

REFERENCES

1 Reynolds HR, Hochman JS Cardiogenic shock: current concepts and improving outcomes Circulation2008; 117:686

2 Goldberg RJ, Spencer FA, Gore JM, et al Thirty-year trends (1975 to 2005) in the magnitude of,

management of, and hospital death rates associated with cardiogenic shock in patients with acute

myocardial infarction: a population-based perspective Circulation 2009; 119:1211

3 Goldberg RJ, Gore JM, Alpert JS, et al Cardiogenic shock after acute myocardial infarction Incidence andmortality from a community-wide perspective, 1975 to 1988 N Engl J Med 1991; 325:1117

4 Hochman JS, Boland J, Sleeper LA, et al Current spectrum of cardiogenic shock and effect of early

revascularization on mortality Results of an International Registry SHOCK Registry Investigators

Circulation 1995; 91:873

The role of IABP is not well studied in the uncommon patient treated with fibrinolytic therapy whose

hemodynamic parameters and clinical status are rapidly deteriorating while on vasopressor and inotropicsupport and for whom transfer to a facility capable of performing urgent revascularization is planned Ourauthors and reviewers have differing approaches, with some recommending placement of an IABP beforetransfer and other not (See 'Use with fibrinolysis' above.)

●

For patients with ST elevation MI, we recommend revascularization as opposed to fibrinolytic therapy (Grade 1A) This recommendation requires that diagnostic coronary angiography be performed within 90 minutes ofinitial hospital presentation For those patients who cannot undergo timely coronary angiography, we

recommend fibrinolytic therapy rather than no immediate reperfusion (Grade 1B)

●

For patients with one or two vessel disease who do not have mechanical complications, we recommendpercutaneous coronary intervention (PCI) of the infarct related artery as opposed to CABG (Grade 1B)

●

For patients with three vessel disease or left main disease who do not have mechanical complications (such

as acute mitral regurgitation or rupture of either the ventricular septal or free walls), we suggest immediatePCI as opposed to CABG (Grade 2C) In many cases it may be appropriate to prefer CABG based on factorssuch as the likelihood of successful revascularization with PCI, the extent of disease, the skill

level/experience of the PCI team, or the availability of immediate CABG