Board Review

Cardiogenic Shock in Acute Myocardial Infarction

Dale T. Ashby,* PhD, Gregg W. Stone, MD, and Jeffrey W. Moses, MD

INTRODUCTION

Cardiogenic shock is estimated to occur in approxi-mately 7–10% of patients with acute myocardial infarc-tion (AMI) [1,2] and is the leading cause of death forhospitalized AMI patients [3–5]. Despite clinical ad-vances in AMI treatment, cardiogenic shock continues tobe associated with a poor prognosis. The underlyingbasis of cardiogenic shock in 50–60% of patients isextensive myonecrosis [6]. Early recognition of cardio-genic shock complicating AMI is important; prompt sup-portive measures and definitive treatment with revascu-larization using percutaneous or surgical techniques canimprove long-term survival [4,7,8]. This article will re-view the definition, etiology, pathophysiology, predictorsof survival, treatment options, and specific conditionsassociated with cardiogenic shock in AMI.

DEFINITION

The clinical definition of cardiogenic shock is com-prised by a combination of decreased cardiac output andevidence of tissue hypoperfusion (cool, mottled extrem-ities, oliguria, clouded mental status) in the presence ofadequate intravascular volume. The most common he-modynamic definition requires a sustained systolic bloodpressure of � 90 mm Hg for at least 30 min (or the needfor vasopressors or intra-aortic balloon counterpulsationto maintain the systolic blood pressure above 90 mmHg), a reduced cardiac index (� 2.2 L/min/m2) with anadequate or increase in left ventricular filling pressure.

INCIDENCE

The exact incidence of cardiogenic shock complicat-ing AMI is difficult to measure, as an unknown propor-tion of patients will die before reaching medical atten-tion. Although early series had reported the incidence ofcardiogenic shock in the setting of AMI to be approxi-mately 20% [9], more recent series report rates of 5–10%[1,2,10].

Although most commonly associated with ST eleva-tion on the presenting electrocardiogram, cardiogenicshock can occur with non-ST elevation infarction andeven unstable angina. In the GUSTO-IIb trial, Holmes etal. [11] reported the presence of cardiogenic shock in4.2% of ST segment elevation MIs and in 2.5% ofpatients without ST segment elevation. Shock developedsignificantly later among patients without ST segmentelevation (median, 76.2 hr after study entry) than inpatients with ST segment elevation AMI (9.6 hr afterstudy entry).

ETIOLOGY OF CARDIOGENIC SHOCK

The degree of hemodynamic impairment followingAMI without a mechanical complication is generallyrelated to the total amount of myocardial damage, bothacute and chronic. Autopsy studies have shown that thereis a loss of more than 40% of the left ventricular myo-cardium among patients dying from cardiogenic shockafter AMI [12–14]. Shock may result from a large initialAMI, from infarct extension (reinfarction in the sameterritory), or after a small AMI in a patient with preex-isting ventricular dysfunction (Table I). Mechanical com-plications of AMI such as mitral regurgitation (due topapillary muscle rupture), ventricular septal defect, free-wall rupture, and pericardial tamponade can also causecardiogenic shock. Other conditions in the differentialdiagnosis are listed in Table I. In the MILIS and SHOCKregistries [15,16], cardiogenic shock was caused by LV

The Lenox Hill Heart and Vascular Institute, New York, NewYork

*Correspondence to: Dr. Dale T. Ashby, Cardiovascular ResearchFoundation, 55 East 59th Street, 6th Floor, New York, NY 10022.E-mail: dashby@crf.org

Received 10 October 2002; Revision accepted 16 January 2003

DOI 10.1002/ccd.10521Published online in Wiley InterScience (www.interscience.wiley.com).

Catheterization and Cardiovascular Interventions 59:34–43 (2003)

© 2003 Wiley-Liss, Inc.

failure in 74% of patients, mitral regurgitation in 9%,VSD in 5%, RV infarction in 3%, and free-wall rupturein � 2%. In the SHOCK trial registry [16] of 1,380patients, shock developed at a median of 6.2 hr after AMIsymptom onset. Early shock (� 24 hr) occurred in 74.1%of patients and was associated with ST segment elevationin two or more leads, multiple infarct locations, inferiorMI, left main disease, and smoking. Late shock (� 24 hr)was associated with recurrent ischemia, Q-waves in twoor more leads, and the left anterior descending artery asthe culprit vessel. Clinical predictors of the developmentof cardiogenic shock after AMI include old age, femalesex, prior angina, diabetes, anterior wall infarction, largerinfarctions, and patients with a past history of stroke andperipheral vascular disease [15,17].

PATHOPHYSIOLOGY

The shock state in most patients with AMI stems fromextensive myocardial injury that directly impairs myo-cardial contractility leading to reduced stroke volumeand arterial pressure. This in turn decreases coronaryperfusion leading to further myocardial ischemia andextension of myocardial dysfunction/necrosis in a vi-cious cycle that ultimately leads to the inability of leftventricular contractility to sustain an arterial blood pres-sure compatible with life (Fig. 1). Reduced cardiac out-put results in decreased systemic tissue perfusion, whichleads to local accumulation of tissue metabolites and aresulting lactic acidosis, which may further compromisesystolic performance. Preexisting cardiac conditions suchas decreased left ventricular ejection fraction, valvularheart disease, or pericardial disease may make the heartsusceptible to shock in AMI. About 30–35% of patients

presenting with cardiogenic shock after AMI have hadprior MIs [18].

The occurrence of cardiogenic shock is intimatelyrelated with the concurrent development of severe hypo-tension during AMI. Therefore, patients initially withoutextensive myocardial damage who later develop severehypotension due to hypovolemia, valvular disease, peri-cardial disease, or severe bradycardia may subsequentlydevelop cardiogenic shock. This occurs as hypotensionper se reduces coronary perfusion and ultimately extendsmyocardial, ischemia, and injury, specifically in areassupplied by significantly stenosed arteries [2,14].

Delayed cardiogenic shock due to progressive myo-cardial necrosis [19] or infarct extension [15] may alsooccur. Infarct extension can occur due to a reocclusion ofthe infarct-related artery, extension, or embolization ofintracoronary thrombus to other coronary branches, or asa result of decreased coronary perfusion pressure second-ary to global hypoperfusion. Given that over 80% pa-tients with cardiogenic shock from AMI have multivesselcoronary disease [4,13,18], areas of myocardium remotefrom the infarct zone that are important for compensatory

TABLE I. Causes of Cardiogenic Shock

Acute myocardial infarctionLeft ventricular failure

Extensive myonecrosisInfarct extension or reinfarctionSmall infarction in setting of prior left ventricular dysfunction

Mechanical complications of AMIMitral regurgitation due to papillary muscle ruptureVentricular septal defectFree-wall rupturePericardial effusion causing tamponade

Other causes of cardiogenic shockSevere cardiomyopathyValvular heart disease (acute and chronic)Hypertrophic obstructive cardiomyopathyMyocarditisMyocardial traumaSystemic sepsis with secondary myocardial dysfunctionBrady- and tachyarrhythmias

Fig. 1. The downward spiral in cardiogenic shock. Adaptedwith permission from Hollenberg et al. [14].

Cardiogenic Shock 35

hyperkinesis may themselves become ischemic as a re-sult of the hypotension, lactic acidosis, and fixed stenosesin the coronary arteries supplying these viable territories,thus exacerbating the shock state.

MANAGEMENT OF CARDIOGENIC SHOCK

Evaluation

Cardiogenic shock complicating AMI is a medicalemergency. Prompt diagnosis and management can im-prove long-term outcomes [20] and thus rapid assess-ment of the patient is mandatory.

The clinical history will usually be that of AMI fol-lowed by the development of shock. The physical find-ings of cardiogenic shock were first described by Herrick[21] in 1912 and include hypotension, cyanosis, a weak,rapid pulse, altered sensorium, and cold clammy skin.Physical findings may include elevated jugular venouspressure, present third or fourth heart sound, a systolicmurmur (from mitral regurgitation or ventricular septaldefect), and a decreased urine output.

Recommended diagnostic studies for suspected car-diogenic shock are shown in Table II. Initial diagnostictests should include basic blood work (complete bloodcount, renal function, cardiac enzymes, coagulation pro-file), arterial blood gas, and a chest X-ray looking forcardiac size and left ventricular failure (interstitial oralveolar edema in the lung fields). In addition, electro-cardiogram, echocardiogram, and invasive hemodynamicmonitoring are indicated (though should not delay revas-cularization therapy, as described below). The electro-cardiogram will provide information on the cardiacrhythm and the site of the AMI, as well as evidence ofprior MI. Echocardiography has the utility to assess leftventricular function, the site of ventricular wall dysfunc-tion, and to exclude other complicating factors such asmitral regurgitation, ventricular septal defect, free-wallrupture, and/or pericardial effusion [22].

The use of invasive monitoring with right heart cath-eterization is controversial. Holmes et al. [23] reportedthat patients in the GUSTO-I trial had better outcomeswhen they were treated more aggressively, including theuse of right heart catheterization. In contrast, in a study ofcritically ill patients (including cardiogenic shock) in anintensive care setting, Connors et al. [24] reported anincrease in mortality associated with the use of right heartcatheterization. To date, there have been no randomizedtrials addressing the issue of the value of right heartcatheterization and cardiogenic shock. Despite the lackof class I evidence of benefit, right heart catheterizationcan provide useful information in the initial assessmentof the cardiogenic shock patient and to monitor compli-cations such as hypovolemia, shunts, right ventricularinfarction, or cardiac tamponade.

Supportive Therapy

Initial therapy. The initial approach to therapy, aftera diagnosis of cardiogenic shock associated with AMI, isto attempt to achieve hemodynamic stability by main-taining a systolic blood pressure � 90 mm Hg andtreating any pulmonary congestion, arrhythmias, and ac-id/base disturbance. Supplemental oxygen should be ap-plied, central venous access obtained, arterial blood pres-sure monitoring commenced, urinary catheter inserted,and intubation and mechanical ventilation should be con-sidered if respiratory failure is present or imminent.Relief of pain with morphine sulfate is important if theblood pressure permits. Intravenous nitroglycerine is aneffective venodilator and can reduce ischemia by reduc-ing left ventricular filling pressures. Its hypotensive ef-fects limits its use in hemodynamically unstable patients.Diuretics should be used to treat pulmonary edema. Betablockers are relatively contraindicated in the setting ofacute cardiogenic shock due to their negative chrono-tropic and hypotensive effects.

Positive inotropic agents and vasodilators. In pa-tients with a systolic blood pressure � 90 mm Hg orsigns of inadequate tissue perfusion with elevated leftventricular filling pressures (pulmonary capillary wedgepressure � 16 mm Hg), cardiac inotropes should beconsidered. Dopamine has both inotropic and vasopres-sor properties, acts directly on myocardial B1-adrenergicreceptors, and indirectly causes release of norepinephrine[25]. Dopamine should be used as the first-line agentwith the addition of dobutamine or norepinephrine inunresponsive patients. A study by Richard et al. [26]showed that in some patients with cardiogenic shock, thecombination of dopamine and dobutamine can be moreeffective than either agent alone. Dobutamine may pro-duce a vasodilatory effect, potentially exacerbating hy-potension and further reducing coronary perfusion pres-sure. Norepinephrine can be used when other therapies

TABLE II. Diagnostic Evaluation

Diagnostic investigations

Initial blood workComplete blood countElectrolytesCardiac enzymesCoagulation profile

Arterial blood gas12-lead electrocardiogramChest-X-raya

Echocardiograma

Arterial blood pressure monitoringa

Right heart cathetera

aImmediate left heart catheterization should precede these tests in mostpatients.

36 Ashby et al.

fail to maintain an arterial diastolic pressure above 50mm Hg. All vasopressor agents should be administeredwith continuous hemodynamic monitoring [6].

Intra-aortic balloon counterpulsation. Intra-aorticballoon pumping (IABP) is beneficial for the initial sta-bilization of patients with cardiogenic shock [27]. Intra-aortic balloon pumping should be considered a stabiliz-ing measure that allows time for definitive measures suchas revascularization rather than a primary treatment forcardiogenic shock. The IABP increases diastolic coro-nary arterial perfusion and reduces systolic afterloadwithout increasing myocardial oxygen demand. It re-quires placement through a femoral arterial sheath. Alarge registry of 9,332 patients with IABP showed sig-nificantly less limb ischemia with 8 Fr size IABP com-pared to 9.5 Fr IABP (1.5% vs. 3.0%; P � 0.005) [28].In this registry, there were no differences between bleed-ing complications or mortality between 8 and 9.5 FrIABP. The risk of ischemic ilio/femoral thrombosis in-creases with the length of time the IABP is left in situ[29].

Although there have been no randomized studies thathave shown a clear mortality benefit with the use ofIABP in cardiogenic shock, a number of studies supportthe hypothesis that IABP is beneficial. Two retrospectivestudies [30,31] demonstrated that patients with AMI andcardiogenic shock treated in community hospitals withIABP followed by thrombolysis had improved in-hospi-tal survival after subsequent transfer to tertiary institu-tions for revascularization. In the GUSTO-I study, pa-tients with cardiogenic shock who received an IABP hada trend toward lower mortality [32]. An analysis from theSHOCK trial registry indicated that patients with cardio-genic shock treated with IABP had a lower in-hospitalmortality than those who did not (50% vs. 72%; P �0.0001) [33]. Potential selection bias in these uncon-trolled studies limits definitive conclusions from beingdrawn, however. Nonetheless, early IABP initiation hasbecome the de facto standard in patients with cardiogenicshock without severe peripheral vascular disease or aor-tic insufficiency.

Thrombolytic Therapy

Thrombolytic therapy has been shown to reduce mor-tality in patients with acute persistent ST elevation AMI[34,35]. In addition, thrombolytic therapy reduces thelikelihood of subsequent development of cardiogenicshock in patients who initially present with AMI withoutshock [35,36]. This is clinically important, since mostpatients develop cardiogenic shock more than 6 hr afterinitial hospital presentation [3,10,37].

Thrombolytic therapy has not been shown to enhancesurvival in patients with established cardiogenic shock atthe time of presentation. Subset analyses in patients with

established cardiogenic shock in large AMI trials dem-onstrated similar mortality with streptokinase as com-pared to placebo and similar mortality between streptoki-nase and tissue plasminogen activator with the 30-daymortality rates ranging from 56% to 78% [10,34,37]. TheSHOCK registry, however, suggests potential benefitfrom thrombolytic therapy [33]. In this large registry,patients in cardiogenic shock treated with thrombolytictherapy had a lower in-hospital mortality than those whodid not receive thrombolytic therapy (54% vs. 64%; P �0.05), though confounding adverse prognostic factors inpatients not receiving lytic therapy makes interpretationof these data difficult.

The reasons for the limited efficacy of thrombolytictherapy in patients with cardiogenic shock may includelimitation of penetration of the drug into the thrombus,possibly in relation to the collapse of the infarct-relatedartery during profound hypotension; diminished conver-sion of plasminogen to plasmin during profound acido-sis; and the low-flow state in the setting of decreasedcoronary perfusion (due to profound hypotension), whichmay favor early reocclusion of the infarct-related arteryeven after successful reperfusion [2,6,13,14,38,39].

REVASCULARIZATION

Given the high mortality of patients with cardiogenicshock despite thrombolytic therapy and IABP support,mechanical revascularization strategies with both percu-taneous transluminal coronary angioplasty (PTCA) andCABG have been studied. Revascularization of the isch-emic but not infarcted myocardium may be important inpatients with multivessel coronary artery disease andcardiogenic shock, as the maintenance of contractility inremote (noninfarct) zones is important for the mainte-nance of adequate cardiac output [40].

The results of PTCA on mortality rates in patients withcardiogenic shock have been reported in a number ofretrospective studies (Table III) [41–52]. The successfulreperfusion rate of the infarct-related artery is less inpatients with shock than nonshock and has ranged from54% to 100%. Survival after successful reperfusion withPTCA was markedly superior to that after unsuccessfulreperfusion. In GUSTO-1, successful PTCA in cases ofcardiogenic shock on arrival to hospital was associatedwith improved 30-day mortality (43% vs. 61% in thosewho did not receive PTCA) [10]. The 30-day mortality ofpatients who develop cardiogenic shock in-hospital wasalso improved by successful PTCA (32% vs. 61% whodid not receive PTCA) [7,53]. Stenting has been shownto reduce 6-month major adverse cardiac event rates overballoon angioplasty in patients with acute ST segmentelevation AMI without cardiogenic shock [54,55]. The

Cardiogenic Shock 37

superiority of stenting over PTCA in cardiogenic shockremains unproven but is widely practiced.

Though no controlled studies exist, a number of ret-rospective studies have suggested a benefit of the plateletglycoprotein IIb/IIIa antagonist abciximab in patientsundergoing PTCA for AMI and cardiogenic shock [56–58]. In the Platelet Glycoprotein IIb/IIIa in UnstableAngina: Receptor Suppression Using Integrilin Therapy(PURSUIT) trial of patients with non-ST elevation acutecoronary syndromes, eptifibatide treatment did not affectthe incidence of cardiogenic shock, but did reduce themortality of patients with cardiogenic shock from 73.5%to 58.5% (P � 0.03) [59].

Several retrospective studies have reported relativelyfavorable outcomes with emergent CABG for AMI andcardiogenic shock [8,60–62]. Left main and triple-vesselcoronary artery disease are a common finding in patientswith cardiogenic shock. The potential contribution ofischemia in the noninfarct zone to myocardial dysfunc-tion would favor complete revascularization [14]. If thepatient can be stabilized on an IABP and an operatingteam mobilized promptly (which is admittedly difficult atmost centers), CABG rather than PTCA is a more ap-propriate method to achieve complete revascularizationin patients with left main or triple-vessel disease [4].

Two multicenter prospective randomized trials havebeen reported comparing initial medical stabilization ver-sus early revascularization for patients with AMI andcardiogenic shock. In both trials, patient recruitment wasdifficult due to physician reluctance to randomize pa-tients. The Swiss Multicenter Evaluation of Early Angio-plasty for Shock Following Myocardial Infarction(SMASH) trial [63] randomized 55 patients developingcardiogenic shock within 48 hr of the onset of AMI atnine European centers over 4 years to either medicaltherapy or revascularization with PTCA. The trial was

terminated due to difficulties with patient recruitment.Sixty-nine percent of the 32 patients randomized toPTCA and 78% of the 25 patients randomized to medicaltherapy died within 30 days (risk ratio � 0.88; 95% CI �0.6–1.2). IABP usage was infrequent in both arms (9% inthe PTCA group and 4% in the medical group).

The larger randomized Should We Emergently Revas-cularize Occluded Coronaries for Shock (SHOCK) trial[4] systematically evaluated 302 patients with cardio-genic shock due to left ventricular failure complicatingAMI and provides the best current data set by which toguide treatment. The study design is shown in Figure 2.Patients were randomly assigned to emergent revascular-ization (n � 152) or initial medical stabilization (n �150). The method of revascularization was either CABGsurgery or angioplasty with or without stent placement(as decided by the operators under protocol guidelines).Early IABP placement was recommended in both groups

Fig. 2. Study design of the SHOCK trial [4].

TABLE III. Retrospective Studies of PTCA for Cardiogenic Shock

Study Patients

Successfulreperfusion

(%)

Survival aftersuccessfulPTCA (%)

Survival afterunsuccessfulPTCA (%)

O’Neil et al. [41], 1985 27 89 75 33Lee et al. [42], 1988 24 54 77 18Landin et al. [43], 1988 34 79 70 14Verna et al. [44], 1989 7 100 86 NAKaplan et al. [45], 1990 88 61 65 29Lee et al. [46], 1991 69 71 69 20Gacioch et al. [47], 1992 48 73 61 7Moosvi et al. [48], 1992 38 78 56 8Laney et al. [49], 1993 52 94 86 0Eltchaninoff et al. [50], 1995 33 75 76 25Antoniucci et al. [51], 1998a 66 94 79 0Ajani et al. [52], 2001b 46 63 89 18aStenting 47%.bStenting 35%.

38 Ashby et al.

and was performed in 86% of patients. The median timeto the onset of shock was 5.6 hr after AMI onset.

Revascularization rates in the emergent revasculariza-tion arm was 61% PTCA and 39% CABG. Angioplastywas successful in 77% of the cases. Thirty-day mortalitywas 38% with successful angioplasty versus 79% withunsuccessful angioplasty (P � 0.003). CABG was asso-ciated with a 36% 30-day mortality.

A marginal statistical benefit with the immediate re-vascularization strategy was present at 30 days (mortalityof 46.7% vs. 56.0%; P � 0.11). Notably, however, thissurvival difference widened at 6 months, with a mortalityoccurring in 50.3% after routine angiography and earlyrevascularization versus 63.1% with initial medical sta-bilization (P � 0.02; Fig. 3).

Subgroup analysis of the SHOCK trial indicated asignificant interaction between patient age and treatmentoutcome (Fig. 4). Patients � 75 years of age had a 15%absolute mortality reduction with revascularization at 30days and 20% at 6 months. In sharp contrast, patients 75years of age or older had a 22% increase in mortality withrevascularization compared to initial medical stabiliza-tion. Patient gender, transfer from a community hospitalto a tertiary center versus on-site revascularization, timefrom AMI onset to randomization, eligibility for throm-bolytic therapy, hypertension, diabetes, prior MI, andgeographic location of the infarct-related artery did notinfluence the benefit of emergent revascularization in thetrial.

Interestingly, the early mortality rate of 56% in themedical therapy group of the SHOCK trial was lowerthan historical controls. This may imply selection bias orraise the possibility that the very high usage of IABP(86%) and thrombolytic therapy in conjunction with de-layed in-hospital revascularization (25%) in the conser-vative arm may be somewhat beneficial.

RIGHT VENTRICULAR INFARCTION

Right ventricular infarction may accompany inferiorleft ventricular infarction and is a predictor of unfavor-able prognosis [64]. Right ventricular infarction is asso-ciated with increased right heart filling pressures whileleft ventricular filling pressure remains normal or onlyslightly raised [65]. RV infarction should be suspectedclinically in a hypotensive patient with clear lung fieldsand an elevated jugular venous pressure. The 12-leadelectrocardiogram will usually show inferior lead STelevation, and right-sided lead placement (V4R-V6R)will show ST segment elevation. Right heart catheteriza-tion is useful for diagnosis, and an elevated right atrialpressure with a right atrial-to-pulmonary capillary wedgepressure ratio of � 0.8 is indicative of right ventricularinfarction [66,67]. The pulmonary capillary wedge pres-sure will be low or normal if there is no left ventricularimpairment of function [65]. If left ventricular failurecoexists, the pulmonary capillary wedge pressure mayalso be elevated as well.

Patients with shock on the basis of right ventricularinfarction have better prognosis than those with de-pressed cardiac contractility resulting from extensive leftventricular injury. Supportive therapy for patients with

Fig. 3. Results of the SHOCK trial [4].

Fig. 4. SHOCK trial, impact of age: (A) 30-day mortality and (B)6-month mortality [4].

Cardiogenic Shock 39

right ventricular infarction includes fluid administrationto maintain the right ventricular preload [67]. This willusually lead to an increase of the forward cardiac output.The development of high-degree atrioventricular blockhas been reported to occur in as many as 48% of rightventricular infarctions [68]. The maintenance of atrio-ventricular synchrony with pacing can improve cardiacoutput and optimize right ventricular filling. Inotropictherapy with dopamine and maintenance of atrioventric-ular synchrony may also be useful to optimize rightventricular filling and increase cardiac output in certainpatients [69]. IABP insertion may be warranted in pa-tients with persistent profound hypertension and rightventricular MI and may increase coronary perfusionpressure and alleviate right ventricular ischemia. Reper-fusion of the occluded coronary artery with thrombolysisor primary angioplasty has been shown to improve theclinical outcomes of patients with right ventricular in-farction [70–72].

MECHANICAL COMPLICATIONS AS CAUSE OFCARDIOGENIC SHOCK AFTER AMI

Mitral regurgitation due to papillary muscle rupture,ventricular septal rupture, or rupture of the left ventric-ular free wall may complicate AMI and result in cardio-genic shock. Rapid surgical treatment is required in mostpatients with these conditions for survival to be possible.Table IV shows the incidence, overall mortality, andsurgical mortality of patients with mechanical complica-tions of AMI from the SHOCK trial registry. The in-hospital survival remained poor with ventricular septalrupture or free-wall rupture even with emergency surgery[73,74]. Patients with mitral regurgitation, however, ben-efited from surgical repair or replacement of the mitralvalve [75].

Coronary angiography should be performed prior tothe cardiothoracic surgery to assess coronary anatomy sothat simultaneous revascularization with CABG can beperformed. If surgical repair is indicated for a mechanicalcomplication, it should generally be performed in anemergent manner before acidosis and multiorgan failuredevelop.

CONCLUSIONS

Despite advances in knowledge of the underlyingpathophysiology and treatment, cardiogenic shock re-mains the most common cause of death in patients hos-pitalized with AMI. In the SHOCK registry, the overallin-hospital mortality for patients with cardiogenic shockhas slightly fallen from 71% in 1992 to 60% in 1997[18]. Of those patients in the registry who were revascu-larized, the in-hospital mortality was 50% in 1992 andhas fallen to 38.5% in 1997.

Early diagnosis and rapid treatment are mandatory ifthe dismal prognosis of cardiogenic shock is to be im-proved. Careful clinical evaluation should be accompa-nied by echocardiographic assessment and aggressivemedical therapy. Right heart catheterization is useful andIABP placement should be performed promptly. Patientsyounger than 75 years should urgently undergo left heartcatheterization and coronary angiography in order toidentify coronary anatomy amenable to percutaneous orsurgical revascularization. Whether aggressive revascu-larization is beneficial in selected patients older than 75years of age is unclear. Thrombolytic therapy with IABPplacement should be considered as early treatment ifPTCA and cardiac surgery are not rapidly (� 4 hr)available, such as in hospitals without PTCA facilities. Insuch centers, however, following initial medical stabili-zation patients with shock should be transferred to inva-sive centers for early angiography and appropriate revas-cularization

The success of the revascularization procedure, ratherthan the method (percutaneous or surgical), determinesprognosis. Left main or extensive coronary artery diseasewith significant obstructive lesions in the noninfarct ter-ritories and mechanical complications of AMI constitutestrong indications for urgent coronary artery bypass sur-gery.

Despite the increasing application of revascularizationtreatment for patients with cardiogenic shock, mortalityremains high. Further improvements in outcome awaitthe development of novel mechanical and/or pharmaco-logic modalities to enhance myocardial cellular recovery[76–83]. Ultimately, the patient presenting late with

TABLE IV. Mechanical Complications Causing Cardiogenic Shock in the SHOCK TrialRegistry [73–75]

Ventricularseptal rupture

(n � 55)

Mitralregurgitation

(n � 98)

Free-wall ruptureor tamponade

(n � 28)

Incidence 3.9% 6.9% 2.7%In-hospital mortality 87.3% 55% 60.7%Surgery performed 56% (31/55) 45.7% (43/94) 75% (21/28)Mortality with surgery 80.6% 39% 60.7%

40 Ashby et al.

extensive myocardial necrosis may require orthotopiccardiac transplantation for survival [84,85].

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