cardiosyok ami.pdf

7/27/2019 cardiosyok ami.pdf

1/9

691

Address for correspondence:

Dr. Laxman Dubey, Consultant, Department of Cardiology,

College of Medical Sciences & Teaching Hospital, Bharatpur, Nepal.

E-mail: [email protected]

Received 29 August 2011; accepted for publication 8 September 2011.

INTRODUCTION

Cardiogenic shock (CS) is the leading cause of deathin patients hospitalized with acute myocardial infarction(AMI). Mortality from CS remains high. The develop-ment of CS is rarely unexpected; most patients whodevelop CS do so within 48 hrs of admission, with only10% shocked on arrival1. CS in AMI occurs when 40%or more of the left ventricle is destroyed. It occurs withinhours of the onset of an infarction due to massive ischae-mia and infarction. A relatively small infarction super-imposed on extensive previous damage may also pre-cipitate CS. Diagnosis of CS is defined as systolic bloodpressure < 90 mm Hg, evidence of hypoperfusion (coldclammy skin, cerebral obtundation), pulse > 100 bpm.

Cardiogenic shock complicating acute myocardial infarction

a review

Laxman DUBEY, MD; Sanjib SHARMA, MD; Mani GAUTAM, MD; Samir GAUTAM, MD;Sogunuru GURUPRASAD, MD, DM; Gangapatnam SUBRAMANYAM, MD, DM

Department of Cardiology, College of Medical Sciences & Teaching Hospital, Bharatpur, Nepal.

Abstract Cardiogenic shock is character ized by inadequate tissue perfusion due to cardiac dysfunction and is the leading cause of death in patientshospitalized with acute myocardial infarction. Mortality from cardiogenic shock still remains high. The development of cardiogenic shock is rarely unex-

pected; most patients who develop cardiogenic shock do so within 48 hrs of admission, with only 10% shocked on arrival. Mortality rate is exceedingly

high and reaches 70-80% in those treated conservatively. Early revascularization is the cornerstone treatment of acute myocardial infarction complicated

by cardiogenic shock. According to the guidelines, revascularization is effective up to 36 hours after the onset of cardiogenic shock and performed within

18 hours after the diagnosis of cardiogenic shock. Primary percutaneous coronary intervention is the most effi cient therapy to restore coronary flow in the

infarct-related artery. However, invasive strategy in a developing country like ours is not only costly but also technically demanding. We present a case of

acute myocardial infarction complicated with cardiogenic shock that underwent primary percutaneous coronary intervention and also review the incidence,

pathophysiology, management and outcome of cardiogenic shock complicating acute myocardial infarction.

Keywords Cardiogenic shock acute myocardial infarction revascularization.

Early revascularization is the cornerstone treatment ofAMI complicated by CS. According to the guidelines,revascularization is effective up to 36 hours after theonset of CS and performed within 18 hours after thediagnosis of CS. Primary percutaneous coronary inter-

vention (PCI) is the most efficient therapy to restorecoronary flow in the infarct-related artery.

CASE PRESENTATION

A 69-year-old female patient presented to the emer-gency department of the College of Medical Sciences &Teaching Hospital, Bharatpur, with a 16-hour history ofretrosternal chest pain, epigastric pain, vomiting withbreathlessness and profuse sweating. The patients med-ical history was significant for long-standing hyperten-sion and type 2 diabetes mellitus as well as occasionalexertional chest pains which were relieved by rest.

Clinical examination revealed an obese restless patientwith a blood pressure (BP) of 110/60 bilaterally and aregular pulse at 90 beats per minute. The jugular veins

were congested with a venous pressure of 21 mm Hgabove the sternal angle and positive Kussmauls sign.

Acta Cardiol 2011; 66(6): 691-699 doi: 10.2143/AC.66.6.2136951

[Review article]


2/9

L. Dubey et al.92

ventricular systolic dysfunction with an ejection fractionof 35% and a severely hypocontractile and dilated rightventricle. After admission in the CCU, the patients BPdecreased to 80/40 mm Hg. Inotropic support with dopa-mine, dobutamine and nor-adrenaline was started.

Cardiac catheterization was carried out under generalanaesthesia with inotropic support with dopamine,dobutamine and nor-adrenaline for BP support. A tem-porary pacemaker was inserted via the right femoral

vein for intermittent complete heart block. Coronaryangiography (CAG) showed an occluded proximal rightcoronary artery (RCA) (figure 2) with minor non-obstructive disease of the left system.

Primary PCI of the RCA, which was considered to bethe infarct-related artery, was undertaken. A 2.0 mm 10 mm balloon catheter was used to dilate the occludedlesion, and a 3.0 mm 20 mm PresillionTMbare metal

stent (Medinol Ltd, Israel) was deployed, with improveddistal coronary flow to TIMI grade III (figure 3). TheBP increased to 110/65 mm Hg. The electrocardio-graphical monitor showed a sinus rhythm with a rate of85 beats per minute. Inotropic support was stopped nextday. The temporary pacemaker was removed and thepatient was extubated on the second and third admissionday, respectively.

INCIDENCE

Mortality rate in AMI complicated with CS is exceed-ingly high and reaches 70-80% in those treated con-servatively2,3.Large thrombolytic trials demonstrate a

Cardiac examination revealed normal first and secondheart sounds and an S3 gallop but no murmurs or per-icardial rub. Chest examination revealed bilaterally equal

air entry with normal vesicular breathing and bibasilarcrepitations and rhonchi.An electrocardiogram was performed in the emer-

gency room and revealed Q waves and ST-segmentelevation in the inferior leads as well as in the right chestleads (V4R and V5R) (figure 1). The clinical picturetogether with electrocardiographic findings suggesteda diagnosis of acute transmural inferior wall MI associ-ated with right ventricular MI.

Laboratory investigations revealed evidence of myo-cardial damage with elevation of cardiac enzymes includ-ing troponin. Random blood sugar was high. The kidney

functions showed evidence of renal dysfunction with ablood urea of 126 mg/dl and serum creatinine of 2.4 mg/dl. Echocardiography was performed and revealed left

Fig. 1 ECG of the patient on presentation. ST-segment elevationwith Q waves in inferior leads ( II, III, aVF) and also ST-segmentelevation in right precordial leads (V4R, V5R).

Fig. 2 CAG revealed total obstruction of proximal RCA. Fig. 3 Post-PCI stenting to RCA (TIMI III flow).


3/9

Cardiogenic shock complicating acute myocardial infarction 693

66% and 73% mortality rate, respectively, in 30 daysfollow-up. The prevention of shock is therefore the mosteffective management strategy. The opportunity for pre-

vention is substantial, given the observation that CSdevelops within 48 hours of hospital admission, withonly 10-15% present to the hospital in cardiac shock1.In the randomized Should We Emergently RevascularizeOccluded Coronaries for Cardiogenic Shock (SHOCK)trial, the median time post MI for occurrence of shockwas 5 hours (interquartile range 2.2 to 12 hours). CS alsocomplicates unstable angina/ non STEMI. Shock com-plicating unstable angina/non STEMI occurs at a latertime period. Shock occurred in unstable angina/nonSTEMI at a median of 76.2 hours (20.6 to 144.5 hours)in the GUSTO II-B trial compared to 9.6 hours (1.8 to67.3 hours) in STEMI, whereas in the PURSUIT trialthe median time to shock in the non STEMI was 94

hours (38 to 206 hours). The primary goal in preventingCS in AMI is to reduce the time to effective treatment,because of the fact that early reperfusion limits ongoingnecrosis and salvages myocardium.

Patients with medical revascularization may developCS due to failed thrombolysis, reinfarction, or the infarctextension and these complications may be reduced sig-nificantly by primary PCI strategy. A growing trend hasbeen to use more aggressive therapeutic interventionsearly in patients who have CS as a result of acute myo-cardial infarction. The recent guidelines of the EuropeanSociety and American College of Cardiology (ACC) and

the American Heart Association (AHA) recommendearly mechanical revascularization for CS for patientsyounger than 75 years with ST-elevation AMI or leftbundle-branch block9,10.

PATHOPHYSIOLOGY

CS is the result of temporary or permanent derange-ments in the entire circulatory system. LV pump failureis the primary insult in most forms of CS, but other partsof the circulatory system contribute to shock with inad-equate compensation or additional defects. Autopsystudies show that CS is generally associated with the lossof more than 40% of the LV myocardial muscle. CS ischaracterized by both systolic and diastolic dysfunction.Patients who develop CS from acute MI consistentlyhave evidence of progressive myocardial necrosis withinfarct extension. Decreased coronary perfusion pres-sure and increased myocardial oxygen demand play arole in the vicious cycle that leads to CS. As depicted infigure 5, a decrease in coronary perfusion lowers cardiacoutput (CO), which further decreases perfusion of the

heart and other vital organs11

. Coronary flow may beadditionally compromised by atherosclerosis of vessels

high mortality. The 30-day mortality in CS with AMIwas 64% for reteplase and 58% for alteplase (P = 0.59) 4,5.Despite the strategies in reducing the time to effectivetreatment to decrease the incidence of CS, the incidenceof CS in AMI is stagnant. The rate of CS complicatingAMI decreased from 20% in the 1960s but then plateauedat ~8% for more than 20 years. Acute myocardial infarc-tion is complicated by CS in 7-10% of patients3. In the

Platelet Glycoprotein IIb/IIIa in Unstable Angina: Recep-tor Suppression Using Integrilin Therapy (PURSUIT)trial, the incidence of CS was 2.9% 6, similar to the 2.5%incidence reported in the non STEMI arm of the GlobalUtilization of Streptokinase and Tissue PlasminogenActivator for Occluded Coronary Arteries (GUSTO)II-B trial7. The incidence now appears to be on thedecline due to the increasing use of PCI for AMI.

Some investigators obtained data from the NationalRegistry of Myocardial Infarction (NRMI) 8, a nationaldatabase tracking practice patterns and outcomes ofpatients with AMI in the United States. Of more than293,633 patients admitted with AMI between 1995 to2004, 25,311 (8.6%) were diagnosed with CS. 29%patients presented in shock condition, while 71% devel-oped shock during their hospital stay. NRMI registryshows that the frequency of CS has remained steady overtime (figure 4).

PREVENTION

The 7.2% of patients developing CS in the GUSTO-I

trial accounted for 58% of the overall deaths at 30 days1

.Similarly, PURSUIT and GUSTO II-B trials reported

Fig. 4 Frequency of CS among patients in the NRMI registry.


4/9

L. Dubey et al.94

dysfunction and shock may be inappropriate. Inotropictherapy is indicated for RV failure when CS persists afterRV end-diastolic pressure has been optimized.

Peripheral vasculature, neurohormones,

and inflammation

Hypoperfusion of the extremities and vital organs isa hallmark of CS. When a critical mass of left ventricu-lar myocardium becomes ischaemic and fails to pumpeffectively, stroke volume and cardiac output are cur-tailed. Vasopressin and angiotensin II levels increase inthe setting of MI and shock, which leads to improvementin coronary and peripheral perfusion at the cost of in-creased afterload, which may further exacerbate myo-cardial ischaemia by compromised myocardial perfusiondue to hypotension and tachycardia. Activation of the

neurohormonal cascade promotes salt and water reten-tion. Fluid retention and impaired left ventricular dias-tolic filling triggered by tachycardia and ischaemia con-tribute to pulmonary venous congestion and hypoxaemia.

Cytokine levels rise more dramatically over the 24 to72 hours after MI. Tumour necrosis factorand inter-leukin-6 have a negative inotropic effect. Tumour necro-sis factoralso induces coronary endothelial dysfunc-tion, which may further diminish coronary flow14.

AETIOLOGY

Important causes of CS in the setting of AMI are LVdysfunction, RV dysfunction, and mechanical complica-tions (figure 6). Predominant LV failure in the settingof a large AMI is the most common cause of CS (74.5%).Other important causes of CS are acute MR (8.3%), VSD(4.6%), RV dysfunction due to RV infarction (3.4%),and LV free wall rupture (1.7%).

other than the infarct artery. These patients often havemultivessel coronary artery disease with limited coro-nary blood flow reserve. Ischaemia remote from theinfarcted zone is an important contributor to shock.Inotropic agents and vasoconstrictors temporarilyimprove CO and peripheral perfusion but do not inter-rupt this vicious circle.

In light of the complex pathophysiology of CS, it is

not surprising that in many cases, severe impairment ofcontractility does not lead to shock, and conversely, LVejection fraction (LVEF) may be only moderatelydepressed in CS. In fact, the mean LVEF in the SHOCKtrial was 30%.

RV dysfunction may cause or contribute to CS. Pre-dominant RV shock represents only 5% of cases of CScomplicating MI12. Shock due to isolated RV dysfunctioncarries nearly as high a mortality risk as LV shock12. Itis suggested that the probable mechanism of the shockassociated with RV infarction is concomitant with severeLV dysfunction. RV failure may limit LV filling via adecrease in CO, ventricular interdependence, or both.Treatment of patients with RV dysfunction and shockhas traditionally focused on ensuring adequate right-sided filling pressures to maintain CO and adequateLV preload; however, patients with CS due to RV dys-function have very high RV end-diastolic pressure, often> 20 mm Hg12. This elevation of RV end-diastolic pres-sure may result in shifting of the interventricular septumtoward the LV cavity, which raises left atrial pressure butimpairs LV filling due to the mechanical effect of theseptum bowing into the LV. This alteration in geometry

also impairs LV systolic function13

. Therefore, the com-mon practice of aggressive fluid resuscitation for RV

Fig. 5 Classic shock paradigm.

Fig. 6 Causes of CS in AMI.


5/9


chest pain at shock onset, ST-segment elevation in twoor more leads, multiple locations of MI (by ECG), infe-rior wall MI, smoking and left main disease. Patients inwhom the right coronary artery was the culprit, or whohad inferior wall MI on clinical grounds, were relativelymore likely to develop shock early. Mortality in thesepatients may be reduced with aggressive medical supportand reperfusion strategies.

More than 25% of patients who developed shock didso relatively late ( 24 h) after MI. Several factors mayfavour the delayed appearance of shock. Late shock wasmore often associated with recurrent ischaemia, thepresence of new Q waves in two or more leads, the useof inotropic agents, and LAD culprit vessel.

MANAGEMENT

Pharmacological treatment

The medical therapies used in the setting of an AMIhave not been specifically studied in the subgroup ofpatients with CS, though their use as it pertains to rep-erfusion should strongly be considered. Aspirin andheparin should be given as routinely recommended forAMI. Clopidogrel may be deferred until after emergencyangiography, because on the basis of angiographic find-ings, coronary artery bypass grafting (CABG) may beperformed immediately. Clopidogrel is indicated in allpatients who undergo PCI. Negative inotropes and

vasodilators (including nitroglycerin) should be avoided.Arterial oxygenation and near-normal pH should bemaintained to minimize ischaemia.

Treatment of the hypotension and low cardiac outputstate accompanying CS is of dire importance in order tomaintain adequate organ perfusion and tissue viability.Inotropic agents have a central role in treatment becausethe initiating event involves contractile failure. TheAmerican College of Cardiology/American Heart Asso-ciation (ACC/AHA) guidelines recommend norepi-nephrine for more severe hypotension because of its

DIAGNOSIS

Clinical definition of CS is a decreased cardiac outputand evidence of tissue hypoperfusion in the presence ofadequate filling pressures: marked and persistent (> 30 min) hypotension with

a systolic BP < 90 mm Hg reduction in the cardiac index (< 2.2 L/min/M2) normal or elevated PCWP (> 15 mm Hg).

CS should be suspected in all patients exhibiting signsof inadequate tissue perfusion irrespective of BP. Somepatients may present in pre-shock condition where sys-tolic BP was maintained but the urine output is typicallylow and the heart rate is > 100 beats per minute. Suchpresentation is associated with a high risk of in-hospitalmorbidity and mortality (43%) 15. When the physicianfails to recognize that the tachycardia is caused by pro-

nounced reduction in the stroke volume and thereforeadministers beta blockers, frank shock may be precipi-tated. Risk factors for CS are heart failure, age > 70,systolic blood pressure < 120, sinus tachycardia > 110 orheart rate < 60, increased time since onset of STEMIsymptoms. In the GUSTO-I mortality model, featuresof end organ hypoperfusion such as cold clammy skin,altered sensorium and oliguria were associated with anincreased 30-day mortality independent of haemody-namic variables16.

Predictor of early and late shock (table 1)

Most patients who develop CS do so relatively earlyafter AMI; however, a therapeutic window is often pre-sent allowing for intervention before CS develops. Shockonset after acute MI occurred within 24 hours in 74%of the patients with predominant LV failure in theSHOCK trial registry. Predictors of early (< 24 h) andlate ( 24 h) development of CS are given in table 1.

Shock might occur early after MI due to occlusion ofa major coronary artery and very extensive myocardialdamage. Early shock was more often associated with

Table 1 Predictors of onset of early and late shock

Predictors of early shock Predictors of late shock

Chest pain at shock onset Recurrent ischaemia

ST-segment elevation in two or more leads Presence of new Q waves in two or more leads

Left main disease LAD culprit vessel

Inferior wall MI Use of inotropic agents

Multiple locations of MI (by ECG)

Smoking


6/9

L. Dubey et al.96

Mechanical support: IABP

Intra-aortic balloon counterpulsation (IABP) haslong been the mainstay of mechanical therapy for CS.Use of an IABP improves coronary and peripheral per-fusion via diastolic balloon inflation and augments LV

performance via systolic balloon deflation with an acutedecrease in afterload. History reveals that the augmen-tation of coronary perfusion pressure was the synergis-tic partner fibrinolysis needed. A study by Prewitt et al.involving canines showed that under moderate hypoten-sion, an IABP enhanced the rate of clot dissolution withthrombolysis22. In 2001, after both the SHOCK trialregistry and the GUSTO-1 trial found similar results,the NRMI-2 database demonstrated a significant reduc-tion in mortality with IABP use in combination withfibrinolysis (67% vs. 49%) in almost 24,000 patients withCS5,23,24.

In many hospitals, initial stabilization is achieved byIABP. However, evidence for improved survival fromrandomized studies on the use of IABP in combinationwith PCI is lacking. In the large National Registry ofMyocardial Infarction, IABP use was independentlyassociated with survival at centres with higher rates ofIABP use, whether PCI, fibrinolytic therapy, or no rep-erfusion had been used25, however, no completed trialsdemonstrate benefit26,27. Neither was there evidence ofbenefit from the use of IABP in the patients developingCS in GUSTO-I23nor in SHOCK once the confounding

effects of cardiac catheterization had been adjusted for.There is thus no indication for IABP insertion in CSexcept in combination with more definitive treatment,or to provide stability during investigation.

Primary PCI

Despite the synergistic effect of fibrinolytic therapyplus IABP use, mortality rates continued to hover around50% and the focus shifted to early revascularization5,23.The GUSTO-I investigators found that while percutane-ous coronary angioplasty (PTCA) was performed in only19% of the 2972 patients with CS, this translated into amortality rate of 31% compared with 61% for patientswho did not undergo dilation.

Meta-analysis of 23 large randomized trials haveshown that primary PCI is superior to fibrinolysis forimmediate treatment of STEMI due to more effectiverestoration of coronary patency, less recurrent myocar-dial ischaemia, less coronary reocclusion, improvedresidual LV function and better clinical outcome includ-ing stroke28-31.

Several studies have reported a decreased mortality

with early revascularization for CS. The SHOCK trial32,33

was conducted to answer the question of whether an

high potency17. Although both dopamine and norepi-nephrine have inotropic properties, dobutamine is oftenneeded in addition. Dopamine works in a dose-depend-ent manner, activating a variety of receptors. At highdoses, dopamine activates alpha receptors in both sys-temic and pulmonary circulations, improving hypoten-sion, though simultaneously increasing pulmonarycapillary wedge pressure (PCWP). Though more evidentat intermediate doses where beta-receptor stimulationis prominent, dopamine has been shown to increasemyocardial contractility18.

Norepinephrine, a stimulator of alpha receptors, isoften used to quickly correct marked hypotension (sys-tolic BP < 70 mm Hg) and CS not responsive to dopa-mine17. Dobutamine is a strong beta1-receptor agonistallowing for both chronotropic and inotropic stimula-tion. Dose-dependent improvements in stroke volume

and PCWP are observed with dobutamine infusion. Thebeta2-receptor properties of dobutamine cause periph-eral vasodilation and reduction in SVR, which is oftencounterproductive to the hypotension associated withCS. As such, dobutamine is not recommended as mon-otherapy in patients with CS18. Dobutamine monother-apy is recommended in low-output heart failure (systolicBP: 70-100 mm Hg), in which there are no signs orsymptoms of shock17.

Fibrinolytics

Although fibrinolytic therapy generally reduces therisk of death in patients with ST- elevation MI, its ben-efits for patients with CS secondary to AMI are disap-pointing. When used early in the course of MI, fibrino-lytic therapy reduces the likelihood of subsequentdevelopment of CS after the initial event.

In a meta-analysis, fibrinolysis was associated witha 7% absolute reduction (54% vs. 61%) in mortality at1 month in patients with a systolic BP of < 100 mm Hgand a heart rate of > 100 bpm19. These findings werecorroborated in apost-hocanalysis of the SHOCK trialin which the use of fibrinolytics was associated withan 18% absolute reduction (60% vs. 78% withoutthrombolysis) in patients treated in the medical armof the study20. In the GISSI-1 study21, 30-day mortalityrates in Killip class IV patients had 69% mortality withstreptokinase and 70% in patients who received aplacebo.

Lower rates of reperfusion of the infarct-relatedartery in patients with CS might help explain the disap-pointing results from fibrinolytic therapy. The otherreasons for the decreased efficacy of fibrinolytic therapyare the presence of haemodynamic, mechanical, and

metabolic factors causative of CS; these factors are unaf-fected by fibrinolytic therapy.


7/9


ventricular failure. Eighty-one patients (63.7%) under-went PCI, while 47 patients (37.3%) underwent CABG.Overall survival was not statistically significant whencomparing CABG to PCI at both 30 days (57 vs. 56%,P = 0.86) and at 1 year (47 vs. 52%, P = 0.71). However,those undergoing CABG differed significantly from thePCI group in that they were more likely to have diabetes,3-vessel disease, and left main coronary disease.

CONCLUSION AND RECOMMENDATIONS

Although the treatment of AMI has improved con-siderably over the last few decades, the in-hospital mor-tality of patients in CS complicating AMI remainsextremely high, even with early interventional therapyand has not changed in recent decades. Given that theSHOCK trial, using a strategy of early revascularization,has demonstrated statistical improvement in long-termoutcomes, the current focus for the management of CSshould remain on timely reperfusion and stricter adher-ence to current ACC/AHA guidelines.

The patient presented has developed CS in the hospitalafter an inferior wall MI with RV infarction. While thepredominance of CS is a complication of an AMI withsubsequent biventricular failure, a mechanical complica-tion cannot be ruled out. In this case, an emergencyechocardiogram revealed biventricular dysfunction withLVEF of 35%. Emergency revascularization by PCI stent-ing or CABG and repair of any mechanical complicationscausing CS (depending on the anatomy) would be recom-mended. Our patient underwent immediate CABG fol-lowed by PCI stenting to RCA and subsequently was dis-charged from the hospital on the tenth day of admission.

CONFLICT OF INTEREST: none declared.

early aggressive strategy improved mortality over max-imal medical management. The SHOCK randomizedtrial demonstrated that in patients with AMI compli-cated by CS, early mechanical revascularization reduced6- and 12-month mortality compared with initialmedical stabilization (including IABP and fibrinolytictherapy) followed by late or no revascularization. TheSHOCK trial reported an increase in 30-day survivalfrom 46.7% to 56% by the adoption of an early revascu-larization strategy32 (figure 7). Moreover, after 1 yearthere was an absolute 13.2% risk reduction in favour ofthe early revascularization (P< 0.05) 33(figure 7).

The SHOCK trial did not show a benefit of earlyrevascularization in the subgroup of elderly (age 75 y),the benefit of early revascularization was large for thosewith age of < 75 years. For patients younger than 75 yearswith STEMI/LBBB, the current ACC/AHA guidelinesconsidered early mechanical revascularization for CS asa class I indication. According to the current ACC/AHAguidelines for PCI, primary PCI is recommended forpatients less than 75 years with STEMI or LBBB or whodevelop shock within 36 hours of MI and are suitablefor revascularization that can be performed within 18hours of shock (class I indication). However, the ACC/AHA guidelines on the management of AMI gave a classIIa recommendation for early revascularization in thoseolder than 75 years who are suitable candidates.

CABG versus PCI

Coronary artery bypass grafting (CABG) in the set-ting of CS is generally associated with high surgicalmorbidity and mortality rates. Because the results of PCIcan be favourable, routine bypass surgery is often dis-couraged for these patients.

In the SHOCK trial34

, emergency revascularizationwas evaluated in 128 patients with predominant left

Fig. 7 Kaplan-Meiercurve showing 30-day

mortality (left) and12-month survival (right)in the earlyrevascularization and

initial medicalstabilization arms ofthe SHOCK trial.


8/9

L. Dubey et al.98

1. Holmes DR Jr, Bates ER, Kleiman NS,

Sadowski Z, Horgan JH, Morris DC,

Califf RM, Berger PB, Topol EJ. Contemporary

reperfusion therapy for cardiogenic shock:

the GUSTO-I trial experience.

J Am Coll Cardiol1995; 26: 668-74. 2. Hasdai D, Topol EJ, Califf RM, Berger PB,

Holmes DR Jr. Cardiogenic shock

complicating acute coronary syndromes.

Lancet2000; 356: 749-56.

3. Goldberg RJ, Samad NA, Yarzebski J,

Gurwitz J, Bigelow C, Gore JM.

Temporal trends in cardiogenic shock

complicating acute myocardial infarction.

N Engl J Med1999; 340: 1162-8.

4. Hasdai D, Holmes DR Jr, Topol EJ, Berger PB,

Criger DA, Hochman JS, Ba tes ER, Vahanian A,

Armstrong PW, Wilcox R, Ohman EM,

Califf RM. Frequency and clinical outcome of

cardiogenic shock during acute myocardial

infarction among patients receiving reteplase

or alteplase. Results from GUSTO-IIIConclusion. Eur Heart J1999; 20: 128-35.

5. Sanborn TA, Sleeper LA, Bates ER, Jacobs AK,

Boland J, French JK, Dens J, Dzavik V,

Palmeri ST, Webb JG, Goldberger M,

Hochman JS. Impact of thrombolysis,

intra-aortic balloon pump counterpulsation,

and their combination in cardiogenic shock

complicating acute myocardial infarction:

a report from the SHOCK trial registry.

J Am Coll Cardiol2000; 36: 1123-9.

6. Hasdai D, Harrington RA, Hochman JS,

Califf RM, Battler A, Box JW, Simoons ML,

Deckers J, Topol EJ, Holmes DR Jr.

Platelet glycoprotein IIb/IIIa blockade and

outcome of cardiogenic shock complicating

acute coronary syndromes without

persistent ST-segment elevation.


7. Holmes DR Jr, Berger PB, Hochman JS,

Granger CB, Thompson TD, Califf RM,

Vahanian A, Bates ER, Topol EJ.

Cardiogenic shock in patients with

acute ischemic syndromes with and

without ST-segment elevation.

Circulation1999; 100: 2067-73.

8. Babaev A, Frederick PD, Pasta DJ, Every N,

Sichrovsky T, Hochman JS; NRMI Investigators.

Trends in management and outcomes of

patients with acute myocardial infarction

complicated by cardiogenic shock.JAMA

2005; 294: 448-54.

9. Silver S, Albertsson P, Aviles FF, Camici PG,

Colombo A, Hamm C, Jrgensen E, Marco J,

Nordrehaug JE, Ruzyllo W, Urban P, Stone GW,

Wijns W; Task Force for Percutaneous

Coronary Interventions of the European

Society of Cardiology. Guidelines for

percutaneous coronary intervention.

The Task Force for Percutaneous Coronary

Interventions of the European Society of

Cardiology. Eur Heart J2005; 26: 804-47.

10. Smith SC Jr, Feldman TE, Hirshfeld JW Jr,

Jacobs AK, Kern MJ, King SB 3rd, Morrison DA,

ONeill WW, Schaff HV, Whitlow PL,

Williams DO, Antman EM, Adams CD,

Anderson JL, Faxon DP, Fuster V, Halperin JL,

Hiratzka LF, Hunt SA, Nishimura R, Ornato JP,

Page RL, Riegel B. ACC/AHA/SCAI 2005

Guideline Update for Percutaneous CoronaryInterventionSummary Article: A Report of

the American College of Cardiology/American

Heart Association Task Force on Practice

Guidelines (ACC/AHA/SCAI Writing

Committee to Update the 2001 Guidelines for

Percutaneous Coronary Intervention).

Circulation2006; 113: 156-75.11. Antman EM, Braunwald E. Acute myocardial

infarction. In: Braunwald E, Fauci A, Kasper D,

et al, eds. Harrisons Principles of Internal

Medicine. 15th ed. New York, NY: McGraw-Hill;

2001: 1395.

12. Jacobs AK, Leopold JA, Bates E, Mendes LA,

Sleeper LA, White H, Davidoff R, Boland J,

Modur S, Forman R, Hochman JS.

Cardiogenic shock caused by right ventricular

infarction: a report from the SHOCK registry.


13. Brookes C, Ravn H, White P, Moeldrup U,

Oldershaw P, Redington A.

Acute right ventricular dilatation in

response to ischemia significantly impairs

left ventricular systolic performance.Circulation1999; 100: 761-7.

14. Zhang C, Xu X, Potter BJ, Wang W, Kuo L,

Michael L, Bagby GJ, Chilian WM. TNF-alpha

contributes to endothelial dysfunction in

ischemia/ reperfusion injury.Arterioscler

Thromb Vasc Biol2006; 26: 475-80.

15. Menon V, Slater JN, White HD, Sleeper LA,

Cocke T, Hochman JS. Acute myocardial

infarction complicated by systemic

hypoperfusion without hypotension:

report from the SHOCK trial registry.

Am J Med2000; 108: 374-80.

16. Hasdai D, Holmes DR Jr, Califf RM,

Thompson TD, Hochman JS, Pfisterer M,

Topol EJ. Cardiogenic shock complicating

acute myocardial infarction: predictors of

death.Am Heart J1999; 138: 21-31.

17. Antman EM, Anbe DT, Armstrong PW,

Bates ER, Green LA, Hand M, Hochman JS,

Krumholz HM, Kushner FG, Lamas GA,

Mullany CJ, Ornato JP, Pearle DL, Sloan MA,

Smith SC Jr, Alpert JS, Anderson JL, Faxon DP,

Fuster V, Gibbons RJ, Gregoratos G,

Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK.

ACC/AHA guidelines for the management of

patients with ST-elevation myocardial

infarction Executive summary: A report of

the American College of Cardiology/American

Heart Association Task Force on Practice

Guidelines (Writing Committee to Revise the

1999 Guidelines for the Management of

Patients With Acute Myocardial Infarction).

Circulation2004; 110: 588-636.

18. Leier CV, Heban PT, Huss P, Bush CA,

Lewis RP. Comparative systemic and

regional hemodynamic effects of

dopamine and dobutamine in patients with

cardiomyopathic heart failure.

Circulation1978; 58: 466-75.

19. Fibrinolytic Therapy Trialists (FTT )

Collaborative Group. Indications for

fibrinolytic therapy in suspected acute

myocardial infarction: Collaborative overview

of early mortality and major morbidity results

from all randomized trials of more than 1000

patients. Lancet1994; 343: 311-22.

20. French JK, Feldman, HA, Assmann, SF,

Sanborn T, Palmeri ST, Miller D, Boland J,

Buller CE, Steingart R, Sleeper LA,Hochman JS; SHOCK Investigators.

Influence of thrombolytic therapy,

with or without intra-aortic balloon

counterpulsation on 12-month survival in

the SHOCK trial.Am Heart J2003; 146: 804-10.

21. Roque M, Sanz GA. Treatment of cardiogenic

shock with thrombolysis and coronaryangioplasty. Rev Esp Cardiol1992; 45: 43-9.

22. Prewitt RM, Gu S, Schick U, Ducas J.

Intraaortic balloon counterpulsation

enhances coronary thrombolysis induced

by intravenous administration of

a thrombolytic agent.


23. Anderson RD, Ohman EM, Holmes DR Jr,

Col I, Stebbins AL, Bates ER, Stomel RJ,

Granger CB, Topol EJ, Califf RM.

Use of intraaortic balloon counterpulsation

in patients presenting with cardiogenic

shock: Observations from the GUSTO-I Study.

Global Utilization of Streptokinase and

TPA for Occluded Coronary Arteries.

J Am Coll Cardiol1997;30

: 708-15.24. Barron HV, Every NR, Parsons LS, Angeja B,

Goldberg RJ, Gore JM, Chou TM; Investigators

in the National Registry of Myocardial

Infarction 2. The use of intra-aortic balloon

counterpulsation in patients with cardiogenic

shock complicating acute myocardial

infarction: Data from the National Registry

of Myocardial Infarction 2.

Am Heart J2001; 141: 933-39.

25. Chen EW, Canto JG, Parsons LS, Peterson ED,

Littrell KA, Every NR, Gibson CM, Hochman JS,

Ohman EM, Cheeks M, Barron HV;

Investigators in the National Registry of

Myocardial Infarction 2. Relation between

hospital intra-aortic balloon counterpulsation

volume and mortality in acute myocardial

infarction complicated by cardiogenic shock.

Circulation2003; 108: 951-7.

26. ORourke MF, Norris RM, Campbell TJ,

Chang VP, Sammel NL. Randomized

controlled trial of intraaortic balloon

counterpulsation in early myocardial

infarction with acute heart failure.

Am J Cardiol1981;47: 815-20.

27. Flaherty JT, Becker LC, Weiss JL, Brinker JA,

Bulkley BH, Gerstenblith G, Kallman CH,

Weisfeldt ML. Results of a randomized

prospective trial of intraaortic balloon

counterpulsation and intravenous

nitroglycerin in patients with

acute myocardial infarction.


28. Keely EC, Boura JA, Grines CL.

Primary angioplasty versus intravenous

thrombolytic therapy for acute myocardial

infarction, a quantitative review of 23

randomized trials. Lancet2003; 361: 13-20.

29. Zijlstra F, Hoorntje JC, de Boer MJ, Reiffers S,

Miedema K, Ottervanger JP, van t Hof AW,

Suryapranata H. Long-term benefit of primary

angioplasty as compared with thrombolytic

therapy for acute myocardial infarction.

N Engl J Med1999; 341: 1413-9.

30. Nunn CM, ONeill WW, Rothbaum D,

Stone GW, OKeefe J, Overlie P, Donohue B,

Grines L, Browne KF, Vlietstra RE, Catlin T,

Grines CL. Long-term outcome after primary

angioplasty: report from primary angioplasty

in myocardial infarction (PAMI-I) trial.J Am Coll Cardiol1999; 33: 640-6.

REFERENCES


9/9


31. Grines CL, Serruys P, ONeill WW. Fibrinolytic

therapy: is it a treatment of the past?

Circulation2003; 107: 2538-42.

32. Hochman JS, Sleeper LA, Webb JG,

Sanborn TA, White HD, Talley JD,

Buller CE, Jacobs AK, Slater JN, Col J,

McKinlay SM, LeJemtel TH.

Early revascularization in acute myocardial

infarction complicated by cardiogenic shock.SHOCK Investigators. Should We Emergently

Revascularize Occluded Coronaries for

Cardiogenic Shock.

N Engl J Med1999; 341: 625-34.

33. Hochman JS, Sleeper LA, White HD, Dzavik V,

Wong SC, Menon V, Webb JG, Steingart R,

Picard MH, Menegus MA, Boland J, Sanborn T,

Buller CE, Modur S, Forman R,

Desvigne-Nickens P, Jacobs AK, Slater JN,

LeJemtel TH; SHOCK Investigators.

One-year survival following earlyrevascularization for cardiogenic shock.

JAMA2001; 285: 190-2.

34. White HD, Assmann SF, Sanborn TA,

Jacobs AK, Webb JG, Sleeper LA, Wong CK,

Stewart JT, Aylward PE, Wong SC,

Hochman JS. Comparison of percutaneous

coronary intervention and coronary artery

bypass grafting after acute myocardial

infarction complicated by cardiogenic shock:

Results from the Should We Emergently

Revascularize Occluded Coronaries forCardiogenic Shock (SHOCK) trial.

Circulation2005; 112: 1992-2001.

cardiosyok ami.pdf

Documents