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144 PART III Coronary Artery Disease
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TABLE 13.2 Hemodynamic Profiles
Left ventricular shock High PCWP, low CO, high SVR Right ventricular shock High RA
RA/PCWP >0.8 Exaggerated RA “y” descent RV square root sign
Ventricular septal defect Large PCWP “v” wave, oxygen saturation
step-up (>5%) from RA to RV
Pericardial tamponade
CO, Cardiac output; PCWP, pulmonary capillary wedge pressure; RA, right atrial; RV, right ventricular; SVR, systemic vascular
resistance.
Equalization of diastolic pressures ~20 mm Hg
as feasible to measure intracardiac pressures, cardiac output, systemic vascular resistance, and mixed venous oxygen saturation. Although use of the pulmonary artery catheter has not been associated with mortality benefit in patients without MI, it is very helpful in the titration of fluids and medications in patients with cardiogenic shock.
The hemodynamic profile of left ventricular shock, as defined
by Forrester and coworkers,
12
includes pulmonary artery wedge
pressure greater than 18 mm Hg and a cardiac index less than
2.2 L/min per m2. Others have used a pulmonary wedge pressure of 15 or 12 mm Hg and a cardiac index of 2.0 or 1.8 L/min per m2. The hemodynamic profile of right ventricular shock includes right atrial pressure of 85% or more of the pulmonary artery wedge pressure, steep Y descent in the right atrial pressure tracing, and the dip and plateau (i.e., square root sign) in the right ventricular wave form. Large V waves in the pulmonary artery wedge tracing suggest the presence of severe mitral regurgitation. An oxygen saturation step-up (>5%) from the right atrium to the right ventricle confirms the diagnosis of ventricular septal rupture. Equalization of right atrial, right ventricular end-diastolic, pulmonary artery diastolic, and pulmonary capillary wedge pressures occurs with severe right ventricular infarction or pericardial tamponade due to free wall rupture or hemorrhagic effusion. Cardiac power (mean arterial pressure × cardiac output/451) is the strongest hemodynamic predictor of hospital mortality.
39
Pharmacologic Support
Vasopressor and inotropic drugs are the major initial interventions for reversing hypotension and improving vital organ perfusion (Table 13.3). Failure to improve blood pressure with these agents is an ominous prognostic sign. Continued hypotension results in progressive myocardial ischemia and deterioration of ven­tricular function. Although many patients temporarily respond to therapy, hospital mortality rates remain unchanged without successful reperfusion therapy.
Dobutamine, a synthetic catecholamine with predominantly
β1-adrenergic effects, is the initial inotropic agent of choice for
patients with systolic pressures greater than 70 mm Hg. Cardiac output is increased and filling pressures are decreased. Dobuta­mine is particularly effective in right ventricular shock.
TABLE 13.3 Pharmacologic Treatment for
Cardiogenic Shock
Drug Dose Side Effects
Dobutamine Dopamine
Norepinephrine
Nitroglycerin
Nitroprusside
Milrinone
Furosemide
Bumetanide
IV, intravenous.
Dopamine, a natural catecholamine, is the initial vasopressor
of choice when the systolic pressure is greater than 70 mm Hg. Low doses (2–5 µg/kg per minute) increase stroke volume and renal perfusion by stimulating dopamine receptors. Intermedi­ate doses have a dose-dependent β1-adrenergic receptor effect, increasing inotropy and chronotropy. High doses (15–20 µg/kg per min) activate α-adrenergic receptors, increasing vascular resistance.
Norepinephrine is a natural catecholamine with predominantly
peripheral α-adrenergic effects. It is used when the systolic pressure is less than 70 mm Hg, because it is a potent venous and arterial vasoconstrictor. Many now prefer norepinephrine over dopamine as initial therapy.
Catecholamine infusions should be carefully titrated. A delicate balance must be obtained between increasing coronary perfu­sion pressure and increasing oxygen demand so that myocardial ischemia is not exacerbated. Moreover, excessive peripheral vasoconstriction decreases tissue perfusion, increased afterload increases filling pressures, and excessive tachycardia or arrhythmias can be stimulated. Extravasation of dopamine or norepinephrine can cause tissue necrosis.
Cardiac glycosides have no significant inotropic effect in patients with severe pump failure and they increase oxygen consumption. Ischemic myocardium is susceptible to the arrhythmogenic effects of digoxin, and intravenous administration causes coronary and peripheral vasoconstriction. Digitalis may be employed for supraventricular tachyarrhythmias to control heart rate.
Vasodilators are useful if adequate blood pressure and coronary artery perfusion pressure can be restored. Nitroprusside is an arterial dilator and a venodilator, whereas nitroglycerin is pre­dominantly a venodilator. Afterload reduction increases stroke volume and is especially important when mitral regurgitation or ventricular septal rupture is present. Preload reduction decreases filling pressures and oxygen demand by reducing wall
5–15 µg/kg/min IV Tolerance 2–20 µg/kg/min IV Increased oxygen
demand
0.5–30 µg/min IV Peripheral and visceral
vasoconstriction
10 µg/min, increased by
10 µg every 10 min, maximum 200 µg/min IV
0.3–10 µg/min IV Hypotension, cyanide
50 µg/kg over 10 min IV,
then 0.375–0.75 µg/ kg/min
20–160 mg/IV Hypokalemia,
1–3 mg IV Nausea, cramps
Headache,
hypotension, tolerance
toxicity
Ventricular arrhythmia
hypomagnesemia
CHAPTER 13 Postmyocardial Infarction Cardiogenic Shock 145
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tension. The major hazard is that reduction in preload and afterload could decrease diastolic arterial pressure, compromising coronary artery perfusion pressure and resulting in extension of ischemic myocardial injury. Reflex tachycardia increases oxygen demand. Nitroglycerin and nitroprusside can be started at low­dose infusions and titrated against blood pressure and pulmonary capillary wedge pressure. Phosphodiesterase inhibitors (e.g., milrinone) are not indicated for acute cardiogenic shock but can be useful in low-output states when the patient is relatively stable by augmenting myocardial contractility and producing peripheral vasodilation.
Mechanical Support
When pharmacologic therapy provides insufficient hemo­dynamic support, mechanical circulatory assistance can be instituted, especially when revascularization or surgical repair of mechanical complications is planned (Figs. 13.3 and 13.4). IABP counterpulsation reduces systolic afterload and augments diastolic perfusion pressure. The usual result is a decrease in filling pressures, systolic blood pressure, heart rate, mitral regurgitation, and left-to-right shunting across a ventricular septal rupture,
along with an increase in diastolic and mean blood pressure, stroke volume, cardiac output, and urine output. Subendocardial blood flow is improved and, in contrast to vasopressor support, oxygen demand is decreased.
Kantrowitz and colleagues9 first reported the use of IABP counterpulsation in treating cardiogenic shock. Mueller and coworkers40 demonstrated improved hemodynamics and myo­cardial metabolism associated with IABP therapy. Improvement in infarct zone regional wall motion, but not adjacent noninfarct zone regional wall motion, was shown by Weiss and associates.41 No improvement in coronary blood flow occurs distal to highly stenotic coronary arteries.42 The IABP favorably influences systemic hemodynamics, but it does not improve ischemic zone blood flow or noninfarct zone wall motion.
The failure to improve ischemic myocardial blood flow probably explains why, despite temporary hemodynamic and clinical improvement in 75% of patients, no obvious difference in enzymatic infarct size or mortality rate with IABP counterpulsa­tion has been noted in the literature.
10,11
The mortality rates in a large cooperative trial were 60% during IABP support, 77% during hospitalization, and 91% at 1 year for 87 patients.11 The only
Cardiogenic
shock
Early shock,
diagnosed on
hospital presentation
Fibrinolytic therapy if all of
the following are present:
1. Greater than 90 minutes to PCI
2. Less than 3 hours post MI onset
3. No contraindications
Arrange prompt transfer
to invasive-capable center
1–2 vessel
CAD
PCI IRA
Fig. 13.3 Recommendations for initial reperfusion therapy. CABG, coronary artery bypass graft
surgery; CAD, coronary artery disease; IABP, intraaortic balloon counterpulsation; IRA, infarct­related artery; LBBB, left bundle branch block; MI, myocardial infarction; PCI, percutaneous coronary intervention. (From Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2004;110;e82.)
Cardiac catheterization and
Moderate 3-
vessel CAD
PCI IRA
Staged
multivessel
PCI
IABP
coronary angiography
Staged
CABG
Delay-onset shock
Echocardiogram to
rule out mechanical
defects
transfer to invasive
capable center
Severe 3-
vessel CAD
Immediate
CABG
Cannot be
performed
Arrange rapid
Left main
CAD
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Maximum Implant Days
Sheath Size
Cardiac Synchrony or Stable Rhythm
3-7 L/min2.5-5 L/min
Myocardial Oxygen Demand
Fig. 13.4 Comparison of mechanical support devices. AO, Aorta; IABP, intraaortic balloon pump;
LA, left atrium; LV, left ventricle; LVEDP, left ventricular end-diastolic pressure; MAP, mean arterial
pressure; PCWP, pulmonary capillary wedge pressure; RA, right atrium; VA-ECMO, venoarterial extracorporeal membrane oxygenation. (From Atkinson TM, Ohman EM, O’Neill WW, et al. A practical approach to mechanical circulatory support in patients undergoing percutaneous coronary intervention: an interventional persepective. JACC Cardiovasc Interv. 2016;9:871-883.)
randomized trial was performed by O’Rourke and colleagues.43 No difference in enzymatic infarct size or mortality was observed.
IABP counterpulsation offers little support to shock patients with extensively scarred ventricles or after late presentation. The best use is in patients with ischemic, viable, but nonfunctioning myocardium that can be revascularized or with mitral regurgita­tion or ventricular septal rupture amenable to surgical repair. Dunkman and colleagues10 showed that the addition of bypass graft surgery to IABP support decreased mortality from 84% to 60%.
Several reports have examined the use of IABP counterpulsa­tion in conjunction with fibrinolytic therapy strategies.
44–48
There were some favorable trends but significantly more bleeding episodes. There has been only one randomized controlled trial comparing IABP counterpulsation plus fibrinolytic therapy to fibrinolysis alone. The Thrombolysis and Counterpulsation to Improve Cardiogenic Shock Survival (TACTICS) trial48 sought to enroll 500 patients with acute STEMI complicated by shock, but only 57 patients were actually enrolled. Six-month follow-up showed a trend toward mortality reduction in the IABP group,
but this was not significant because of small sample size. The strategy of early fibrinolytic therapy and IABP counterpulsation, followed by immediate transfer for PCI or CABG, may be appropriate for hospitals that do not have revascularization capability.
The use of IABP therapy in patients undergoing primary or rescue PCI has also been evaluated. Early studies with balloon angioplasty suggested a reduction in infarct artery reocclusion rates and improvement in clinical outcome in patients without cardiogenic shock.
49,50
However, a recent trial in the stent era failed to demonstrate a survival benefit in cardiogenic shock.51 In patients with cardiogenic shock, insertion of the IABP catheter before angiography provides optimal hemodynamic support during PCI and in the early treatment period even if it does not reduce mortality rates.
The American College of Cardiology/American Heart Associa­tion (ACC/AHA) STEMI guidelines have given a class IIa recom­mendation (can be useful) for use of IABP counterpulsation in patients with cardiogenic shock who do not quickly stabilize with pharmacologic therapy.
52
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Contraindications for IABP counterpulsation therapy include aortic regurgitation, aortic dissection, and peripheral vascular disease. Complications occur in 10% to 30% of patients with cardiogenic shock and include limb ischemia, femoral artery laceration, aortic dissection, infection, hemolysis, thrombocy­topenia, thrombosis, and embolism.
Devices that offer greater circulatory support than IABP counterpulsation are available and have been used in cardiogenic shock as a bridge to recovery or to transplantation (see Fig.
13.4). These devices may be classified into those that can be
placed percutaneously and those that require surgical placement. It is critical to recognize early which patients will require greater hemodynamic support than provided by IABP therapy.
Percutaneous cardiopulmonary bypass with venoarterial extracorporeal membrane oxygenation (VA-ECMO) can be initiated at the bedside via the femoral artery and vein and can provide 3 to 5 L/min of nonpulsatile flow and a mean aortic pressure of 50 to 70 mm Hg despite cardiac standstill.53 A review of 52 studies (533 patients) suggested a mean survival to discharge of 51% (median 38%) among patients with cardiogenic shock treated with percutaneous bypass.54 A single-center retrospective comparison of 219 patients treated with VA-ECMO versus a historical control of 115 patients without VA-ECMO supported a survival benefit (70% vs. 58%).55 These results are encouraging since VA-ECMO is more commonly used emergently for cardiac arrest or near-arrest circumstances. Left ventricular decompression is not possible with these devices.
Another strategy has been to use ventricular assist devices (VADs) as a bridge to recovery or to transplant or even as destina­tion therapy. These devices can be placed percutaneously or surgically. The TandemHeart device (CardiacAssist, Inc.) utilizes a 21 Fr femoral cannula placed across the interatrial septum into the left atrium, while a shorter 15 Fr or 17 Fr cannula is placed in the femoral artery, allowing left atrial to arterial assist pumping by an extracorporeal centrifugal continuous flow pump. Two small randomized trials compared IABP counterpulsation and the TandemHeart device in patients undergoing primary PCI for acute MI complicated by cardiogenic shock. While the TandemHeart device provided better hemodynamic support, the risk of complications was higher and there was no difference in 30-day mortality.
56,57
The microaxial flow pump catheter (Impella; Abiomed, Inc.) is placed into the left ventricle across the aortic valve in retrograde fashion and pumps blood from the left ventricle into the aorta. The Impella EURO-SHOCK Registry included 120 patients treated with the Impella device: 30-day mortality was 64%.58 A small randomized trial with 25 patients showed no difference in mortality compared with IABP counterpulsation.
59
Surgically implanted VADs have also been used in cardiogenic shock. These devices require placement via thoracotomy but can be left in place long term. In a single-center series, the Thoratec biventricular assist device was used as a successful bridge to cardiac transplantation in 11 of 19 patients in cardiogenic shock.60 Both percutaneous and surgical VADs are available only at select centers; early transfer of patients to these facilities should be considered for patients failing standard supportive measures.
REPERFUSION STRATEGIES
Fibrinolytic Therapy
Several multicenter randomized megatrials have demonstrated that fibrinolytic therapy reduces mortality from acute MI. Moreover, the greatest survival benefit has been confirmed for patients with the most jeopardized myocardium (e.g., anterior infarction, new left bundle branch block). It is paradoxical and disappointing that no obvious survival benefit has been realized for the subset of patients with cardiogenic shock.
61
Mathey and colleagues14 first reported that the shock state could be reversed with successful reperfusion due to intracoronary streptokinase administration. However, a multicenter registry report on 44 patients treated with intracoronary streptokinase documented a 66% in-hospital mortality rate,62 but the impor­tance of successful reperfusion and outcome was first suggested by this report. Only 43% of the patients had successful reperfusion compared with 71% for the entire study, but their mortality rate was 42%, compared with 84% for unsuccessful reperfusion.
Compared with placebo, intravenous fibrinolytic therapy reduces the risk of subsequent cardiogenic shock in patients who initially present without shock.
3,4,63
Comparative trials of fibrinolytic agents have shown variable results. Those that show no difference in mortality between agents also do not show a reduction in the incidence of cardiogenic shock with any one
64–66
agent.
In contrast, those comparative trials that show a mortal­ity benefit in favor of one agent also showed a significant reduction in the incidence of cardiogenic shock in favor of that agent. Thus one can conclude that therapy with fibrinolytic agents in acute MI significantly reduces the subsequent development of cardiogenic shock and that those agents that are associated with higher patency rates and improved survival in comparative studies also lead to lower rates of shock.
Fibrinolytic therapy for patients presenting in manifest car­diogenic shock is associated with relatively low reperfusion rates and no clear-cut treatment benefit.61 Mean arterial pressure must be above 65 mm Hg for coronary blood flow to be maintained; flow ceases when mean arterial pressure is below 30 mm Hg. Furthermore, vasoconstriction and passive collapse of the arterial wall are additional factors that may limit the ability of the fibrin­olytic agent to penetrate an intracoronary thrombus.70 Canine studies demonstrated that restoration of blood pressure to normal ranges with norepinephrine infusion improved reperfusion rates, suggesting that coronary perfusion pressure, not cardiac output, is the major determinant of fibrinolytic efficacy.
71,72
Interestingly, the trials that compared streptokinase with alteplase showed mortality benefit for shock patients randomized to streptokinase, despite the fact that patients treated with alteplase fared better. Streptokinase may be beneficial in this subset of patients because it causes a prolonged finbrinolytic state in the setting of low coronary blood flow (which may reduce the risk of reocclusion) and because it is less fibrin specific and may therefore penetrate the thrombus better because it does not bind preferentially to the surface of the clot. Because of the limitations of fibrinolytic therapy for cardiogenic shock, it should be considered as a second­ary treatment option when revascularization therapy with PCI or CABG is not rapidly available. Viable patients should then
2–5
67–69
64,68
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be transferred to a hospital with revascularization capability as soon as possible so that the potential benefits of revascularization therapy might still be obtained.
Percutaneous Coronary Intervention
Meyer et al.15 were the first to use PCI to treat cardiogenic shock. The first treatment series were reported in 1985. O’Neill and colleagues73 obtained successful reperfusion in 24 (88%) of 27 patients, with an in-hospital mortality rate of 25%. Brown and coworkers74 had a 61% successful reperfusion rate, associated with a 42% mortality rate; the mortality rate was 82% when reperfusion was unsuccessful. Multiple small observational reports since then have consistently shown a survival benefit for patients in whom PCI was successful compared with patients in whom PCI was unsuccessful or with historical controls.
There have been a few large observational reports on reperfu­sion therapy for cardiogenic shock. The Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-1) trial75 included 2972 patients with cardiogenic shock treated with fibrinolytic therapy. There was a lower 30-day mortality rate for the 22% of patients who were subsequently treated with PCI compared with those receiving only medical therapy (43% vs. 61% with shock on arrival, 32% vs. 61% for those who developed shock after arrival). Another GUSTO-1 analysis included 2200 patients with cardiogenic shock.76 Compared with a delayed strategy, angiography within 24 hours of shock onset with revascularization by PCI or CABG when deemed appropriate was independently associated with reduced 30-day mortality (38% vs. 62%).
A large registry evaluated the outcome of 1333 patients undergoing primary PCI for cardiogenic shock.77 The in-hospital mortality in this cohort was 46%. The independent predictors of mortality were left main disease, thrombolysis in myocardial infarction (TIMI) less than grade 3 flow after PCI, older age, three-vessel disease, and longer time interval between symptom onset and PCI.
None of these reports represent randomized, controlled studies of PCI. A selection bias favoring PCI over historical controls could easily have resulted from excluding the elderly or patients in extremis or with comorbid disease. Hochman and colleagues have documented that patients with cardiogenic shock who are selected for cardiac catheterization are younger and less likely to die (51% vs. 85%), even when not revascularized. Nevertheless, several studies and clinical experience clearly demonstrate the favorable impact that a patent infarct artery can have on reversing the shock state.
Two small randomized trials have been performed. The Swiss Multicenter trial of Angioplasty SHock (SMASH)
79
randomized 55 patients to either undergo emergency angiography and revascularization when indicated or initial medical management but was terminated prematurely because of poor enrollment. Mortality at 30 days was 69% in the invasive arm versus 78% in the medical arm. At 1 year, the mortality figures were 74% and 83%, respectively. Although the study failed to reach statistical significance because of sample size, the trend was clinically important. The Should We Emergently Revascularize Occluded
17–19
Coronaries for Cardiogenic Shock (SHOCK) trial
randomized
78
302 patients to emergent revascularization or immediate medical stabilization. Concurrently, the 30 participating sites collected registry data on 1190 patients presenting with cardiogenic shock who were not randomized.80 Medical stabilization included fibrinolytic therapy in over half the patients as well as inotropic and vasopressor agents. IABP counterpulsation was used in 86% of the patients. In the revascularization arm, 97% of patients underwent early angiography; 64% underwent PCI and 36% had CABG. There was no statistically significant difference in 30-day mortality between the revascularization and medical therapy groups (46.7% vs. 56.0%; P = 0.11), but by the 6-month endpoint, a significant survival advantage had emerged for patients randomized to revascularization (50.3% vs. 63.1%, P = .027) that was maintained at 1 year (53.3% vs. 66.4%).
Emergency PCI is recommended by the ACC/AHA STEMI guidelines for those who are suitable for revascularization unless further support is deemed futile (class I).52 The best candidates for PCI are patients without prior MI who are younger than 75 years of age with fewer comorbidities and symptom duration less than 12 hours. The severity, distribution, and diffuseness of coronary artery disease and the degree of left ventricular dysfunc­tion also influence outcome. Poor candidates because of very high mortality risk are those with rapidly progressive hemody­namic deterioration despite therapeutic interventions and elderly patients with comorbid disease. Additionally, patients with life-shortening illnesses, no vascular access, previously defined coronary anatomy that was unsuitable for revascularization, anoxic brain damage, and prior cardiomyopathy are poor candidates. Except for the elderly, all other subgroups had treat­ment benefit with revascularization in the SHOCK trial.
Analysis of the elderly patient subgroup in the SHOCK registry81 was performed to gain further insight in patients at least 75 years of age. Whereas the randomized trial included only 56 patients in that age group, the registry included 277 patients. Overall, in-hospital mortality in the elderly versus the younger age group was 76% versus 55% (P < .001). The 44 elderly patients selected for early revascularization, however, showed a significantly lower mortality rate than those who did not undergo revascularization (48% vs. 81%; P = .0002). Other
82–84
reports
also support the use of primary PCI in selected elderly patients with cardiogenic shock complicating MI; thus, age alone should not be an exclusion for selecting patients for cardiac catheterization. Prior functional status, comorbidity, and patient and family preferences are important selection criteria.
Emergency angiography determines revascularization suit­ability. Angiographic exclusions for PCI include infarct artery stenosis less than 70% with TIMI grade 3 flow or lesion morphol­ogy that is high risk for no reflow or other complications. Emergency CABG surgery may be considered for patients with severe coronary anatomy unsuitable for PCI, multivessel disease, mechanical complications, or failed PCI if there is ongoing myocardial ischemia.
The procedure is most safely performed with the patient ventilated and sedated or paralyzed. Gas exchange is maximized, risk of aspiration is minimized, cardioversion can be performed easily, and patient movements do not interfere with the procedure.
17
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Both femoral arteries and veins are cannulated with vascular sheaths. An IABP or Impella device is inserted through one femoral artery for hemodynamic support and a pulmonary artery catheter is inserted through a femoral vein. Interventions to control volume and pressure are titrated against the systemic and pulmonary artery wedge pressures. Electrolytes and blood gases are monitored and abnormalities are corrected. A temporary pacemaker is inserted if necessary.
PCI is best performed when the patient is maximally supported. Using a low osmolar ionic contrast medium, two orthogonal injections of the left coronary artery and one left anterior oblique injection of the right coronary artery are made in an attempt to identify the infarct artery. Left ventriculography should usually be avoided because of the contrast load. If PCI is to be attempted, it should be performed as quickly and efficiently as possible, with limited contrast injections. Although PCI for STEMI is usually limited to the infarct artery, patients in cardiogenic shock with multivessel disease may have the best survival chance with PCI of all proximal discrete lesions. Early resolution of arrhyth­mias, conduction blocks, or hypotension suggests an important therapeutic benefit. Conversely, failure to improve within the first 24 hours usually predicts mortality.
Coronary stents decrease restenosis rates in elective PCI compared with balloon angioplasty but have not reduced mortality rates in primary PCI.
85
Some observational studies in cardiogenic shock that have not completely corrected for confounding variables suggest lower mortality rates with stents than percutane­ous transluminal coronary angioplasty (PTCA),
86–88
but others show no benefit89 or higher mortality rates.90 Randomized studies have not been performed. Most patients undergoing primary PCI for cardiogenic shock will receive stents because they improve the immediate angiographic result and decrease subsequent target vessel revascularization in survivors.
The use of platelet glycoprotein (GP) IIb/IIIa inhibitors may improve outcomes with primary PCI.91 Observational studies suggested a benefit of abciximab in primary stenting for cardio­genic shock.
87,89,90,92
While there are no randomized controlled trials evaluating use of abciximab or other GP IIb/IIIa inhibitors in cardiogenic shock, they can be used as adjunctive therapy when unfractionated heparin is used instead of bivalirudin for anticoagulation. However, the use of GP IIb/IIIa inhibitors has greatly decreased since the introduction of oral platelet P2Y12 receptor inhibitors.
Surgery
Dunkman and associates10 were the first to report the use of CABG for cardiogenic shock. Emergency CABG is associated with mortality rates ranging from 25% to 60%. In the SHOCK trial,17 one-third of the patients randomized to revascularization were treated with a surgical approach. Patients were more likely to have left main disease or three-vessel disease than those treated with PCI. Thirty-day mortality for patients undergoing surgery was equivalent to PCI mortality (42% vs. 45%). The high degree of surgical expertise required, inherent time delays, increasing hesitancy of surgeons to operate on patients with high operative mortality risk because of “scorecard” medicine, and favorable results with PCI make emergency CABG an increasingly rare
intervention. It is more often performed electively in survivors with multivessel disease.
Surgical repair of acute mitral regurgitation,22 ventricular septal defect,23 and free wall rupture24 can be accomplished, although mortality rates are high. The use of emergency cardiac transplantation has been reported.
93
NEW APPROACHES
New approaches to cardiogenic shock have focused on mecha­nisms beyond mechanical support and revascularization. A significant proportion of patients in the SHOCK trial exhibited a systemic inflammatory response syndrome (SIRS) marked by fever, leukocytosis, and low systemic vascular resistance.36 Comple­ment activation, release of inflammatory cytokines, expression of inducible nitric oxide synthase (NOS), and inappropriate vasodilation were deemed culpable and inhibition of NO produc­tion was explored as a therapeutic strategy. Early single-center clinical studies indicated a dramatic benefit from inhibition of
94,95
NOS.
The phase 2, dose-ranging trial SHould we inhibit nitric Oxide synthase in cardiogenic shoCK 2 (SHOCK-2) demonstrated modest early changes in hemodynamic parameters, but no effect on survival.96 The large multicenter Tilarginine Acetate Injection in a Randomized International Study in Unstable MI Patients with Cardiogenic Shock (TRIUMPH) trial was halted after no benefit was seen during an interim analysis.
97
There is intense clinical and basic science activity exploring delivery of stem cells to the infarcted myocardium to improve left ventricular recovery. While the early studies remain incon­clusive, it is likely that cardiogenic shock survivors will be enrolled in the pivotal trials once an effective strategy to salvage or revive the infarcted myocardium is discovered.
It is important to note that recent emphasis on reperfusion therapy for all patients with STEMI, the importance of time to treatment, and the increasing use of primary PCI as the reperfu­sion modality have dramatically decreased the number of patients developing cardiogenic shock as a complication of STEMI.98 Because cardiogenic shock is usually an in-hospital complication of MI occurring hours after infarct artery occlusion, early restora­tion of infarct artery patency to prevent development of the shock state is the best approach to this complication.
PROGNOSIS
The historical early mortality rate for cardiogenic shock complicat­ing acute MI treated with medical therapy was 65% to 80%. Current rapid reperfusion strategies and adjunctive therapies have reduced that rate to 40% to 50%. Rigorous observation of high-risk patients (e.g., age >75 years, history of prior MI, ejection fraction <35%, large myocardial infarction, diabetes, female gender); rapid diagnosis (e.g., careful physical exami­nation, hemodynamic monitoring, echocardiography, cardiac catheterization); and prompt correction of arrhythmias, electrolyte and blood gas abnormalities, volume status, and hypotension may prevent the patient from spiraling into the shock state. When cardiogenic shock is present, early circulatory support to increase mean arterial pressure, reduction in left ventricular
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volume (preload) and pressure (afterload) to reduce myocardial oxygen demand, and coronary artery reperfusion decrease the risk of developing multiorgan dysfunction syndrome (MDS) and the SIRS.
In the SHOCK registry, in-hospital mortality rates rose from 34% to 51% as the number of diseased arteries increased from one to three.99 After PCI, the mortality rate was 86% with absent reperfusion (TIMI grade 0/1 flow), 50% with incomplete reperfu­sion (TIMI grade 2 flow), and 33% with complete reperfusion (TIMI grade 3 flow). Similarly, final TIMI flow was a major predictor of outcome in a German registry with mortality rates of 78%, 66%, and 37% for TIMI grade 0/1, TIMI grade 2 and TIMI grade 3 flow, respectively.
77
A total of 87% of the 1-year survivors in the SHOCK trial were in New York Heart Association (NYHA) functional class I
100
or II.
The 13 lives saved per 100 patients treated with early revascularization in the SHOCK trial at 6 months and 1 year was maintained at 3 and 6 years.19 Overall survival rates at 6 years were 32.8% in the early revascularization group and 19.6% in the initial medical stabilization group. The 6-year survival rates for the hospital survivors were 62.4% versus 44.4%, respectively.
At 30 days in the GUSTO-1 trial, 20,360 patients without
shock (88.9%) and 953 (50.4%) patients with shock were alive.
101
After a median of 11 years, 69.4% without and 55.2% with shock remained alive. Patients receiving PCI were less likely to die (24.1% vs. 34.6%). Beginning in the second year, mortality rates were 2% to 4% per year for all patients regardless of shock status (Fig. 13.5).
CONCLUSION
Shock
12
9
6
3
0
12345678910 11
Fig. 13.5 Long-term mortality rate in 30-day survivors in the
GUSTO-I trial (From Singh M, White J, Hasdai D, et al. Long-term outcome and its predictors among patients with ST-segment elevation myocardial infarction complicated by shock. J Am Coll Cardiol. 2007;50:1752.)
Non-shock
revascularization. These patients need to be directly admitted or transferred to tertiary care shock centers with expertise in acute revascularization and advanced intensive care unless further care is deemed futile. Novel therapies are needed to further decrease mortality rates in patients who develop cardiogenic shock, which remain high despite successful reperfusion therapy.
The full reference list for this chapter is available at
ExpertConsult.com.
Patients with cardiogenic shock complicating MI have a substantial survival benefit with PCI compared with no or late in-hospital
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REFERENCES
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