Amar R. Chadaga, MD, Jamil B. Dihu, MD, Timothy A. Sanborn, MD

Abstract

Cardiogenic shock represents the most ominous challenge of acute myocardial infarction (AMI), with an incidence of 8–9% and a mortality rate approaching 50%. The majority of cases of cardiogenic shock are secondary to AMI complicated by left ventricular failure leading to refractory hypoperfusion and hypotension. Placement of an intra-aortic balloon pump (IABP) and primary percutaneous coronary intervention (PCI), particularly in young patients, remain the American College of Cardiology (ACC)/American Heart Association (AHA) Class 1 recommendations in those suffering from cardiogenic shock. Prompt triage of all patients in cardiogenic shock for early angiography, IABP counterpulsation, and early revascularization with PCI or bypass surgery is now the preferred management strategy. The purpose of this review is to summarize the care of these critically ill patients, including the consideration of basic pharmacologic and interventional techniques and novel therapies as well.

Key words: myocardial infarction, anticoagulation, percutaneous coronary intervention, new devices

VASCULAR DISEASE MANAGEMENT 2010;7:E46–E54

Case Presentation

A 78-year-old female with no prior cardiac history presented with 1 week of intermittent burning in the chest, which progressed to remaining constant on the day she presented to our center. The pain, however, had abated upon her arrival to the emergency department. The patient’s blood pressure was 102/64 mmHg, she had a heart rate of 114 beats/minute, and no murmurs or gallops were heard on auscultation. An electrocardiogram (ECG) revealed ST depression in the lateral leads. Her troponin was 2.5 µg/L, while her CK-MB U/L was 22.50 and her myoglobin was 170 µg/L. The patient was started on oxygen, intravenous fluids, aspirin, beta-blockade, heparin, integrilin, clopidogrel, and a statin. At 5:00 am her blood pressure was 64/27 mmHg and her pulmonary examination revealed rales.

Question: What treatment strategy would be most appropriate in this case?

Introduction

A diagnosis of cardiogenic shock portends a grave outcome in acute myocardial infarction (AMI), with historic mortality rates ranging from 70– 90%.^1–3 Though the pathophysiology varies, this article will focus primarily on cardiogenic shock as a complication of an AMI with subsequent left ventricular failure leading to refractory hypotension and hypoperfusion.^4–6 Historically, the frequency with which cardiogenic shock complicates AMI has remained unchanged at approximately 8–9%.^1,3,7

An encouraging trend in recent investigations has emerged to show a decreased incidence of cardiogenic shock and a lower mortality rate as well.^7–10 Improvements in mortality and incidence are thought to reflect the increased use of intra-aortic balloon pump (IABP) counterpulsation and emergent coronary reperfusion strategies.¹¹ Data from 775 hospitals with revascularization capabilities found that mortality rates from cardiogenic shock dropped from 60.3% in 1995 to 47.9% in 2004, according to data retrieved from the Second, Third, and Fourth National Registry of Myocardial Infarction (NRMI-2, NRMI-3, NRMI-4).¹² Not surprisingly, placement of an IABP and primary percutaneous coronary intervention (PCI) in patients ≤ 75 years of age are American College of Cardiology (ACC)/American Heart Association (AHA) Class 1 recommendations in those suffering from cardiogenic shock.^13,14

Despite noted improvements, the mortality rates from cardiogenic shock continue to be unacceptably high. The medical community has responded with a variety of measures including evaluating the appropriate mode and time of revascularization in patients with cardiogenic shock. Improvement in the understanding and management of cardiogenic shock has also been achieved through the use of pharmacologic regimens and percutaneous ventricular assist devices. A description of the current pharmacologic and percutaneous interventional techniques, consensus guidelines, and emerging technologies relating to cardiogenic shock is presented in this article.

Pharmacologic Therapy

Aspirin, heparin, and GP IIb/IIIa inhibitors. The medical therapies used in the setting of an AMI have not been specifically studied in the subgroup of patients with cardiogenic shock, though their use as it pertains to reperfusion should strongly be considered. These therapies are outlined in the AHA/ACC Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction and Unstable Angina/Non-ST-Elevation Myocardial Infarction.^13,15

Aspirin, through its ability to irreversibly block thromboxane A2 production, has long been studied to prevent platelet adhesion after the rupture of an atherosclerotic plaque. Meta-analyses of several trials evaluating the role of aspirin in acute coronary syndromes (ACS) have revealed reduced vascular events, recurrent ischemia, and coronary reocclusion rates in patients receiving aspirin.^16,17 Data supporting the use of aspirin in ACS has led to a Class 1 designation within the ACC/AHA Guidelines for the use of chewable aspirin (dose 162–325 mg) in patients with unstable angina (UA)/non-ST-elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI) who are not known to be intolerant.^13,15 A preference for chewable aspirin is guided by the fact that buccal absorption is more rapid than is the case with enteric-coated aspirin.¹⁸

Anticoagulant therapy in addition to antiplatelet measures is also recommended in patients with AMI. Though not specifically studied in patients with cardiogenic shock complicating AMI, it is reasonable to consider the use of unfractionated heparin (UFH), especially as invasive strategies are often used to assist in revascularization. The use of UFH in patients undergoing percutaneous or surgical revascularization, or with concomitant fibrinolytic therapy, is an AHA/ACC Class 1 recommendation.¹³ Alternative anticoagulants have also been studied in patients with AMI including low-molecular-weight heparins (LMWH), direct thrombin inhibitors, and fondaparinux.^19–21 Some trials have limited their use in patients with cardiogenic shock, therefore the data are insufficient to assess their safety and efficacy in this setting. Their use must be evaluated carefully in the patient population including type of AMI (STEMI vs. UA/NSTEMI), mode of revascularization planned, age, bleeding risk, and renal function. Quick and reliable levels of these anticoagulants may be difficult to obtain in the setting of cardiogenic shock where hemodynamic and renal function are unpredictably compromised.

The cascade of events and platelet adhesion after plaque rupture are mediated by several glycoprotein receptors. The final and main receptor in platelet adhesion and aggregation is the glycoprotein IIb/IIIa receptor (GP IIb/IIIa).^22,23 Though not specificially studied in patients with cardiogenic shock, a retrospective subgroup analysis of the Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial analyzed the impact of the GP IIb/IIIa inhibitor eptifibatide on the frequency and outcome of cardiogenic shock developing after enrollment in the trial. Analysis showed that randomization to eptifibatide did not affect the occurrence of cardiogenic shock, which developed in 2.5% of patients enrolled in the trial. However, in patients who did develop shock and had been treated with eptifibatide, a significantly reduced incidence of death at 30 days was observed.24
Thienopyridines, which inhibit platelet aggregation by ADP P2Y12 antagonism, have been used successfully in patients with ACS and those undergoing PCI.^25,26 In patients with STEMI in whom PCI is planned, the use of the thienopyridine, clopidogrel, is an ACC/AHA Class 1 (level of evidence B) recommendation, with the duration of therapy dependent on the type of stent used.¹³ Though PCI is routinely performed in the setting of cardiogenic shock, the ACC/AHA guidelines do not recommend routine administration of clopidogrel as pretreatment in patients who have not yet undergone diagnostic cardiac catheterization and in whom coronary artery bypass graft (CABG) surgery would be performed within 5 to 7 days.

Sympathomimetic inotropic and vasopressor agents. Treatment of the hypotension and low cardiac output state accompanying cardiogenic shock is of dire importance in order to maintain adequate organ perfusion and tissue viability. Sympathomimetic, inotropic, and vasopressor agents are used to improve the altered hemodynamic parameters which accompany cardiogenic shock.

Dopamine works in a dose-dependent manner, activating a variety of receptors. At high doses, dopamine activates alpha receptors in both systemic and pulmonary circulations, improving hypotension, though simultaneously increasing pulmonary capillary wedge pressure (PCWP). Though more evident at intermediate doses where beta-receptor stimulation is prominent, dopamine has been shown to increase myocardial contractility.²⁷

Norepinephrine, a stimulator of alpha-receptors, is often used to quickly correct marked hypotension (systolic blood pressure < 70 mmHg) and cardiogenic shock not responsive to dopamine.¹³

Inodilators, agents with positive inotropic and vasodilator properties such as dobutamine and milrinone, have been used in the treatment of cardiogenic shock in conjunction with other sympathomimetics and vasopressor agents. Dobutamine is a strong beta1-receptor agonist allowing for both chronotropic and inotropic stimulation. Dose-dependent improvements in stroke volume and PCWP are observed with dobutamine infusion. The beta2-receptor properties of dobutamine cause peripheral vasodilation and reduction in SVR, which is often counterproductive to the hypotension associated with cardiogenic shock. As such, dobutamine is not recommended as monotherapy in patients with cardiogenic shock.²⁷ Dobutamine monotherapy is recommended in low-output heart failure (systolic blood pressure 70–100 mmHg), in which there are no signs or symptoms of shock.¹³

Milrinone, a phosphodiesterase inhibitor, increases intracellular calcium concentrations, myocardial contractility, and accelerates myocardial contractility. This is done by selectively inhibiting the phosphodiesterase III enzyme, which results in an increase in intracellular cAMP. Milrinone is often used in patients not taking beta-blockers because the mechanism of action, unlike dobutamine, does not involve beta-receptors. Because milrinone lacks adrenergic stimulation, there is less effect on myocardial work.²⁸ Both dobutamine and milrinone cause vasodilation, reduction in SVR, and left and right ventricular filling pressures, resulting in an increase in cardiac output.²⁹

Though helpful and often necessary for hemodynamic support, these drugs are not without limitations and adverse effects. Each of the agents discussed above are associated with effects ranging from arrhythmias, ischemic necrosis, and in the case of dobutamine and milrinone, hypotension. An increase in cardiac work and myocardial oxygen consumption are also noted adverse effects seen with the use of dobutamine, which can be especially deleterious in the setting of AMI.²⁹

Nitric oxide synthase inhibitors. The pathophysiology of cardiogenic shock is a complex mechanism that is not completely understood. Elevation in SVR is a compensatory feature present in cardiogenic shock to maintain tissue viability and organ perfusion. A complex inflammatory response occurs in patients with myocardial infarction. This results in the release of several inflammatory markers including nitric oxide, which in cardiogenic shock, reduces SVR and leads to hypoperfusion of the systemic and coronary vasculature and inhibition of myocardial contractility.³⁰ The hypothesis that the inhibition of nitric oxide synthase (NOS) would lead to better outcomes in patients with cardiogenic shock was evaluated in The Tilarginine Acetate Injection in a Randomized International Study in Unstable MI Patients With Cardiogenic Shock (TRIUMPH) trial. In the trial, patients were randomized to receive the nitric oxide syntase inhibitor tilarginine or placebo. The trial was terminated early due to a prespecified futility analysis and no statistically significant difference in all-cause mortality was appreciable at 30 days.³¹

Reperfusion with Thrombolysis and Intra-aortic Balloon Pump Counterpulsation

Thrombolytics. Prior to augmentation of coronary perfusion pressure as well as revascularization, thrombolysis alone enjoyed limited efficacy in patients who experienced cardiogenic shock. In a 1994 meta-analysis, thrombolysis was associated with a 7% absolute reduction (54% vs. 61%) in mortality at 1 month in patients with a systolic blood pressure of < 100 mmHg and a heart rate of > 100 beats per minute (bpm).³² These findings were corroborated in a post-hoc analysis of the SHOCK trial in which the use of fibrinolytics was associated with an 18% absolute reduction (60% vs. 78% without thrombolysis) in patients treated in the medical arm of the study.³³ The impact of thrombolytic therapy on mortality when used in combination with revascularization is discussed in detail below. Fibrinolytic therapy alone is an ACC/AHA Class 1 recommendation (Level of Evidence B) in STEMI patients with cardiogenic shock who are unsuitable for further invasive care and do not have contraindications to fibrinolysis13 (Figure 1) .

Intra-aortic balloon pump. History reveals that the augmentation of coronary perfusion pressure was the synergistic partner fibrinolysis needed. In 1994, a study by Prewitt et al involving canines showed that under moderate hypotension, an IABP enhanced the rate of clot dissolution with thrombolysis.³⁴ In 2001, after both the SHOCK trial registry and the GUSTO-1 trial found similar results, the NRMI-2 database demonstrated a significant reduction in mortality with IABP use in combination with fibrinolysis (67% vs. 49%) in almost 24,000 patients with cardiogenic shock.^35–37 Chen and colleagues further studied the NRMI-2 database and, after dividing the NRMI-2 hospitals into three tertiles (low-, intermediate-, and high-IABP volume hospitals), found that in AMI complicated by cardiogenic shock, the crude mortality rate decreased with increasing IABP volume (65.4%, lowest volume tertile; 54.1%, intermediate volume tertile; and 50.6%, highest volume tertile [P for trend < 0.001]).³⁸ Placement of an IABP is an ACC/AHA Class 1 recommendation (Level of evidence B) in cardiogenic shock refractory to pharmacologic therapy¹³ (Figure 1).

Reperfusion with PCI, CABG

Notwithstanding the synergistic effect of fibrinolytic therapy plus IABP use, mortality rates continued to hover around 50% and the focus shifted to early revasculization.^35,36 The GUSTO-I investigators found that while percutaneous coronary angioplasty (PTCA) was performed in only 19% of the 2,972 patients with cardiogenic shock, this translated into a mortality rate of 31% compared with 61% for patients who did not undergo dilation.⁴ Berger and colleagues further investigated the startling results in the GUSTO-I data, and after adjusting for differences between the two groups, the 30-day mortality rate was 38% with early angiography, and an aggressive strategy was independently associated with reduced 30-day mortality.³⁹ This independent survival benefit associated with aggressive revascularization strategies was also noted in several other studies, including GUSTO-III, the California State Database, and NRMI-2.^9,40,41

The SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK (SHOCK) trial was conducted to answer the question of whether an early aggressive strategy improved mortality over maximal medical management given that inherent and undetectable selection bias appeared to confound the outcomes in the nonrandomized trials above. The SHOCK trial randomly assigned 302 patients (inclusion and exclusion criteria provided in Table 1) with acute STEMI, or new left bundle branch block complicated by shock to either an early revascularization strategy (angioplasty 55%, CABG 38%) within 6 hours of randomization, or initial medical stabilization and delayed revascularization. At 30 days, 53% of the emergency revascularization group survived versus 44% of the initial medical stabilization group, which did not translate into a statistically significant 30-day survival rate (95% confidence interval, 0.96, 1.53; p = 0.109) (Figure 2).¹¹ However, by 6 months and continuing out to 12 months, the survival differences had increased and had reached statistical significance (Figure 2).⁴² Further solidifying these results were the findings that at 1 year, survivors in the emergency revascularization arm had good functional status and had a lower rate of deterioration than the initial medically stabilized patients.⁴³ Even more recently, the statistical advantage conferred by early revasculization was found to persist at 60 months.⁴⁴ The survival benefit in the SHOCK trial was limited to patients < 75 years of age. Thus, primary PCI is a Class 1 recommendation (Level of Evidence A) for patients < 75 years of age with cardiogenic shock.

The survival benefit seen in the SHOCK trial did not extend to the subset of elderly patients who experience acute MI complicated by cardiogenic shock. A mortality rate of 75% in the emergency revascularization arm versus 53% in the initial medication therapy group (p = 0.01) was discovered in patients ≥ 75 years of age.¹¹ This subgroup was composed of only 56 patients. Larger, but nonrandomized, studies contradict these findings. A mortality rate of 48% in the 103 elderly patients undergoing early revascularization was found in the SHOCK registry, which enrolled patients during the same time frame as the SHOCK randomized trial. In comparison, a mortality rate of 81% was discovered for those aged > 75 years undergoing late or no revascularization.45 Prasad and colleagues found a similar mortality rate (47%) in a series of 61 consecutive elderly patients with cardiogenic shock undergoing PCI.⁴⁶ And finally, The Northern New England Cardiovascular Disease Study Group studied a total of 310 patients (74 of whom were ≥ 75 years of age) who underwent PCI for cardiogenic shock.⁴⁷ The mortality rate of the elderly subgroup was 46%, similar to the observational results above and significantly less than the 75% mortality rate reported in the SHOCK trial. Given the discrepancy between the randomized subset in the SHOCK trial and the nonrandomized trials above, primary PCI is a Class IIa recommendation (level of evidence B) for patients aged 75 years and older with cardiogenic shock.^12–14

CABG versus PCI. Data on emergent revascularization was analyzed for 128 patients with predominant left ventricular failure in the SHOCK randomized trial.⁴⁸ Eighty-one patients (63.7%) underwent PCI, while 47 patients (37.3%) underwent CABG. Overall survival was not statistically significant when comparing 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 the PCI group in that they were more likely to have diabetes, 3-vessel disease, and left main coronary disease. Given the similar survival between the two groups, despite worse disease in the CABG cohort, the authors of this analysis concluded that emergency CABG is an important component of an optimal treatment strategy in patients with cardiogenic shock, and should be considered a complementary treatment option in patients with extensive coronary disease.

Advances in PCI — Stents TIMI flow, thrombectomy and thrombus aspiration. Since the SHOCK trial, there has been an increased use of stents, with or without GP IIb/IIIa inhibitors, rather than conventional PTCA.49 Stents have been found to decrease infarct artery reocclusion, while also improving thrombolysis in myocardial infarction (TIMI) flow and are now used in the majority of patients receiving percutaneous coronary revasculization.^50,51 Specific to cardiogenic shock, Chan and colleagues demonstrated a mortality benefit when prospectively examining 96 consecutive patients who underwent emergent PCI for cardiogenic shock.⁵² At 2.5 years, mortality in those treated with conventional PTCA was 68%, while those receiving stents faired far better, with a mortality rate of 43%. Given the salutary effects of GP IIb/IIIa inhibitors discussed above, in a subgroup analysis of the PURSUIT trial,²⁴ Chan and colleagues included two other arms and patients were classified as receiving stent plus abciximab, a stent alone, PTCA plus abciximab, or PTCA alone. Over the 2.5 years after emergent PCI for cardiogenic shock, the mortality rates for stent plus abciximab, stent only, PTCA plus abciximab, and PTCA alone were 33%, 43%, 61% and 68%, respectively (p = 0.028).

Post-procedural flow of the infarct-related artery (IRA) has been measured using the TIMI flow-grade scoring system. In the SHOCK trial, one criteria indicating successful angioplasty was a TIMI flow grade of 2 or 3. Previous studies have also shown an inverse relationship between TIMI flow grades and mortality, with TIMI flow grades of 0 to 2 being independently associated with an increase in mortality.⁵³ A large analysis of post-procedural TIMI flow in patients with STEMI and cardiogenic shock was conducted using the American College of Cardiology National Cardiovascular Database Cath PCI Registry. Data from the registry showed that post-PCI TIMI flow grades of 0 to 2 in the IRA were associated with a a 2.3-fold higher mortality rate than in patients with a TIMI flow score of 3. Patients with TIMI flow grades of 0 to 2 were more likely to undergo CABG than those with TIMI 3 flow (20% vs. 5.4%).⁵⁴ Drawbacks pertaining to PCI that have limited post-procedural flow in this patient population have been attributed to distal embolization and microvascular damage. In order to reduce this complication, studies have been conducted to evaluate the efficacy of thrombectomy to prevent thrombus embolization and microvascular damage. These studies, although not specifically conducted in the setting of cardiogenic shock, have shown improvement in reperfusion represented by improvement in myocardial blush grade, reduction in infarct size, and mortality.^55–58 Whether a patient population with cardiogenic shock will benefit from thrombus aspiration has yet to be determined.

Revascularization in cardiogenic shock caused by mechanical complication. Although this article, along with the aforementioned randomized SHOCK trial, focuses on cardiogenic shock as a complication of AMI with subsequent left ventricular failure, a mechanical complication can be the etiology of cardiogenic shock. Indeed, utilizing the SHOCK Trial Registry, Hochman and colleagues showed that while predominant left ventricular failure was the most common etiology of cardiogenic shock at 78.5%, mechanical complications such as severe mitral regurigitation, ventricular septal rupture, isolated ventricular shock, and tampanode were the culprits in 6.9%, 3.9%, 2.8%, and 1.4% of cases of cardiogenic shock, respectively.⁵⁹ Ventricular septal rupture, in particular, portended a significantly higher mortality at 87.3%. In an early experience with three patients in severe mitral regurgitation (two of whom were in cardiogenic shock), Heuser and colleagues were able to expertly demonstrate resolution of the mitral regurgitation after utilizing PTCA.⁶⁰ Hochman and colleagues were able to further demonstrate a lower mortality rate and risk profile for Registry patients who were managed with thrombolytic therapy and/or IABP, coronary angiography, angioplasty and/or CABG.

Novel Percutaneous Mechanical Support Systems

Despite aggressive pharmacological measures, percutaneous intervention, and mechanical support with IABP, mortality rates remain elevated in patients with cardiogenic shock.¹² Mechanical assistance has generally been limited to the use of IABP and has been considered the method of choice as outlined by the current ACC/AHA guidelines.¹³ Although IABP is considered helpful in improving cardiac function, there are limitations to its benefits and uses. IABP counterpulsation lacks the ability to provide active cardiac support in patients with very severe depression of left ventricular function and other hemodynamic abnormalities such as arrhythmias. Because of the continued high mortality rates and limited improvement with the use of an IABP, mechanical circulatory support systems have been designed to assist patients with severe acute heart failure not responding to current therapies. Two mechanical support systems designed as short-term ventricular assist devices and studied in cardiogenic shock include the TandemHeart PTVA (CardiacAssist, Inc., Pittsburgh, Pennsylvania) and the Impella Recover LP 2.5 (Abiomed, Inc., Danvers, Massachusetts). A third device not yet studied in the setting of cardiogenic shock, but recently investigated in patients requiring substantial cardiac support undergoing high-risk PCI, is the Reitan catheter pump (RCP) (CardioBridge GmbH, Hechingen, Germany). Although beyond the scope of this review, the RCP device was safely implanted percutaneously in 9 high-risk PCI patients. Further investigational analysis utilizing the RCP in prolonged cardiac support is currently being conducted.⁶¹

The TandemHeart. A description of the TandemHeart PTVA System and its percutaneous implantation has previously been described in detail elsewhere.⁶² Briefly, this system involves a low-speed centrifugal continuous-flow pump in which a venous inflow cannula is inserted into the left atrium after transseptal puncture. Oxygenated blood is withdrawn from the left atrium via the cannula into a centrifugal pump and then returned through a femoral cannula to the lower abdominal aorta at a flow of up to 4 L/min. The feasibility of the TandemHeart device was assessed in the treatment of hemodynamic instability after percutaneous revascularization and in patients who had presented in cardiogenic shock prior to therapeutic intervention. In both studies the TandemHeart showed statistically significant improvements in CI, MAP, and PCWP.^62,63 These studies showed that the TandemHeart device provided a useful mechanical means for hemodynamic support in these two patient populations. Subsequently, a randomized comparison was conducted to assess the hemodynamic and mortality effects of the TandemHeart PTVA as compared to the IABP. Patients in cardiogenic shock after AMI with intended PCI of the IRA were randomized to either IABP (n = 20) or the TandemHeart PTVA device (n = 21). Though data from the trial did show improvement in hemodynamic parameters from the TandemHeart PTVA, namely an increase in the cardiac power index, there was no trend in mortality benefit. The TandemHeart PTVA was associated with more complications as opposed to the IABP, including distal limb ischemia and severe bleeding.⁶⁴

The Impella Recover. A description of the Impella LP 2.5 and its percutaneous implantation have been provided previously.65 Briefly, the Impella LP 2.5 is able to provide 2.5 L/min of flow through a catheter-mounted rotary blood pump inserted percutaneously through the femoral artery and positioned across the aortic valve in the left ventricle (Figure 3). The safety and feasibility of the Impella LP 2.5 have been demonstrated previously.⁶⁶ Studies have shown the Impella LP 2.5 to provide adequate hemodynamic support while improving a variety of hemodynamic parameters. The Impella LP 2.5 has also been found to be safe and feasible in patients with cardiogenic shock. Specifically, The Efficacy Study of LV Assist Device to Treat Patients with Cardiogenic Shock (ISAR-SHOCK) trial compared the Impella LP 2.5 to the IABP. Patients with AMI of < 48 hours and cardiogenic shock were randomized to receive treatment with an IABP (n = 13) or Impella LP 2.5 (n = 12). The Impella LP 2.5 showed a statistically significant improvement in the primary endpoint, which was a change in CI from baseline at 30 minutes after implantation. No significant differences were noted between treatment arms in regard to organ dysfunction or mortality. The trial did not show failure of the device during use, an increase in bleeding, distal limb ischemia, arrhythmias, or infection. There was noted to be a transitory increase in hemolysis and an increase in the use of both fresh frozen plasma and packed red blood cells in patients treated with the Impella LP 2.5.⁶⁷ The investigators have proposed a larger prospective, randomized trial comparing the Impella LP 2.5 with the IABP in patients with cardiogenic shock after MI to better assess the devices’ role on clinical outcomes and effects on mortality.⁶⁸

Conclusion and Recommendations

The novel technologies above and the emerging therapies of cell therapy and cooling devices represent a promising future for the challenging entity of cardiogenic shock complicating AMI. However, these technologies have yet to show a distinct mortality benefit and their roles in the treatment of cardiogenic shock have yet to be defined. Given that the SHOCK trial, using a strategy of early revascularization, has demonstrated statistical improvement in long-term outcomes, the current focus for the management of cardiogenic shock should remain on timely reperfusion and stricter adherence to current ACC/AHA guidelines.

The patient presented in the vignette has developed cardiogenic shock in the hospital after a NSTEMI. While the predominance of cardiogenic shock is a complication of an AMI with subsequent left ventricular failure, a mechanical complication cannot be ruled out. In this case, an emergency echocardiogram revealed severe mitral regurgitation due to papillary muscle dysfunction. Regardless, IABP support, minimal required doses of sympathomimetic, inotropic, and vasopressor support, rapid coronary angiography, and emergent revascularization by PTCA ± stenting or CABG and repair of any mechanical complications causing cardiogenic shock (depending on the anatomy) would be recommended. If the patient is in cardiogenic shock at a hospital without a cardiac catheterization laboratory, thrombolytic therapy, IABP, and immediate transfer to a hospital with angiography and revascularization capabilities would be recommended.

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From the Division of Cardiology, University of Chicago, Evanston, Illinois.

Address for correspondence: Timothy A. Sanborn, MD, Division of Cardiology, University of Chicago, 2650 Ridge Ave., Walgreen Building, Third Floor, Evanston, IL 60201. E-mail: TSanborn@northshore.org

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