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Medical Studies/Studia Medyczne
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Postępowanie u chorych ze wstrząsem kardiogennym

Marcin Sadowski
1, 2
Agnieszka Janion-Sadowska

Department of Interventional Cardiology, Świętokrzyskie Cardiology Centre, Kielce, Poland
Department of Anatomy, Institute of Medicine Science, Faculty of Medicine and Health Science, Jan Kochanowski University, Kielce, Poland
Acute Cardiac Care Unit, Świętokrzyskie Cardiology Centre, Kielce, Poland
Medical Studies/Studia Medyczne 2017; 33 (1): 55–62
Data publikacji online: 2017/03/31
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Cardiogenic shock (CS) is a life-threatening condition of heterogeneous aetiology with acute left or right heart failure as a key point leading to decreased and insufficient peripheral perfusion and multiple organ failure. Many disorders contribute to CS development; however, acute coronary syndromes (ACS), i.e. acute myocardial infarction (MI), are the leading cause [1, 2] (Table 1). Cardiogenic shock complicates up to 10% of ST-segment elevation myocardial infarction (STEMI) [3] and 2.5% of non-STEMI cases [4]. Typically, 50% of patients with STEMI develop CS during the first 6 h and 75% during the first 24 h from myocardial infarction symptoms onset [5]. Although in-hospital and short-term mortality is very high, ranging from 70–80% in patients treated conservatively [6] to 40–60% in patients receiving early reperfusion therapy [7], there is a chance for acceptable long-term survival in those treated aggressively [8].
The aim of this review is to outline pathophysiological changes during CS and to present step by step initial diagnosis, treatment strategies according to aetiology, and to discus novel research directions.

Aetiology of cardiogenic shock

Several acute conditions may contribute to the decrease in peripheral tissue perfusion. Most of them are primary cardiac. The most frequent are clinical manifestations of coronary artery disease. They include acute heart failure due to myocardial infarction and its complications, myocarditis, cardiomyopathies, blunt trauma, brady- and tachyarrhythmias, and severe mitral or aortic regurgitation. Some of them are related to prosthetic valve dysfunction, unintentional or intentional drug overdose, or, in rare cases, transplant rejection. In many cases the heart is not initially involved; however, it cannot remain free of the haemodynamic complications in pericardial tamponade, pneumothorax, pulmonary embolism, etc. Regardless of the initial aetiology, the final path includes the heart’s failure as a pump [1] (Table 1).


Recent investigations provide convincing data that in CS acute left- or right-ventricular failure is in parallel with neurohormone and cytokine system activation and peripheral vasculature compensatory response, which are all trapped in a vicious circle. Systemic inflammatory response due to myocardial and peripheral ischaemia mediated by catecholamines, vasopressin, angiotensin II, interleukin 6, tumour necrosis factor , nitric oxide, and many others interfere with reflex vasoconstriction and left ventricular contractility, and therefore sustain and aggravate both myocardial injury and haemodynamic collapse. This complex pathophysiology has been presented in detail in an excellent paper by Reynolds and Hochmann in Circulation [9].

Clinical presentation and initial diagnosis

There are a variety of symptoms, signs, and measurements that define CS and characterise its severity. Although some haemodynamic parameters, i.e. cardiac index (CI) < 2.2 l/min/m2 and pulmonary capillary wedge pressure (PCWP) > 18 mm Hg, are helpful to confirm the diagnosis and to monitor the response to the therapy applied, they are not mandatory in the initial phase of CS. A history of recent chest pain, persistent arterial hypotension < 90 mm Hg, tachycardia, cool extremities, diuresis less than 20 ml/h, and altered mental status are typical signs of peripheral hypoperfusion and should focus the attending physician on the active search for possible causes of CS [1, 10, 11]. Prompt 12-lead ECG and physical examination remain the basics to establish or to eliminate many conditions presented in Table 1. ECG provides initial information on STEMI/NSTEMI or arrhythmias and may suggest the suspicion of pulmonary embolism or cardiac tamponade. Some negative prognostic factors may also be noted, such as heart rate, QRS complex duration, and the voltage sum of ST-segment depression [12]. Bed-side echocardiography plays a key role in confirming diagnosis, identifying high-risk patients, and excluding mechanical complications of MI or acute valve disease and identifying signs of pulmonary embolism to plan the revascularisation and further treatment strategy (class I C according to European Society of Cardiology guidelines, [10]). The most powerful echocardiographic predictors of short- and long-term mortality are stroke volume index, stroke work index, and the severity of mitral regurgitation [13]. Some baseline laboratory parameters (blood smear, cardiac troponins, serum creatinine, electrolytes, bilirubin, C-reactive protein, natriuretic peptides, glucose, transaminases activity, and blood gases) should be repeated frequently to assess the dynamics of multiple organ failure. Chest computed tomography (CT) scan may help in differential diagnosis when ACS is not probable and provide life-saving data if aortic dissection or pulmonary embolism is present. Continuous monitoring of heart rate, blood pressure, respiratory rate, temperature, ECG, blood oxygen saturation, and urine output is mandatory. Invasive blood pressure measurement (class IIa C) is useful in haemodynamically unstable patients or in patients receiving inotropic agents. Central venous catheter (class IIa C) should be used when catecholamine infusion is present or to obtain central venous pressure (CVP) and venous oxygenation measurements. However, CVP may be inadequate during positive end-expiratory pressure ventilation or in patients with significant tricuspid regurgitation. Some haemodynamic parameters (CVP, right atrial pressure, PAWP) provided by Swan-Ganz catheter (class IIb B) are helpful in monitoring response to treatment and allow the calculation of mean arterial pressure, stroke volume, systemic and pulmonary vascular resistance, and many others. An ongoing discussion on the usefulness of the Swan-Ganz catheter has been summarised in a meta-analysis by Shah et al. [14] and in a review by Payen and Gayat [15] with the conclusion that the Swan-Ganz catheter should not be used in a routine manner and that most of the parameters can be obtained by other non-invasive measurements, including echocardiography and central venous catheter.

Treatment of patients with cardiogenic shock

An aetiology-guided treatment should start during first medical contact. A temporary pacing should be initiated in patients with bradycardia, and an electrical cardioversion should be performed in most cases of ventricular tachycardia or atrial fibrillation with rapid ventricular response. Patients with acute valve insufficiency or acute aortic root dissection should undergo surgical repair regardless of the cause provided in Table 1. Other non left-ventricular causes are rare; however, attempts should be made to ensure proper right-sided filling pressures by fluid resuscitation and removing the primary cause (i.e. tamponade, pulmonary embolism, etc.). Maintaining appropriate oxygenation using both non-invasive and invasive ventilation techniques is mandatory to prevent respiratory failure and further shock progression.

Cardiogenic shock due to acute coronary syndrome

The current treatment of patients with CS related to acute coronary syndromes has been summarised in both American and European guidelines for the management of patients with STEMI [10, 16]. In general, there is agreement that prompt haemodynamic stability achieved by immediate revascularisation and supporting pharmacotherapy is the primary goal. Invasive and non-invasive methods must start simultaneously, because the classic DeLuca’s finding that every minute of delay counts remains valid [17]. Before aggressive antithrombotic and antiplatelet therapy and primary percutaneous coronary intervention (PCI) is initiated mechanical complications of MI must be excluded.

Mechanical complications of myocardial infarction

A free wall rupture (FWR) complicates 1–6% of STEMI. Older people without reperfusion therapy or treated with lytics, systemic steroids, or non-steroid anti-inflammatory drugs are prone to the development of this complication. In acute cases chest pain, blood pressure drop, and pulseless electrical activity are usually followed by death. In subacute FWR a continuous blood leakage to the pericardium may lead to tamponade; however, a surgical intervention is possible when performed on time. In chronic form a false aneurysm may be formed. An early invasive strategy, optimal blood pressure control, and quick relief from the anginal pain are the most efficient methods of FWR prevention. A ventricular septum rupture (VSR) is rare in a primary PCI era (less than 1% of all STEMI cases, mainly in multi-vessel disease cases). A progression of biventricular heart failure, or right bundle branch or complete heart block and a loud systolic murmur make a typical clinical picture. A papillary muscle rupture often accompanies the right or circumflex coronary artery closure and results in an acute mitral regurgitation (MR) manifested as pulmonary oedema or CS. The treatment of choice in all cases mentioned is an immediate surgical intervention because the mortality in patients treated conservatively reaches 90% [18–20].

Myocardial infarction of the right ventricle

A right ventricular MI may coincide with up to 50% of inferior MIs and is characterised by an increase in right atrial and ventricular pressures, and decreased PCWP and stroke volume. When isolated it is usually well tolerated because the right ventricle receives support from the left one via interventricular septum movements and thus by increasing right ventricular pressures. In large MIs often accompanied by atrial fibrillation or atrioventricular blocks this mechanism fails and severe CS develops with high mortality [21, 22].

Reperfusion and revascularization

Emergency revascularisation, either by PCI or coronary artery bypass graft (CABG), irrespective of time delay or prior lysis, is recommended in all cases in CS due to acute myocardial infarction, in both European and American guidelines (class I B) [10, 16]. The beneficial impact of an early revascularisation strategy was observed regardless of baseline left ventricular function [23]. In the Should We Emergently Revascularise Occluded Coronaries for Cardiogenic Shock Trial (SHOCK) there was no significant difference in 30-day mortality; however, early revascularisation strategy was superior to conservative management (6-month mortality: 50.3% vs. 63.1%, p = 0.027; 12-month mortality 53.3% vs. 66.4%, p < 0.03) and this trend was sustained in 3-year and 6-year observations [7, 8, 24]. The 30-day mortality was lower in a subgroup of patients younger than 75 (41.4% vs. 56.8%, p < 0.02). Data by Dauerman et al. from the Global Registry of Acute Coronary Events (GRACE) show lower in-hospital mortality in revascularised patients (45% vs. 69%, p < 0.001) [25] regardless of age as well as in Dzavik’s et al. sub-analysis (48% vs. 81%, p < 0.0003) [5]. Similar observations on in-hospital mortality in older patients with CS come from the Polish Registry of Acute Coronary Syndromes (PL-ACS): 54.6% vs. 69.9%, p < 0.0001 [26]. These outcomes are even better when platelet glycoprotein IIb/IIIa inhibitors (abciximab) are added to the adjunctive pharmacotherapy [27]. In cases of primary PCI failure or in patients who are not eligible for PCI due to multivessel disease or/and the left main involvement CABG should not be postponed (class I C) [10, 28].

Adjunctive pharmacotherapy

Antithrombotic therapy with aspirin and heparin should be administered as a standard of care in ACS patients. Both clopidogrel and novel ADP-receptor inhibitors may be deferred until coronary angiography is performed, to decrease bleeding complications during emergent coronary artery by-pass grafting. Negative inotropes and blood pressure-lowering agents should be avoided. An appropriate arterial oxygenation (including non-invasive and invasive positive pressure ventilation), adequate glycaemic control and near-normal pH are mandatory to support the results of invasive treatment. A variety of pharmacological agents improving cardiac output and increasing blood pressure are available. In cases with CS and PCWP < 14 mm Hg and CI < 2.2 l/min/m2 a continuous fluid infusion is recommended to fulfil the vascular bed. When PCWP exceeds 18 mm Hg vasodilators may be helpful in cases without hypotension and severe valve stenosis. In patients with CI < 2.2 l/min/m2, PCWP > 18–20 mm Hg, and systolic blood pressure (SBP) < 85 mm Hg a continuous infusion of inotropic agents through a central venous catheter should be initiated. An adequate CVP (ca 10–14 mm Hg) is mandatory to avoid peripheral hypoperfusion. Haemodynamic benefit may be diminished by potential side effects (ventricular arrhythmia, tachycardia). The most popular agents, their dosage, and special issues are summarised in Table 2 [10, 29].

Mechanical support

Mechanical support to improve systemic blood flow and to decrease peripheral hypoperfusion may be a life-saving option in patients in whom CS persists despite early revascularisation and optimal medical therapy. A history of left ventricular support begins with extracorporeal membrane oxygenation (ECMO), and evolves via intra-aortic balloon pump (IABP) and Hemopump to TandemHeart, Impella, and Ventricular Assist Devices (VAD). Currently, various modifications are available on the market.

Intra-aortic balloon pump

Forty years of experience after IABP introduction has made it easy to implant a device with relatively low cost and complication rate. Peak diastolic pressure is increased and the end-systolic pressure is decreased during continuous inflation-deflation cycles, which results in a reduction of afterload and improved coronary flow. Previously reported as a first line strategy (class I C) [30] with scientific support from the SHOCK Trial Registry [31] and the National Registry of Myocardial Infarction-2 (NRMI-2) [32], IABP lost its position in guidelines due to several meta-analyses [33, 34] and IABP-SHOCK II Trial [35] results with no further support of any IABP benefit. Unfortunately, while IABP is not efficient to ensure long-term survival, there is no well defined reason why the improvement in the haemodynamic status after IABP insertion is not a suitable predictor of better survival. Several limitations of the SHOCK Trial Registry may be a partial explanation: IABP inserted after PCI, IABP group represents a high-risk population, bleeding complication, stroke or inflammatory response to IABP components. Of note, classic indications for IABP, i.e. mechanical complications of MI, are still valid.

Novel devices and areas of future research

In theory, veno-arterial extracorporeal membrane oxygenation may maintain cardiac output up to 6 l/min and exchange carbon dioxide and oxygen. Whether it has a beneficial effect on long-term survival in STEMI complicated by CS remains unclear due to the scarcity of data. In a single-centre study in a population with deep CS of a heterogenous aetiology, the majority of 68 patients who were successfully weaned from ECMO were discharged alive. In-hospital mortality in the STEMI subgroup was 40.5% [36], which was also confirmed in a small STEMI-only oriented study on 27 subjects (37% 30-day mortality in those successfully weaned from ECMO) [37] and in another one on 33 patients (1-year mortality 36.4% in patients treated with ECMO and IABP vs. 76% in those without ECMO; p < 0.001) [38]. Although these data are encouraging, better survival was assigned for successful weaning from ECMO. Whether it was an ECMO-related benefit remains undetermined. However, ECMO may be followed by different modifications of ventricular assist device. Data from large well powered randomised controlled trials on novel devices in CS management are lacking. The reports available come from observational studies and retrospective analyses or small trials [39–43]. The Impella (Abiomed, Germany) is a catheter-based, percutaneously implanted axial pump facilitating the blood flow from the left ventricle to the aorta. The TandemHeart (Cardiac Assist, USA) is a percutaneously or surgically implanted by-pass from the left atrium to the femoral artery via centrifugal continuous flow pump. Both systems may be implanted by interventional cardiologists prior to or after PCI; however, TandemHeart requires the operator to be skilled in transseptal puncture because the by-pass is implanted via the femoral vein through the interatrial septum at an activated clotting time of over 400 s. Despite encouraging results, bleeding complications, in-hospital, and long-term mortality still remain unacceptably high in this population [44]. This is best summarised in a meta-analysis by Cheng et al., with a conclusion that despite better haemodynamic profile mortality does not decrease significantly [45]. However, these devices may be a bridge to heart transplantation or – if the donor is lacking – to total artificial heart implantation and staged transplantation with an excellent long-term survival [46–48].
Another important area of research involves mild therapeutic hypothermia via percutaneous catheter located in the inferior vena cava. It has been shown to improve the neurological outcome in out-of-hospital cardiac arrest survivors, and neuroprotection is the primary goal of its emergent application [49]. Its effect on myocardial performance during the acute phase of MI remains unknown. In animal models the results are conflicting [50, 51]. In trials that proved hypothermia benefit patients with CS were excluded [10]. Moreover, hypothermia might have a deleterious influence on haemodynamic status due to hypotension, bradycardia, vasoconstriction, or shivering and its management (deep analgo-sedation or neuromuscular blocking agents). This may raise concerns about the efficacy and safety in patients with initial haemodynamic collapse. Inter-hospital differences in cooling protocols, no standard in sequence (prior to or after primary PCI), and lack of data from well-powered trials may cause difficulties in drawing conclusions. Therefore, extrapolating data must be done with caution. Nevertheless, Norwegian and Czech reports encourage further investigate this issue [52, 53].


Can the 50% mortality barrier be broken? An effort to achieve early reperfusion with final TIMI 3 flow, experience in PCI techniques, and new generations of stents and multilevel platelet activation inhibition has resulted in a mortality decrease in recent decades. Unfortunately, some patients with patent infarct-related artery do not improve their haemodynamic status and have a very poor prognosis. Many conclusions on CS were drawn from SHOCK analyses. Randomised controlled trials involving patients with CS are difficult to conduct due to ethical reasons, so the national registries play an important role [54]. It is not clear whether research in mechanical support combined with therapeutic hypothermia in cardiac arrest comatose survivors or experimental therapies in the inhibition of the systemic inflammatory response (i.e. inducible nitric oxide synthase), or even bone marrow stromal cells auto-transplantation, will further improve survival. So far, we can “only” exclude mechanical complications, optimise oxygenation, and achieve TIMI 3 flow, preferably by immediate culprit lesion stenting and staged procedure (PCI or CABG) for multivessel disease (unless there is TIMI flow less than 3 in non-culprit vessels with significant narrowing). A need for a prompt mechanical support is intuitively defined; however, no strong data supporting novel techniques is present.

Conflict of interest

The authors declare no conflict of interest.


1. Antmann EM, Braunwald E. Acute myocardial infarction. In: Heart Disease. A Textbook of Cardiovascular Medicine. Braunwald E, Zipes DP, Libby P (eds.) 6th ed. W.B. Saunders Company, 2001.
2. Hochman JS, Buller CE, Sleeper LA, Boland J, Dzavik V, Sanborn TA, Godfrey E, White HD, Lim J, LeJemtel T. Cardiogenic shock complicating acute myocardial infarction: etiologies, management and outcome: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol 2000; 36 (3 Suppl A): 1063-70.
3. Goldberg RJ, Spencer FA, Gore JM, Lessard D, Yarzebski J. Thirty-year trends (1975-2005) in the magnitude of, management of, and hospital death rates associated with cardiogenic shock in patients with acute myocardial infarction: a population-based perspective. Circulation 2009; 119: 1211-9.
4. 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. J Am Coll Cardiol 2000; 36: 685-92.
5. Dzavik V, Sleeper LA, Cocke TP, Moscucci M, Saucedo J, Hosat S, Jiang X, Slater J, LeJemtel T, Hochman JS; SHOCK Investigators. Early revascularization is associated with improved survival in elderly patients with acute myocardial infarction complicated by cardiogenic shock: a report from the SHOCK Trial Registry. Eur Heart J 2003; 24: 828-37.
6. Goldberg RJ, Gore JM, Alpert JS, Osganian V, de Groot J, Bade J, Chen Z, Frid D, Dalen JE. Cardiogenic shock after acute myocardial infarction. Incidence and mortality from a community-wide perspective, 1975 to 1988. N Engl J Med 1991; 325: 1117-22.
7. 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. Should we emergently revascularize occluded coronaries for cardiogenic shock. One-year survival following early revascularization for cardiogenic shock. JAMA 2001; 285: 190-2.
8. Hochman JS, Sleeper LA, Webb JG, Dzavik V, Buller CE, Aylward P, Col J, White HD; SHOCK Investigators. Early revascularization and long-term survival in cardiogenic shock complicating acute myocardial infarction. JAMA 2006; 295: 2511-5.
9. Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circulation 2008; 117: 686-97.
10. Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology (ESC), Steg PG, James SK, Atar D, Badano LP, Blömstrom-Lundqvist C, Borger MA, Di Mario C, Dickstein K, Ducrocq G, Fernandez-Aviles F, Gershlick AH, Giannuzzi P, Halvorsen S, Huber K, Juni P, Kastrati A, Knuuti J, Lenzen MJ, Mahaffey KW, Valgimigli M, van ‘t Hof A, Widimsky P, Zahger D. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J 2012; 33: 2569-619.
11. Gheorghiade M, Zannad F, Sopko G, Klein L, Pińa IL, Konstam MA, Massie BM, Roland E, Targum S, Collins SP, Filippatos G, Tavazzi L; International Working Group on Acute Heart Failure Syndromes. Acute heart failure syndromes: current state and framework for future research. Circulation 2005; 112: 3958-68.
12. White HD, Palmeri ST, Sleeper LA, French JK, Wong CK, Lowe AM, Crapo JW, Koller PT, Baran KW, Boland JL, Hochman JS, Wagner GS; SHOCK Trial Investigators. Electrocardiographic findings in cardiogenic shock, risk prediction, and the effects of emergency revascularization: results from the SHOCK trial. Am Heart J 2004; 148: 810-7.
13. Picard MH, Davidoff R, Sleeper LA, Mendes LA, Thompson CR, Dzavik V, Steingart R, Gin K, White HD, Hochman JS; SHOCK Trial. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK. Echocardiographic predictors of survival and response to early revascularization in cardiogenic shock. Circulation 2003; 107: 279-84.
14. Shah MR, Hasselblad V, Stevenson LW, Binanay C, O’Connor CM, Sopko G, Califf RM. Impact of the pulmonary artery catheter in critically ill patients: meta-analysis of randomized clinical trials. JAMA 2005; 294: 1664-70.
15. Payen D, Gayat E. Which general intensive care unit patients can benefit from placement of the pulmonary artery catheter? Crit Care 2006; 10 Suppl. 3: S7.
16. O’Gara PT, Kushner FG, Ascheim DD, Casey DE Jr, Chung MK, de Lemos JA, Ettinger SM, Fang JC, Fesmire FM, Franklin BA, Granger CB, Krumholz HM, Linderbaum JA, Morrow DA, Newby LK, Ornato JP, Ou N, Radford MJ, Tamis Holland JE, Tommaso JE, Tracy CM, Woo YJ, Zhao DX; CF/AHA Task Force. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013; 127: 529-55.
17. De Luca G, Suryapranata H, Ottervanger JP, Antman EM. Time delay to treatment and mortality in primary angioplasty for acute myocardial infarction: every minute of delay counts. Circulation 2004; 109: 1223-5.
18. Labovitz AJ. Mechanical complications of acute myocardial infarction. Cardiovasc Rev Rep 1984; 5: 948-64.
19. Sugiura T, Nagahama Y, Nakamura S, Kudo Y, Yamasaki F, Iwasaka T. Left ventricular free wall rupture after reperfusion therapy for acute myocardial infarction. Am J Cardiol 2003; 92: 282-4.
20. Stańczak P, Janion-Sadowska A, Sadowski M, Sadowski J, Janion M. Postinfarction left ventricular pseudoaneurysm. Pol Arch Med Wewn 2005; 113: 68-72.
21. 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. J Am Coll Cardiol 2003; 41: 1273-9.
22. Gadsbøll N, Høilund-Carlsen PF, Madsen EB, Marving J, Pedersen A, Lønborg-Jensen H, Dige-Petersen H, Jensen BH. Right and left ventricular ejection fractions: relation to one-year prognosis in acute myocardial infarction. Eur Heart J 1987; 8: 1201-9.
23. Jeger RV, Lowe AM, Buller CE, Pfisterer ME, Dzavik V, Webb JG, Hochman JS, Jorde UP; SHOCK Investigators. Hemodynamic parameters are prognostically important in cardiogenic shock but similar following early revascularization or initial medical stabilization: a report from the SHOCK Trial. Chest 2007; 132: 1794-803.
24. 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 Med 1999; 341: 625-34.
25. Dauerman HL, Goldberg RJ, White K, Gore JM, Sadiq I, Gurfinkel E, Budaj A, Lopez de Sa E, Lopez-Sendon J; Global Registry of Acute Coronary Events. GRACE Investigators. Revascularization, stenting, and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock. Am J Cardiol 2002; 90: 838-42.
26. Gasior M, Slonka G, Wilczek K, Gierlotka M, Ruzyllo W, Zembala M, Osadnik T, Dubiel J, Zdrojewski T, Kalarus Z, Polonski L. Comparison of invasive and non-invasive treatment strategies in older patients with acute myocardial infarction complicated by cardiogenic shock (from the Polish Registry of Acute Coronary Syndromes - PL-ACS). Am J Cardiol 2011; 107: 30-6.
27. Chan AW, Chew DP, Bhatt DL, Moliterno DJ, Topol EJ, Ellis SG. Long-term mortality benefit with the combination of stents and abciximab for cardiogenic shock complicating acute myocardial infarction. Am J Cardiol 2002; 89: 132-6.
28. Hochman JS. Cardiogenic shock complicating acute myocardial infarction: expanding the paradigm. Circulation 2003; 107: 2998-3002.
29. McMurray JJ, Adamopoulos S, Anker SD, Auricchio A, Böhm M, Dickstein K, Falk V, Filippatos G, Fonseca C, Gomez-Sanchez MA, Jaarsma T, Køber L, Lip GY, Maggioni AP, Parkhomenko A, Pieske BM, Popescu BA, Rønnevik PK, Rutten FH, Schwitter J, Seferovic P, Stepinska J, Trindade PT, Voors AA, Zannad F, Zeiher A; ESC Committee for Practice Guidelines. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC. Eur Heart J 2012; 33: 1787-847.
30. Van de Werf F, Bax J, Betriu A, Blomstrom-Lundqvist C, Crea F, Falk V, Filippatos G, Fox K, Huber K, Kastrati A, Rosengren A, Steg PG, Tubaro M, Verheugt F, Weidinger F, Weis M; ESC Committee for Practice Guidelines (CPG). Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation: the Task Force on the Management of ST-Segment Elevation Acute Myocardial Infarction of the European Society of Cardiology. Eur Heart J 2008; 29: 2909-45.
31. 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. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol 2000; 36 (3 Suppl. A): 1123-9.
32. 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 J 2001; 141: 933-9.
33. Sjauw KD, Engström AE, Vis MM, van der Schaaf RJ, Baan J Jr, Koch KT, de Winter RJ, Piek JJ, Tijssen JG, Henriques JP. A systematic review and meta-analysis of intraaortic balloon pump therapy in ST-elevation myocardial infarction: should we change the guidelines? Eur Heart J 2009; 30: 459-68.
34. Bahekar A, Singh M, Singh S, Bhuriya R, Ahmad K, Khosla S, Arora R. Cardiovascular outcomes using intra-aortic balloon pump in high-risk acute myocardial infarction with or without cardiogenic shock: a meta-analysis. J Cardiovasc Pharmacol Ther 2012; 17: 44-56.
35. Thiele H, Zeymer U, Neumann FJ, Ferenc M, Olbrich HG, Hausleiter J, Richardt G, Hennersdorf M, Empen K, Fuernau G, Desch S, Eitel I, Hambrecht R, Fuhrmann J, Böhm M,Ebelt H, Schneider S, Schuler G, Werdan K; IABP-SHOCK II Trial Investigators. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med 2012; 367: 1287-96.
36. Chung SY, Sheu JJ, Lin YJ, Sun CK, Chang LT, Chen YL, Tsai TH, Chen CJ, Yang CH, Hang CL, Leu S, Wu CJ, Lee FY, Yip HK. Outcome of patients with profound cardiogenic shock after cardiopulmonary resuscitation and prompt extracorporeal membrane oxygenation support. A singlecenter observational study. Circ J 2012; 76: 1385-92.
37. Kim H, Lim SH, Hong J, Hong YS, Lee CJ, Jung JH, Yu S. Efficacy of veno-arterial extracorporeal membrane oxygenation in acute myocardial infarction with cardiogenic shock. Resuscitation 2012; 83: 971-5.
38. Tsao NW, Shih CM, Yeh JS, Kao YT, Hsieh MH, Ou KL, Chen JW, Shyu KG, Weng ZC, Chang NC, Lin FY, Huang CY. Extracorporeal membrane oxygenation-assisted primary percutaneous coronary intervention may improve survival of patients with acute myocardial infarction complicated by profound cardiogenic shock. J Crit Care 2012; 27: 530.e1-11.
39. Engström AE, Cocchieri R, Driessen AH, Sjauw KD, Vis MM, Baan J, de Jong M, Lagrand WK, van der Sloot JA, Tijssen JG, de Winter RJ, de Mol BA, Piek JJ, Henriques JP. The Impella 2.5 and 5.0 devices for ST-elevation myocardial infarction patients presenting with severe and profound cardiogenic shock: the Academic Medical Center intensive care unit experience. Crit Care Med 2011; 39: 2072-9.
40. Cheng JM, den Uil CA, Hoeks SE, van der Ent M, Jewbali LS, van Domburg RT, Serruys PW. Percutaneous left ventricular assist devices vs. intra-aortic balloon pump counterpulsation for treatment of cardiogenic shock: a meta analysis of controlled trials. Eur Heart J 2009; 30: 2102-8.
41. Takayama H, Truby L, Koekort M, Uriel N, Colombo P, Mancini DM, Jorde UP, Naka Y. Clinical outcome of mechanical circulatory support for refractory cardiogenic shock in the current era. J Heart Lung Transplant 2013; 32: 106-11.
42. Kar B, Gregoric ID, Basra SS, Idelchik GM, Loyalka P. The percutaneous ventricular assist device in severe refractory cardiogenic shock. J Am Coll Cardiol 2011; 57: 688-96.
43. Seyfarth M, Sibbing D, Bauer I, Fröhlich G, Bott-Flügel L, Byrne R, Dirschinger J, Kastrati A, Schömig A. A randomized clinical trial to evaluate the safety and efficacy of a percutaneous left ventricular assist device versus intra aortic balloon pumping for treatment of cardiogenic shock caused by myocardial infarction. J Am Coll Cardiol 2008; 52: 1584-8.
44. Lauten A, Engström AE, Jung C, Empen K, Erne P, Cook S, Windecker S, Bergmann MW, Klingenberg R, Lüscher TF, Haude M, Rulands D, Butter C, Ullman B, Hellgren L, Modena MG, Pedrazzini G, Henriques JP, Figulla HR, Ferrari M. Percutaneous left-ventricular support with the Impella-2.5-assist device in acute cardiogenic shock: results of the Impella-EUROSHOCK-registry. Circ Heart Fail 2013; 6: 23-30.
45. Cheng JM, den Uil CA, Hoeks SE, van der Ent M, Jewbali LS, van Domburg RT, Serruys PW. Percutaneous left ventricular assist devices vs. intra-aortic balloon pump counterpulsation for treatment of cardiogenic shock: a meta-analysis of controlled trials. Eur Heart J 2009; 30: 2102-8.
46. Tayara W, Starling RC, Yamani MH, Wazni O, Jubran F, Smedira N. Improved survival after acute myocardial infarction complicated by cardiogenic shock with circulatory support and transplantation: comparing aggressive intervention with conservative treatment. J Heart Lung Transplant 2006; 25: 504-9.
47. Copeland JG, Smith RG, Arabia FA, Nolan PE, Sethi GK, Tsau PH, McClellan D, Slepian MJ; CardioWest Total Artificial Heart Investigators. Cardiac replacement with a total artificial heart as a bridge to transplantation. N Engl J Med 2004; 351: 859-67.
48. Kirklin JK, Naftel DC, Kormos RL, Stevenson LW, Pagani FD, Miller MA, Baldwin JT, Young JB. The Fourt INTERMACS Annual Report: 4,000 implants and counting. J Heart Lung Transplant 2012; 31: 117-26.
49. Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G, Smith K. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002; 346: 557-63.
50. Hale SL, Dave RH, Kloner RA. Regional hypothermia reduces myocardial necrosis even when instituted after the onset of ischemia. Basic Res Cardiol 1997; 92: 351-7.
51. Maeng M, Mortensen UM, Kristensen J, Kristiansen SB, Andersen HR. Hypothermia during reperfusion does not reduce myocardial infarct size in pigs. Basic Res Cardiol 2006; 101: 61-8.
52. Hovdenes J, Laake JH, Aaberge L, Haugaa H, Bugge JF. Therapeutic hypothermia after out-of-hospital cardiac arrest: experiences with patients treated with percutaneous coronary intervention and cardiogenic shock. Acta Anaesthesiol Scand 2007; 51: 137-42.
53. Skulec R, Kovarnik T, Dostalova G, Kolar J, Linhart A. Induction of mild hypothermia in cardiac arrest survivors presenting with cardiogenic shock syndrome. Acta Anaesthesiol Scand 2008; 52: 188-94.
54. Kołodziej M, Kurzawski J, Janion-Sadowska A, Gierlotka M, Poloński L, Gąsior M, Sadowski M. Mortality of women with ST-segment elevation myocardial infarction and cardiogenic shock – results from the PL-ACS registry. Medical Studies/Studia Medyczne 2016; 32: 157-63.

Address for correspondence:

Marcin Sadowski MD, PhD
Department of Interventional Cardiology
Świętokrzyskie Cardiology Centre
ul. Grunwaldzka 45, 25-736 Kielce, Poland
Phone: +48 606 906 454
E-mail: emsad@o2.pl
Copyright: © 2017 Jan Kochanowski University in Kielce This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (http://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
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