Interleukin-6, -7, -8 and -10 predict outcome in acute myocardial infarction complicated by cardiogenic shock

Prondzinsky, Roland; Unverzagt, Susanne; Lemm, Henning; Wegener, Nikolas-Arne; Schlitt, Axel; Heinroth, K. M.; Dietz, Sebastian; Buerke, Ute; Kellner, Patrick; Loppnow, Harald; Fiedler, Georg Martin; Thiery, Joachim; Werdan, Karl; Buerke, Michael

doi:10.1007/s00392-011-0403-3

Cited by 98 publications

(62 citation statements)

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“…Second, we did not obtain hemodynamic measurements or assess laboratory inflammatory markers other than blood pressure, heart rate, and C-reactive protein levels, although data on these variables are available from previous trials. [24][25][26][27] Third, the slightly lower mortality in our trial -approximately 40%, as compared with 42 to 48% in other randomized trials and registries -might suggest that our trial included a higher percentage of patients with mild or moderately severe cardiogenic shock, a factor that could preclude generalization of the results to patients with the most severe forms of cardiogenic shock. [1][2][3][4]28 However, on the basis of a post hoc analysis, there was no mortality benefit of intraaortic balloon counterpulsation among patients with a systolic blood pressure of less than 80 mm Hg.…”

Section: Discussionmentioning

confidence: 75%

Intraaortic Balloon Support for Myocardial Infarction with Cardiogenic Shock

et al. 2012

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Section: Discussionmentioning

confidence: 75%

Intraaortic Balloon Support for Myocardial Infarction with Cardiogenic Shock

et al. 2012

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“…Cardiogenic shock is also associated with a systemic inflammatory response, characterized by dramatic increases in the levels of proinflammatory cytokines. In patients with cardiogenic shock, circulating IL-6 levels independently predict mortality (133); levels of other proinflammatory cytokines and chemokines (such as TNF-α and IL-8/CXCL8) are also markedly increased (75,298). Because proinflammatory cytokines are potent myocardial depressants, patients with overactive systemic inflammation following myocardial infarction may be more susceptible to cardiogenic shock.…”

Section: Cardiogenic Shockmentioning

confidence: 96%

Pathophysiology of Myocardial Infarction

Frangogiannis

2015

Comprehensive Physiology

500

391

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Myocardial infarction is defined as sudden ischemic death of myocardial tissue. In the clinical context, myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function. Prolonged myocardial ischemia activates a "wavefront" of cardiomyocyte death that extends from the subendocardium to the subepicardium. Mitochondrial alterations are prominently involved in apoptosis and necrosis of cardiomyocytes in the infarcted heart. The adult mammalian heart has negligible regenerative capacity, thus the infarcted myocardium heals through formation of a scar. Infarct healing is dependent on an inflammatory cascade, triggered by alarmins released by dying cells. Clearance of dead cells and matrix debris by infiltrating phagocytes activates anti-inflammatory pathways leading to suppression of cytokine and chemokine signaling. Activation of the renin-angiotensin-aldosterone system and release of transforming growth factor-β induce conversion of fibroblasts into myofibroblasts, promoting deposition of extracellular matrix proteins. Infarct healing is intertwined with geometric remodeling of the chamber, characterized by dilation, hypertrophy of viable segments, and progressive dysfunction. This review manuscript describes the molecular signals and cellular effectors implicated in injury, repair, and remodeling of the infarcted heart, the mechanistic basis of the most common complications associated with myocardial infarction, and the pathophysiologic effects of established treatment strategies. Moreover, we discuss the implications of pathophysiological insights in design and implementation of new promising therapeutic approaches for patients with myocardial infarction.

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“…26 Other inflammatory mediators such as interleukins and tumor necrosis factor can also contribute to systemic vasodilation and have been associated with mortality in CS. 30 In addition, bleeding and transfusions may be associated with mortality. 31,32 Alterations in erythrocyte NO biology of stored blood can lead to vasoconstriction, platelet aggregation, and ineffective oxygen delivery, whereas transfusion of stored blood may also contribute to inflammation.…”

Section: Pathophysiologymentioning

confidence: 99%

Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association

Diepen¹,

Katz²,

Albert³

et al. 2017

Circulation

1,274

1,165

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Cardiogenic shock is a high-acuity, potentially complex, and hemodynamically diverse state of end-organ hypoperfusion that is frequently associated with multisystem organ failure. Despite improving survival in recent years, patient morbidity and mortality remain high, and there are few evidence-based therapeutic interventions known to clearly improve patient outcomes. This scientific statement on cardiogenic shock summarizes the epidemiology, pathophysiology, causes, and outcomes of cardiogenic shock; reviews contemporary best medical, surgical, mechanical circulatory support, and palliative care practices; advocates for the development of regionalized systems of care; and outlines future research priorities. Cardiogenic shock (CS) is a low-cardiac-output state resulting in life-threatening end-organ hypoperfusion and hypoxia.1,2 Acute myocardial infarction (MI) with left ventricular (LV) dysfunction remains the most frequent cause of CS. 1,3 Advances in reperfusion therapy have been associated with improvements in survival, but significant regional disparities in evidence-based care have been reported, and in-hospital mortality remains high (27%-51%).1,4-9 Management recommendations are distributed between disease-specific statements and guidelines, and a dedicated and comprehensive clinical resource in this area is lacking. Thus, consolidating the evidence to define contemporary best medical and surgical CS practices for both MI-associated CS and other types of CS may be an important step in knowledge translation to help attenuate disparities in evidence-based care.Regional systems of care coupled with treatment algorithms have improved survival in high-acuity time-sensitive conditions such as MI, out-of-hospital cardiac arrest (OHCA), and trauma.10-12 Applying a similar framework to CS management may lead to similar improvements in survival, and CS systems of care are emerging within existing regional cardiovascular emergency care networks; however, guidance from a national expert group on structure and systems of care has not been available. 13,14 Accordingly, the purposes of this American Heart Association (AHA) scientific statement on CS are to summarize our contemporary understanding of the epidemiology, pathophysiology, and in-hospital best care practices into a single clinical resource document; to suggest a stepwise management algorithm that integrates medical, surgical, and mechanical circulatory support (MCS) therapies; and to propose a Mission: Lifelinesupported pathway for the development of integrated regionalized CS systems of care. DEFINITION OF CSAcute cardiac hemodynamic instability may result from disorders that impair function of the myocardium, valves, conduction system, or pericardium, either in isolation HISTORICAL PERSPECTIVESBefore the routine use of early revascularization, MIassociated CS had an in-hospital mortality exceeding 80%. A registry trial of 250 patients with acute MI described the association between bedside physical examination (Killip classification) for the as...

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Interleukin-6, -7, -8 and -10 predict outcome in acute myocardial infarction complicated by cardiogenic shock

Abstract: The inflammatory response in patients with myocardial infarction complicated by cardiogenic shock, as reflected by the inflammatory markers IL-6, IL-7, IL-8 and IL-10, demonstrates a clinically relevant prognostic contribution to clinical outcome.

Cited by 98 publications

References 44 publications

Intraaortic Balloon Support for Myocardial Infarction with Cardiogenic Shock

Intraaortic Balloon Support for Myocardial Infarction with Cardiogenic Shock

Pathophysiology of Myocardial Infarction

Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association

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