Impaired microcirculation predicts poor outcome of patients with acute myocardial infarction complicated by cardiogenic shock

Uil, Corstiaan A. den; Lagrand, Wim K.; Ent, Martin van der; Jewbali, Lucia S.D.; Cheng, Jin M.; Spronk, Peter E.; Simoons, Maarten L.

doi:10.1093/eurheartj/ehq324

Cited by 188 publications

(104 citation statements)

References 43 publications

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“…Both values incorporate the density of the vascular network as well as its perfusion status. Both have prognostic relevance (13,24) and allow the monitoring of changes following pharmacological therapy (reviewed in Ref. 25).…”

Section: Discussionmentioning

confidence: 99%

Increase of cortical cerebral blood flow and further cerebral microcirculatory effects of Serelaxin in a sheep model

Bischoff

Schmidt

Irintchev

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

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Serelaxin, recombinant human relaxin-2, modulates endothelial vasodilatory functionality and is under evaluation for treatment of acute heart failure. Little is known about acute effects on cerebral perfusion. We tested the hypothesis that Serelaxin might also have effects on the cerebral microcirculation in a sheep model, which resembles human brain structure quite well. We used laser Doppler flowmetry and sidestream dark-field (SDF) imaging techniques, which are reliable tools to continuously assess dynamic changes in cerebral perfusion. Laser Doppler flowmetry shows that bolus injection of 30 g Serelaxin/kg body wt induces an increase (P ϭ 0.006) to roughly 150% of cortical cerebral blood flow (CBF), whereas subcortical CBF remains unchanged (P ϭ 0.688). The effects on area-dependent CBF were significantly different after the bolus injection (P ϭ 0.042). Effects on cortical CBF were further confirmed by SDF imaging. The bolus injection of Serelaxin increased total vessel density to 127% (P ϭ 0.00046), perfused vessel density to 145% (P ϭ 0.024), and perfused capillary density to 153% (P ϭ 0.024). Western blotting confirmed the expression of relaxin receptors RXFP1 and truncated RXFP2-variants in the respective brain regions, suggesting a possible contribution of RXFP1 on the effects of Serelaxin. In conclusion, the injection of a high dose of Serelaxin exerts quick effects on the cerebral microcirculation. Therefore, Serelaxin might be suitable to improve cortical microcirculation and exert neuroprotective effects in clinically relevant scenarios that involve cortical hypoperfusion. These findings need to be confirmed in relevant experimental settings involving cerebral cortical hypoperfusion and can possibly be translated into clinical practice. RELAXIN-2 IS A HUMAN HORMONE that mediates cardiovascular adaptations during pregnancy and particularly systemic and renal vasodilatation (7). Moreover, these effects are observed in nonpregnant animals and in ex vivo studies following the artificial administration of the substance as well (33). An intravenous bolus injection of a recombinant form of human relaxin-2, Serelaxin (Novartis Pharma, Basel, Switzerland), modulates a sustained endothelial vasodilatory function. Serelaxin mediates systemic hemodynamic changes and increases renal blood flow through a fall in systemic intravascular resistance with a concomitant increase in arterial compliance (15,22,31,38,39). In the RELAX-AHF study, cardiovascular and all-cause mortality was reduced 37% in patients treated with Serelaxin (42). Furthermore, initial positive studies on the cerebral effects of this peptide hormone in a stroke model (47) and in a high blood pressure situation (6) have already been published. Serelaxin induces a nitric oxide-mediated vasodilatation (40) and can particularly reduce the infarction size of the cerebral cortex, suggesting a neuroprotective effect (47).Nonetheless, studies on the influence of Serelaxin on the cerebral blood flow (CBF) have not been performed to this day. Moreover, desp...

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Section: Discussionmentioning

confidence: 99%

Increase of cortical cerebral blood flow and further cerebral microcirculatory effects of Serelaxin in a sheep model

Bischoff

Schmidt

Irintchev

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

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“…3 Emerging evidence has also shown that impairment of tissue microcirculation is associated with 30-day mortality and temporal changes in SOFA (SepsisRelated Organ Failure Assessment) scores and may be improved with MCS. 28,29 In fact, it is now well established that CS can result in both acute and subacute derangements to the entire circulatory system, including the peripheral vasculature. Extremity and vital organ hypoperfusion remains a clinical hallmark.…”

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confidence: 99%

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

Diepen¹,

Katz²,

Albert³

et al. 2017

Circulation

1,343

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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“…This approach is unfortunately potentially biased when alterations in microvascular perfusion alter oxygen extraction capabilities such as in sepsis [40]. Microcirculatory alterations also occur in cardiogenic shock and severe heart failure [41,42], but these have less impact on SvO2, as SvO2 is already low due to the low cardiac output. The second factor to take into account is lactate levels.…”

Section: Characterization Of the Type Of Shockmentioning

confidence: 99%

Is There a Role for Invasive Hemodynamic Monitoring in Acute Heart Failure Management?

Backer

2015

Curr Heart Fail Rep

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The place of invasive hemodynamic monitoring in patients with acute heart failure is still debated, even though frequently used. Invasive techniques, which include the pulmonary artery catheter and transpulmonary thermodilution, provide important information on cardiac output and intravascular pressures or volume. These techniques should be used in combination with echocardiography and allow nurse-driven semicontinuous hemodynamic monitoring. These techniques are useful not only in the diagnosis of circulatory or respiratory failure but also for the evaluation of the effects of therapies. Admittedly, large-scale randomized trials failed to demonstrate a survival benefit with the pulmonary artery catheter (and were even not yet performed with transpulmonary thermodilution). However, these trials may be subjected to selection bias, as patients from recruiting centers not included in the trial but receiving the pulmonary artery catheter were more severe and had higher mortality rates than patient included in the trial. Hence, invasive techniques may still have a place in selected patients with acute circulatory failure and especially in the most severe cases.

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Impaired microcirculation predicts poor outcome of patients with acute myocardial infarction complicated by cardiogenic shock

Abstract: diminished sublingual PCD, at baseline or following treatment, is associated with development of multi-organ failure and is a predictor of poor outcome in patients with acute myocardial infarction complicated by cardiogenic shock.

Cited by 188 publications

References 43 publications

Increase of cortical cerebral blood flow and further cerebral microcirculatory effects of Serelaxin in a sheep model

Increase of cortical cerebral blood flow and further cerebral microcirculatory effects of Serelaxin in a sheep model

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

Is There a Role for Invasive Hemodynamic Monitoring in Acute Heart Failure Management?

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