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Intra aortic balloon pumps in cardiogenic shock
- Truls Myrmel, Stig E. Hermansen (14 October 2009)
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Intra-aortic balloon pump therapy and systemic inflammatory response syndrome.
- Alberto Dominguez-Rodriguez, Pedro Abreu-Gonzalez and Juan Carlos Kaski (14 October 2009)
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Truls Myrmel, Professor University Hospital North Norway, 9038 Tromsø, Norway, Stig E. Hermansen
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We read with some concern the meta-analysis by Sjauw and co-workers on the use of intra-aortic balloon pumps (IABP) in ST-elevation infarction and cardiogenic shock (1). We do not agree with the authors that their meta-analysis challenge existing guidelines. First, the title of the paper concerns ST-elevation infarction, but their arguments against the guidelines relates to the use of IABP in the setting of post infarct revascularized cardiogenic shock, the patient group where IABP has the strongest physiological rationale and support by observational data (2). The 7 cited RCTs include almost no such patients. In 4 of the STEMI trials patients with cardiogenic shock were excluded. Their reference 11 was conducted before the revascularization era. Importantly, in their reference 17 patients in cardiogenic shock were prespecified to IABP treatment, and in reference 14, 9 of the 27 patients randomized to fibrinolysis alone crossed over to IABP because of a deteriorating clinical condition. Thus, in the complete set of studies there was a strong bias towards treating patients in shock with IABP and this severely limits the overall value of these studies. In our view, these design factors are stripping the studies from the possibility to show a clinically relevant benefit from using IABP in ST-elevation infarction. Second, the analysis of observational data demonstrates a survival benefit for IABP in the setting of thrombolysis. The observational studies addressing the use of IABP as an adjunct to primary PCI included their own Amsterdam Medical Center (AMC) CS registry and the US National Registry of Myocardial Infarction 2. Their AMC CS publications concern the risk stratification of elevated glucose (reference 20) and low hemoglobin (reference 21), not the use of IABP, and as such have no peer reviewed data for us to assess. These data are an important reason for the authors to conclude that IABP is a characteristic for an increased mortality. The NRMI 2 data have been thoroughly discussed (2), and the lack of an IABP effect could quite possibly be due to a selection bias towards IABP treatment in patients with incomplete revascularization and/or complex untreated coronary pathology remaining after PCI. In our opinion, the extensive IABP data on the physiological effect of the pump, the long and established effect in surgical patients, and the supportive observational data in cardiological patients (2) are not challenged by this meta-analysis, and the guidelines should not be changed at this time. The concern is more related to the fact that too few patients in cardiogenic shock receive this treatment, as stated in the accompanying editorial. References 1. Sjauw KD, Engström AE, Vis MM, van der Schaaf RJ, Baan Jr J, Koch KT, de Winter RJ, Piek JJ, Tijssen JGP, Henriques JPS. A systematic review and meta-analysis of intra-aortic balloon pump therapy in ST-elevation myocardial infarction: should we change the guidelines? Eur Heart J 2009; 30: 459-68. 2. Ohman EM, Hochman JS. Aortic counter pulsation in acute myocardial infarction: physiological important but does the patient benefit? Am Heart J 2001; 141: 889-892 Conflict of Interest:None declared |
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Alberto Dominguez-Rodriguez, MD, PhD, FESC University Hospital of Canarias, Dept. of Cardiology. Tenerife. E- 38320. Spain, Pedro Abreu-Gonzalez and Juan Carlos Kaski
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Sjauw et al (1) should be congratulated on their study on intra- aortic balloon pump (IABP) support for ST-elevation myocardial infarction (STEMI) with and without cardiogenic shock (CS). They indicate that available observational data concerning IABP therapy in the setting of CS is affected by bias and confounding. Moreover, they highlight the fact that there is insufficient evidence to endorse current therapeutic recommendations for the use of IABP therapy in the setting of STEMI complicated by CS. We concur with their views but also believe that not only a redefinition of the guidelines is required, but a better understanding of the pathophysiological processes associated with IABP therapy in the setting of STEMI and CS. CS in the setting of STEMI has traditionally been viewed simply as a “mechanical” problem, i.e. an acute reduction in myocardial contractility caused by the ischaemic/necrotic process leads to reduced stroke volume and cardiac output, which, in turn, leads to systemic tissue hypoperfusion (2). Emerging evidence, however, suggests that this paradigm should be expanded (3). During acute myocardial infarction the release of inflammatory mediators results in the production of high levels of inducible nitric oxide (NO) synthase (4). NO and peroxynitrites produced in this process reduce the inotropic activity of the heart, suppress mitochondrial respiration in nonischemic myocardium, alter myocardial glucose metabolism, and reduce the myocardial response to catecholamines (3). These abnormalities, which contribute substantially to the mortality associated with CS, are not reversed even when a more physiological haemodynamic state is achieved with treatment. The use of mechanical circulatory support in patients with STEMI complicated by CS is predicated on the assumption that mortality will improve as a result of the improved haemodynamic status. We should realize, however, that an improved haemodynamic status is not necessarily a marker for improved survival (1,5,6). Of interest, it has been shown that despite initial beneficial effects on haemodynamic variables, the use of mechanical circulatory support could promote systemic inflammatory responses that may lead to multi- organ dysfunction (6). Systemic inflammation triggered by mechanical circulatory support may have deleterious effects in some patients leading to further clinical deterioration. IABP therapy in such patients should perhaps be combined with pharmacological interventions aimed at antagonising the negative effects of systemic inflammation. It is conceivable that the combination of effective haemodynamic support and appropriate anti-inflammatory interventions could result in better clinical outcomes. However, these interventions need to be identified and further investigation is therefore required. Well planned research into the mechanisms responsible for the less than optimal results observed with the use of IABP is probably the only way to make significant progress in this field. References 1.Sjauw KD, Engstrom AE, Vis MM, van der Schaaf RJ, Baan Jr J, Koch KT, de Winter RJ, Piek JJ, Tijssen JGP, Henriques JPS. A systemic review and meta-analysis of intra-aortic balloon pump therapy in ST-elevation myocardial infarction: should we change the guidelines? Eur Heart J 2009;30:459-468. 2.Hollenberg SM, Kavinsky CJ, Parrillo JE. Cardiogenic shock. Ann Intern Med 1999;131:47-59. 3.Hochman JS. Cardiogenic shock complicating acute myocardial infarction: expanding the paradigm. Circulation 2003;107:2998-3002. 4.Neumann FJ, Ott I, Gawaz M, RichardT G, Holzapfel H, Jochum M, Schomig A. Cardiac release of cytokines and inflammation responses in acute myocardial infarction. Circulation 1995;92:748-755. 5.Thiele H, Schuler G. Cardiogenic shock: to pump or not to pump?. Eur Heart J 2009;30:389-390. 6.Thiele H, Sick P, Boudriot E, Diederich KW, Hambrecht R, Niebauer J, Schuler G. Randomized comparison of intraaortic balloon support versus a percutaneous left ventricular assist device in patients with revascularized acute myocardial infarction complicated by cardiogenic shock. Eur Heart J 2005;26:1276-1283. Conflict of Interest:None declared |
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