Q J Med 2001; 94: 57-67
© 2001 Association of Physicians
Review |
Revascularization for cardiogenic shock
From the Department of Cardiology, Oregon Health Sciences University, Portland, Oregon, USA
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Introduction |
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 Top Introduction Diagnosis and aetiologyPathophysiology of shock due...Management of shock due...Prospects for maximizing...ConclusionsTrials glossaryReferences |
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Despite the availability of invasive circulatory monitoring, inotropes and thrombolysis, mortality from cardiogenic shock remains in excess of 50%, and continues to account for the deaths of between 7% and 11% of patients admitted with myocardial infarction.1–3 In the majority of these patients, the problem is one of overwhelming left ventricular damage and, intuitively, revascularization should be the primary therapeutic strategy. However, attempts to prove this have been fraught with difficulty, and the randomized trial paradigm that revolutionized our approach to acute cardiology appears to have faltered. This review examines the features of cardiogenic shock that have hindered attempts to improve its outcome, discusses whether current evidence is sufficient to support a policy of revascularization and explores the potential value of approaches aimed at minimizing reperfusion damage.
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Diagnosis and aetiology |
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TopIntroductionDiagnosis and aetiologyPathophysiology of shock due...Management of shock due...Prospects for maximizing...ConclusionsTrials glossaryReferences |
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The development of cardiogenic shock is rarely unexpected, most patients who develop shock do so within 48 hours of admission, with only 10% shocked on arrival.2 As would be expected, shock is associated with larger infarcts, prior infarction, diabetes and infarct extension.4,5 The diagnosis itself is straightforward, with a systolic blood pressure <90 mmHg for more than 30 min in the absence of hypovolaemia or other potential causes of hypotension. Additional features such as oliguria and impaired peripheral perfusion identify those at particularly high risk of death.6 The widespread availability of bedside echocardiography has rendered the use of invasive haemodynamics, and in particular a requirement for a cardiac index of less than 2.2 l/min/m2, virtually obsolete in the decision-making process. Echocardiography readily identifies the mechanism of shock and those patients that might benefit from surgery for intra- or extra-myocardial rupture (Figure 1
).4,7,8
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Pathophysiology of shock due to overwhelming ventricular damage |
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TopIntroductionDiagnosis and aetiologyPathophysiology of shock due...Management of shock due...Prospects for maximizing...ConclusionsTrials glossaryReferences |
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We are then left with the largest group of patients, those with insufficient contracting myocardium to survive. This group comprises those patients with overwhelming left ventricular damage and the 50% of those with severe right ventricular damage that do not respond to fluid loading (whose prognosis is often worse than commonly perceived). The pathogenesis of shock in these patients can be considered at the level of the occluded epicardial artery, in the damaged microvasculature and in individual myocytes. This initiating insult is then compounded by a maladaptive endocrine response with additional damage produced by reperfusion and the myocardial depressant effects of hypotension itself.
Coronary occlusion
The initiating insult is persistent occlusion of an epicardial coronary artery,9,10 reflected in the presence of ST segment elevation in 80% of patients.11 The potential factors underlying thrombolytic failure in normotensive individuals have been recently reviewed,12 but once shock develops, further intense thrombolytic resistance supervenes. This occurs due to failure of the lytic agent to gain access to the thrombus and a hostile biochemical environment13 (Figure 2). In non-shocked patients, a pressure gradient exists between the proximal and distal margins of the thrombus, permitting both thrombolytics and their plasminogen substrate direct access to a large volume of clot via pores in the fibrin mesh. However, coronary blood flow falls off steeply below an aortic pressure of 85 mmHg,14 and the pressure gradient declines, restricting access to only the proximal blood/clot boundary plane.15 Under both in vitro conditions16 and in animal models17,18 this produces a substantial reduction in the rate of thrombolysis. In addition, acidosis impairs conversion of plasminogen to plasmin and produces disassociation of the streptokinase-plasminogen complex.19
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Microvascular damage
Following epicardial occlusion, platelet and neutrophil microthrombi aggregate in the capillaries and release vasoconstrictors, resulting in microvascular spasm. Leukocytes adhere to the endothelium via selectin and integrin receptors, producing endothelial dysfunction before migrating into the myocardium to produce direct myocardial damage. Combined with myocardial oedema, these events produce an additional impedance to flow at the level of the microvasculature which persists even after the restoration of epicardial flow (the ‘no-reflow’ phenomenon).
Myocyte necrosis and ischaemic dysfunction
Failure of perfusion results in necrosis of, on average, 50% of the left ventricular myocardium, although the range is surprisingly wide (35–66%).9,20,21 Anaerobic metabolism results in accumulation of H+ ions within the myocyte, activating the Na+/H+ exchange system. This results in a net Na+ influx which in turn is removed by the Na+/Ca2+ exchanger, producing Ca2+ influx, overload, hypercontracture and death. Gap-junction-mediated communication of this calcium overload may be responsible for the characteristic wave-front progression of necrosis. However, in addition to this irreversible damage, a proportion of the myocytes will be viable but not contracting due to varying degrees of stunning (impaired function despite restoration of flow) and hibernation (impaired function due to severely impaired flow).22 Importantly, the timecourse of recovery of left ventricular myocardial function in shock (a component of which may extend over weeks23) parallels other situations where stunning occurs. This has implications for the protracted support that may be required if reperfusion were actually achieved.
Neuroendocrine responses
Meanwhile, the fall in tissue perfusion induces a compensatory neuro-endocrine activation which attempts to maintain cardiac output by myocardial stimulation and increased peripheral resistance.24 The ability of the remaining myocardium to generate a compensatory hyperkinesis25,26 in response to this neuro-endocrine activation is probably responsible for the much of the variability in the degree of myocardial damage required to produce shock9,20,21 and is particularly impaired in patients with multivessel disease.27 Progressive myocardial depression then occurs by a combination of hypotension producing infarct extension,21 the neuroendocrine activation producing direct myocardial damage20,28,29 and an inappropriately high afterload.
Reperfusion injury
Paradoxically, reperfusion is associated with a burst of free radical production, further neutrophil adhesion and complement formation.30 In addition, the restoration of free fatty acid metabolism precedes that of glucose oxidation. This further depresses intracellular pH and the potential for calcium overload via an activated Na+-H+ exchanger.31 As a result, the proportion of viable myocardium actually falls during the first 2 h of reperfusion32 and apoptotic mechanisms may be particularly prominent here.
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Management of shock due to overwhelming left ventricular damage |
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TopIntroductionDiagnosis and aetiologyPathophysiology of shock due...Management of shock due...Prospects for maximizing...ConclusionsTrials glossaryReferences |
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Attempts to improve the outcome of cardiogenic shock need to address this multi-faceted pathophysiology: circulatory support is required during restoration of reperfusion at both the macro- and microvascular levels, while at the same time attempts are made to limit ongoing myocyte necrosis and minimize reperfusion damage.
Inotropes and supportive therapies
Whilst catecholamines33,34 and other agents35 increase cardiac output acutely, there is no evidence that they improve survival. This point is underscored by the static mortality of shock during the period of increasing inotrope use.1 Indeed, the role of catecholamine excess in the pathogenesis of shock suggests that inotropes will accelerate myocardial dysfunction, due to the rapid development of ß-adrenoceptor desensitization,36 and the need for dosage escalation. Inotropes do have a role in stabilizing patients during assessment or transfer, and in situations where a reversible aetiology has been identified; however, as a treatment in isolation, they should be regarded as essentially palliative. Similar comments can be applied to the use of mechanical ventilation and haemofiltration in the absence of a remediable cause of shock. The inappropriately high peripheral resistance in cardiogenic shock has been viewed as a potential target for vasodilators, although in practice the prevailing hypotension makes these of no practical use.37
Mechanical LV assist devices and transplantation
The use of mechanical ventricular assist devices, usually as a bridge to transplantation, remains experimental. Although successful series have been published,38–40 other reports have been less encouraging.41–43 The mismatch between the numbers of patients developing cardiogenic shock and the availability of donor organs means that this will never be an option for the majority of patients.
Myocardial reperfusion
Reperfusion, either chemically or mechanically, is intuitively the rational approach to a condition caused by arterial occlusion, a fact appreciated for almost a century.44 However, for this to become a realistic option, flow must be restored at both the epicardial and microvascular levels while attempts are made to minimize myocyte injury. As a result, progress to establish reperfusion as a viable strategy has been frustratingly slow.
Thrombolysis
As the absolute benefits of successful medical treatments tend to be accentuated in high-risk subgroups of cardiovascular trials, one might predict that thrombolysis would be particularly efficacious in patients at such a high risk of death. This effect is seen up to a point in the FTT thrombolytic meta-analysis, where some of the highest absolute benefits occurred in those with a systolic BP <100 mmHg (66 lives saved per 1000) or heart rate >100/min (33 lives/100).45 Judging by their overall mortality of <35%, however, this group fell short of established cardiogenic shock and the subgroup with established shock (both BP <100 mmHg and heart rate >100/min and a 60% mortality) failed to show benefit.46 This meta-analysis defined the clinical lower limit limit of thrombolytic efficacy, where the biochemical effects of thrombolytic resistance negate the high-risk subgroup effect. This important conclusion is also apparent in the one trial to specifically include shocked patients47 and has not been altered by subsequent trials using more aggressive lytic regimens.2,48–50 Further support for the futility of thrombolysis in shock is derived from SHOCKR,7 where patients receiving thrombolysis had a similar mortality to thrombolytic-eligible patients (61%) who did not receive thrombolysis (71%, p=0.334).
Intra-aortic balloon pumping
The combination of reduced afterload, increased diastolic pressure available for coronary perfusion and improved cardiac output makes the use of an intra-aortic balloon pump (IABP) an attractive option in cardiogenic shock. Unfortunately, early experience demonstrated that although patients can frequently be stabilized, they cannot subsequently be weaned, and that the overall outlook remains unchanged.51–55 Two randomized trials have also failed to demonstrate benefit from the use of an IABP,56,57 although strictly speaking the patients enrolled fell short of the criteria for cardiogenic shock. Neither was there evidence of benefit from the use of balloon pumping in the patients developing cardiogenic shock in GUSTO-158 nor in SHOCKR once the confounding effects of cardiac catheterization had been adjusted for.58 Pooling of all of the above data still fails to demonstrate any benefit.59 There is thus no indication for IABP insertion in cardiogenic shock except in combination with more definitive treatment, or to provide stability during investigation.60
Intra-aortic balloon-pump-assisted thrombolysis
In canine models, the thrombolytic resistance encountered in shock is substantially reversed by intra-aortic balloon pumping.18,61,62 This effect is not mediated by significant increases in coronary flow, suggesting that the benefit was due to the augmentation of diastolic pressure or to a doubling of the number of pressure waves in each diastolic period. One attraction of a combination of thrombolysis and IABP (‘balloon-assisted thrombolysis’) is that it does not require transfer of patients to a regional centre or the provision of 24-h interventional facilities. Nevertheless, enthusiasm has been tempered by the potential for haemorrhagic complications: IABP insertion was an independent predictor of severe bleeding in the TAMI-1 trial of alteplase63 and of moderate bleeding in GUSTO-1.64 Surprisingly, this has not been a consistent finding65 and the availability of balloons which can be inserted through smaller puncture sizes has promoted a re-evaluation of this combination.
The clinical evidence for balloon-assisted thrombolysis is derived from three retrospective series and the prosective data from SHOCKR. In the first of these, Stomel et al.66 examined the records of 64 patients treated with either thrombolysis or IABP alone or the two in combination. Mortality was similar for patients receiving either treatment in isolation (70%) but reduced (32%) in those who receiving both. Kovak et al. have reported similar findings, with an in-hospital mortality of 93% for thrombolysis alone but 37% for balloon-assisted thrombolysis.67 Of the 21178 patients who developed cardiogenic shock in the Second National Registry of Myocardial Infarction, mortality was lower in patients receiving a combination of thrombolysis and balloon pumping when compared to thrombolysis alone (49% vs. 69%).68 Lastly, in the 857 patients in SHOCKR, the combination of IABP and thrombolysis was associated with a 46% mortality compared to 76% for patients who received neither (p<0.001), but this result was potentially confounded by younger age, earlier onset of shock and a higher frequency of revascularization in patients in the combined treatment group.69
The combination of a coherent scientific rationale combined with these encouraging studies made this a promising avenue of investigation, and the publication of the randomized TACTICS trial was eagerly awaited. Unfortunately, this has now been abandoned due to poor recruitment, and the role of balloon-assisted thrombolysis in the management of shock remains undefined. It remains worth considering if interventional facilities are not immediately available, particularly for the 10% of patients who present in shock, as only a single dose of thrombolytic is required, thus minimizing the haemorrhagic risk. A variant on this theme is the use of inotropes to increase the blood pressure transiently to a point at which thrombolysis might be effective. This is potentially a more logical use of inotropes than our current practice, and is supported by evidence from a canine model.62 To date, this has only been investigated in a small series of eight patients, of whom reperfusion was demonstrated in six,70 and the role of this approach must await further studies.
Mechanical revascularization
The information suggesting a benefit from mechanical revascularization (the majority of which relate to PTCA) can be considered in three sections: small case series, registry data and the two randomized controlled trials (Table 1).
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There were 31 small single-centre series between 1985 and 1999, involving a total of 1267 patients with an in-hospital mortality of 50% (many only available as abstracts). Although these are frequently presented as an improvement on the 90% mortality of historical controls, the small numbers of patients and the likelihood of selection bias makes interpretation difficult. What these data do confirm is that PTCA for patients in cardiogenic shock is technically feasible, but that unsuccessful PTCA carries a very high mortality. One interesting observation is that in those studies examining longer-term prognosis, the benefits of revascularization are still apparent at 6 and 12 months.71–76
The registry data is derived from the SHOCKR, Worcester, MITRA, Californian and Second National Registry studies, with additional data from the four publications relating to shock from GUSTO-1 (Figure 4). SHOCKR was first published in 1995,7 with an update in 1999,77 and now includes a total of 1380 patients. Those undergoing revascularization (which was by PTCA in 69%) had a lower mortality than those managed conservatively (41% vs. 79%). In addition, the use of revascularization increased over time, and was paralleled by a reduction in mortality in both SHOCKR and the Worcester registry.1 A similar pattern emerges in MITRA,3 the Second National Registry68 and in GUSTO-1.2,78 Importantly, the one-year follow-up data from GUSTO-1 confirm the impression from the smaller studies that the prognosis of patients who were successfully revascularized remains favourable (with 88% of those alive at 30 days surviving at one year).79 Subgroup analysis of the GUSTO-180 and GUSTO-350 data by country also reveals improved survival for the more intensively treated patients in the USA compared to elsewhere (50% vs. 66%). However, the limitations of this type of data are illustrated by the fact that those patients selected to undergo catheterization in SHOCKR had a lower mortality than those not selected (51% vs. 85%), even if they were not subsequently revascularized. Similarly, patients selected for aggressive treatment in GUSTO-1 were younger, had a lower incidence of prior infarction and a shorter time to treatment.78 Those being considered for aggressive management thus constitute a subgroup with an intrinsically favourable outlook, with the suspicion that the sickest patients either died before revascularization could be undertaken, or were rejected as being unsalvageable. The data examining mortality between countries are equally problematic, as the incidence of shock was higher in the USA and the mortality in medically-managed patients lower, further fuelling suspicion that a lower-risk population was revascularized. These studies illustrate that in a condition with a high intrinsic mortality, even small changes in inclusion characteristics can translate into marked variations in outcome—a fact that can also be inferred from the wide differences in mortality between individual studies.
Thus, despite data involving almost 27 000 patients, a definite answer remained elusive, setting the scene for the two randomized trials. The first of these, SMASH,43 enrolled 55 patients over a 4-year period in nine European centres. Virtually all of the patients in the invasive arm underwent PTCA, with only one undergoing bypass surgery. The study was terminated prematurely due to inadequate recruitment, with no significant mortality difference between the invasive and non-invasive groups (69% vs. 78%). In a small parallel registry, the differences between invasive and non-invasive groups were more marked (50% vs. 74%), again emphasizing the preselection that must have been present in previous series.
In the second of the randomized trials, SHOCKT,81 302 patients with ST elevation were randomized within 36 h of infarction and within 18 h of the onset of shock (Box 1). Strictly speaking, the comparison was between immediate revascularization (of which 64% was by PTCA) and revascularization preceded by a period of medical management (21% of patients in this latter group were subsequently revascularized). Mortality was not significantly different between the two groups at the primary end point of 30 days (47% vs. 56%), but was reduced by the secondary end-points of 6 months (50% vs. 63%, p<0.03) and 1 year (53% vs. 66%, p<0.03). Looked at optimistically, this equates with needing to treat approximately eight patients to prevent one death at 6 months, but conversely the absolute difference in numbers between the two groups is too small for this type of analysis to be meaningful (an extra five deaths in the intervention group against 10 in the medically-managed group between 30 days and 6 months). It should be noted that benefit was concentrated in those below 75 years of age, which is in accord with both prior studies and clinical experience. The caveat that the ongoing improvements in PTCA technology result in trials underestimating the benefits of intervention is frequently cited when a PTCA trial fails to deliver the expected results. Although favourable results from the use of both abciximab and stenting82,83 have been described in the context of shock, only stenting appeared to confer additional benefit in SHOCKT.84 More important perhaps was the frequent use of thrombolysis (63%) and balloon pumping (86%) in the medical therapy group, which may have attenu ated the apparent benefit from revascularization.
With the benefit of hindsight, the fundamental problem with both randomized trials is that they were underpowered, as the expectation generated by the registry studies of a 20% mortality reduction never materialized (to reliably detect the 9% difference that actually occurred would require a trial of >1000 patients). The enormous effort to randomize the 300 patients in SHOCK should not be underestimated, and there is no realistic prospect of a 1000-patient trial ever being undertaken (the HEROICS trial has been abandoned). In addition, the registry data and published opinion remind us that most major US centres now regard revascularization for cardiogenic shock as the norm.
We are thus left in the uncomfortable position of deciding whether to adopt an expensive and high-risk procedure on the basis of incomplete information. On balance, with the prospect of significantly improved survival at 6 and 12 months, the evidence favours early revascularization in selected patients, but this begs the question of what selection criteria are appropriate. Criteria based on the measurement of cardiac reserve have been proposed,85 but these are based on studies of only 28 patients, with no evidence that they can predict suitability for revascularization. The inclusion criteria for SHOCKT provide a starting point (Box 1) and shocked patients falling outside these should not be considered for revascularization, whereas patients falling within them should be discussed with a regional cardiology centre. However, many cardiologists would feel that the optimal time window for intervention is significantly less than the 18-h duration of SHOCKT and that a 10-h ceiling would be more appropriate.
However if they tell us anything at all, what these trials clearly demonstrate is that even with revascularization, mortality remains unacceptably high, and this serves to focus attention on efforts to maximize myocardial salvage once reperfusion has been achieved.
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Prospects for maximizing myocardial salvage |
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TopIntroductionDiagnosis and aetiologyPathophysiology of shock due...Management of shock due...Prospects for maximizing...ConclusionsTrials glossaryReferences |
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Attempts to improve myocardial salvage have centred on reducing platelet and neutrophil adhesion/migration whilst maximizing the ischaemic tolerance of the myocyte.
Neutrophil and platelet function
Abxicimab prevents platelet and neutrophil adhesion, and might be expected to mitigate against the no-reflow phenomenon by reducing the formation of microthrombi. There is some preliminary evidence of improved outcomes in cardiogenic shock angioplasty with the use of abciximab,86 although as noted above, this was not apparent in retrospective analysis of the SHOCK data. For the future, inhibition of leucocyte adhesion using a monoclonal antibody directed against the integrin receptor is being investigated in the HALT-MI,87 while complement inhibition has been shown to improve myocardial salvage in animal models of reperfusion.88
Myocyte protection (Figure 3)
Pharmacological attempts to mimic the powerful protection afforded by the preconditioning phenomenon using adenosine have demonstrated a reduction in infarct size,89 while its intracoronary use has been claimed to mitigate against the no-reflow phenomenon. Both nicorandil,90 an ATP-sensitive K+ channel opener, and the L-type calcium antagonist verapamil91 result in a reduction of the no-reflow zone and improved left ventricular function following angioplasty in acute MI, although the precise mechanisms underlying this remain unclear. In addition, there has been renewed interest in the use of glucose/insulin/potassium infusions, which aim to stimulate glycolytic activity whilst reducing free fatty acid consumption and consequently intracellular acidosis.92 Lastly, there is a substantial body of animal evidence to support direct inhibition of the Na+-H+ exchanger.31 Clinical experience with Na+-H+ exchanger inhibition, however, has produced conflicting results. Initial results in patients undergoing primary PTCA showed improvements in left ventricular function,93 but no evidence of benefit was apparent in a larger unselected group of patients in the GUARDIAN trial.94 These disappointing results probably reflect the need to initiate exchanger inhibition prior to the ischaemic insult—a strategy unlikely to prove viable in the context of shock.
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Thus the potential for improving myocardial salvage following reperfusion already exists, although much remains to be done before this emerges as a coherent clinical strategy.95 At present, clinical use is restricted to the use of adenosine and verapamil for angiographic no-reflow.
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Conclusions |
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TopIntroductionDiagnosis and aetiologyPathophysiology of shock due...Management of shock due...Prospects for maximizing...ConclusionsTrials glossaryReferences |
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Mortality from cardiogenic shock remains frustratingly high, while attempts to demonstrate benefit from revascularization have been fraught with difficulty. We have arrived at a point where we should accept that in shocked patients, inotropes are essentially palliative, that thrombolysis is of no value and that on balance, the evidence favours a policy of revascularization in selected patients. We still lack a sound basis on which to perform this selection. However, even with revascularization, mortality remains in excess of 50%, and in order to make further progress, our attention must now shift from the open artery to one of maximizing microvascular integrity and optimizing myocardial protection.
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Trials glossary |
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TopIntroductionDiagnosis and aetiologyPathophysiology of shock due...Management of shock due...Prospects for maximizing...ConclusionsTrials glossaryReferences |
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AMISTAD, acute myocardial infarction study of adenosine; FTT, fibrinolytic therapy trialists collaborative group; GISSI, groupo Italiano per lo studio della streptochinasi nell'infarcto miocardio; GUSTO, global utilization of streptokinase and tPA for occluded arteries; GUARDIAN, guard during ischaemia against necrosis; HEROICS, how effective are revascularization options in cardiogenic shock; INJECT, international joint efficacy comparison of thrombolytics; MILIS, multicenter investigation of limitation of infarct size; MITRA, maximal individual therapy of acute myocardial infarction; TAMI, thrombolysis and myocardial infarction; SHOCK, should we emergently revascularize occluded coronary arteries for cardiogenic shock [trial (SHOCKT) and registry (SHOCKR)]; SMASH, Swiss multicenter trial of angioplasty for shock [trial (SMASHT) and registry (SMASHR)]; TACTICS, thrombolysis and counterpulsation to improve cardiogenic shock survival (confusingly, there is also a TIMI trial in unstable angina with the same acronym).
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Notes |
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Address correspondence to Dr C.H. Davies, Department of Cardiology, Mail Code UHN 62, Oregon Health Sciences University, 3181 SW Sam Jackson Park Road, Portland, Oregon 97201–3098, USA. e-mail: daviesc{at}ohsu.edu
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References |
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TopIntroductionDiagnosis and aetiologyPathophysiology of shock due...Management of shock due...Prospects for maximizing...ConclusionsTrials glossaryReferences |
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1. Goldberg RJ, Samad NA, Yarzebski J, Gurwitz J, Bigelow, Gore JM. Temporal trends in cardiogenic shock complicating acute myocardial infarction. N Engl J Med1999; 340:1162–8.
2. Holmes DRJ, Bates ER, Kleiman NS, et al. Contemporary reperfusion therapy for cardiogenic shock: the GUSTO-I trial experience. The GUSTO-I Investigators. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries. J Am Coll Cardiol1995; 26:668–74.[Abstract]
3. Gitt AK, Schiele R, Seidl K, Glunz HJ, Limbourg P, Sengens J. Influence of recanalisation therapy on prognosis of cardiogenic shock in acute myocardial infarction in unselected patients of the MITRA-study. J Am Coll Cardiol1999; 33 (Suppl. A):375A(abstract).
4. Hands ME, Rutherford JD, Muller JE, et al. The in-hospital development of cardiogenic shock after myocardial infarction: Incidence, predictors of occurrence, outcome and prognostic factors. J Am Coll Cardiol1989; 14:40–6.[Abstract]
5. Leor J, Goldbourt U, Reicher-Reiss H, Kaplinsky E, Behar. Cardiogenic shock complicating acute myocardial infarction in patients without heart failure on admission: incidence, risk factors and outcome. SPRINT Study Group. Am J Med1993; 94:265–73.[Web of Science][Medline]
6. Hasdai D, Holmes DRJ, Califf RM, et al. Cardiogenic shock complicating acute myocardial infarction: predictors of death. GUSTO Investigators. Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries. Am Heart J1999; 138:21–31.[Web of Science][Medline]
7.
Hochman JS, Boland J, Sleeper LA, et al. Current spectrum of cardiogenic shock and effect of early revascularization on mortality. Results of an International Registry. SHOCK Registry Investigators. Circulation1995; 91:873–81.
8.
Hochman JS, Buller CE, Dzavik V, et al. Cardiogenic shock (CS) complicating acute MI-etiologies, management and outcome; Overall findings of the Shock trial registry. Circulation1998; 98 (Suppl. 1):1–778(abstract).
9.
Hanarayan C, Bennett MA, Pentecost BL, Brewer DB. Quantitative study of infarcted myocardium in cardiogenic shock. Br Heart J1970; 32:728–32.
10. Kennedy JW, Gensini GG, Timmis GC, Maynard C. Acute myocardial infarction treated with intracoronary streptokinase: a report of the Society for Cardiac Angiography. Am J Cardiol1985; 55:871–7.[Web of Science][Medline]
11.
Holmes DRJ, Berger PB, Hochman JS, et al. Cardiogenic shock in patients with acute ischaemic syndromes with and without ST segment elevation. Circulation1999; 100:2067–73.
12.
Cannon CP. Overcoming thrombolytic resistance: rationale and initial clinical experience combining thrombolytic therapy and glycoprotein IIb/IIIa receptor inhibition for acute myocardial infarction. J Am Coll Cardiol1999; 34:1395–402.
13. Becker RC. Hemodynamic, mechanical and metabolic determinants of thrombolytic efficacy: a theoretic framework for assessing the limitations of thrombolysis in patients with cardiogenic shock. Am Heart J1993; 125:919–29.[Web of Science][Medline]
14. Mueller H, Ayres SM, Conklin EF, et al. The effects of intra-aortic counterpulsation on cardiac performance and metabolism in shock associated with acute myocardial infarction. J Clin Invest1971; 50:1885–900.
15. Blinc A, Planinsic G, Keber D, et al. Dependence of blood clot lysis on the mode of transport of urokinase into the clot—a magnetic resonance imaging study in vitro. Thrombosis & Haemostasis1991; 65:549–52.[Web of Science][Medline]
16. Kornowski R, Mendelevich L, Zaretsky U, Einav S, Laniado, Keren G. Hemodynamic changes determine the efficacy of thrombolysis: results from an in-vitro flow model. Coronary Artery Dis1998; 9:43–8.[Web of Science][Medline]
17. Prewitt RM, Gu S, Garber PJ, Ducas J. Marked systemic hypotension depresses coronary thrombolysis induced by intracoronary administration of recombinant tissue-type plasminogen activator. J Am Coll Cardiol1992; 20:1626–33.[Abstract]
18.
Gurbel PA, Anderson RD, MacCord CS, et al. Arterial diastolic pressure augmentation by intraaortic balloon counterpulsation enhances the onset of coronary artery reperfusion by thrombolytic therapy. Circulation1994; 89:361–5.
19.
Wohl RC, Summaria L, Robbins KC. Kinetics of activation of human plasminogen by different activator species at pH 7.4 and 37 degrees C. J Biol Chem1980; 255:2005–13.
20. Page DL, Caufield JB, Kastor JA, DeSanctis RW, Saunders CA. Myocardial changes associated with cardiogenic shock. N Engl J Med1971; 285:133–7.
21.
Alonso DR, Scheidt S, Post M, Killip T. Pathophysiology of cardiogenic shock: Quantitation of myocardial necrosis, clinical, pathologic and electrocardiographic correlations. Circulation1973; 48:588–96.
22.
Kloner RA, Bolli R, Marban E, Reinlib L, Braunwald E. Medical and cellular implications of stunning, hibernation, and preconditioning: an NHLBI workshop. Circulation1998; 97:1848–67.
23.
Bowers TR, O'Neill WW, Grines C, Pica MC, Safian RD, Goldstein JA. Effect of reperfusion on biventricular function and survival after right ventricular infarction. N Engl J Med1998; 338:933–40.
24.
Benedict CR, Grahame-Smith DG. Plasma adrenaline and noradrenaline concentrations and dopamine-beta-hydroxylase activity in myocardial infarction with and without cardiogenic shock. Br Heart J1979; 42:214–20.
25. Widimsky P, Gregor P, Cervenka V, et al. Severe diffuse hypokinesis of the remote myocardium—the main cause of cardiogenic shock? An echocardiographic study of 75 patients with extremely large myocardial infarctions. Cor et Vasa1988; 30:27–34.[Web of Science][Medline]
26. Gibson RS, Bishop HL, Stamm RB, Crampton RS, Beller GA, Martin RP. Value of early two dimensional echocardiography in patients with acute myocardial infarction. Am J Cardiol1982; 49:1110–19.[Web of Science][Medline]
27.
Grines CL, Topol EJ, Califf RM, et al. Prognostic implications and predictors of enhanced regional wall motion of the noninfarct zone after thrombolysis and angioplasty of acute myocardial infarction. Circulation1989; 80:245–53.
28. Yates JC, Beamish RE, Dhalla NS. Ventricular dysfunction and necrosis produced by adrenochrome metabolite of epinephrine: relation to pathogenesis of catecholamine cardiomyopathy. Am Heart J1981; 102:210–21.[Web of Science][Medline]
29. Van Vliet PD, Burchell HB, Titus JL. Focal myocarditis associated with pheochromocytoma. N Engl J Med1966; 274:1102–8.
30. Ambrosio G, Tritto I. Reperfusion injury: experimental evidence and clinical implications. Am Heart J1999; 138:69–75.[Web of Science][Medline]
31. Avkiran M. Rational basis for use of sodium-hydrogen exchange inhibitors in myocardial ischemia. Am J Cardiol1999; 83:10–17G.
32.
Matsumura K, Jeremy RW, Schaper J, Becker LC. Progression of myocardial necrosis during reperfusion of ischemic myocardium [see comments]. Circulation1998; 97:795–804.
33. Gillespie TA, Ambos HD, Sobel BE, Roberts R. Effects of dobutamine in patients with acute myocardial infarction. Am J Cardiol1977; 39:588–94.[Web of Science][Medline]
34.
Richard C, Ricome JL, Rimailho A, Bottineau G, Auzepy P. Combined hemodynamic effects of dopamine and dobutamine in cardiogenic shock. Circulation1983; 67:620–6.
35.
Gage J, Rutman H, Lucido D, LeJemtel TH. Additive effects of dobutamine and amrinone on myocardial contractility and ventricular performance in patients with severe heart failure. Circulation1986; 74:367–73.
36. Harding SE, Brown LA, Wynne DG, Davies CH, Poole-Wilson PA. Mechanisms of beta-adrenoceptor desensitisation in the failing human heart. Cardiovasc Res1994; 28:1451–60.[Web of Science][Medline]
37. Keung EC, Ribner HS, Schwartz W, Sonnenblick EH, LeJemtel TH. Effects of combined dopamine and nitroprusside therapy in patients with severe pump failure and hypotension complicating acute myocardial infarction. J Cardiovasc Pharmacol1980; 2:113–19.[Web of Science][Medline]
38. Hendry PJ, Masters RJ, Mussivand TV, Davies RA, Finlay S, Keon WJ. Circulatory support for cardiogenic shock due to acute myocardial infarction: a Canadian experience. Canadian Journal of Cardiology1999; 10:1090–4.
39.
Champagnac D, Claudel JP, Chevalier P, et al. Primary cardiogenic shock during acute myocardial infarction: results of emergency cardiac transplantation. Eur Heart J1993; 14:925–9.
40. Overlie PA, Shawl FA, George BS, et al. Cardiogenic shock: survival rates from the national registry for emergency cardiopulmonary bypass investigators. J Am Coll Cardiol1997; 29:398A(abstract).
41. Boehemer JP, Pae WP, Silber D, Christenson D, Sun BC. Poor outcome with left ventricular assist devices as a bridge to transplant following myocardial infarction with cardiogenic shock. J Am Coll Cardiol1999; 33:208A (abstract).
42. Gacioch GM, Ellis SG, Lee L, et al. Cardiogenic shock complicating acute myocardial infarction: the use of coronary angioplasty and the integration of the new support devices into patient management. J Am Coll Cardiol1992; 19:647–53.[Abstract]
43.
Urban P, Stauffer JC, Bleed D, et al. A randomized evaluation of early revascularization to treat shock complicating acute myocardial infarction. The (Swiss) Multicenter Trial of Angioplasty for Shock-(S)MASH. Eur Heart J1999; 20:1030–8.
44. Herrick JB. Clinical features of sudden obstruction of the coronary arteries. JAMA1912; 59:2015–20(abstract).
45. FTT Collaborative Group. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group. Lancet1994; 343:311–22.[Web of Science][Medline]
46.
White HD, Van de Werf FJ. Thrombolysis for acute myocardial infarction. Circulation1998; 97:1632–46.
47. Anonymous. Long-term effects of intravenous thrombolysis in acute myocardial infarction: final report of the GISSI study. Gruppo Italiano per lo Studio della Streptochi-nasi nell’Infarto Miocardico (GISSI). Lancet1987; 2:871–4.[Medline]
48.
Anonymous. Six-month survival in 20 891 patients with acute myocardial infarction randomized between alteplase and streptokinase with or without heparin. GISSI-2 and International Study Group. Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto. Eur Heart J1992; 13:1692–7.
49. AnonymousRandomised, double-blind comparison of reteplase double-bolus administration with streptokinase in acute myocardial infarction (INJECT): trial to investigate equivalence. International Joint Efficacy Comparison of Thrombolytics. Lancet1995; 346:329–36.[Web of Science][Medline]
50.
Hasdai D, Holmes DRJ, Topol EJ, et al. Frequency and clinical outcome of cardiogenic shock during acute myocardial infarction among patients receiving reteplase or alteplase. Results from GUSTO-III. Global Use of Strategies to Open Occluded Coronary Arteries. Eur Heart J1999; 20:128–35.
51. Scheidt S, Wilner G, Mueller H, et al. Intra-aortic balloon counterpulsation in cardiogenic shock. Report of a co-operative clinical trial. N Engl J Med1973; 288:979–84.
52.
DeWood MA, Notske RN, Hensley GR, et al. Intraaortic balloon counterpulsation with and without reperfusion for myocardial infarction shock. Circulation1980; 61:1150–12.
53. Willerson JT, Curry GC, Watson JT, et al. Intraaortic balloon counterpulsation in patients in cardiogenic shock, medically refractory left ventricular failure and/or recurrent ventricular tachycardia. Am J Med1975; 58:183–91.[Web of Science][Medline]
54. Hagemeijer F, Laird JD, Haalebos MM, Hugenholtz PG. Effectiveness of intraaortic balloon pumping without cardiac surgery for patients with severe heart failure secondary to a recent myocardial infarction. Am J Cardiol1997; 40:951–6.
55. Goldberger M, Tabak SW, Shah PK. Clinical experience with intra-aortic balloon counterpulsation in 112 consecutive patients. Am Heart J1986; 111:497–502.[Web of Science][Medline]
56. O'Rourke MF, Norris RM, Campbell TJ, Chang VP, Sammel NL. Randomized controlled trial of intraaortic balloon counterpulsation in early myocardial infarction with acute heart failure. Am J Cardiol1981; 47:815–20.[Web of Science][Medline]
57. Flaherty JT, Becker LC, Weiss JL, et al. Results of a randomized prospective trial of intraaortic balloon counterpulsation and intravenous nitroglycerin in patients with acute myocardial infarction. J Am Coll Cardiol1985; 6:434–46.[Abstract]
58. Anderson RD, Ohman EM, Holmes DRJ, et al. Use of intraaortic balloon counterpulsation in patients presenting with cardiogenic shock: observations from the GUSTO-I Study. Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries. J Am Coll Cardiol1997; 30:708–15.[Abstract]
59. Bates ER, Stomel RJ, Hochman JS, Ohman EM. The use of intraaortic balloon counterpulsation an adjunct to reperfusion therapy in cardiogenic shock. Int J Cardiol1998; 65 (Suppl. 1):S37–42.
60. Brodie BR, Stuckey TD, Hansen C, Muncy D. Intra-aortic balloon counterpulsation before primary percutaneous transluminal coronary angioplasty reduces catheterization laboratory events in high-risk patients with acute myocardial infarction. Am J Cardiol1999; 84:18–23.[Web of Science][Medline]
61. Prewitt RM, Gu S, Schick U, Ducas J. Intraaortic balloon counterpulsation enhances coronary thrombolysis induced by intravenous administration of a thrombolytic agent. J Am Coll Cardiol1994; 23:794–8.[Abstract]
62.
Prewitt RM, Gu S, Schick U, Ducas J. Effect of a mechanical vs a pharmacologic increase in aortic pressure on coronary blood flow and thrombolysis induced by IV administration of a thrombolytic agent. Chest1997; 111:449–53.
63. Ohman EM, Califf RM, George BS, et al. The use of intraaortic balloon pumping as an adjunct to reperfusion therapy in acute myocardial infarction. The Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) Study Group. Am Heart J1991; 121:895–901.[Web of Science][Medline]
64.
Berkowitz SD, Granger CB, Pieper KS, et al. Incidence and predictors of bleeding after contemporary thrombolytic therapy for myocardial infarction. The Global Utilization of Streptokinase and Tissue Plasminogen activator for Occluded coronary arteries (GUSTO) I Investigators. Circulation1997; 95:2508–16.
65. Goodwin M, Hartmann J, McKeever L, et al. Safety of intraaortic balloon counterpulsation in patients with acute myocardial infarction receiving streptokinase intravenously. Am J Cardiol1989; 64:937–8.[Web of Science][Medline]
66.
Stomel RJ, Rasak M, Bates ER. Treatment strategies for acute myocardial infarction complicated by cardiogenic shock in a community hospital. Chest1994; 105:997–1002.
67. Kovack PJ, Rasak MA, Bates ER, Ohman EM, Stomel RJ. Thrombolysis plus aortic counterpulsation: improved survival in patients who present to community hospitals with cardiogenic shock. J Am Coll Cardiol1997; 29:1454–8.[Abstract]
68. Barron HV, Pizarda SR, Lomnitz DJ, Every NR, Gore JM, Chou TM. Use of intra-aortic balloon counterpulsation in patients with acute myocardial infarction complicated by cardiogenic shock. J Am Coll Cardiol1998; 31:135A(abstract).
69. Sanborn T, Sleeper L, Webb JG, et al. Impact of thrombolysis, aortic balloon counterpulsation and their combination in cardiogenic shock: The SHOCK trial registry. Circulation1998; 98 (Suppl. 1):1–778(abstract).
70. Garber PJ, Mathieson AL, Ducas J, Patton JN, Geddes JS, Prewitt RM. Thrombolytic therapy in cardiogenic shock: effect of increased aortic pressure and rapid tPA administration. Canad J Cardiol1995; 11:30–6.
71. Moosvi AR, Khaja F, Villanueva L, Gheorghiade M, Douthat, Goldstein S. Early revascularization improves survival in cardiogenic shock complicating acute myocardial infarction. J Am Coll Cardiol1992; 19:907–14.[Abstract]
72. Hibbard MD, Holmes DRJ, Bailey KR, Reeder GS, Bresnahan JF, Gersh BJ. Percutaneous transluminal coronary angioplasty in patients with cardiogenic shock. J Am Coll Cardiol1992; 19:639–46.[Abstract]
73. Yamamoto H, Hayashi Y, Oka Y, et al. Efficacy of percutaneous transluminal coronary angioplasty in patients with acute myocardial infarction complicated by cardiogenic shock. Japan Circ J1992; 56:815–21.[Medline]
74.
Antoniucci D, Valenti R, Santoro GM, et al. Systematic direct angioplasty and stent-supported direct angioplasty therapy for cardiogenic shock complicating acute myocardial infarction: in-hospital and long-term survival. J Am Coll Cardiol1998; 31:294–300.
75. Laney PJ, Dell’Italia LJ, Brooks RS, et al. Follow-up exercise function in patients presenting with cardiogenic shock and acute transmural myocardial infarction. J Am Coll Cardiol1993; 21:77A(abstract).
76. Stack RS, Califf RM, Hinohara T, et al. Survival and cardiac event rates in the first year after emergency coronary angioplasty for acute myocardial infarction. J Am Coll Cardiol1988; 11:1141–9.[Abstract]
77. Carnendran L, Gurunathan R, Webb J, et al. Trends in cardiogenic shock: Report from the SHOCK trial registry. J Am Coll Cardiol1999; 33:366A(abstract).
78.
Berger PB, Holmes DR, Jr., Stebbins AL, Bates ER, Califf RM, Topol EJ. Impact of an aggressive invasive catheterization and revascularization strategy on mortality in patients with cardiogenic shock in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) trial. An observational study. Circulation1997; 96:122–7.
79.
Berger PB, Tuttle RH, Holmes DR, et al. One-year survival among patients with acute myocardial infarction complicated by cardiogenic shock, and its relation to early revascularisation. Results from GUSTO-1. Circulation1999; 99:873–8.
80. Holmes DR, Califf RM, Van de Werf F, et al. Differences in countries’ use of resources and clinical outcome for patients with cardiogenic shock after myocardial infarction: results from the GUSTO trial. Lancet1997; 349:75–8.[Web of Science][Medline]
81.
Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med1999; 341:625–34; and Hochman JS, Sleeper LA, White HD, et al. J Am Med Assn 2001; 285:190–2.
82. Giri S, Kiernan FJ, Mitchell JF, et al. Synergistic interaction between intracoronary stenting and IIb/IIIa inhibition for improving clinical outcomes in primary angioplasty for cardiogenic shock. Circulation1999; 100:1–380(abstract).
83. Silva JA, Nunez E, Vivekanathan K, et al. Cardiogenic shock complicating acute myocardial infarction: A comparison of primary angioplasty versus primary stenting in in-hospital outcomes. J Am Coll Cardiol1999; 33(Suppl. A):368A (abstract).
84. Webb JG, Sanborn TA, Carere RG, et al. Coronary stenting in the SHOCK trial. Circulation1999; 100(Suppl. 1):1–87(abstract).
85.
Tan LB, Littler WA. Measurement of cardiac reserve in cardiogenic shock: implications for prognosis and management. Br Heart J1990; 64:121–8.
86. Giri S, Mitchell JF, Kiernan FJ, et al. Adjunctive use of abciximab improves clinical outcomes in acute myocardial infarction patients presenting with cardiogenic shock. J Am Coll Cardiol1999; 23:12A(abstract).
87. Faxon DP, Gibbons RJ, Chronos NA, Gurbel PA, Martin JS. The effect of a CD11/CD18 inhibitor (Hu23F2G) on infarct size following direct angioplasty: The HALT MI study. Circulation1999;100(Suppl. 1):1–791.
88.
Lazar HL, Bao Y, Gaudiani J, Rivers S, Marsh H. Total complement inhibition: an effective strategy to limit ischemic injury during coronary revascularization on cardiopulmonary bypass. Circulation1999; 100:1438–42.
89.
Mahaffey KW, Puma JA, Barbagelata A, et al. Adenosine as an adjunct to thrombolytic therapy for acute myocardial infarction. J Am Coll Cardiol1999; 34:1711–20.
90.
Ito H, Taniyama Y, Iwakura K, et al. Intravenous nicorandil can preserve microvascular integrity and myocardial viability in patients with reperfused anterior wall myocardial infarction. J Am Coll Cardiol1999; 33:654–60.
91. Taniyama Y, Ito H, Iwakura K, et al. Beneficial effect of intracoronary verapamil on microvascular and myocardial salvage in patients with acute myocardial infarction. J Am Coll Cardiol1997; 30:1193–9.[Abstract]
92.
Apstein CS. Glucose-insulin-potassium for acute myocardial infarction: remarkable results from a new prospective, randomized trial [editorial]. [Review] [27 refs]. Circulation1998; 98:2223–6.
93. Buerke M, Rupprecht HJ, vom Dahl J, et al. Sodium-hydrogen exchange inhibition: novel strategy to prevent myocardial injury following ischaemia and reperfusion. Am J Cardiol1999; 83:19–22G.
94. Erhardt LR. GUARD During Ischemia Against Necrosis (GUARDIAN) trial in acute coronary syndromes. Am J Cardiol1999; 83:23–5G.
95.
Yellon DM, Baxter GF. Protecting the ischaemic and reperfused myocardium in acute myocardial infarction: distant dream or near reality?. Heart2000; 83:381–7.
96. Edep ME, Brown DL. Effect of early revascularisation on mortality from cardiogenic shock complicating acute myocardial infarction. Am J Cardiol2000; 85:1185–8.[Web of Science][Medline]
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