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Communications to the Editor |

Cardiogenic ShockCardiogenic Shock FREE TO VIEW

Francisco José Munoz, MD; Boban Thomas, MD, FCCP
Author and Funding Information

Affiliations: Hospital Fernando Fonseca, Amadora, Portugal,  Free University of Brussels, Brussels, Belgium

Correspondence to: Boban Thomas, MD, FCCP, Av Almirante Gago Coutinho, 101, 2 A Dto, 1700–029 Lisbon, Portugal; e-mail: boban_thomas@lycos.com.



Chest. 2004;126(1):312-313. doi:10.1378/chest.126.1.312
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To the Editor:

We wish to clarify a few points in the data presented by Lim and colleagues (November 2003).1Eighteen patients presented with acute myocardial infarction that developed into cardiogenic shock (CS). No mention is made about the method of reperfusion or revascularization, information that is absolutely essential in light of the findings of the Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock (SHOCK) trial.2An institutional protocol that uses intra-aortic balloon pumps (IABPs) only in those patients with refractory CS, despite the use of therapy with vasopressors, is not dispensing state-of-the art care to patients with CS. While the benefit of therapy with vasopressors on outcome in patients with CS is doubtful, a survival benefit is evident in patients who are supported with an IABP, and this is included in the current American College of Cardiology/American Heart Association guidelines. Data from the SHOCK trial and Registry demonstrated that the reversal of systemic hypoperfusion following IABP therapy is associated with improved 30-day survival, independent of early revascularization.3

Hochman also has proposed alterations to the current model and has suggested expanding the paradigm in a recent review.4 Large myocardial infarctions that are complicated by CS may be accompanied by a substantial inflammatory response with the release of various mediators, including cytokines, leading to high levels of nitric oxide and peroxynitrite with deleterious effects. A nitric oxide synthase inhibitor will be utilized in the SHOCK-2 trial to test this hypothesis.

A recent concept introduced into the lexicon of shock terminology is the cardiac power output. This parameter is calculated by multiplying the mean arterial pressure by the cardiac output. This parameter was found on multivariate analysis to be the single hemodynamic factor associated with in-hospital mortality among patients in the SHOCK Registry.5 It would be interesting to know whether Lim and colleagues will confirm this finding in their cohort of patients as they have data on the mean arterial pressure and CO for each patient.

Lim, N, Dubois, M-J, De Backer, D, et al (2003) Do all nonsurvivors of cardiogenic shock die with a low cardiac index?Chest124,1885-1891. [CrossRef] [PubMed]
 
Hochman, J, Sleeper, L, Webb, J, et al Early revascularization in acute myocardial infarction complicated by cardiogenic shock.N Engl J Med1999;341,625-634. [CrossRef] [PubMed]
 
Ramanathan, K, Cosmi, J, Harkness, SM, et al Reversal of systemic hypoperfusion following intra-aortic balloon pumping is associated with improved 30-day survival independent of early revascularization in cardiogenic shock complicating acute myocardial infarction [abstract]. Circulation. 2003;;108 ,.:3059. [CrossRef] [PubMed]
 
Hochman, JS Cardiogenic shock complicating acute myocardial infarction: expanding the paradigm.Circulation2003;107,2998-3002. [CrossRef] [PubMed]
 
Cotter, G, Finke, R, Lowe, AM, et al Cardiac power output is the strongest hemodynamic predictor of in-hospital mortality: a report from the SHOCK Trial Registry [abstract]. Circulation. 2003;;108 ,.:2458
 

Cardiogenic Shock

To the Editor:

We thank Drs. Munoz and Thomas for their comments on our article. Indeed, the 18 patients with acute myocardial infarction whose conditions evolved into cardiogenic shock were treated according to the guidelines that were in effect at the time of the study. The patients were admitted to the hospital in one of the following three ways: (1) most were revascularized using percutaneous angioplasty unless coronary angiography disclosed diffuse and/or distal lesions; (2) several patients developed shock a few days after apparently successful thrombolysis; and (3) a small groups of patients did not receive any revascularization intervention due to the long delay between the onset of symptoms and hospital admission. All patients were treated with antiplatelet agents and heparin. Intra-aortic balloon counterpulsation was used when possible, but this procedure was contraindicated in some patients (in more nonsurvivors than survivors). These factors do not invalidate our findings, as the aim of the study was to describe the hemodynamic evolution of nonsurvivors, regardless of the results of any revascularization procedure they may have received. Nine of the 23 nonsurviving patients developed hyperdynamic shock, suggesting that pump failure was not the primary cause of death. As both BP and cardiac output were relatively preserved, cardiac power was not significantly decreased in these patients.

Finally, we agree, and indeed discussed briefly in our article, that nitric oxide and peroxynitrite may be involved in this process. It will be interesting to see the results of the SHOCK-2 trial.


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References

Lim, N, Dubois, M-J, De Backer, D, et al (2003) Do all nonsurvivors of cardiogenic shock die with a low cardiac index?Chest124,1885-1891. [CrossRef] [PubMed]
 
Hochman, J, Sleeper, L, Webb, J, et al Early revascularization in acute myocardial infarction complicated by cardiogenic shock.N Engl J Med1999;341,625-634. [CrossRef] [PubMed]
 
Ramanathan, K, Cosmi, J, Harkness, SM, et al Reversal of systemic hypoperfusion following intra-aortic balloon pumping is associated with improved 30-day survival independent of early revascularization in cardiogenic shock complicating acute myocardial infarction [abstract]. Circulation. 2003;;108 ,.:3059. [CrossRef] [PubMed]
 
Hochman, JS Cardiogenic shock complicating acute myocardial infarction: expanding the paradigm.Circulation2003;107,2998-3002. [CrossRef] [PubMed]
 
Cotter, G, Finke, R, Lowe, AM, et al Cardiac power output is the strongest hemodynamic predictor of in-hospital mortality: a report from the SHOCK Trial Registry [abstract]. Circulation. 2003;;108 ,.:2458
 
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