Mortality in patients with acute myocardial infarction has declined substantially with the introduction of very early and effective reperfusion.
1
However, cardiogenic shock (CS) remains the most common cause of death in patients with acute myocardial infarction.2
In the era of primary coronary angioplasty for acute myocardial infarction, the incidence of CS has declined,3
yet it still occurs in 5% to 8% of patients and has a mortality of approximately 50%.4
Left ventricular failure is the cause in the majority of patients who develop CS, and the myocardial damage that initiates CS is usually, but not necessarily, severe.5
CS is end-organ hypoperfusion due to cardiac failure and is recognized by the development of hypotension (systolic blood pressure [BP] < 80-90 mm Hg), a severe reduction of cardiac output (cardiac index < 1.8 L/min/m2), and evidence of organ hypoperfusion (cool peripheries, low urine output, and clouded sensorium). A reflex tachycardia usually accompanies CS. In the Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries (GUSTO) study,
6
CS developed an average of 12 hours after enrollment in the study in ST-segment elevation myocardial infarction (STEMI) patients who were not considered to have CS at the time of their initial assessment. Some of the patients who developed CS may have had subclinical shock with a low BP at the time of presentation yet no signs of organ hypoperfusion. Iatrogenic CS may have developed in patients from the administration of β-blockers or angiotensin-converting enzyme inhibitors or because of overzealous diuresis. Further coronary ischemic events with extension of myocardial injury might have been responsible in others. Recognition of the patient with subclinical shock is important as appropriate measures may prevent the development of full-blown CS, with its dire prognosis.In the current issue of the Canadian Journal of Cardiology, Bilkova and colleagues describe an analysis of 644 patients with STEMI undergoing primary percutaneous coronary intervention (PCI) in 92% and rescue PCI in 7%.
7
Independent predictors of mortality in this cohort were the shock index (heart rate divided by systolic BP at hospital admission), age, and a history of diabetes. Those with a shock index ≥ 0.8 had a 20% in-hospital mortality, whereas the group with a shock index < 0.8 had a 4% mortality. With the use of a value of 0.8 to predict early mortality, the shock index was 75% sensitive and 61% specific.The Thrombolysis in Myocardial Infarction (TIMI) group, in the fibrinolytic era, devised a score to predict mortality.
8
Ten variables accounted for 97% of the predictive model. The model was externally validated in an external data set and shown to have similar predictive accuracy. The TIMI score for STEMI has a 40-fold range in mortality, from 0.8% with a score of 0 and 36% with a score of > 8. Systolic BP < 100 mm Hg and heart rate > 100 beats per minute contributed to the score (3 and 2 points, respectively) in similar amounts as age did (65-74 years, 2 points; > 75 years, 3 points). Other risk factors, such as time to treatment > 4 hours, anterior MI or left bundle-branch block, weight < 67 kg, as well as a history of diabetes, hypertension, or angina, contributed only 1 point each. Subsequently Morrow9
devised a simple risk index, [heart rate × (age/10)2]/systolic BP, that was proposed to be useful in simplifying initial risk assessment and guiding early clinical decision making. However, further assessment of the risk index in a community-based cohort10
showed it to have poor discrimination (c = 0.62) and calibration. This analysis emphasized the need to validate prognostic scores in community-based cohorts before the score is integrated into clinical practice.The GUSTO group devised a simple scoring system to predict the development of CS.
11
The parameters shown to independently predict the development of CS were age, systolic BP, heart rate, and Killip class. In a validation cohort, these 4 variables accounted for 95% of the predictive information for the development of shock, which is a major predictor of early mortality.The study by Bilkova et al.
7
also describes a simple shock index to predict in-hospital mortality that includes only systolic BP and heart rate, despite age and a history of diabetes also being independently predictive. The analysis provides no indication of the discrimination power or calibration of this index. However, the index is modestly sensitive (75%) and poorly specific (60%) for the prediction of early mortality. Furthermore, there is no comparison of the effectiveness of the shock index to other prognostic indices, such as TIMI STEMI, GUSTO shock, or the Global Registry of Acute Coronary Events (GRACE). Although the index was derived in a community-based population, it should not be applied clinically until an external validation study is performed and clear estimates of the discrimination and calibration are provided.How should we apply a reliable prognostic index in the early management of patients with acute myocardial infarction? The study by Bilkova et al.
7
suggests that patients with a high shock index should be transferred immediately to a primary PCI centre without any comment on transfer time. In general, early effective revascularization performed within a short time-frame after symptom onset reduces mortality, especially in high-risk patients with acute myocardial infarction. However, when it is likely that there will be an excessive time delay before primary PCI can be performed, it is recommended that fibrinolysis be administered immediately to high-risk patients and the patient then be transferred for PCI.12
Whether delayed primary PCI has a greater benefit than immediate fibrinolysis in this population is controversial. In patients at an especially high risk, with TIMI scores of > 7, thrombolysis did not appear to be beneficial compared with placebo.- Welsh R.C.
- Travers A.
- Huynh T.
- Cantor W.J.
Canadian Cardiovascular Society Working Group: providing a perspective on the 2007 focused update of the American College of Cardiology and American Heart Association 2004 guidelines for the management of ST elevation myocardial infarction.
Can J Cardiol. 2009; 25: 25-32
13
Yet the Danish Trial in Acute Myocardial Infarction-2 (DANAMI 2) showed that primary PCI did not prevent the development of CS complicating acute MI, compared with fibrinolysis.14
Patients with acute myocardial infarction who have a low BP and high heart rate are at risk of developing CS and have a high early mortality. Although early effective revascularization must remain the most important therapeutic goal, the use an intra-aortic counterpulsation balloon pump may provide hemodynamic support to allow the severely ischemic myocardium to recover. No clinical trial has proven this hypothesis. In patients with established CS, there has been a trend toward multivessel primary PCI, despite guideline recommendations indicating that a staged procedure following PCI of the infarct related artery is preferable.
15
However, no guideline or study has suggested any benefit from such an approach in patients at risk of developing CS.Prevention of iatrogenic CS by avoidance of the use of β-blockers and angiotensin-converting enzyme inhibitors in the very early management of high-risk patients with relative hypotension and tachycardia is important. The Clopidogrel and Metoprolol in Myocardial Infarction Trial (COMMIT)
16
showed that early β-blockade use in patients with acute myocardial infarction had no impact on mortality, reduced the risk of reinfarction and life-threatening arrhythmias, yet increased the incidence of CS, especially in patients with Killip class II and III at entry. In patients with established CS, “complete revascularization,” with primary PCI of stenosed arteries other than the culprit vessel, is recommended. However, no study or recommendation has suggested any benefit from such an approach in patients at risk of developing CS.Beware the patient with recent infarction and both sinus tachycardia and a low BP. However, before we start using a new, simplified risk index to change management, we need to be sure that it has been externally validated in the population in which we wish to apply the tool. Furthermore, we need to know that the tool adds value to existing validated indices (eg, Killip class and TIMI risk score), as simpler is not always better.
Disclosures
The author has no conflicts of interest to disclose.
References
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- A simple risk index for rapid initial triage of patients with ST-elevation myocardial infarction: an InTIME II substudy.Lancet. 2001; 358: 1571-1575
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- Canadian Cardiovascular Society Working Group: providing a perspective on the 2007 focused update of the American College of Cardiology and American Heart Association 2004 guidelines for the management of ST elevation myocardial infarction.Can J Cardiol. 2009; 25: 25-32
- Application of the TIMI risk score for ST-elevation MI in the National Registry of Myocardial Infarction 3.JAMA. 2001; 286: 1356-1359
- Percutaneous coronary intervention for acute MI does not prevent in-hospital development of cardiogenic shock compared to fibrinolysis.Eur J Heart Fail. 2008; 10: 668-674
- ACC/AHA guidelines for the management of patients with ST elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.Circulation. 2004; 110: 588-636
- Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial.Lancet. 2005; 366: 1622-1632
Article info
Publication history
Published online: September 26, 2011
Accepted:
August 2,
2011
Received:
August 2,
2011
Footnotes
See article by Bilkova et al., pages 739-742 in this issue.
See page 676 for disclosure information.
Identification
Copyright
© 2011 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
