Document Detail

Myocardial infarction on the ICU: can we do better?
Jump to Full Text
MedLine Citation:
PMID:  18394186     Owner:  NLM     Status:  MEDLINE    
Myocardial infarction remains a major cause of death despite contemporary therapeutic strategies. Diagnosis in the intensive care unit is challenging, but is essential to target therapy accurately. In this issue of Critical Care Lim and colleagues present the results of a prospective non-interventional screening study for acute myocardial infarction in patients admitted to the intensive care unit. Myocardial infarction is observed to occur frequently, often without being clinically apparent, with a high associated mortality. Such approaches may facilitate accurate diagnosis of myocardial infarction in this setting, hence opening the way to improved therapy.
Ian Webb; James Coutts
Related Documents :
8279356 - Expanding indications for thrombolytic therapy in acute myocardial infarction. how late...
2468836 - Beta-blockade in myocardial ischemia: acute interventions in myocardial infarction.
8942226 - Causes of death from myocardial infarction before and after thrombolysis era: a patholo...
14694276 - Biochemical changes and inflammatory response as markers for brain ischaemia: molecular...
23640146 - Hyperkalemia and ventricular tachycardia after outpatient ureteral valve reimplantation...
18377526 - Evaluation of right ventricular fibrosis in adult congenital heart disease using gadoli...
Publication Detail:
Type:  Journal Article     Date:  2008-04-03
Journal Detail:
Title:  Critical care (London, England)     Volume:  12     ISSN:  1466-609X     ISO Abbreviation:  Crit Care     Publication Date:  2008  
Date Detail:
Created Date:  2008-06-30     Completed Date:  2008-10-20     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  9801902     Medline TA:  Crit Care     Country:  England    
Other Details:
Languages:  eng     Pagination:  129     Citation Subset:  IM    
Department of Cardiology, St Thomas' Hospital, Guys and St Thomas' NHS Foundation Trust, London, SE1 7EH, UK.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Biological Markers / blood
Critical Illness*
Hospital Mortality
Intensive Care Units
Middle Aged
Myocardial Infarction / blood,  diagnosis*,  epidemiology
Outcome and Process Assessment (Health Care)
Troponin / blood*
Reg. No./Substance:
0/Biological Markers; 0/Troponin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Full Text
Journal Information
Journal ID (nlm-ta): Crit Care
ISSN: 1364-8535
ISSN: 1466-609X
Publisher: BioMed Central
Article Information
Download PDF
Copyright ? 2008 BioMed Central Ltd
Print publication date: Year: 2008
Electronic publication date: Day: 3 Month: 4 Year: 2008
Volume: 12 Issue: 2
First Page: 129 Last Page: 129
ID: 2447569
Publisher Id: cc6832
PubMed Id: 18394186
DOI: 10.1186/cc6832

Myocardial infarction on the ICU: can we do better?
Ian Webb1
James Coutts1 Email:
1Department of Cardiology, St Thomas' Hospital, Guys and St Thomas' NHS Foundation Trust, London, SE1 7EH, UK

Myocardial infarction (MI) in the critically ill presents a diagnostic challenge to the physician and is associated with a particularly adverse outcome for the patient [1]. Such patients have high metabolic demands and are often subject to sustained adverse physiology. Typical signs and symptoms can be difficult to elicit and surrogate physiological markers of impaired coronary perfusion masked or misinterpreted in the context of the index pathology. Cardiac troponin measurements and the 12-lead echocardiogram (ECG) remain sensitive in this setting, but specificity decreases, resulting in diagnostic uncertainty.

Recent consensus guidelines from the European Society of Cardiology, American College of Cardiology Foundation, American Heart Association and World Heart Federation emphasise the role of cardiac biomarkers in defining MI [2]. Diagnosis requires a rise and/or fall in serum levels (preferably troponin) together with evidence of myocardial ischaemia defined: clinically by patient history; electrocardiographically (new ST-T wave changes, new left bundle branch block or evolving pathological Q waves); or by imaging evidence of new regional wall motion abnormality.

Current troponin assays provide a highly sensitive marker of even microscopic levels of myocardial necrosis [3]. This does not define the mechanism of injury, however, and troponin elevation is reported in a variety of non-acute coronary syndrome (non-ACS) pathologies common in the intensive care unit (ICU), including pulmonary embolus, severe sepsis and renal impairment [4,5]. All-cause mortality and duration of ICU admission are increased in critically ill patients with elevated troponin, irrespective of the cause. Lim and colleagues [6] have previously reported on a meta-analysis of 20 studies with 3,278 general ICU patients, where the median incidence of troponin-positivity was 43%. This was associated in an adjusted analysis of 6 of these studies (1,706 patients) with a significant increase in mortality (odds ratio of dying 2.5, 95% confidence interval (CI) 1.9 to 3.4; p < 0.001), and in a further unadjusted analysis of 8 of these studies (1,019 patients) with an increase in ICU stay (3 days, 95% CI 1 to 5.1, p = 0.004) and a trend towards longer overall hospital admission (2.2 days, 95% CI -0.6 to 4.9; p = 0.12). Whether the adverse outcome was due to concomitant ACS, or the severity of the index condition, resulting in troponin elevation, is a critical question in targeting appropriate therapies.

The problems of troponin specificity dictate the requirement for additional diagnostic criteria in defining MI, and nowhere is this more true than on the ICU. Clearly, treatment strategies appropriate for ACS may not improve outcome where elevated troponin is due to an alternative pathology.

Myocardial ischaemia in the setting of mechanical ventilation and weaning is well described [7,8]. Contemporary analyses of ICU patients with current definitions of myocardial infarction are limited. Booker and colleagues [9] prospectively screened 76 consecutive patients admitted to a general ICU. ST-segment changes on continuous telemetry and 12-lead ECGs for the first 24 to 48 hours of admission were recorded with troponin I (TnI) assays 8 to 12 hours after monitoring. There were 37 ECG-defined ischaemic events detected in 8 patients (10.5%), of which 96% were asymptomatic. Out of the 8 patients, 6 had significant troponin I elevation, and this accounted for 50% of all troponin-positive results. More recently, Lim et al. [1] reported on the combined results of ECG, troponin testing and new regional wall motion defects on echocardiography in general ICU patients. Investigations were clinically driven, but of 93 patients included, 24 (25.8%) were diagnosed with coincident MI, and this was associated with a significantly higher ICU (37.5% versus 17.6%; p = 0.05) and in-hospital (50% versus 22%; p = 0.01) mortality, even after correction for APACHE II score and inotrope/vasopressor requirement.

The current paper by Lim and colleagues [10] continues a series of publications from the McMaster group analysing MI and the diagnostic components in the critically ill patient. A robust screening protocol for MI was devised, defined according to consensus-guidelines by the presence of positive troponin assay and ischaemic ST-T wave changes on ECG. The study includes 103 patients admitted to general ICU and enrolled over a two month period. Serial 12-lead ECGs and cardiac troponin T (cTnT) assays were performed. Tests were performed additionally, and blinded to ICU staff, if not ordered on clinical grounds. Only one patient had an index diagnosis of MI.

Patients were analysed according to: diagnosis of MI (35.9% of patients); presence of positive troponin only (14.6%); and troponin-negative status (49.5%). ICU staff made a clinical diagnosis of MI in 18 patients (17.5%), although 4 did not fulfil diagnostic criteria. Screening identified an additional 23 patients with true infarction. MI was associated with a longer ICU stay (median 5 versus 2 days; p = 0.001) and increased hospital mortality (43.2% versus 2%; p < 0.0001) compared to troponin-negative patients. MI patients also required a longer period of mechanical ventilation (median 4 days versus 2 versus 1; p < 0.0001) with increased ICU mortality (37.8% versus 6.7% versus 2.0%; p < 0.0001) compared to the troponin positive and negative groups, respectively.

This paper supports existing literature regarding adverse outcomes for ICU patients with coincident MI, and importantly highlights the additional detection rate afforded by simple screening investigations. Whether this will translate into better patient outcomes through targeted therapy ? pharmacological and interventional ? will surely be the subject of future studies. Interestingly, in the current paper, mortality rates were similar for MI patients irrespective of whether this was diagnosed prospectively by ICU staff or not. Indeed, there was actually a trend towards better outcome in those not identified, which one would speculate reflects a less unwell subset of patients with smaller infarcts (rather than any iatrogenic effect).

Invasive strategies (coronary angiography and percutaneous intervention) have a clear role in the patient with ACS outside of the ICU. Their role in the ICU setting is less clear ? although the potential benefits are very high, so are the risks. Interventional approaches in this population are beset with difficulties arising from the lack of specificity of troponin elevation, and the difficulty in early diagnosis of MI. The work of Lim and colleagues [10] provides further clarification as to which patients could be targeted; further studies are required to ascertain the way in which this should be undertaken.


ACS = acute coronary syndrome; CI = confidence interval; ECG = echocardiogram; ICU = intensive care unit; MI = myocardial infarction.

Competing interests

The authors declare that they have no competing interests.

Lim W,Qushmaq I,Cook DJ,Crowther MA,Heels-Ansdell D,Devereaux PJ. Elevated troponin and myocardial infarction in the intensive care unit: a prospective studyCrit Care 2005;9:R636–R644. [pmid: 16280062] [doi: 10.1186/cc3816]
Thygesen K,Alpert JS,White HD,Jaffe AS,Apple FS,Galvani M,Katus HA,Newby LK,Ravkilde J,Chaitman B,Clemmensen PM,Dellborg M,Hod H,Porela P,Underwood R,Bax JJ,Beller GA,Bonow R,Van der Wall EE,Bassand JP,Wijns W,Ferguson TB,Steg PG,Uretsky BF,Williams DO,Armstrong PW,Antman EM,Fox KA,Hamm CW,Ohman EM,et al. Universal definition of myocardial infarctionCirculation 2007;116:2634–2653. [pmid: 17951284] [doi: 10.1161/CIRCULATIONAHA.107.187397]
Jaffe AS,Ravkilde J,Roberts R,Naslund U,Apple FS,Galvani M,Katus H. It's time for a change to a troponin standardCirculation 2000;102:1216–1220. [pmid: 10982533]
Ammann P,Maggiorini M,Bertel O,Haenseler E,Joller-Jemelka HI,Oechslin E,Minder EI,Rickli H,Fehr T. Troponin as a risk factor for mortality in critically ill patients without acute coronary syndromesJ Am Coll Cardiol 2003;41:2004–2009. [pmid: 12798573] [doi: 10.1016/S0735-1097(03)00421-2]
Jeremias A,Gibson CM. Narrative review: alternative causes for elevated cardiac troponin levels when acute coronary syndromes are excludedAnn Intern Med 2005;142:786–791. [pmid: 15867411]
Lim W,Qushmaq I,Devereaux PJ,Heels-Ansdell D,Lauzier F,Ismaila AS,Crowther MA,Cook DJ. Elevated cardiac troponin measurements in critically ill patientsArch Intern Med 2006;166:2446–2454. [pmid: 17159009] [doi: 10.1001/archinte.166.22.2446]
Hurford WE,Lynch KE,Strauss HW,Lowenstein E,Zapol WM. Myocardial perfusion as assessed by thallium-201 scintigraphy during the discontinuation of mechanical ventilation in ventilator-dependent patientsAnesthesiology 1991;74:1007–1016. [pmid: 2042755] [doi: 10.1097/00000542-199106000-00007]
Hurford WE,Favorito F. Association of myocardial ischemia with failure to wean from mechanical ventilationCrit Care Med 1995;23:1475–1480. [pmid: 7664548] [doi: 10.1097/00003246-199509000-00006]
Booker KJ,Holm K,Drew BJ,Lanuza DM,Hicks FD,Carrigan T,Wright M,Moran J. Frequency and outcomes of transient myocardial ischemia in critically ill adults admitted for noncardiac conditionsAm J Crit Care 2003;12:508–516. [pmid: 14619356]
Lim W,Holinski P,Devereaux PJ,Tkaczyk A,McDonald E,Clarke F,Qushmaq I,Terrenato I,Schunemann H,Crowther M,Cook D. Detecting myocardial infarction in critical illness using screening troponin measurements and ECG recordingsCrit Care 2008;12:R36. [pmid: 18318915] [doi: 10.1186/cc6815]

Article Categories:
  • Commentary

Previous Document:  Knowing who would respond to a recruitment maneuver before actually doing it--this might be a way to...
Next Document:  Inflammation and breast cancer: metalloproteinases as common effectors of inflammation and extracell...