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Acute Med, All Updates, Guidelines, ICU, PHARM, Resus

STEMI criteria vary with age and sex

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On reading through the 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science – Part 10: Acute Coronary Syndromes, I found a reminder that the ECG criteria for diagnosing ST-elevation myocardial infarction (STEMI) vary according to age and sex. From the original article in the Journal of the American College of Cardiology:

The threshold values of ST-segment elevation of 0.2 mV (2 mm) in some leads and 0.1 mV (1 mm) in others results from recognition that some elevation of the junction of the QRS complex and the ST segment (the J point) in most chest leads is normal. Recent studies have revealed that the threshold values are dependent on gender, age, and ECG lead ([8], [9], [10], [11] and [12]). In healthy individuals, the amplitude of the ST junction is generally highest in leads V2 and V3 and is greater in men than in women.
Recommendations

  1. For men 40 years of age and older, the threshold value for abnormal J-point elevation should be 0.2 mV (2 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads.
  2. For men less than 40 years of age, the threshold values for abnormal J-point elevation in leads V2 and V3 should be 0.25 mV (2.5 mm).
  3. For women, the threshold value for abnormal J-point elevation should be 0.15 mV (1.5 mm) in leads V2 and V3 and greater than 0.1 mV (1 mm) in all other leads.
  4. For men and women, the threshold for abnormal J-point elevation in V3R and V4R should be 0.05 mV (0.5 mm), except for males less than 30 years of age, for whom 0.1 mV (1 mm) is more appropriate.
  5. For men and women, the threshold value for abnormal J- point elevation in V7 through V9 should be 0.05 mV (0.5 mm).
  6. For men and women of all ages, the threshold value for abnormal J-point depression should be −0.05 mV (−0.5 mm) in leads V2 and V3 and −0.1 mV (−1 mm) in all other leads.

What does establishment of abnormal J-point mean for STEMI diagnosis? The AHA/ECC guidelines state the following:

ST-segment elevation… is characterized by ST-segment elevation in 2 or more contiguous leads and is classified as ST-segment elevation MI (STEMI). Threshold values for ST-segment elevation consistent with STEMI are:

  • J-point elevation 0.2 mV (2 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men ≥40 years old);
  • J-point elevation 0.25 mV (2.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men <40 years old);
  • J-point elevation 0.15 mV (1.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (women).

So, in summary:

Older men – 2mm in V2/V3 and 1mm everywhere else
Younger men – 2.5 mm in V2/V3 and 1mm everywhere else
Women – 1.5 mm in V2/V3 and 1mm everywhere else

Shouldn’t be too difficult to remember.
Part 10: acute coronary syndromes: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
Circulation. 2010 Nov 2;122(18 Suppl 3):S787-817
AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part VI: acute ischemia/infarction: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology.
J Am Coll Cardiol. 2009 Mar 17;53(11):1003-11

All Updates

'Sensitive' troponin assays do not rule out at ED presentation

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An assessment of new ‘sensitive’ troponin assays at presentation of chest pain patients in a real-world ED setting showed that a single troponin I assay at ED presentation has insufficient sensitivity for clinical use to rule out MI. Author Anne-Maree Kelly discusses the current requirement for a minimum interval after an episode of chest pain to ensure adequate sensitivity: Currently in Australia the recommended minimum interval is 8 h after symptom onset. New evidence suggests that a shorter interval might be appropriate with the sensitive assays. Keller et al. reported 100% sensitivity at 3 h after ED presentation. Macrae et al. suggested that an assay 6 h from pain onset or serial assays 3 h apart with one at least 6 h from pain onset has high diagnostic accuracy. Although further research in an ED chest pain cohort is needed, the weight of evidence suggests a reduction in the minimum interval from pain onset to 6 h might be appropriate.

Aim: Troponin assays have high diagnostic value for myocardial infarction (MI), but sensitivity has been weak early after chest pain onset. New, so-called ‘sensitive’ troponin assays have recently been introduced. Two studies report high sensitivity for assays taken at ED presentation, but studied selected populations. Our aim was to evaluate the diagnostic performance for MI of a sensitive troponin assay measured at ED presentation in an unselected chest pain population without ECG evidence of ischaemia.
Methods: This is a sub-study of a prospective cohort study of adult patients with potentially cardiac chest pain who underwent evaluation for acute coronary syndrome. Patients with clear ECG evidence of acute ischaemia or an alternative diagnosis were excluded. Data collected included demographic, clinical, ECG, biomarker and outcome data. A ‘positive’ troponin was defined as >99th percentile of the assay used. MI diagnosis was as judged by the treating cardiologist. The outcomes of interest were sensitivity, specificity and likelihood ratios (LR) for positive troponin assay taken at ED presentation. Data were analysed by clinical performance analysis.
Results: Totally 952 were studied. Median age was 61 years; 56.4% were male and median TIMI score was 2. There were 129 MI (13.6, 95% CI 11.5-15.9). Sensitivity of TnI at ED presentation was 76.7% (95% CI 68.5-83.7%), specificity 93.6% (95% CI 91.7-95.1%), with LR positive 11.92 and LR negative 0.25.
Conclusion: Sensitive TnI assay at ED presentation has insufficient diagnostic accuracy for detection of MI. Serial biomarker assays in patients with negative initial TnI are required.

Performance of a sensitive troponin assay in the early diagnosis of acute myocardial infarction in the emergency department.
Emerg Med Australas. 2011 Apr;23(2):181-5

Acute Med, All Updates, Resus

Triple marker panel for AMI

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A large Asian/Australasian study examined a 2hr triple-marker test in patients presenting with chest pain.

BACKGROUND: Patients with chest pain contribute substantially to emergency department attendances, lengthy hospital stay, and inpatient admissions. A reliable, reproducible, and fast process to identify patients presenting with chest pain who have a low short-term risk of a major adverse cardiac event is needed to facilitate early discharge. We aimed to prospectively validate the safety of a predefined 2-h accelerated diagnostic protocol (ADP) to assess patients presenting to the emergency department with chest pain symptoms suggestive of acute coronary syndrome.
METHODS: This observational study was undertaken in 14 emergency departments in nine countries in the Asia-Pacific region, in patients aged 18 years and older with at least 5 min of chest pain. The ADP included use of a structured pre-test probability scoring method (Thrombolysis in Myocardial Infarction [TIMI] score), electrocardiograph, and point-of-care biomarker panel of troponin, creatine kinase MB, and myoglobin. The primary endpoint was major adverse cardiac events within 30 days after initial presentation (including initial hospital attendance). This trial is registered with the Australia-New Zealand Clinical Trials Registry, number ACTRN12609000283279.
FINDINGS: 3582 consecutive patients were recruited and completed 30-day follow-up. 421 (11.8%) patients had a major adverse cardiac event. The ADP classified 352 (9.8%) patients as low risk and potentially suitable for early discharge. A major adverse cardiac event occurred in three (0.9%) of these patients, giving the ADP a sensitivity of 99.3% (95% CI 97.9-99.8), a negative predictive value of 99.1% (97.3-99.8), and a specificity of 11.0% (10.0-12.2).
INTERPRETATION: This novel ADP identifies patients at very low risk of a short-term major adverse cardiac event who might be suitable for early discharge. Such an approach could be used to decrease the overall observation periods and admissions for chest pain. The components needed for the implementation of this strategy are widely available. The ADP has the potential to affect health-service delivery worldwide.

A 2-h diagnostic protocol to assess patients with chest pain symptoms in the Asia-Pacific region (ASPECT): a prospective observational validation study.
Lancet. 2011 Mar 26;377(9771):1077-84
Full text link available at time of writing
In an accompanying editorial, nicely entitled ‘Acute MI: triple-markers resurrected or Bayesian dice?’ Dr Rick Body notes that the point-of-care triple-marker test has a relatively low sensitivity, at just 82.9%, when used alone, and the sensitivity only increased to 99.3% in the current study because it was used in an already-selected low-risk population. He writes: “Most people will probably consider this net risk to be statistically acceptable. However, if properly informed, low-risk patients might feel differently about the relative merits of waiting for definitive six-hour laboratory-based troponin testing or going home after two hours on the basis of results from a test that correctly identifies serious coronary disease, when present, in just over eight of 10 occasions.”
Dr Body has a new blog at The Bodsblog where we’re likely to be informed other data relevant to emergency cardiology as they emerge.
Point-of-care panel assessment using a similar triple-marker test at presentation and 90 minutes was also examined in the RATPAC study, in which it increased successful discharge home and reduced median length of stay, but did not alter overall hospital bed use.

Acute Med, All Updates, ICU, PHARM, Resus

Which cardiac arrest survivors have a positive angio?

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A retrospective study of out-of-hospital cardiac arrest patients attended by a French pre-hospital system was performed to assess the predictive factors for positive coronary angiography.

OBJECTIVES: Coronary angiography is often performed in survivors of out-of-hospital cardiac arrest, but little is known about the factors predictive of a positive coronary angiography. Our aim was to determine these factors.
METHODS: In this 7-year retrospective study (January 2000-December 2006) conducted by a French out-of-hospital emergency medical unit, data were collected according to Utstein style guidelines on all out-of-hospital cardiac arrest patients with suspected coronary disease who recovered spontaneous cardiac activity and underwent early coronary angiography. Coronary angiography was considered positive if a lesion resulting in more than a 50% reduction in luminal diameter was observed or if there was a thrombus at an occlusion site.
RESULTS: Among the 4621 patients from whom data were collected, 445 were successfully resuscitated and admitted to hospital. Of these, 133 were taken directly to the coronary angiography unit, 95 (71%) had at least one significant lesion, 71 (53%) underwent a percutaneous coronary intervention, and 30 survived [23%, 95% confidence interval (CI): 16-30]. According to multivariate analysis, the factors predictive of a positive coronary angiography were a history of diabetes [odds ratio (OR): 7.1, 95% CI: 1.4-36], ST segment depression on the out-of-hospital ECG (OR: 5.4, 95% CI: 1.1-27.8), a history of coronary disease (OR: 5.3, 95% CI: 1.4-20.1), cardiac arrest in a public place (OR: 3.7, 95% CI: 1.3-10.7), and ventricular fibrillation or ventricular tachycardia as initial rhythm (OR: 3.1, 95% CI: 1.1-8.6).
CONCLUSION: Among the factors identified, diabetes and a history of coronary artery were strong predictors for a positive coronary angiography, whereas ST segment elevation was not as predictive as expected.

Predictive factors for positive coronary angiography in out-of-hospital cardiac arrest patients
Eur J Emerg Med. 2011 Apr;18(2):73-6

Acute Med, All Updates, ICU, PHARM, Resus

Supplemental oxygen decreases LV perfusion in volunteers

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Oxygen therapy in normoxic acute coronary syndrome patients is controversial, and a previous systematic review cautioned against it in uncomplicated MI. A volunteer study using cardiac imaging demonstrates the effects of supplemental oxygen on coronary blood flow.
 

OBJECTIVES: Oxygen (O2) is a cornerstone in the treatment of critically ill patients, and the guidelines prescribe 10-15 l of O2/min even to those who are initially normoxic. Studies using indirect or invasive methods suggest, however, that supplemental O2 may have negative cardiovascular effects. The aim of this study was to test the hypothesis, using noninvasive cardiac magnetic resonance imaging, that inhaled supplemental O2 decreases cardiac output (CO) and coronary blood flow in healthy individuals.
METHODS: Sixteen healthy individuals inhaled O2 at 1, 8 and 15 l/min through a standard reservoir bag mask. A 1.5 T magnetic resonance imaging scanner was used to measure stroke volume, CO and coronary sinus blood flow. Left ventricular (LV) perfusion was calculated as coronary sinus blood flow/LV mass.
RESULTS: The O2 response was dose-dependent. At 15 l of O2/min, blood partial pressure of O2 increased from an average 11.7 to 51.0 kPa with no significant changes in blood partial pressure of CO2 or arterial blood pressure. At the same dose, LV perfusion decreased by 23% (P=0.005) and CO decreased by 10% (P=0.003) owing to a decrease in heart rate (by 9%, P<0.002), with no significant changes in stroke volume or LV dimensions. Owing to the decreased CO and LV perfusion, systemic and coronary O2 delivery fell by 4 and 11% at 8 l of O2/min, despite the increased blood oxygen content.
CONCLUSION: Our data indicate that O2 administration decreases CO, LV perfusion and systemic and coronary O2 delivery in healthy individuals. Further research should address the effects of O2 therapy in normoxic patients.

Effects of oxygen inhalation on cardiac output, coronary blood flow and oxygen delivery in healthy individuals, assessed with MRI
European Journal of Emergency Medicine 2011, 18:25–30

Acute Med, All Updates, PHARM

Delayed door-to-balloon even with helicopters

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For a whole bunch of reasons, patients with ST-elevation myocardial infarction who undergo interhospital transfer for primary percutaneous coronary intervention may not meet the required 90 minute door-to-balloon time. In a new study of patients transferred by helicopter, only 3% of STEMI patients transferred for reperfusion met the 90-minute goal. Should this result in an increase in the use of fibrinolysis at non–percutaneous coronary intervention hospitals?

Opportunity for gratuitous helicopter shot never knowingly declined

STUDY OBJECTIVE: Early reperfusion portends better outcomes for ST-segment elevation myocardial infarction (STEMI) patients. This investigation estimates the proportions of STEMI patients transported by a hospital-based helicopter emergency medical services (EMS) system who meet the goals of 90-minute door-to-balloon time for percutaneous coronary intervention or 30-minute door-to-needle time for fibrinolysis.
METHODS: This was a multicenter, retrospective chart review of STEMI patients flown by a hospital-based helicopter service in 2007. Included patients were transferred from an emergency department (ED) to a cardiac catheterization laboratory for primary or rescue percutaneous coronary intervention. Out-of-hospital, ED, and inpatient records were reviewed to determine door-to-balloon time and door-to-needle time. Data were abstracted with a priori definitions and criteria.
RESULTS: There were 179 subjects from 16 referring and 6 receiving hospitals. Mean age was 58 years, 68% were men, and 86% were white. One hundred forty subjects were transferred for primary percutaneous coronary intervention, of whom 29 had no intervention during catheterization. For subjects with intervention, door-to-balloon time exceeded 90 minutes in 107 of 111 cases (97%). Median door-to-balloon time was 131 minutes (interquartile range 114 to 158 minutes). Thirty-nine subjects (21%) received fibrinolytics before transfer, and 19 of 39 (49%) received fibrinolytics within 30 minutes. Median door-to-needle time was 31 minutes (interquartile range 23 to 45 minutes).
CONCLUSION: In this study, STEMI patients presenting to non-percutaneous coronary intervention facilities who are transferred to a percutaneous coronary intervention-capable hospital by helicopter EMS do not commonly receive fibrinolysis and rarely achieve percutaneous coronary intervention within 90 minutes. In similar settings, primary fibrinolysis should be considered while strategies to reduce the time required for subsequent interventional care are explored.

Reperfusion Is Delayed Beyond Guideline Recommendations in Patients Requiring Interhospital Helicopter Transfer for Treatment of ST-segment Elevation Myocardial Infarction.
Ann Emerg Med. 2011 Mar;57(3):213-220

Acute Med, All Updates, Guidelines, Resus

Testing of Low-Risk Chest Pain Patients

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A summary of the literature on low risk chest pain, including history, physical exam, ECG, biomarkers, and investigations such as exercise tolerance testing, myocardial perfusion imaging, and other investigations, is provided in the American Heart Association’s recently published scientific statement.
The document contains a number of useful statistics on the limitations of clinical assessment in ruling out coronary artery disease, such as these:
“…the Multicenter Chest Pain Study found that 22% of patients presenting with symptoms described as sharp or stabbing pain (13% with pleuritic pain and 7% with pain reproduced on palpation) were eventually diagnosed with ACS.”

Testing of Low-Risk Patients Presenting to the Emergency Department With Chest Pain
A Scientific Statement From the American Heart Association
Circulation. 2010;122:1756-1776 – Full Text

Acute Med, All Updates, Resus

RV involved in AMI more often than you think

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We know that inferior STEMI may be complicated by right ventricular involvement, which is why I whack a V4R lead on all my inferior AMI patients. A recent study using cardiac magnetic resonance imaging showed that RV oedema and regional or global RV dysfunction were common in anterior infarcts too, although the proportion significantly decreased at four month follow up.

T2w image of patient with LAD occlusion. Hyperintense appearance of jeopardised anteroseptal and anterior LV myocardium (arrowheads), extending to adjacent RV lateral free wall (arrows)

RV abnormalities are contiguous to the jeopardized LV myocardium and do not occur exclusively in inferior LV infarcts, but are found in up to 33% of anterior LV infarcts as well. The presence of RV ischemic injury is associated with early RV dysfunction as well as with RV functional recovery at follow-up.
Right Ventricular Ischemic Injury in Patients With Acute ST-Segment Elevation Myocardial Infarction: Characterization With Cardiovascular Magnetic Resonance.
Circulation. 2010 Oct 5;122(14):1405-12

Acute Med, All Updates, ICU

'AMI' on ICU

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ECG machines may give a printed report saying ***ACUTE MI***. In a retrospective study, patients on the ICU whose 12 lead ECGs contained this electronic interpretation did not have an elevated troponin 85% of the time. Even in the minority of patients whose electronic ECG diagnosis of MI was agreed with by a cardiologist, only one third developed an elevated troponin.
The authors state ‘In contrast to nonintensive care unit patients who present with chest pain, the electrocardiographic ST-segment elevation myocardial infarction diagnosis seems to be a nonspecific finding in the intensive care unit that is frequently the result of a variety of nonischaemic processes. The vast majority of such patients do not have frank ST-segment elevation myocardial infarction.’
Electrocardiographic ST-segment elevation myocardial infarction in critically ill patients: An observational cohort analysis
Crit Care Med. 2010 Dec;38(12):2304-230

Acute Med, All Updates, Guidelines, Resus

GPIIb/IIIa inhibitors

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A systematic review on use of GPIIb/IIIa inhibitors in NSTEACS has been updated as part of the Annals of Emergency Medicine‘s Evidence Based Emergency Medicine series. The bottom line:
In patients with non-ST-segment elevation acute coronary syndromes who do not undergo early percutaneous coronary intervention, administration of platelet glycoprotein IIb/IIIa (GPIIb/IIIa) inhibitors, given in addition to aspirin and unfractionated heparin, does not reduce 30-day or 6-month mortality. For the composite endpoint of myocardial infarction or death, there was modest benefit at 30 days and 6 months; however, there was an increased risk of major hemorrhage among those receiving GPIIb/IIIa inhibitors.
Update: Use of Platelet Glycoprotein IIb/IIIa Inhibitors in Patients With Unstable Angina and Non-ST-Segment Elevation Myocardial Infarction
Annals of Emergency Medicine Volume 56, Issue 5 , Pages e1-e2, November 2010

Compare this with the recommendations of the European Resuscitation Council who provide the following summary regarding this class of drug:
Gp IIB/IIIA receptor inhibition is the common final link of platelet aggregation. Eptifibatide and tirofiban lead to reversible inhibition, while abciximab leads to irreversible inhibition of the Gp IIB/IIIA receptor. Older studies from the pre-stent era mostly support the use of this class of drugs. Newer studies mostly document neutral or worsened outcomes. Finally in most supporting, as well as neutral or opposing studies, bleeding occurred in more patients treated with Gp IIB/IIIA receptor blockers. There are insufficient data to support routine pre-treatment with Gp IIB/IIIA inhibitors in patients with STEMI or non-STEMI-ACS. For high-risk patients with non-STEMI-ACS, in-hospital upstream treatment with eptifibatide or tirofiban may be acceptable whereas abciximab may be given only in the context of PCI. Newer alternatives for antiplatelet treatment should be considered because of the increased bleeding risk with Gp IIB/IIIA inhibitors when used with heparins.
European Resuscitation Council Guidelines for Resuscitation 2010 Section 5. Initial management of acute coronary syndromes
Resuscitation 81 (2010) 1353–1363 – full text downloadable