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    Vancouver Chest Pain Rule

    Identifies chest pain patients who are low risk and safe for early discharge.
    When to Use
    Why Use
    • Use in adult patients ≥25 years old presenting to the ED with chest pain.
    • Should not be used in patients with trauma or other radiographically-identified cause for chest pain such as pneumothorax, pleural effusion, and/or pneumonia.
    • Should not be used in patients with any of the following findings on EKG: ST elevation, ST depression >0.5mm, Q waves, left ventricular hypertrophy, paced rhythm, left bundle branch block.
    • Original derivation study was intended to derive a prediction rule allowing for safe discharge of ED chest pain patients within 2 hours and without the need for further provocative testing.
    • The original derivation study tested with troponin T, but an external validation study showed no difference in the performance of the rule with high-sensitivity troponin.
    • The incidence of disease may be higher in the countries where the rule was developed and tested (Canada, Australia, New Zealand) compared to the United States.
    • Primary outcome was diagnosis of ACS (acute MI or unstable angina) within 30 days. Acute MI was defined as positive troponin, EKG consistent with acute MI, or death without any other cause or event, and unstable angina was defined as coronary angiogram showing 70% lesion or revascularization with either percutaneous coronary intervention or coronary artery bypass grafting”
    • Adverse events include: tachycardia or bradycardia requiring medical intervention, respiratory failure requiring assisted ventilation, pulmonary embolism, aortic dissection or aneurysm, new congestive heart failure requiring intravenous medications, hypotension requiring vasoactive agents or an intra-aortic balloon pump, chest compressions, percutaneous coronary intervention, or coronary artery bypass grafting.

    The Vancouver Chest Pain Rule identifies low-risk chest pain patients that can be safely discharged from the ED after the standard initial evaluation of history and physician exam, EKG, and one cardiac biomarker (normal sensitivity troponin).

    Step One
    Step Two
    Step Three


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    Next Steps
    Creator Insights


    • Patients with an abnormal EKG, positive troponin at 2 hours, or history of prior ACS or nitrate use do not qualify for early discharge.
    • Patients with a normal EKG, negative 2-hour troponin, no prior history of ACS or nitrate use, and reproducible pain to palpation can be discharged from the ED without further provocative testing.
    • Patients with a normal EKG, negative 2-hour troponin, no prior history of ACS or nitrate use, with non-reproducible chest pain who are age <50 years and have chest pain that does not radiate to the neck, jaw, or arm, can be discharged from the ED without further provocative testing.

    Critical Actions

    • Low-risk patients can be considered for discharge from the ED without further provocative testing for ACS.
    • Consider other etiologies of chest pain, including aortic, esophageal, pulmonary, cardiac, abdominal, and musculoskeletal sources.
    • Patients who are not low risk should be managed as per usual chest pain protocols, including but not limited to consideration of aspirin, nitroglycerin, and serial EKGs and biomarkers.


    Step-wise analysis of EKG, biomarker, history and physical exam; if all questions are answered “No,” the patient is low-risk by the Vancouver Chest Pain Rule.

    Facts & Figures

    Step 1: If no to all, move to Step 2. Otherwise proceed with standard chest pain evaluation:

    • Abnormal initial EKG?
    • Positive troponin at 2 hours?
    • Prior ACS or nitrate use?

    Step 2: If yes, proceed to early discharge. If no, move to Step 3.

    • Does palpation reproduce pain?

    Step 3: If no to all, proceed with early discharge. Otherwise proceed with standard chest pain evaluation.

    • Age ≥50?
    • Does pain radiate to neck, jaw, or left arm

    Evidence Appraisal

    Scheuermeyer et al (2014) derived the Vancouver Chest Pain Rule in a prospective cohort study of 763 ED patients at St. Paul’s Hospital, an urban tertiary care center, and internally validated the rule in a prospective cohort of 906 ED patients at the same hospital. They included ED patients complaining of anterior or lateral chest pain who were suspected of possibly having ischemic chest pain. Patients were excluded for any of the following: age under 25 years old, traumatic etiology, radiologically evident alternate cause of chest pain, previous enrollment in past 30 days, terminal illness, or communication barriers. The primary outcome was the diagnosis of ACS defined as an acute myocardial infarction (AMI) or unstable angina (UA) within 30 days.

    EKGs were labeled as having ischemic factors if there were any of the following: ST elevation >2 mm in two consecutive precordial leads or >1mm in two consecutive limb leads, ST depression >2 mm in V1/V2, ST depression >0.5 mm or Q waves or T-wave inversions in 2 contiguous leads, left bundle branch block (LBBB), left ventricular hypertrophy (LVH), or a paced rhythm. Of note, “ischemic EKG changes” in this study are not the same as those in the American Heart Association (AHA) guidelines. The AHA uses 1 mm as the measurement cutoff for significant ST elevation, except in the anterior leads, which are age and sex-dependent. Also, the AHA does not consider a paced rhythm or the existence of a LBBB or LVH as a sign of acute ischemia.

    In the derivation cohort, 10.1% had an AMI and 11.5% had unstable angina. Based on the Vancouver Chest Pain Rule, no cases of ACS were missed, and 18.6% of patients without ACS would have been able to be discharged within 2 hours without the need for additional provocative testing, resulting in 100% sensitivity, 18.6% specificity, 100% negative predictive value, and 25.3% positive predictive value.

    In the internal validation cohort, 4.3% had an AMI and 8.8% had UA. The Vancouver Chest Pain Rule missed one case of unstable angina: a 48-year-old male who screened as low risk but was taken to the catheterization lab because of documented prehospital hypotension, and was found to have a 50% lesion to the left anterior descending coronary artery. Based on the validation cohort, the Vancouver Chest Pain Rule had 99.2% sensitivity, 23.4% specificity, NPV of 99.5%, and PPV of 16.4%.

    Cullen et al (2014) externally validated the Vancouver Chest Pain Rule in a prospective cohort of 1,635 ED patients in Brisbane, Australia and Christchurch, New Zealand, comparing sensitive and highly-sensitive troponin assays. They included ED patients with ≥5 minutes of suspected ischemic chest pain. Patients were excluded if there was a clear non-ACS etiology of chest pain, previous enrollment in past 45 days, terminal illness, unable/unwilling to consent, or pregnancy. All patients had troponins drawn on presentation and at ≥6 hours. Blood was also drawn at 2 hours for the highly-sensitive troponin assay. Cullen et al looked at the same primary outcome of ACS, defined as AMI or UA, within 30 days. With the usual sensitive troponin assay, 20.4% had ACS, resulting in 98.8% sensitivity, 15.8% specificity, NPV of 98.1%, and PPV 23.2%. The Vancouver Chest Pain Rule using the usual sensitive troponin assay missed 4 cases of unstable angina. When the highly-sensitive troponin assay was used, 20.2% were identified with ACS, resulting in 99.1% sensitivity, 16.1% specificity, NPV 98.6%, and PPV 23.3%. The Vancouver Chest Pain Rule using the highly-sensitive troponin assay missed 3 cases of unstable angina. There was no statistically significant difference in the function of the Vancouver Chest Pain Rule between the use of the usual sensitive troponin versus the highly-sensitive troponin.

    Dr. Frank Scheuermeyer

    From the Creator

    Why did you develop the Vancouver Chest Pain Rule? Was there a clinical experience that inspired you to create this tool for clinicians? Was it directly related to the “old” Vancouver Chest Pain Rule that used older enzyme assays?
    The Vancouver Chest Pain Rule (VCPR) was developed in response to work by Pope (NEJM 2000) and Christenson (CMAJ 2004) that demonstrated a 2 - 5% of emergency department patients with an acute coronary syndrome were inappropriately discharged with a minimizing diagnosis and no further follow-up. The initial VCPR decribed by Christenson (Ann Emerg Med 2006), which used creatinine kinase as a key decision point, was clinically appropriate, but the disuse of CK ensured that an additional rule had to be derived.
    Overall, the declining prevalence of ACS in chest pain patients (likely due to better community control of risk factors such as cholesterol and hypertension), as well as the diversion of STEMI patients directly to the catheterization laboratory, ensures that emergency physicians will likely be faced with an increased proportion of low risk chest pain patients with clinically vague presentations. In these cases, a 2-hour risk stratification approach may be welcomed, since it can result in safe discharge of 20 - 40% of chest pain patients within 2 hours, rather than subjecting these patients to prolonged observation, repeated investigations, and potential hospital admissions.
    What pearls, pitfalls and/or tips do you have for users of the Vancouver Chest Pain Rule? Are there cases in which it has been applied, interpreted, or used inappropriately?
    Many clinicians will be tempted to use the VCPR in patients they have already decided are low-risk - for example, patients that are younger, have lower Framingham risk factors, etc. - but the rule is designed to perform in any ED patient with potential ischemic chest pain. It cannot be used to “rule-in” an ACS diagnosis, but works better as a “rule out” test. Rare but lethal causes of chest pain including aortic dissection, pneumothorax, and pericarditis, cannot reliably be identified with the VCPR.
    A few questions about definitions: how are “prior ACS” or “nitrate use” defined. For the former, was this any anginal symptom in the past? For the latter, was this any prior prescription for nitrates?
    Prior acute coronary syndrome was defined as a history of acute myocardial infarction or unstable angina, or prior percutaneous coronary intervention or coronary artery bypass grafting. Prior nitrate use (or any prior nitrate prescription) was a proxy marker for stable angina, since many patients could not remember they had angina, but patients COULD remember that they inhaled liquid from a reddish bottle that gave them a headache.
    What recommendations do you have for health care providers once they have applied the Vancouver Chest Pain Rule? Are there any adjustments or updates you would make to the rule given recent changes in medicine?
    One advantage of the VCPR is that no additional investigations are required - the patient does not need to be admitted for provocative testing, cardiac CT angiography, or echocardiography - and the patient can simply be discharged home. However, the use of rapid ED-based advance imaging may affect the VCPR. Currently, chest pain outcomes are typically studied until 30 days, but a normal cardiac CT, for instance, could provide reassurance that no ACS event is likely in the next several years.
    Any other comments? Any new research or papers on this topic in the pipeline? Any thoughts on comparisons to other risk scores like the HEART or GRACE Scores?
    Currently other scores like HEART and GRACE appear to be appropriate as well, although the variables in GRACE may be difficult to obtain in the ED. The team led by Drs Martin Than and Louise Cullen have a practical approach with the ADAPT and EDACS, which are other 2-hour ACS rule-out tests. These different techniques have so far not been compared to one another.

    About the Creator

    Frank Xavier Scheuermeyer, MD, is an assistant professor of emergency medicine at the University of British Columbia in Vancouver, Canada. He also practices at St. Paul's and Mount St. Joseph's Hospital Emergency Departments. Dr. Scheuermeyer conducts research on atrial fibrillation and other cardiac emergencies.

    To view Dr. Frank Scheuermeyer's publications, visit PubMed

    About the Creator
    Dr. Frank Scheuermeyer
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