References

1. Kloner RA, Poole WK, Perritt RL. When throughout the year is coronary death most likely to occur? A 12-year population-based analysis of more than 220 000 cases. Circulation 1999;100:1630 – 4.
2. Muller JE, Stone PH, Turi ZG, et al. Circadian variation in the frequency of onset of acute myocardial infarction. N Engl J Med 1985;313:1315 – 22.
3. Tanaka A, Kawarabayashi T, Fukuda D, et al. Circadian variation of Plaque rupture in acute myocardial infarction. Am J Cardiol 2004; 93:1 – 5.
4. Alves DW, Allegra JR, Cochrane DG, Cable G. Effect of lunar cycle on temporal variation in cardiopulmonary arrest in seven emergency departments during 11 years. Eur J Emerg Med 2003;10:225 – 8.
5. Eisenburger P, Schreiber W, Vergeiner G, et al. Lunar phases are not related to the occurrence of acute myocardial infarction and sudden cardiac death. Resuscitation 2003;56:187 – 9.
6. Miles LE, Raynal DM, Wilson MA. Blind man living in normal society has Circadian rhythms of 24.9 hours. Science 1977;198:421 – 3.
7. Middlekauff HR, Sontz EM. Morning sympathetic nerve activity is not increased in humans. Implications for mechanisms underly- ing the circadian pattern of cardiac risk. Circulation 1995;91: 2549 – 55.
8. Fernandez-Ortiz A, Badimon JJ, Falk E, et al. Characterization of the relative thrombogenicity of atherosclerotic plaque components: implications for consequences of plaque rupture. J Am Coll Cardiol 1994;23:1562 – 9.
9. Tofler GH, Brezinski D, Schafer AI, et al. Concurrent morning increase in platelet aggregability and the risk of myocardial infarction and sudden cardiac death. N Engl J Med 1987;316:1514 – 8.
10. Rosing DR, Brakman P, Redwood DR, et al. Blood fibrinolytic activity in man. Diurnal variation and the response to varying intensities of exercise. Circ Res 1970;27:171 – 84.

    Internet-based survey on the use of additional lead electrocardiograms and fibrinolysis of posterior and right ventricular acute myocardial infarctions

    To the Editor,

    We write to you with results from an internet-based survey of practicing emergency physicians (EPs) and their use of additional lead Electrocardiograms in patients with chest pain suspected of acute coronary syndromes; after review of the clinical information and ECG, the physician was then asked if he/she would consider fibrinolysis.

    The ECG is an essential tool for evaluating the patient with chest pain. The standard 12-lead ECG assists the physician in making certain diagnoses, selecting both appropriate therapies and inpatient disposition locations, and establishing prognoses. However, the 12-lead ECG has many limitations–a significant one being the detection of acute myocardial infarction (AMI) to either the right ventricle or posterior wall of the left ventricle. Using additional ECG leads may reduce this regional limitation. Posterior and right ventricular ECG leads are an inexpensive and rapid aid to diagnosis [1,2]. We hypothesized that a significant number of emergency physicians (EPs) may not recognize the value of

    additional ECG leads with subsequent impact on thera- peutic decisions.

    We developed an internet-based survey that consisted of 3 similar hypothetical scenarios of AMI occurring in an emergency department where a cardiologist was unavailable and transport to another hospital was impos- sible. The 3 scenarios were isolated posterior AMI (Fig. 1A), posterior AMI with concomitant inferior AMI (Fig. 1B), and right ventricular AMI with concomitant inferior AMI (Fig. 1C). The 12-lead ECG was displayed for each of the scenarios (Fig. 1A-C). Invitations for participation in the survey were emailed to EPs from the Society for Academic Emergency Medicine 2002 directo- ry. Fisher exact test was used to determine statistical significance ( P b .01). The study was considered exempt by the institutional review board.

    The response rate was 14.7% (n = 3470 invitations with 448 responses) over 3 successive notifications. The percentage of respondents who requested posterior wall and right ventricular leads was 79.2% for isolated posterior AMI, 61.4% for posterior AMI with inferior AMI, and 62.7% for right ventricular AMI with inferior AMI. The percentage of respondents who decided to fibrinolyse the patient was 55.6% for isolated posterior AMI, 94.9% for posterior AMI with inferior AMI, and 86.4% for right ventricular AMI with inferior AMI. Significantly fewer EPs chose reperfusion therapy in the case of isolated posterior AMI than when there was inferior wall involvement (55.6% vs 94.9% [ P b .0001] and 86.4% [ P b .0001]). Significantly more ( P b .0001) of those who requested additional ECG leads decided to thrombolyse posterior AMI (68.4%) vs those who chose not to order additional leads (28.0%). Refer to Fig. 2A and C for a listing of the response rates to the clinical questions.

    Less respondents thrombolysed isolated posterior AMI (case 1, question 2) than posterior AMI with concomitant inferior AMI (case 2, question 4). Perhaps the 12-lead ECG for the isolated posterior AMI was interpreted as an ST- segment depression syndrome, for which fibrinolysis is detrimental. It is interesting that more ( P b .0001) of the respondents who wanted additional leads decided to fibrinolyse isolated posterior AMI (68.4%) vs those who chose not to order additional leads (28.0%) (Table 1). This result is consistent with a prior survey that showed many cardiologists and EPs would be more likely to administer fibrinolytic agents if they were provided with ECG evidence suggestive of posterior AMI [3].

    Additional leads did not impact treatment for inferior AMI with posterior or right ventricular AMI. There were similar fibrinolysis rates for case 2, question 4 (94.9%), and case 3, question 6 (86.4%). This result suggests that there is not a widespread appreciation of the literature that indicates that concomitant posterior AMI and right ventricular AMI portend worse morbidity and mortality than isolated inferior AMI [4 -6].

    

    Fig. 1 A, Presentation of Case One with clinical questions. 1. A 52-year-old male presents to the emergency department complaining of two hours of crushing substernal chest pain and shortness of breath. The patient has a past medical history of hypertension, diabetes mellitus, hypercholesterolemia and 40+ pack years of smoking cigarettes. Physical exam reveals the patient to be anxious and diaphoretic with a blood pressure of 138/96, heart rate 88, a normal precordial exam, clear lung auscultation and no Lower extremity edema. The patient’s electrocardiogram is displayed below. What Diagnostic modality performed in the emergency department would you pursue in the next five minutes to more completely identify the possibility of myocardial injury? Please select the single most appropriate answer. 2. Given the same history and ECG presented in question 1, which treatment would you employ within the next 30 minutes to most completely treat the patient’s condition? Assume that the patient has no contraindication to all medical agents that could increase the chance of bleeding and that he has already received aspirin. Also assume that a cardiologist is not available at your facility and the closest transfer facility is at least 6 hours away by ground transport due to a severe winter storm. Please select the single most appropriate answer. B, Presentation of Case Two with clinical questions. 3. A 52-year-old male presents to the emergency department complaining of two hours of crushing substernal chest pain and shortness of breath. The patient has a past medical history of hypertension, diabetes mellitus, hypercholesterolemia and 40+ pack years of smoking cigarettes. Physical exam reveals the patient to be anxious and diaphoretic with a blood pressure of 138/96, heart rate 88, a normal precordial exam, clear lung auscultation and no lower extremity edema. The patient’s electrocardiogram is displayed below. What diagnostic modality performed in the emergency department would you pursue in the next five minutes to more completely identify the possibility of myocardial injury? Please select the single most appropriate answer. 4. Given the same history and ECG presented in question 3, which treatment would you employ within the next 30 minutes to most completely treat the patient’s condition? Assume that the patient has no contraindication to all medical agents that could increase the chance of bleeding and that he has already received aspirin. Also assume that a cardiologist is not available at your facility and the closest transfer facility is at least 6 hours away by ground transport due to a severe winter storm. Please select the single most appropriate answer. C, Presentation of Case Three with clinical questions. 5. A 52-year-old male presents to the emergency department complaining of two hours of crushing substernal chest pain and shortness of breath. The patient has a past medical history of hypertension, diabetes mellitus, hypercholesterolemia and 40+ pack years of smoking cigarettes. Physical exam reveals the patient to be anxious and diaphoretic with a blood pressure of 138/96, heart rate 88, a normal precordial exam, clear lung auscultation and no lower extremity edema. The patient’s electrocardiogram is displayed below. The patient is given oxygen, aspirin, sublingual nitroglycerin and IV fluid at KVO rate. The patient’s subsequent blood pressure is 74/42. What diagnostic modality performed in the emergency department would you pursue in the next five minutes to more completely identify the possibility of myocardial injury? Please select the single most appropriate answer. 6. Given the same history and ECG presented in question 5, which treatment would you employ within the next 30 minutes to most completely treat the patient’s condition? Assume that the patient has no contraindication to all medical agents that could increase the chance of bleeding and that he has already received aspirin. Also assume that a cardiologist is not available at your facility and the closest transfer facility is at least 6 hours away by ground transport due to a severe winter storm. Please select the single most appropriate answer.

    For unknown reasons, people are opting not to fibrinolyse case 2, question 4 (5.1%), and case 3, question

    Table 1 Subgroup analysis of fibrinolysis rate for isolated

    posterior wall AMI

    Those who requested

    additional leads (n = 335)

    Those who did not request additional leads (n = 93)

    Fibrinolysis

    n 229

    P

    %

    68.4

    .0001

    26

    28.0

    6 (13.6%). Perhaps recent literature on the use of low- molecular-weight heparin, glycoprotein inhibitors, and intravenous Antiplatelet agents has confused EPs about the management of acute coronary syndromes, even in the setting of obvious AMI needing prompt revascularization. Less respondents fibrinolysed case 3, question 6 (86.4%),

    than did case 2, question 4 (94.9%). Perhaps some respondents were hesitant in the setting of cardiogenic

    

    Fig. 2 A, B, C, Results of clinical questions.

    shock. Nitrate-induced hypotension has been well de- scribed in patients with right ventricular AMI. STE in lead V₄R should prompt the EP to restrict the use of nitrates and other vasodilating agents while judiciously adminis- tering crystalloid infusions to avoid systemic hypotension. Case 3 was designed to prompt the respondent to consider right ventricular AMI and select bElectrocardiogram with posterior and right ventricular leadsQ as the most appropriate answer to question 5. Treatment of nitrate- induced hypotension with intravenous fluids should not preclude prompt revascularization therapy for right ven- tricular AMI.

    This study is limited by several issues, primarily involving study design. The 14.7% response rate is low and may be subject to a reporting bias due to the internet- based design that relies on uncompensated volunteer participation. A conventional, paper-based survey distributed by US mail may have yielded a higher response rate. Also, the scenarios were hypothetical, contrived situations– highly artificial–and very much unlike actual emergency department encounters. In real-time evaluation of the patient, the EP may use numerous diagnostic tools simultaneously or in close succession. Our survey only allowed the respondent to choose a single diagnostic modality.

    This survey suggests that EPs less often recognize posterior wall and right ventricular AMI, whether it be isolated or concomitant with other STEMI patterns. This lack of recognition of these infarction patterns, however, only appears to affect management in one area–that of the isolated posterior AMI–in which fibrinolysis was less often used.

    Michael P. Somers MD Jesse M. Pines MD, MBA William J. Brady MD

    Department of Emergency Medicine University of Virginia Health System Charlottesville, VA 22908-0699, USA

    Dominique Caovan MD School of Medicine University of Virginia Charlottesville, VA, USA

    doi:10.1016/j.ajem.2005.04.010

    References

    Somers MP, Brady WJ, Bateman DC, et al. Additional electrocardio- graphic leads in the ED chest pain patient: right ventricular and posterior leads. Am J Emerg Med 2003;21:563 – 73.

11. Brady WJ, Erling B, Pollack M, et al. Electrocardiographic manifes- tations: acute posterior wall myocardial infarction. J Emerg Med 2001;20:391 – 401.
12. Novak PG, Davies C, Ken GG. Survey of British Columbia cardiologists’ and emergency physicians’ practice of using nonstandard EKG leads (V₄R to V₆R and V₇ to V₉) in the diagnosis and treatment of acute myocardial infarction. Can J Cardiol 1999;15:967 – 72.
13. Zehender M, Kasper W, Kauder E, et al. Eligibility for and benefit of thrombolytic therapy in Inferior myocardial infarction: focus on the Prognostic importance of Right ventricular infarction. J Am Coll Cardiol 1994;24:362 – 9.
14. Matetzky S, Freimark D, Chouraqui P, et al. Significance of ST segment elevations in posterior chest leads (V₇ to V₉) in patients with acute inferior myocardial infarction: application for thrombolytic therapy. J Am Coll Cardiol 1998;31:506 – 11.
15. Boden WE, Kleiger RE, Gibson RS, et al. electrocardiographic evolution of posterior acute myocardial infarction: importance of early precordial ST-segment depression. Am J Cardiol 1987;59:782.