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Asymptomatic ST elevation myocardial infarction
ARTICLE IN PRESS Heart & Lung ■■ (2018) ■■–■■
Contents lists available at ScienceDirect
Heart & Lung j o u r n a l h o m e p a g e : w w w. h e a r t a n d l u n g . c o m
Case Report
Asymptomatic ST elevation myocardial infarction Kenton L. Anderson, MD a,*, Neel A. Shah, MD b, Moises Gallegos, MD b, I-Hui Chiang, MD c a Department
of Emergency Medicine, Stanford University School of Medicine, 900 Welch Road, Palo Alto, CA 94304, USA Department of Emergency Medicine, Baylor College of Medicine, 1504 Taub Loop, Houston, TX 77030, USA c Department of Medicine, Division of Cardiology, Baylor College of Medicine, 1220 Main St., Houston, TX 77030, USA b
A R T I C L E
I N F O
Article history: Received 27 January 2018 Accepted 28 April 2018 Available online Keywords: ST elevation myocardial infarction Asymptomatic Silent
A B S T R A C T
Background: A 71-year-old non-smoking female with a history of diabetes, hypertension, hyperlipidemia and end-stage renal disease presented to the emergency department for right leg pain due to an ankle fracture. Case: The patient’s initial electrocardiogram (ECG) revealed ST segment elevations in the anterior leads. She denied any chest pain, shortness of breath, fatigue, lightheadedness, palpitations, nausea or diaphoresis. Her initial laboratory Troponin I resulted 35.9 ng/mL. Coronary catheterization demonstrated 99% occlusion of the left anterior descending (LAD) coronary artery. The patient had 2 drug eluting stents placed in the LAD with 10% residual stenosis. Conclusion: Although witnessing an ongoing asymptomatic ST elevation myocardial infarction (STEMI) is rare, this case highlights the importance of early revascularization when the ECG demonstrates a STEMI, even in the absence of symptoms for patients at risk for silent myocardial infarctions. © 2018 Elsevier Inc. All rights reserved.
Introduction
Case report
The incidence of asymptomatic ST-segment elevation myocardial infarction (STEMI) is unknown. Asymptomatic myocardial infarctions (MIs) have a highly variable prevalence depending on the population studied; however, it is clear that the prevalence of silent MI increases markedly with increasing age. Reported prevalences range from 0.3–0.5% among younger subjects and 3.4–6.4% in older subjects.1–5 Silent MI is usually discovered inadvertently during routine electrocardiogram (ECG) examinations which reveal the existence of abnormal Q waves.1 Unfortunately silent myocardial ischemia is an independent predictor of increased morbidity and mortality.6 Only two previous reports have revealed an ongoing asymptomatic STEMI; one was complicated by hyperkalemia.7,8 We report a case of an ongoing STEMI in a patient whose only complaint was leg pain from a recent fracture.
A 71-year-old non-smoker female with a history of diabetes, hypertension, hyperlipidemia, and end-stage renal disease (ESRD) presented to the emergency department (ED) for right leg pain due to leg fractures. The patient had been evaluated for acute right bimalleolar ankle and right patellar fractures at another ED, nine days earlier, where she was placed in a splint and referred to an orthopedic clinic for further management of the fractures. The patient was unable to follow-up with the orthopedic surgeon as arranged and had missed a hemodialysis session the day prior to presentation because she was having difficulty ambulating due to leg pain. On the day of her presentation to the ED, she had called the local fire department to help her transfer from a chair to her bed because she was having difficulty ambulating; the paramedics from the fire department brought her to the ED for further evaluation of her leg pain. An electrocardiogram (ECG) was performed in the ED because the patient had missed her scheduled dialysis session the day prior. The ECG demonstrated ST elevations in the anterior leads which were not present on prior ECGs (Figure 1). Her point-of-care potassium level was 5.2 mEq/L. The attending emergency physician had the ECG repeated to verify that the ECG had been performed on the correct patient since she was denying any symptoms other than leg pain. The patient denied any chest discomfort, shortness of breath, fatigue, lightheadedness, palpitations, nausea or diaphoresis. No family or past medical history of cardiac disease was known,
Conflict of interests: None. Funding: This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. Author contributions: Each of the authors contributed to drafting the article, revising it critically for important intellectual content, and final approval of the version to be submitted. * Corresponding author. Fax: (650) 723-0121. E-mail address: [email protected] (K.L. Anderson). 0147-9563/$ – see front matter © 2018 Elsevier Inc. All rights reserved. https://doi.org/10.1016/j.hrtlng.2018.04.012
ARTICLE IN PRESS K.L. Anderson et al. / Heart & Lung ■■ (2018) ■■–■■
2
Fig. 1. The 12-lead ECG performed on presentation to the emergency department showing ST segment elevation predominantly in the anterior leads.
however the patient had abnormal ankle-brachial indices suggestive of peripheral artery disease. An abnormal nuclear stress test had been followed by a negative coronary catheterization a decade prior. The repeat ECG was identical to the initial ECG performed, and the cardiac catheterization team was immediately mobilized. On physical exam, the patient was not in any distress, and her vital signs were within normal limits. On auscultation, her heart sounds were normal without murmurs, gallops or rubs. Her lungs were clear and her extremities were non-edematous. While the catheterization team was mobilizing, the attending cardiologist performed a point-of-care echocardiogram (echo) in the ED which did not show any wall motion abnormalities. While the echo was being performed, the patient’s point-of-care Troponin I resulted 8.31 ng/mL. Sixteen minutes later her laboratory Troponin I resulted 35.9 ng/mL; she was taken to the catheterization laboratory shortly thereafter where she was found to have 99% stenosis of the mid left anterior descending (LAD) coronary artery (Figure 2). She had two drug eluting stents placed in the LAD with 10% residual stenosis. An echo performed on hospital day 3 revealed mid to distal septum/apex as well as anterior/anterolateral wall akinesis, impaired relaxation of the left ventricle (LV), increased LV filling pressures and a severely dilated left atrium. Due to a lack of funding and her dependence on dialysis, the patient was unable to be discharged to a nursing facility or rehabilitation center, but she was eventually discharged on hospital day 18 with a house call program established for her ongoing medical care. There were no adverse cardiac events until 2 months after discharge, when the patient was admitted with MI. The patient died of complications from presumed dialysis catheter associated sepsis approximately 3 months after discharge.
and had missed a dialysis session, her potassium levels were normal. In all three cases the patients had multiple risk factors for silent MI including old age, hypertension, and diabetes.1 These similarities highlight the recommendation that patients with multiple risk factors for silent MI, especially diabetes, have a need for interdisciplinary care, including prevention, early detection and active management of cardiovascular disease.9–11 Little is known about the phenomenon of silent myocardial infarction and less is known about asymptomatic STEMI. One retrospective analysis demonstrated that painless STEMI is more common in diabetics, women, non-smokers, normolipidemics, and the elderly and that painless STEMI is associated with worse outcomes than painful STEMI.6 This analysis highlights the presence or absence of pain as a symptom but does not specifically explore
Discussion We present a case of an ongoing asymptomatic STEMI. There have only been two other cases reported of an ongoing asymptomatic STEMI; one was confounded by hyperkalemia which can cause a pseudo-infarction pattern of ST elevation without MI.7,8 In that case, bedside echo was used to identify a regional wall motion abnormality and ultimately led to cardiac catheterization revealing a culprit lesion. In our case, although the patient had a history of ESRD
Fig. 2. Cardiac catheterization revealing the left coronary system. The left anterior descending artery is marked by the black arrow, and the filling defect is marked by the black circle.
ARTICLE IN PRESS K.L. Anderson et al. / Heart & Lung ■■ (2018) ■■–■■
truly asymptomatic STEMI devoid of even atypical symptoms. Similarly, analyses that examine unrecognized MI focus on angina pectoris as the symptom in question and do not explore the presence of other symptoms.2,12 This case also highlights the importance for early revascularization when the ECG demonstrates STEMI, even in the absence of symptoms for patients at risk for silent MI. Extensive evidence and the most recent ACC/AHA Guidelines demonstrate and reiterate that the expeditious restoration of flow in the obstructed infarct artery is a key determinant of short and long-term outcomes in STEMI.13–17 Unfortunately, silent STEMI patients have significantly longer door-to-balloon times and higher rates of adverse short and long-term outcomes than painful STEMI patients; the exact cause for higher rates of adverse outcomes in painless STEMI is unclear but may represent longer ischemic duration and subsequent total ischemic burden.18 Conclusion Witnessing an ongoing asymptomatic STEMI is a rare event. Although there are several conditions that cause elevated ST segments on ECG, suspicion for STEMI should be high among patients at high risk for painless MI. These patients deserve the same rapid intervention that patients with symptomatic STEMI would receive. References 1. Valensi P, Lorgis L, Cottin Y. Prevalence, incidence, predictive factors and prognosis of silent myocardial infarction: a review of the literature. Arch Cardiovasc Dis. 2011;104:178–188. doi:10.1016/j.acvd.2010.11.013. 2. Sigurdsson E, Thorgeirsson G, Sigvaldason H, Sigfusson N. Unrecognized myocardial infarction: epidemiology, clinical characteristics, and the prognostic role of angina pectoris. The Reykjavik Study. Ann Intern Med. 1995;122:96–102. 3. Jónsdóttir LS, Sigfusson N, Sigvaldason H, Thorgeirsson G. Incidence and prevalence of recognised and unrecognised myocardial infarction in women. The Reykjavik Study. Eur Heart J. 1998;19:1011–1018. 4. Sheifer SE, Gersh BJ, Yanez ND 3rd, Ades PA, Burke GL, Manolio TA. Prevalence, predisposing factors, and prognosis of clinically unrecognized myocardial infarction in the elderly. J Am Coll Cardiol. 2000;35:119–126.
3
5. Nadelmann J, Frishman WH, Ooi WL, et al. Prevalence, incidence and prognosis of recognized and unrecognized myocardial infarction in persons aged 75 years or older: the Bronx Aging Study. Am J Cardiol. 1990;66:533–537. 6. Gottlieb SO, Gottlieb SH, Achuff SC, et al. Silent ischemia on Holter monitoring predicts mortality in high-risk postinfarction patients. JAMA. 1988;259:1030– 1035. 7. Abdallah M, Raza R, Abdallah T, McCord D, Khoueiry G. A rare case of silent transmural myocardial infarction with diffuse ST elevations complicated by concomitant severe hyperkalemia. Heart Lung. 2014;43:286–288. doi:10.1016/ j.hrtlng.2014.04.017. 8. Draman MS, Thabit H, Kiernan TJ, O’Neill J, Sreenan S, McDermott JH. A silent myocardial infarction in the diabetes outpatient clinic: case report and review of the literature. Endocrinol Diabetes Metab Case Rep. 2013;2013:130058. doi:10 .1530/EDM-13-0058. 9. Arenja N, Mueller C, Ehl NF, et al. Prevalence, extent, and independent predictors of silent myocardial infarction. Am J Med. 2013;126:515–522. doi:10.1016/j .amjmed.2012.11.028. 10. Zellweger MJ, Hachamovitch R, Kang X, et al. Prognostic relevance of symptoms versus objective evidence of coronary artery disease in diabetic patients. Eur Heart J. 2004;25:543–550. 11. Jeger RV, Bonetti PO, Zellweger MJ, et al. Influence of revascularization on long-term outcome in patients > or =75 years of age with diabetes mellitus and angina pectoris. Am J Cardiol. 2005;96:193–198. 12. Sheifer SE, Manolio TA, Gersh BJ. Unrecognized myocardial infarction. Ann Intern Med. 2001;135:801–811. 13. O’Gara PT, Kushner FG, Ascheim DD, et al. American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127:e362–e425. doi:10.1161/CIR.0b013e3182742cf6. 14. De Luca G, Suryapranata H, Zijlstra F, et al. Symptom-onset-to-balloon time and mortality in patients with acute myocardial infarction treated by primary angioplasty. J Am Coll Cardiol. 2003;42:991–997. 15. Boersma E, Mercado N, Poldermans D, Gardien M, Vos J, Simoons ML. Acute myocardial infarction. Lancet. 2003;361:847–858. 16. De Luca G, Suryapranata H, Ottervanger JP, Antman EM. Time delay to treatment and mortality in primary angioplasty for acute myocardial infarction: every minute of delay counts. Circulation. 2004;109:1223–1225. 17. Conlon PJ, Krucoff MW, Minda S, Schumm D, Schwab SJ. Incidence and long term significance of transient ST segment deviation in haemodialysis patients. Clin Nephrol. 1998;49:236–239. 18. Cho JY, Jeong MH, Ahn YK, et al. Korea Acute Myocardial Infarction Registry Investigators. Comparison of outcomes of patients with painless versus painful ST-segment elevation myocardial infarction undergoing percutaneous coronary intervention. Am J Cardiol. 2012;109:337–343. doi:10.1016/j.amjcard.2011.09 .017.
Contents lists available at ScienceDirect
Heart & Lung j o u r n a l h o m e p a g e : w w w. h e a r t a n d l u n g . c o m
Case Report
Asymptomatic ST elevation myocardial infarction Kenton L. Anderson, MD a,*, Neel A. Shah, MD b, Moises Gallegos, MD b, I-Hui Chiang, MD c a Department
of Emergency Medicine, Stanford University School of Medicine, 900 Welch Road, Palo Alto, CA 94304, USA Department of Emergency Medicine, Baylor College of Medicine, 1504 Taub Loop, Houston, TX 77030, USA c Department of Medicine, Division of Cardiology, Baylor College of Medicine, 1220 Main St., Houston, TX 77030, USA b
A R T I C L E
I N F O
Article history: Received 27 January 2018 Accepted 28 April 2018 Available online Keywords: ST elevation myocardial infarction Asymptomatic Silent
A B S T R A C T
Background: A 71-year-old non-smoking female with a history of diabetes, hypertension, hyperlipidemia and end-stage renal disease presented to the emergency department for right leg pain due to an ankle fracture. Case: The patient’s initial electrocardiogram (ECG) revealed ST segment elevations in the anterior leads. She denied any chest pain, shortness of breath, fatigue, lightheadedness, palpitations, nausea or diaphoresis. Her initial laboratory Troponin I resulted 35.9 ng/mL. Coronary catheterization demonstrated 99% occlusion of the left anterior descending (LAD) coronary artery. The patient had 2 drug eluting stents placed in the LAD with 10% residual stenosis. Conclusion: Although witnessing an ongoing asymptomatic ST elevation myocardial infarction (STEMI) is rare, this case highlights the importance of early revascularization when the ECG demonstrates a STEMI, even in the absence of symptoms for patients at risk for silent myocardial infarctions. © 2018 Elsevier Inc. All rights reserved.
Introduction
Case report
The incidence of asymptomatic ST-segment elevation myocardial infarction (STEMI) is unknown. Asymptomatic myocardial infarctions (MIs) have a highly variable prevalence depending on the population studied; however, it is clear that the prevalence of silent MI increases markedly with increasing age. Reported prevalences range from 0.3–0.5% among younger subjects and 3.4–6.4% in older subjects.1–5 Silent MI is usually discovered inadvertently during routine electrocardiogram (ECG) examinations which reveal the existence of abnormal Q waves.1 Unfortunately silent myocardial ischemia is an independent predictor of increased morbidity and mortality.6 Only two previous reports have revealed an ongoing asymptomatic STEMI; one was complicated by hyperkalemia.7,8 We report a case of an ongoing STEMI in a patient whose only complaint was leg pain from a recent fracture.
A 71-year-old non-smoker female with a history of diabetes, hypertension, hyperlipidemia, and end-stage renal disease (ESRD) presented to the emergency department (ED) for right leg pain due to leg fractures. The patient had been evaluated for acute right bimalleolar ankle and right patellar fractures at another ED, nine days earlier, where she was placed in a splint and referred to an orthopedic clinic for further management of the fractures. The patient was unable to follow-up with the orthopedic surgeon as arranged and had missed a hemodialysis session the day prior to presentation because she was having difficulty ambulating due to leg pain. On the day of her presentation to the ED, she had called the local fire department to help her transfer from a chair to her bed because she was having difficulty ambulating; the paramedics from the fire department brought her to the ED for further evaluation of her leg pain. An electrocardiogram (ECG) was performed in the ED because the patient had missed her scheduled dialysis session the day prior. The ECG demonstrated ST elevations in the anterior leads which were not present on prior ECGs (Figure 1). Her point-of-care potassium level was 5.2 mEq/L. The attending emergency physician had the ECG repeated to verify that the ECG had been performed on the correct patient since she was denying any symptoms other than leg pain. The patient denied any chest discomfort, shortness of breath, fatigue, lightheadedness, palpitations, nausea or diaphoresis. No family or past medical history of cardiac disease was known,
Conflict of interests: None. Funding: This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. Author contributions: Each of the authors contributed to drafting the article, revising it critically for important intellectual content, and final approval of the version to be submitted. * Corresponding author. Fax: (650) 723-0121. E-mail address: [email protected] (K.L. Anderson). 0147-9563/$ – see front matter © 2018 Elsevier Inc. All rights reserved. https://doi.org/10.1016/j.hrtlng.2018.04.012
ARTICLE IN PRESS K.L. Anderson et al. / Heart & Lung ■■ (2018) ■■–■■
2
Fig. 1. The 12-lead ECG performed on presentation to the emergency department showing ST segment elevation predominantly in the anterior leads.
however the patient had abnormal ankle-brachial indices suggestive of peripheral artery disease. An abnormal nuclear stress test had been followed by a negative coronary catheterization a decade prior. The repeat ECG was identical to the initial ECG performed, and the cardiac catheterization team was immediately mobilized. On physical exam, the patient was not in any distress, and her vital signs were within normal limits. On auscultation, her heart sounds were normal without murmurs, gallops or rubs. Her lungs were clear and her extremities were non-edematous. While the catheterization team was mobilizing, the attending cardiologist performed a point-of-care echocardiogram (echo) in the ED which did not show any wall motion abnormalities. While the echo was being performed, the patient’s point-of-care Troponin I resulted 8.31 ng/mL. Sixteen minutes later her laboratory Troponin I resulted 35.9 ng/mL; she was taken to the catheterization laboratory shortly thereafter where she was found to have 99% stenosis of the mid left anterior descending (LAD) coronary artery (Figure 2). She had two drug eluting stents placed in the LAD with 10% residual stenosis. An echo performed on hospital day 3 revealed mid to distal septum/apex as well as anterior/anterolateral wall akinesis, impaired relaxation of the left ventricle (LV), increased LV filling pressures and a severely dilated left atrium. Due to a lack of funding and her dependence on dialysis, the patient was unable to be discharged to a nursing facility or rehabilitation center, but she was eventually discharged on hospital day 18 with a house call program established for her ongoing medical care. There were no adverse cardiac events until 2 months after discharge, when the patient was admitted with MI. The patient died of complications from presumed dialysis catheter associated sepsis approximately 3 months after discharge.
and had missed a dialysis session, her potassium levels were normal. In all three cases the patients had multiple risk factors for silent MI including old age, hypertension, and diabetes.1 These similarities highlight the recommendation that patients with multiple risk factors for silent MI, especially diabetes, have a need for interdisciplinary care, including prevention, early detection and active management of cardiovascular disease.9–11 Little is known about the phenomenon of silent myocardial infarction and less is known about asymptomatic STEMI. One retrospective analysis demonstrated that painless STEMI is more common in diabetics, women, non-smokers, normolipidemics, and the elderly and that painless STEMI is associated with worse outcomes than painful STEMI.6 This analysis highlights the presence or absence of pain as a symptom but does not specifically explore
Discussion We present a case of an ongoing asymptomatic STEMI. There have only been two other cases reported of an ongoing asymptomatic STEMI; one was confounded by hyperkalemia which can cause a pseudo-infarction pattern of ST elevation without MI.7,8 In that case, bedside echo was used to identify a regional wall motion abnormality and ultimately led to cardiac catheterization revealing a culprit lesion. In our case, although the patient had a history of ESRD
Fig. 2. Cardiac catheterization revealing the left coronary system. The left anterior descending artery is marked by the black arrow, and the filling defect is marked by the black circle.
ARTICLE IN PRESS K.L. Anderson et al. / Heart & Lung ■■ (2018) ■■–■■
truly asymptomatic STEMI devoid of even atypical symptoms. Similarly, analyses that examine unrecognized MI focus on angina pectoris as the symptom in question and do not explore the presence of other symptoms.2,12 This case also highlights the importance for early revascularization when the ECG demonstrates STEMI, even in the absence of symptoms for patients at risk for silent MI. Extensive evidence and the most recent ACC/AHA Guidelines demonstrate and reiterate that the expeditious restoration of flow in the obstructed infarct artery is a key determinant of short and long-term outcomes in STEMI.13–17 Unfortunately, silent STEMI patients have significantly longer door-to-balloon times and higher rates of adverse short and long-term outcomes than painful STEMI patients; the exact cause for higher rates of adverse outcomes in painless STEMI is unclear but may represent longer ischemic duration and subsequent total ischemic burden.18 Conclusion Witnessing an ongoing asymptomatic STEMI is a rare event. Although there are several conditions that cause elevated ST segments on ECG, suspicion for STEMI should be high among patients at high risk for painless MI. These patients deserve the same rapid intervention that patients with symptomatic STEMI would receive. References 1. Valensi P, Lorgis L, Cottin Y. Prevalence, incidence, predictive factors and prognosis of silent myocardial infarction: a review of the literature. Arch Cardiovasc Dis. 2011;104:178–188. doi:10.1016/j.acvd.2010.11.013. 2. Sigurdsson E, Thorgeirsson G, Sigvaldason H, Sigfusson N. Unrecognized myocardial infarction: epidemiology, clinical characteristics, and the prognostic role of angina pectoris. The Reykjavik Study. Ann Intern Med. 1995;122:96–102. 3. Jónsdóttir LS, Sigfusson N, Sigvaldason H, Thorgeirsson G. Incidence and prevalence of recognised and unrecognised myocardial infarction in women. The Reykjavik Study. Eur Heart J. 1998;19:1011–1018. 4. Sheifer SE, Gersh BJ, Yanez ND 3rd, Ades PA, Burke GL, Manolio TA. Prevalence, predisposing factors, and prognosis of clinically unrecognized myocardial infarction in the elderly. J Am Coll Cardiol. 2000;35:119–126.
3
5. Nadelmann J, Frishman WH, Ooi WL, et al. Prevalence, incidence and prognosis of recognized and unrecognized myocardial infarction in persons aged 75 years or older: the Bronx Aging Study. Am J Cardiol. 1990;66:533–537. 6. Gottlieb SO, Gottlieb SH, Achuff SC, et al. Silent ischemia on Holter monitoring predicts mortality in high-risk postinfarction patients. JAMA. 1988;259:1030– 1035. 7. Abdallah M, Raza R, Abdallah T, McCord D, Khoueiry G. A rare case of silent transmural myocardial infarction with diffuse ST elevations complicated by concomitant severe hyperkalemia. Heart Lung. 2014;43:286–288. doi:10.1016/ j.hrtlng.2014.04.017. 8. Draman MS, Thabit H, Kiernan TJ, O’Neill J, Sreenan S, McDermott JH. A silent myocardial infarction in the diabetes outpatient clinic: case report and review of the literature. Endocrinol Diabetes Metab Case Rep. 2013;2013:130058. doi:10 .1530/EDM-13-0058. 9. Arenja N, Mueller C, Ehl NF, et al. Prevalence, extent, and independent predictors of silent myocardial infarction. Am J Med. 2013;126:515–522. doi:10.1016/j .amjmed.2012.11.028. 10. Zellweger MJ, Hachamovitch R, Kang X, et al. Prognostic relevance of symptoms versus objective evidence of coronary artery disease in diabetic patients. Eur Heart J. 2004;25:543–550. 11. Jeger RV, Bonetti PO, Zellweger MJ, et al. Influence of revascularization on long-term outcome in patients > or =75 years of age with diabetes mellitus and angina pectoris. Am J Cardiol. 2005;96:193–198. 12. Sheifer SE, Manolio TA, Gersh BJ. Unrecognized myocardial infarction. Ann Intern Med. 2001;135:801–811. 13. O’Gara PT, Kushner FG, Ascheim DD, et al. American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127:e362–e425. doi:10.1161/CIR.0b013e3182742cf6. 14. De Luca G, Suryapranata H, Zijlstra F, et al. Symptom-onset-to-balloon time and mortality in patients with acute myocardial infarction treated by primary angioplasty. J Am Coll Cardiol. 2003;42:991–997. 15. Boersma E, Mercado N, Poldermans D, Gardien M, Vos J, Simoons ML. Acute myocardial infarction. Lancet. 2003;361:847–858. 16. De Luca G, Suryapranata H, Ottervanger JP, Antman EM. Time delay to treatment and mortality in primary angioplasty for acute myocardial infarction: every minute of delay counts. Circulation. 2004;109:1223–1225. 17. Conlon PJ, Krucoff MW, Minda S, Schumm D, Schwab SJ. Incidence and long term significance of transient ST segment deviation in haemodialysis patients. Clin Nephrol. 1998;49:236–239. 18. Cho JY, Jeong MH, Ahn YK, et al. Korea Acute Myocardial Infarction Registry Investigators. Comparison of outcomes of patients with painless versus painful ST-segment elevation myocardial infarction undergoing percutaneous coronary intervention. Am J Cardiol. 2012;109:337–343. doi:10.1016/j.amjcard.2011.09 .017.