Myocardial infarction management

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Myocardial infarction management involves salvaging as much myocardium as possible and to prevent further complications, thus the phrase "time is muscle".[1] Oxygen, aspirin, and nitroglycerin are usually administered as soon as possible. Morphine was classically used if nitroglycerin was not effective however it may increase mortality in the setting of NSTEMI.[2] A 2009 and 2010 review of high flow oxygen in myocardial infarction found increased mortality and infarct size, calling into question the recommendation about its routine use.[3][4]

Antiplatelet agents[edit]

Aspirin is useful not only for the primary prevention of vascular events but is also effective across the entire spectrum of acute coronary syndromes and forms part of the initial management strategy for patients with suspected STEMI. Aspirin has been shown to markedly reduce mortality and thus should be taken as soon as possible in those without an allergy to it.[5][6] Aspirin has an antiplatelet effect which inhibits formation of further thrombi (blood clots) that clog arteries. Chewing is the preferred method of administration, so that it can be absorbed quickly. Dissolved soluble preparations or sublingual administration can also be used. Because low doses take several days to achieve full antiplatelet effect, U.S. guidelines recommend a dose of 162–325 mg.[7] Australian guidelines recommend a dose of 150–300 mg.[8] Additionally, the antiplatelet agent clopidogrel improves outcomes in those who will be conservatively managed or undergo percutaneous coronary intervention.[9] It however may worsen outcomes in those who need urgent coronary artery bypass surgery.[9]


Nitroglycerin is used in the treatment of ACS/IHD to relieve anginal symptoms. It is associated with the decrease in myocardial stress due to peripheral vasodilation. The decrease of stress also decreases oxygen demand of the heart. The first line treatment for symptomatic relief of angina is sub-lingual nitroglycerin. Other formulations such as spray and IV can also be used.[10] In the body nitroglycerin donates three nitric oxide molecules, which activate a second messenger system leading to release of calcium ions. The release of calcium ions leads to a relaxation of vascular smooth muscles and vasodilation. Nitroglycerin should not be given if any phosphodiesterase type 5 inhibitors such as Viagra,[11] Cialis, Stondra, and Levitra have been taken by the casualty within the previous 24–48 hours[12] as the combination of the two could cause a serious drop in blood pressure. It should not be given to patients with systolic blood pressure (SBP) less than 90mmHg or 30mmHg or more below baseline.

Beta Blockers[edit]

In theory β-blockers decrease the effect of the sympathetic nervous system on the heart. Since it is known that the sympathetic nervous system increases the heart rate and blood pressure in order to increase the cardiac output. Hence its blockage spares the heart the extra work load. So, the immediate intravenous administration of beta blockers reduces cardiac index, heart rate and blood pressure.[13] Favorable effects are reduction in chest pain, in the proportion of patients with threatened infarction who actually evolve STEMI and in the development of ventricular arrhythmias.[14] It is reasonable to administer iv beta blockers promptly to STEMI patients, especially if a tachyarrhythmia or hypertension is present, in the absence of signs of heart failure or low output, increased risk of developing shock or other relative contraindications to beta blockers.[15]

Some new data showed that early treatment of heart attack patients with an inexpensive beta-blocker drug called metoprolol, while in transit to the hospital, can significantly reduce damage to the heart during a myocardial infarction[16] Inpatient beta-blocker use can be coupled with transvenous pacing, where a temporary pacemaker allows for the benefits of beta-blocker therapy while preventing uncontrolled bradycardia and maintaining sufficient cardiac output.[17]


Unfractionated heparin and enoxaparin result in similar outcomes at one year post MI.[18]

Myocardial Energy Metabolism Regulator[edit]

Mildronate is a clinically used pharmacological preconditioning agent and anti-ischemic drug.[19] It acts as a myocardial energy metabolism regulator by inhibiting fatty acid oxidation, and the carnitine biosynthesis and transport pathways,[20][21][22] in particular gamma-butyrobetaine dioxygenase[23][24][25] and carnitine acetyltransferase.[26] By regulating the effective carnitine concentration, treatment with mildronate shifts the myocardial energy metabolism from fatty acid oxidation to the more favourable glucose oxidation under ischemic conditions.[27]


Main article: Reperfusion therapy

The concept of reperfusion has become so central to the modern treatment of acute myocardial infarction, that we are said to be in the reperfusion era.[28][29] Patients who present with suspected acute myocardial infarction and ST segment elevation (STEMI) or new bundle branch block on the 12 lead ECG are presumed to have an occlusive thrombosis in an epicardial coronary artery. They are therefore candidates for immediate reperfusion, either with thrombolytic therapy, percutaneous coronary intervention (PCI) or when these therapies are unsuccessful, bypass surgery.

Individuals without ST segment elevation are presumed to be experiencing either unstable angina (UA) or non-ST segment elevation myocardial infarction (NSTEMI). They receive many of the same initial therapies and are often stabilized with antiplatelet drugs and anticoagulated. If their condition remains (hemodynamically) stable, they can be offered either late coronary angiography with subsequent restoration of blood flow (revascularization), or non-invasive stress testing to determine if there is significant ischemia that would benefit from revascularization. If hemodynamic instability develops in individuals with NSTEMIs, they may undergo urgent coronary angiography and subsequent revascularization. The use of thrombolytic agents is contraindicated in this patient subset, however.[30]

The basis for this distinction in treatment regimens is that ST segment elevations on an ECG are typically due to complete occlusion of a coronary artery. On the other hand, in NSTEMIs there is typically a sudden narrowing of a coronary artery with preserved (but diminished) flow to the distal myocardium. Anticoagulation and antiplatelet agents are given to prevent the narrowed artery from occluding.

At least 10% of patients with STEMI do not develop myocardial necrosis (as evidenced by a rise in cardiac markers) and subsequent Q waves on EKG after reperfusion therapy. Such a successful restoration of flow to the infarct-related artery during an acute myocardial infarction is known as "aborting" the myocardial infarction. If treated within the hour, about 25% of STEMIs can be aborted.[31]


Additional objectives are to prevent life-threatening arrhythmias or conduction disturbances. This requires monitoring in a coronary care unit and protocolised administration of antiarrhythmic agents. Antiarrhythmic agents are typically only given to individuals with life-threatening arrhythmias after a myocardial infarction and not to suppress the ventricular ectopy that is often seen after a myocardial infarction.[32][33][34]

Cardiac rehabilitation aims to optimize function and quality of life in those afflicted with a heart disease. This can be with the help of a physician, or in the form of a cardiac rehabilitation program.[35]

Physical exercise is an important part of rehabilitation after a myocardial infarction, with beneficial effects on cholesterol levels, blood pressure, weight, stress and mood.[35] Some patients become afraid of exercising because it might trigger another infarct.[36] Patients are stimulated to exercise, and should only avoid certain exerting activities. Local authorities may place limitations on driving motorised vehicles.[37] In most cases, the advice is a gradual increase in physical exercise during about 6–8 weeks following an MI.[38] If it doesn't feel too hard for the patient, the advice about exercise is then the same as applies to anyone else to gain health benefits, that is, at least 20–30 minutes of moderate exercise on most days (at least five days per week) to the extent of getting slightly short of breath.[38]

Some people are afraid to have sex after a heart attack. Most people can resume sexual activities after 3 to 4 weeks. The amount of activity needs to be dosed to the patient's possibilities.[39]

Emergency services[edit]

When symptoms of myocardial infarction occur, people wait an average of three hours, instead of doing what is recommended: calling for help immediately.[40][41] Acting immediately by calling the emergency services can improve outcomes for two reasons. First and most importantly, the emergency services can immediately save life from ventricular fibrillation, most often primary ventricular fibrillation, which occurs unexpectedly in more than 10% of all infarctions especially during the first hour of symptoms[citation needed][42] and second, immediate treatment of myocardial infarction can prevent sustained damage to the heart ("time is muscle").[1]

Emergency Medical Services (EMS) Systems vary considerably in their ability to evaluate and treat patients with suspected acute myocardial infarction. Some provide as little as first aid and early defibrillation. Others employ highly trained paramedics with sophisticated technology and advanced protocols.[43] Paramedic services are capable of providing oxygen, IV access, sublingual nitroglycerine, morphine, and aspirin. Some advanced paramedic systems can also perform 12-lead ECGs.[44] If a STEMI is recognized the paramedic may be able to contact the local PCI hospital and alert the emergency room physician, and staff of the suspected AMI. Some Paramedic services are capable of providing thrombolytic therapy in the prehospital setting, allowing reperfusion of the myocardium.[45][46]

With primary PCI emerging as the preferred therapy for ST-segment elevation myocardial infarction, EMS can play a key role in reducing door-to-balloon intervals (the time from presentation to a hospital ER to the restoration of coronary artery blood flow) by performing a 12-lead ECG in the field and using this information to triage the patient to the most appropriate medical facility.[47][48][49][50] In addition, the 12-lead ECG can be transmitted to the receiving hospital, which enables time saving decisions to be made prior to the arrival of the patient. This may include a "cardiac alert" or "STEMI alert" that calls in off duty personnel in areas where the cardiac cath lab is not staffed 24 hours a day.[51] Even in the absence of a formal alerting program, prehospital 12-lead ECGs are independently associated with reduced door to treatment intervals in the emergency department.[52]

Special cases[edit]


Cocaine associated myocardial infarction should be managed in a manner similar to other patients with acute coronary syndrome except beta blockers should not be used and benzodiazepines should be administered early.[53] The treatment itself may have complications. If attempts to restore the blood flow are initiated after a critical period of only a few hours, the result may be a reperfusion injury instead of amelioration.[54]

Wilderness setting[edit]

In wilderness first aid, a possible heart attack justifies evacuation by the fastest available means, often meaning the initiation of a MEDEVAC. The suspicion or provisional diagnosis of an MI means that it is inappropriate for the patient to walk out of the wilderness setting and will require them to be carried or conveyed in a vehicle. Aspirin, nitroglycerin, and oxygen can all be given with relative ease in a wilderness setting and should be administered as soon as possible in suspected cases of MI. Wilderness management of cardiac arrest differs slightly from that carried out in an urban setting in that it is generally considered acceptable to terminate a resuscitation attempt after 30 minutes if there has been no change in the patient's condition.

Air travel[edit]

Certified personnel traveling by commercial aircraft may be able to assist an MI patient by using the on-board first aid kit, which may contain some cardiac drugs (such as glyceryl trinitrate spray, aspirin, or opioid painkillers), an AED,[55] and oxygen. Pilots may divert the flight to land at a nearby airport. Cardiac monitors are being introduced by some airlines, and they can be used by both on-board and ground-based physicians.[56]

See also[edit]


  1. ^ a b TIME IS MUSCLE TIME WASTED IS MUSCLE LOST[dead link]. Early Heart Attack Care, St. Agnes Healthcare. Retrieved November 29, 2006.
  2. ^ Meine TJ, Roe MT, Chen AY, et al. (2005). "Association of intravenous morphine use and outcomes in acute coronary syndromes: results from the CRUSADE Quality Improvement Initiative". Am Heart J 149 (6): 1043–9. doi:10.1016/j.ahj.2005.02.010. PMID 15976786. 
  3. ^ "Routine use of oxygen in the treatment of myocardial infarction: systematic review -- Wijesinghe et al. 95 (3): 198 -- Heart". 
  4. ^ Cabello JB, Burls A, Emparanza JI, Bayliss S, Quinn T (2010). "Oxygen therapy for acute myocardial infarction". In Cabello, Juan B. Cochrane Database Syst Rev 6 (6): CD007160. doi:10.1002/14651858.CD007160.pub2. PMID 20556775. 
  5. ^ ISIS-2 Collaborative group (1988). "Randomized trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2". Lancet 2 (8607): 349–60. PMID 2899772. 
  6. ^ Brown AL, Mann NC, Daya M, Goldberg R, Meischke H, Taylor J, Smith K, Osganian S, Cooper L. (2000). "Demographic, belief, and situational factors influencing the decision to utilize emergency medical services among chest pain patients. Rapid Early Action for Coronary Treatment (REACT) study". Circulation 102 (2): 173–8. doi:10.1161/01.cir.102.2.173. PMID 10889127. 
  7. ^ Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, Hochman JS, Krumholz HM, Kushner FG, Lamas GA, Mullany CJ, Ornato JP, Pearle DL, Sloan MA, Smith SC Jr (2004). "ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction)". J Am Coll Cardiol 44 (3): 671–719. doi:10.1016/j.jacc.2004.07.002. PMID 15358045. 
  8. ^ Rossi S, editor. Australian Medicines Handbook 2006. Adelaide: Australian Medicines Handbook; 2006. ISBN 0-9757919-2-3.
  9. ^ a b Hoekstra J, Cohen M (April 2009). "Management of patients with unstable angina / non-ST-elevation myocardial infarction: a critical review of the 2007 ACC /AHA guidelines". Int. J. Clin. Pract. 63 (4): 642–55. doi:10.1111/j.1742-1241.2009.01998.x. PMC 2705816. PMID 19222616. 
  10. ^ Anderson JL, Adams CD, Antman EM, et al. (August 2007). "ACC/AHA 2007 guidelines for the management of patients with unstable angina/non ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non ST-Elevation Myocardial Infarction): developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons: endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine". Circulation 116 (7): e148–304. doi:10.1161/CIRCULATIONAHA.107.181940. PMID 17679616. 
  11. ^ Cheitlin, Melvin. "Use of Sildenafil (Viagra) in Patients With Cardiovascular Disease". Retrieved 9/6/2012. 
  12. ^ Cheitlin, Melvin. "Use of Sildenafil (Viagra) in Patients With Cardiovascular Disease". AHA. Retrieved 6 September 2012. 
  13. ^ Bates ER: Role of intravenous beta-blockers in the treatment of ST-elevation myocardial infarction: Of mice and men. Circulation 115:2904, 2007.
  14. ^ Freemantle N et al: Beta blockade after myocardial infarction: Systematic review and meta regression analysis. BMJ 318:1730, 1999.
  15. ^ Braunwald, E. (2012). ST-Segment Elevation Myocardial Infarction: Management. Braunwald's Heart disease: a textbook of cardiovascular medicine (9th ed., ). Philadelphia: Saunders.
  16. ^ B. Ibanez, C. Macaya, V. Sanchez-Brunete, G et al. (2013) Effect of Early Metoprolol on Infarct Size in ST-Segment-Elevation Myocardial Infarction Patients Undergoing Primary Percutaneous Coronary Intervention: The Effect of Metoprolol in Cardioprotection During an Acute Myocardial Infarction (METOCARD-CNIC) Tri. Circulation, 128 (14): 1495 OI:10.1161/%u200BCIRCULATIONAHA.113.003653
  17. ^ D. Overbay & L. Criddle (2004). Mastering Temporary Invasive Cardiac Pacing. Critical Care Nurse 24 (3): 25-32.
  18. ^ Morrow DA, Antman EM, Fox KA, et al. (September 2010). "One-year outcomes after a strategy using enoxaparin vs. unfractionated heparin in patients undergoing fibrinolysis for ST-segment elevation myocardial infarction: 1-year results of the ExTRACT-TIMI 25 trial". Eur. Heart J. 31 (17): 2097–102. doi:10.1093/eurheartj/ehq098. PMID 20400762. 
  19. ^ JSC Grindeks. (accessed May 17, 2012).
  20. ^ Sesti C, Simkhovich BZ, Kalvinsh I, Kloner RA (March 2006). "Mildronate, a novel fatty acid oxidation inhibitor and antianginal agent, reduces myocardial infarct size without affecting hemodynamics". J. Cardiovasc. Pharmacol. 47 (3): 493–9. doi:10.1097/01.fjc.0000211732.76668.d2. PMID 16633095. 
  21. ^ Liepinsh E, Vilskersts R, Loca D, Kirjanova O, Pugovichs O, Kalvinsh I, Dambrova M (December 2006). "Mildronate, an inhibitor of carnitine biosynthesis, induces an increase in gamma-butyrobetaine contents and cardioprotection in isolated rat heart infarction". J. Cardiovasc. Pharmacol. 48 (6): 314–9. doi:10.1097/01.fjc.0000250077.07702.23. PMID 17204911. 
  22. ^ Hayashi Y, Kirimoto T, Asaka N, Nakano M, Tajima K, Miyake H, Matsuura N (May 2000). "Beneficial effects of MET-88, a gamma-butyrobetaine hydroxylase inhibitor in rats with heart failure following myocardial infarction". Eur. J. Pharmacol. 395 (3): 217–24. doi:10.1016/S0014-2999(00)00098-4. PMID 10812052. 
  23. ^ Vaz FM, Wanders RJA (2002). "Carnitine biosynthesis in mammals". Biochem. J. 361: 417–29. doi:10.1042/0264-6021:3610417. 
  24. ^ Leung IK, Krojer TJ, Kochan GT, Henry L, von Delft F, Claridge TD, Oppermann U, McDonough MA, Schofield CJ (December 2010). "Structural and mechanistic studies on γ-butyrobetaine hydroxylase". Chem. Biol. 17 (12): 1316–24. doi:10.1016/j.chembiol.2010.09.016. PMID 21168767. 
  25. ^ Tars K, Rumnieks J, Zeltins A, Kazaks A, Kotelovica S, Leonciks A, Sharipo J, Viksna A, Kuka J, Liepinsh E, Dambrova M (August 2010). "Crystal structure of human gamma-butyrobetaine hydroxylase". Biochem. Biophys. Res. Commun. 398 (4): 634–9. doi:10.1016/j.bbrc.2010.06.121. PMID 20599753. 
  26. ^ Jaudzems K, Kuka J, Gutsaits A, Zinovjevs K, Kalvinsh I, Liepinsh E, Liepinsh E, Dambrova M (December 2009). "Inhibition of carnitine acetyltransferase by mildronate, a regulator of energy metabolism". J. Enzyme Inhib. Med. Chem. 24 (6): 1269–75. doi:10.3109/14756360902829527. PMID 19912061. 
  27. ^ Dambrova M, Liepinsh E, Kalvinsh I (August 2002). "Mildronate: Cardioprotective Action through Carnitine-Lowering Effect". Trends Cardiovasc. Med. 12 (6): 257–9. doi:10.1016/S1050-1738(02)00175-5. PMID 12242052. 
  28. ^ Lee KL, Woodlief LH, Topol EJ et al. (1995). "Predictors of 30-Day Mortality in the Era of Reperfusion for Acute Myocardial Infarction". Circulation 91 (6): 1659–1668. doi:10.1161/01.cir.91.6.1659. PMID 7882472. 
  29. ^ Stone GW, Grines CL, Browne KF et al. (1995). "Predictors of in-hospital and 6-month outcome after acute myocardial infarction in the reperfusion era: the Primary Angioplasty in Myocardial Infarction (PAMI) trail". J Am Coll Cardiol 25 (2): 370–377. doi:10.1016/0735-1097(94)00367-Y. PMID 7829790. 
  30. ^ "Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Fibrinolytic Therapy Trialists' (FTT) Collaborative Group.". Lancet 343 (8893): 311–22. February 1994. doi:10.1016/s0140-6736(94)91161-4. PMID 7905143. 
  31. ^ Verheugt FW, Gersh BJ, Armstrong PW (2006). "Aborted myocardial infarction: a new target for reperfusion therapy". Eur Heart J 27 (8): 901–4. doi:10.1093/eurheartj/ehi829. PMID 16543251. 
  32. ^ Echt DS, Liebson PR, Mitchell LB, Peters RW, Obias-Manno D, Barker AH, Arensberg D, Baker A, Friedman L, Greene HL, et al. (1991). "Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial". N Engl J Med 324 (12): 781–8. doi:10.1056/NEJM199103213241201. PMID 1900101. 
  33. ^ Waldo AL, Camm AJ, deRuyter H, Friedman PL, MacNeil DJ, Pauls JF, Pitt B, Pratt CM, Schwartz PJ, Veltri EP. (1996). "Effect of d-sotalol on mortality in patients with left ventricular dysfunction after recent and remote myocardial infarction. The SWORD Investigators. Survival With Oral d-Sotalol". Lancet 348 (9019): 7–12. doi:10.1016/S0140-6736(96)02149-6. PMID 8691967. 
  34. ^ Julian DG, Camm AJ, Frangin G, Janse MJ, Munoz A, Schwartz PJ, Simon P. (1997). "Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT. European Myocardial Infarct Amiodarone Trial Investigators". Lancet 349 (9053): 667–74. doi:10.1016/S0140-6736(96)09145-3. PMID 9078197. 
  35. ^ a b Life after a Heart Attack. U.S. National Heart, Lung and Blood Institute. Retrieved December 2, 2006.
  36. ^ Trisha Macnair. Recovering after a heart attack. BBC, December 2005. Retrieved December 2, 2006.
  37. ^ "Classification of Drivers' Licenses Regulations". Nova Scotia Registry of Regulations. May 24, 2000. Retrieved April 22, 2007. 
  38. ^ a b Patient UK > After a Myocardial Infarction Reviewed: 19 May 2010
  39. ^ "Heart Attack: Getting Back Into Your Life After a Heart Attack". American Academy of Family Physicians, updated March 2005. Retrieved December 4, 2006.
  40. ^ Heart attack first aid. MedlinePlus. Retrieved December 3, 2006.
  41. ^ Act In Time to Heart Attack Signs - NHLBI. Retrieved December 13, 2006.
  42. ^ Gheeraert, Peter. [http:// "Ventricular fibrillation during acute myocardial infarction"]. Retrieved 13 August 2010. 
  43. ^ Antman EM, Anbe DT, Armstrong PW, et al. (August 2004). "ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction--executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1999 guidelines for the management of patients with acute myocardial infarction)". J. Am. Coll. Cardiol. 44 (3): 671–719. doi:10.1016/j.jacc.2004.07.002. PMID 15358045. 
  44. ^ Alberta Occupational Competency Profile EMT Paramedic. Alberta College Of Paramedics. Updated January 2007, Retrieved June 29, 2011.
  45. ^ Morrow DA, Antman EM, Sayah A, et al. (July 2002). "Evaluation of the time saved by prehospital initiation of reteplase for ST-elevation myocardial infarction: results of The Early Retavase-Thrombolysis in Myocardial Infarction (ER-TIMI) 19 trial". J. Am. Coll. Cardiol. 40 (1): 71–7. doi:10.1016/S0735-1097(02)01936-8. PMID 12103258. 
  46. ^ Morrison LJ, Verbeek PR, McDonald AC, Sawadsky BV, Cook DJ. (2000). "Mortality and prehospital thrombolysis for acute myocardial infarction: A meta-analysis" (PDF). JAMA 283 (20): 2686–92. doi:10.1001/jama.283.20.2686. PMID 10819952. 
  47. ^ Rokos IC, Larson DM, Henry TD, et al. (2006). "Rationale for establishing regional ST-elevation myocardial infarction receiving center (SRC) networks". Am. Heart J. 152 (4): 661–7. doi:10.1016/j.ahj.2006.06.001. PMID 16996830. 
  48. ^ Moyer P, Feldman J, Levine J, et al. (June 2004). "Implications of the Mechanical (PCI) vs Thrombolytic Controversy for ST Segment Elevation Myocardial Infarction on the Organization of Emergency Medical Services: The Boston EMS Experience". Crit Pathw Cardiol 3 (2): 53–61. doi:10.1097/01.hpc.0000128714.35330.6d. PMID 18340140. 
  49. ^ Terkelsen CJ, Lassen JF, Nørgaard BL, et al. (April 2005). "Reduction of treatment delay in patients with ST-elevation myocardial infarction: impact of pre-hospital diagnosis and direct referral to primary percutanous coronary intervention". Eur. Heart J. 26 (8): 770–7. doi:10.1093/eurheartj/ehi100. PMID 15684279. T
  50. ^ Henry TD, Atkins JM, Cunningham MS, et al. (April 2006). "ST-segment elevation myocardial infarction: recommendations on triage of patients to heart attack centers: is it time for a national policy for the treatment of ST-segment elevation myocardial infarction?". J. Am. Coll. Cardiol. 47 (7): 1339–45. doi:10.1016/j.jacc.2005.05.101. PMID 16580518. 
  51. ^ Rokos I. and Bouthillet T., "The emergency medical systems-to-balloon (E2B) challenge: building on the foundations of the D2B Alliance," STEMI Systems, Issue Two, May 2007. Accessed June 16, 2007.
  52. ^ Cannon, Christopher (1999). Management of acute coronary syndromes. Totowa, NJ: Humana Press. ISBN 0-89603-552-2. 
  53. ^ McCord J, Jneid H, Hollander JE, et al. (April 2008). "Management of cocaine-associated chest pain and myocardial infarction: a scientific statement from the American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology". Circulation 117 (14): 1897–907. doi:10.1161/CIRCULATIONAHA.107.188950. PMID 18347214. 
  54. ^ Faxon DP (November 2005). "Coronary interventions and their impact on post myocardial infarction survival.". Clinical Cardiology 28 (11 Suppl 1): I38–44. PMID 16450811. 
  55. ^ Youngwith, Janice (2008-02-06). "Saving hearts in the air". Retrieved 2008-06-12. [dead link]
  56. ^ Dowdall N (November 2000). ""Is there a doctor on the aircraft?" Top 10 in-flight medical emergencies.". BMJ (Clinical research ed.) 321 (7272): 1336–7. doi:10.1136/bmj.321.7272.1336. PMC 1119071. PMID 11090520.