Myocardial Infarction Workup

  • Author: A Maziar Zafari, MD, PhD; Chief Editor: Eric H Yang, MD   more...
 
Updated: Feb 13, 2012
 

Approach Considerations

The objectives of laboratory testing and imaging include the following:

  • To determine the presence or absence of myocardial infarction for diagnosis and differential diagnosis (point–of-care testing and testing in central laboratory of cardiac biomarkers)
  • To characterize the locus, nature (STEMI or NSTEMI), and extent of myocardial infarction (ie, to estimate infarct size)
  • To detect recurrent ischemia or myocardial infarction (extension of myocardial infarction)
  • To detect early and late complications of myocardial infarction
  • To estimate the patient's prognosis

Laboratory evaluation is particularly helpful in the presence of comorbid conditions that may affect the patient's prognosis and influence his or her care. Such comorbidities include the following:

  • Diabetes
  • Renal or hepatic failure
  • Anemia
  • Bleeding disorders
  • Respiratory failure

Cardiac imaging

The role of imaging in ACSs is broad, but the procedures are primarily used to confirm or rule out coronary disease. Furthermore, it may help define the anatomy and degree of myocardial perfusion abnormalities. In lower-risk individuals in whom ACS is suspected and who do not have serial ECG changes or positive serial cardiac biomarker findings, the ACC/AHA guidelines recommend some form of stress testing to help confirm the diagnosis and guide therapy.[22] In individuals with highly probable or confirmed ACS, consultation to a cardiologist is made to so that coronary angiography can be performed m to definitively diagnose or rule out coronary artery disease. Based on the angiographic result and patient comorbidities, subsequent treatment recommendations can be made, which may include medical therapy, percutaneous coronary intervention (PCI), or coronary artery bypass grafting (CABG) surgery.

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Cardiac Biomarkers/Enzymes

The American College of Cardiology/American Heart Association (ACC/AHA) guidelines on unstable angina/NSTEMI recommend that in patients with suspected myocardial infarction, cardiac biomarkers should be measured at presentation. The guidelines recommend a total turnaround time of less than 1 hour and preferably less than 30 minutes for the cardiac biomarker measurements.

Several studies have shown that implementation of point-of-care testing (POCT) for cardiac biomarkers may improve early diagnosis as well as decrease patient length of stay.[25] Additional studies are needed to determine the relative analytic performance of different POCT assays for troponins, creatine phosphokinase–myocardial band (CPK-MB) and myoglobin alone or in combination in the current state of analytical technologies.

If initial markers are negative and have been measured within 6 hours of symptom onset, the biomarkers should be remeasured within 8-12 hours after symptom onset. Remeasuring cardiac enzyme levels at regular intervals for the first 24 hours is a reasonable approach to improving the sensitivity of detection of myocardial necrosis, and the degree of positivity can be important for prognostication. Note the graph below.[22]

Graph Graph

In addition, biomarkers alone or as part of accelerated diagnostic protocols (ADP) can reduce the number of patients with a missed diagnosis of NSTEMI who are at increased risk of major adverse cardiac events. Furthermore, such approaches can facilitate early discharge from the ED in patients who a have a low short-term risk of a major cardiac event as reported in The Asia-Pacific Evaluation of Chest Pain Trial (ASPECT).[26]

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Troponin Levels

Troponin is a contractile protein that normally is not found in serum. It is released only when myocardial necrosis occurs.

Troponin levels are now considered to be the criterion standard for defining and diagnosing myocardial infarction, according to the American College of Cardiology (ACC)/American Heart Association (AHA) consensus statement on myocardial infarction.[27, 28]

Positive troponin levels are considered virtually diagnostic of myocardial infarction, according to a revised version of the ACC/AHA consensus statement, as they are without equal in combined specificity and sensitivity in this diagnosis. Reichlan et al suggest that absolute changes in troponin levels have a significantly higher diagnostic accuracy for acute myocardial infarction than relative changes.[29]

Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to baseline over 5-14 days.

Improved cardiac troponin assays offer even greater diagnostic accuracy than the standard assays do, according to a study by Reichlin et al. This is especially true for the early diagnosis of acute myocardial infarction, particularly in patients with a recent onset of chest pain, according to the investigators.[30]

Keller et al suggest that among patients with suspected acute coronary syndrome, highly sensitive troponin I assay (hsTnI) or contemporary troponin I assay (cTnI) determination 3 hours after admission for chest pain may facilitate early rule-out of acute myocardial infarction. A serial change in hsTnI or cTnI levels from admission (using the 99th percentile diagnostic cutoff value) to 3 hours postadmission may aid in early diagnosis of acute myocardial infarction.[31]

According to Hubbard et al, in patients without heart failure with marginally increased troponin levels, a low BNP level (BNP ≤80 pg/mL) cannot identify patients at low-risk for 30-day acute MI or death.[32]

MI is a strong trigger of N-terminal pro-B-type natriuretic peptide (NT-proBNP) release, and checking these levels may improve the early diagnosis and risk stratification of patients with suspected acute MI.[33]

For more information, see Use of Cardiac Markers in the Emergency Department.

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Creatine Kinase Levels

The 3 CK isoenzymes are as follows:

  • CK with muscle subunits (CK-MM), which is found mainly in skeletal muscle
  • CK with brain subunits (CK-BB), which is found predominantly in the brain
  • CK-MB, which is found mainly in the heart

Serial measurements of CK-MB isoenzyme levels were previously the standard criterion for the diagnosis of myocardial infarction. CK-MB levels increase within 3-12 hours of the onset of chest pain, reach peak values within 24 hours, and return to baseline after 48-72 hours. levels peak earlier (wash out) if reperfusion occurs. Sensitivity is approximately 95%, with high specificity. However, sensitivity and specificity are not as high as they are for troponin levels, and, as mentioned above, the trend has favored using troponins for the diagnosis of myocardial infarction.

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Myoglobin levels

Myoglobin, a low-molecular-weight heme protein found in cardiac and skeletal muscle, is released more rapidly from infarcted myocardium than is troponin. Urine myoglobin levels rise within 1-4 hours from the onset of chest pain. Myoglobin levels are highly sensitive but not specific; they may be useful within the context of other studies and in the early detection of myocardial infarction in the emergency department (ED).

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Other Significant Laboratory Studies

Complete blood cell count

Obtain a complete blood cell (CBC) count if myocardial infarction is suspected in order to rule out anemia as a cause of decreased oxygen supply and prior to giving thrombolytics. Leukocytosis is also common, but not universal, in the setting of acute myocardial infarction.

A platelet count is necessary if a IIb/IIIa agent is considered; furthermore, the patient's white blood cell (WBC) count may be modestly elevated in the setting of myocardial infarction, signifying an acute inflammatory state. The platelet count may become dangerously low after the use of heparin because of heparin-induced thrombocytopenia (HIT). The leukocyte count may be normal initially, but it generally increases within 2 hours and peaks in 2-4 days, with predominance of polymorphonuclear leukocytes and a shift to the left. Elevations generally persist for 1-2 weeks.

Chemistry profile

In the setting of myocardial infarction, closely monitor potassium and magnesium levels. The creatinine level is also needed, prior to initiating treatment with an ACE inhibitor.

The erythrocyte sedimentation rate (ESR) rises above reference range values within 3 days and may remain elevated for weeks.

The serum lactate dehydrogenase (LDH) level rises above the reference range within 24 hours of myocardial infarction, reaches a peak within 3-6 days, and returns to the baseline within 8-12 days.

Blood oxygenation should be checked and repeatedly corrected if any clinical findings suggest hypoxemia; hypoxemia may result from pulmonary congestion, atelectasis, or ventilatory impairment secondary to complications of myocardial infarction or excessive sedation or analgesia. Fingertip oximetry may be adequate in the absence of carbon dioxide retention and may obviate puncture to assess arterial blood gases (ABGs). Such puncturing may lead to bleeding in patients being treated with thrombolytic drugs. However, normal oxygen saturation does not exclude impending respiratory failure.

Lipid profile

This may be helpful if obtained upon presentation, because levels can change after 12-24 hours of an acute illness.

C-reactive protein and other inflammation markers

Consider measuring C-reactive protein (CRP) levels and other inflammation markers upon presentation if an ACS is suspected.

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Electrocardiogram

As recommended by the most recent ACC/AHA guidelines for the management of unstable angina/NSTEMI, last updated in 2007, patients with active ongoing symptoms suggestive of an acute coronary syndrome should have early risk stratification by checking cardiac enzyme levels and undergoing a 12-lead ECG within 10 minutes of presentation of the emergency department. For patients with ongoing symptoms, serial ECGs should be performed to look for dynamic changes in the ST segment.[22]

The ECG is the most important tool in the initial evaluation and triage of patients in whom an ACS is suspected. It is confirmatory of the diagnosis in approximately 80% of cases. The electrocardiographic evidence of myocardial infarction is seen in the images below.

Acute anterior myocardial infarction. Acute anterior myocardial infarction. Acute inferior myocardial infarction. Acute inferior myocardial infarction. Posterolateral myocardial infarction. Posterolateral myocardial infarction. Acute inferior myocardial infarction on an electroAcute inferior myocardial infarction on an electrocardiogram.

Obtain an ECG immediately if myocardial infarction is considered or suspected. In patients with inferior myocardial infarction, record a right-sided ECG to rule out right ventricular infarct. Qualified personnel should review the ECG as soon as possible.

Electrocardiography should be performed serially upon presentation to evaluate progression and assess changes with and without pain. Obtain daily serial ECGs for the first 2-3 days and additionally as needed.

Because the symptoms of acute myocardial infarction can be subtle or protean, electrocardiography should be performed on any patient who is older than age 45 years and is experiencing any form of thoracoabdominal discomfort, including new epigastric pain or nausea.

In younger patients, an ECG should be considered when suggestive symptoms are present or when risk factors exist for early coronary artery disease. Younger patients are disproportionately represented in missed cases. An ECG is a rapid, low-risk, relatively low-cost measure.

Electrocardiographic abnormalities

The diagnosis may be established with certainty when typical ST-segment elevation persists for hours and is followed by inversion of T waves during the first few days and by the development of Q waves. However, initial ST depression or T-wave inversion associated with myocardial infarction is difficult to differentiate from that seen in the presence of ischemia without myocardial infarction or in unrelated conditions. ST-segment depression followed by T-wave inversion without the evolution of Q waves may result from non–Q-wave myocardial infarction or from subendocardial ischemia without myocardial infarction. True posterior-wall myocardial infarctions may cause precordial ST depression, inverted and hyperacute T waves, or both. ST-segment elevation and upright hyperacute T waves may be evident with the use of right-sided chest leads.

High probability of myocardial infarction is indicated either by ST-segment elevation greater than 1 mm in 2 anatomically contiguous leads or by the presence of new Q waves. Results that indicate intermediate probability of myocardial infarction are ST-segment depression, T-wave inversion, and other nonspecific ST-T wave abnormalities. Results that indicate low probability of myocardial infarction are normal findings on ECGs; however, normal or nonspecific findings on ECGs do not exclude the possibility of myocardial infarction.

Localization based on distribution of electrocardiographic abnormalities is as follows:

  • Inferior wall - II, III, aVF (See the image below.)The right-sided leads indicate ST-segment elevatioThe right-sided leads indicate ST-segment elevations in RV4 and RV5, which are consistent with a right ventricular infarct.
  • Lateral wall - I, aVL, V4 through V6 (See the image below.)The electrocardiogram shows lateral ST-segment eleThe electrocardiogram shows lateral ST-segment elevation that is consistent with a lateral wall acute myocardial infarction.
  • Anteroseptal - V1 through V3
  • Anterolateral - V1 through V6
  • Right ventricular - RV4, RV5 (See the image below.)This patient has a symptom duration of fewer than This patient has a symptom duration of fewer than 12 hours. In the setting of active chest pain and electrocardiographic changes showing acute myocardial infarction, he would still benefit from thrombolysis. His history of surgery is not a contraindication and his blood pressure can be controlled with nitrates and beta-blockers.
  • Posterior wall - R/S ratio greater than 1 in V1 and V2; T-wave changes (ie, upright) in V1, V8, and V9 (See the image below.)

Right ventricular myocardial infarction commonly is manifested by ST-segment elevation or Q waves detectable in right-sided precordial leads. The appearance of abnormalities in a large number of ECG leads often indicates extensive injury or concomitant pericarditis.

Anterior and anterolateral myocardial infarctions tend to involve more left ventricular myocardium than do inferior or true posterior myocardial infarctions. Hyperacute (symmetrical and often but not necessarily pointed) T waves are frequently an early sign of myocardial infarction at any locus. The characteristic electrocardiographic changes may be seen in conditions other than acute myocardial infarction. For example, patients with previous myocardial infarction and left ventricular aneurysm may have persistent ST elevation resulting from dyskinetic wall motion, rather than from acute ischemic injury. ST-segment changes may also be the result of misplaced precordial leads, hypothermia (elevated J point or Osborne waves), or hypothyroidism.

False q waves may be seen in septal leads in hypertrophic-obstructive cardiomyopathy (HOCM). They may also result from cardiac rotation.

Substantial T-wave inversion may be seen in some forms of left ventricular hypertrophy with secondary changes. The Q-T segment may be prolonged because of ischemia or hypomagnesemia. Saddleback ST-segment elevation (Brugada epsilon waves) may be seen in leads V1 -V3 in patients with a congenital predisposition to life-threatening arrhythmias. This elevation may be confused with that observed in acute anterior myocardial infarction. Brugada electrocardiographic changes may be seen during the administration of procainamide or a beta-blocker in patients whose ECG was previously normal. Brain injuries also may trigger changes in T waves.

Convex ST-segment elevation with upright or inverted T waves is generally indicative of myocardial infarction in the appropriate clinical setting. ST depression and T-wave changes may also indicate evolution of NSTEMI.

Unfortunately, in a series of missed myocardial infarction, the failure to recognize ischemic changes is frequent. The inferior leads, in particular, must be scrutinized carefully for any evidence of ST-segment elevation by using a straight edge across the T-P segments.

Another common error is to recognize ischemic changes and then discharge the patient without definitively proving that the changes were preexistent.

Nonischemic causes of ST-segment elevation include left ventricular hypertrophy, pericarditis, ventricular-paced rhythms, hypothermia, hyperkalemia, and left ventricular aneurysm. Nonischemic causes may lead to overtreatment.

Patients with a permanent pacemaker in place may confound recognition of STEMI by 12-lead ECG due to the presence of paced ventricular contractions.

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Cardiac Imaging

The roles and appropriateness of imaging in acute coronary syndromes (ACSs) are broad but primarily are used to confirm or rule out coronary disease. Furthermore, it may help define the anatomy and degree of myocardial perfusion abnormalities. In lower-risk individuals in whom ACS is suspected, serial ECG changes are not present, and serial cardiac biomarkers are negative, the ACC/AHA guidelines recommend for some form of stress testing to help confirm diagnosis and guide therapy.[22] In individuals with highly probable or confirmed ACS, consultation to a cardiologist is made to perform a coronary angiogram to definitively diagnose or rule out coronary artery disease. Based on the angiographic result and patient comorbidities, subsequent treatment recommendations can be made: medical therapy, percutaneous coronary intervention (PCI), or coronary artery bypass grafting (CABG) surgery.

To see complete information on Imaging in Myocardial Infarction, please go to the main article by clicking here .

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Coronary Artery Calcium Scoring

Coronary artery calcium scoring is an emerging technique that appears to add some predictive value in identifying patients at low risk for coronary artery disease. However, in high-risk patients or in those who have established coronary artery disease, the test does not appear to be helpful at this time.[27, 28]

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Contributor Information and Disclosures
Author

A Maziar Zafari, MD, PhD  Professor, Department of Medicine, Emory University School of Medicine; Chief, Section of Cardiology, Atlanta Veterans Affairs Medical Center

A Maziar Zafari, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American Heart Association, American Society of Echocardiography, and Association of Professors of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Luis C Afonso, MD  Assistant Professor, Department of Internal Medicine-Cardiology, Program Director of Cardiology Fellowship Program, Wayne State University; Director of Echocardiography Laboratory, Harper University Hospital

Luis C Afonso, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, and American Society of Echocardiography

Disclosure: Nothing to disclose.

Kul Aggarwal, MD, FACC  Professor of Clinical Medicine, Department of Internal Medicine, Division of Cardiology, University of Missouri-Columbia School of Medicine; Chief, Cardiology Section, Harry S Truman Veterans Hospital

Kul Aggarwal, MD, FACC is a member of the following medical societies: American College of Cardiology and American College of Physicians

Disclosure: Nothing to disclose.

Edward Bessman, MD  Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David L Coven, MD, PhD  Assistant Professor of Medicine, Columbia University College of Physicians and Surgeons; Attending Physician in Interventional Cardiology, St Luke's-Roosevelt Hospital Center

David L Coven, MD, PhD is a member of the following medical societies: American College of Physicians, American Medical Association, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Kenneth B Desser, MD  Clinical Professor, Director of Cardiology Fellowship, Banner Good Samaritan Medical Center, Phoenix, Arizona

Disclosure: Nothing to disclose.

Claudia Dima, MD  Fellow in Interventional Cardiology, Department of Cardiology, Banner Good Samaritan Medical Center

Disclosure: Nothing to disclose.

Samer Garas, MD, FACC  Chief of Cardiology, Department of Interventional Cardiology, St Vincent's Hospital

Samer Garas, MD, FACC is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, and American Medical Association

Disclosure: Nothing to disclose.

Pawan Hari, MD, MPH  Resident Physician, Department of Internal Medicine, Wayne State University School of Medicine

Disclosure: Nothing to disclose.

Ahmad M Jeroudi, MD  Fellow in Cardiovascular Disease, Emory University School of Medicine

Disclosure: Nothing to disclose.

Ashok K Kondur, MD  Clinical Assistant Professor, Department of Internal Medicine, Detroit Medical Center, Wayne State University

Ashok K Kondur, MD is a member of the following medical societies: American College of Physicians and Michigan State Medical Society

Disclosure: Nothing to disclose.

David S Levey, MD, PhD  Orthopedic/Neurospinal MRI TeleRadiologist, Poolside MRI, San Antonio, TX

David S Levey, MD, PhD is a member of the following medical societies: American Roentgen Ray Society, Radiological Society of North America, and Texas Medical Association

Disclosure: Nothing to disclose.

Suzanne M Miller, MD  Clinical Instructor, Emergency Medicine, George Washington University School of Medicine and Health Sciences; Attending Physician, Department of Emergency Medicine, INOVA Fairfax Hospital; Chief Executive Officer, MDadmit

Suzanne M Miller, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Brian Olshansky, MD  Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences

Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

Justin D Pearlman, MD, ME, PhD, FACC, MA  Chief, Division of Cardiology, Director of Cardiology Consultative Service, Director of Cardiology Clinic Service, Director of Cardiology Non-Invasive Laboratory, Director of Cardiology Quality Program KMC, Dartmouth-Hitchcock Medical Center, Dartmouth Medical School

Justin D Pearlman, MD, ME, PhD, FACC, MA is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, International Society for Magnetic Resonance in Medicine, and Radiological Society of North America

Disclosure: Nothing to disclose.

Ashish Pershad, MD  Consulting Staff, Heart and Vascular Center of Arizona

Ashish Pershad, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Donald Schreiber, MD, CM  Associate Professor of Surgery (Emergency Medicine), Stanford University School of Medicine

Donald Schreiber, MD, CM is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Abbott Point of Care Inc Research Grant and Speakers Bureau Speaking and teaching; Nanosphere Inc Grant/research funds Research; Singulex Inc Grant/research funds Research; Abbott Diagnostics Inc Grant/research funds None

Gary Setnik, MD  Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

Specialty Editor Board

Eric Vanderbush, MD, FACC  Chief, Department of Internal Medicine, Division of Cardiology, Harlem Hospital Center; Clinical Assistant Professor of Cardiology, Columbia University College of Physicians and Surgeons

Eric Vanderbush, MD, FACC is a member of the following medical societies: American College of Cardiology and American Heart Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

David FM Brown, MD  Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Eugene C Lin, MD  Attending Radiologist, Teaching Coordinator for Cardiac Imaging, Radiology Residency Program, Virginia Mason Medical Center; Clinical Assistant Professor of Radiology, University of Washington School of Medicine

Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, and Society of Nuclear Medicine

Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD  Associate Professor of Medicine, Director of Interventional Cardiology Fellowship Program, Henry Ford Hospital

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Sumanth R Daram, MD, Rex C Liu, MD, Sridevi R Pitta, MD, Vibhuti N Singh, MD, MPH, FACC, FSCAI, and coauthor George A Stouffer III, MD , to the development and writing of the source articles.

References

  1. Rathore SS, Gersh BJ, Weinfurt KP, Oetgen WJ, Schulman KA, Solomon AJ. The role of reperfusion therapy in paced patients with acute myocardial infarction. Am Heart J. Sep 2001;142(3):516-9. [Medline].

  2. Ryan TJ. Percutaneous coronary intervention in st-elevation myocardial infarction. Curr Cardiol Rep. Jul 2001;3(4):273-9. [Medline].

  3. Siddiqui MA, Tandon N, Mosley L, Sheridan FM, Hanley HG. Interventional therapy for acute myocardial infarction. J La State Med Soc. Jun 2001;153(6):292-9. [Medline].

  4. Costa e Silva R, Pellanda L, Portal V, Maciel P, Furquim A, Schaan B. Transdisciplinary approach to the follow-up of patients after myocardial infarction. Clinics (Sao Paulo). Aug 2008;63(4):489-96. [Medline]. [Full Text].

  5. Sleight P. Medical interventions in acute myocardial infarction. J Cardiovasc Pharmacol. 1990;16 Suppl 5:S113-9. [Medline].

  6. Bonaca MP, Wiviott SD, Braunwald E, et al. American College of Cardiology/American Heart Association/European Society of Cardiology/World Heart Federation Universal Definition of Myocardial Infarction Classification System and the Risk of Cardiovascular Death: Observations From the TRITON-TIMI 38 Trial (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel-Thrombolysis in Myocardial Infarction 38). Circulation. Jan 31 2012;125(4):577-83. [Medline].

  7. Chatzizisis YS, Coskun AU, Jonas M, Edelman ER, Feldman CL, Stone PH. Role of endothelial shear stress in the natural history of coronary atherosclerosis and vascular remodeling: molecular, cellular, and vascular behavior. J Am Coll Cardiol. Jun 26 2007;49(25):2379-93. [Medline].

  8. Wang JC, Normand SL, Mauri L, Kuntz RE. Coronary artery spatial distribution of acute myocardial infarction occlusions. Circulation. Jul 20 2004;110(3):278-84. [Medline].

  9. Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation. Aug 1 1995;92(3):657-71. [Medline].

  10. McDaniel MC, Willis P, Walker B, et al. Plaque necrotic core content is greater immediately distal to bifurcations compared to bifurcations in the proximal lad of patients with CAD. Am J Cardiol. 2008;102(8):242i.

  11. Concheiro-Guisán A, Sousa-Rouco C, Fernández-Santamarina I, González-Carreró J. Intrauterine myocardial infarction: unsuspected diagnosis in the delivery room. Fetal Pediatr Pathol. Jul-Aug 2006;25(4):179-84. [Medline].

  12. Gharacholou SM, Lopes RD, Alexander KP, Mehta RH, Stebbins AL, Pieper KS, et al. Age and Outcomes in ST-Segment Elevation Myocardial Infarction Treated With Primary Percutaneous Coronary Intervention: Findings From the APEX-AMI Trial. Arch Intern Med. Mar 28 2011;171(6):559-67. [Medline].

  13. Chughtai H, Ratner D, Pozo M, et al. Prehospital delay and its impact on time to treatment in ST-elevation myocardial infarction. Am J Emerg Med. May 2011;29(4):396-400. [Medline].

  14. Antman EM, Cohen M, Bernink PJ, McCabe CH, Horacek T, Papuchis G. The TIMI risk score for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA. Aug 16 2000;284(7):835-42. [Medline].

  15. Jaber WA, Prior DL, Marso SP, Houghtaling PL, Menon V, Harrington RA. CHF on presentation is associated with markedly worse outcomes among patients with acute coronary syndromes: PURSUIT trial findings. Circulation 1999:100(suppl I):I-433 .

  16. Killip T 3rd, Kimball JT. Treatment of myocardial infarction in a coronary care unit. A two year experience with 250 patients. Am J Cardiol. Oct 1967;20(4):457-64. [Medline].

  17. James SK, Lindahl B, Siegbahn A, Stridsberg M, Venge P, Armstrong P, et al. N-terminal pro-brain natriuretic peptide and other risk markers for the separate prediction of mortality and subsequent myocardial infarction in patients with unstable coronary artery disease: a Global Utilization of Strategies To Open occluded arteries (GUSTO)-IV substudy. Circulation. Jul 22 2003;108(3):275-81. [Medline].

  18. de Lemos JA, Morrow DA, Bentley JH, Omland T, Sabatine MS, McCabe CH, et al. The prognostic value of B-type natriuretic peptide in patients with acute coronary syndromes. N Engl J Med. Oct 4 2001;345(14):1014-21. [Medline].

  19. Haaf P, Reichlin T, Corson N, et al. B-type Natriuretic Peptide in the Early Diagnosis and Risk Stratification of Acute Chest Pain. Am J Med. May 2011;124(5):444-52. [Medline].

  20. Morrow DA, Rifai N, Antman EM, Weiner DL, McCabe CH, Cannon CP, et al. C-reactive protein is a potent predictor of mortality independently of and in combination with troponin T in acute coronary syndromes: a TIMI 11A substudy. Thrombolysis in Myocardial Infarction. J Am Coll Cardiol. Jun 1998;31(7):1460-5. [Medline].

  21. [Best Evidence] Beck JA, Meisinger C, Heier M, Kuch B, Hörmann A, Greschik C, et al. Effect of blood glucose concentrations on admission in non-diabetic versus diabetic patients with first acute myocardial infarction on short- and long-term mortality (from the MONICA/KORA Augsburg Myocardial Infarction Registry). Am J Cardiol. Dec 15 2009;104(12):1607-12. [Medline].

  22. Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, et al. 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. J Am Coll Cardiol. Aug 14 2007;50(7):e1-e157. [Medline].

  23. Smith SC Jr, Allen J, Blair SN, Bonow RO, Brass LM, Fonarow GC, et al. AHA/ACC guidelines for secondary prevention for patients with coronary and other atherosclerotic vascular disease: 2006 update: endorsed by the National Heart, Lung, and Blood Institute. Circulation. May 16 2006;113(19):2363-72. [Medline].

  24. Moholdt T, Aamot IL, Granoien I, et al. Aerobic interval training increases peak oxygen uptake more than usual care exercise training in myocardial infarction patients: a randomized controlled study. Clin Rehabil. Jan 2012;26(1):33-44. [Medline].

  25. Lee-Lewandrowski E, Januzzi JL, Grisson R, Mohammed AA, Lewandrowski G, Lewandrowski K. Evaluation of First-Draw Whole Blood, Point-of-Care Cardiac Markers in the Context of the Universal Definition of Myocardial Infarction: A Comparison of a Multimarker Panel to Troponin Alone and to Testing in the Central Laboratory. Arch Pathol Lab Med. Apr 2011;135(4):459-63. [Medline].

  26. Than M, Cullen L, Reid CM, Lim SH, Aldous S, Ardagh MW, et al. A 2-h diagnostic protocol to assess patients with chest pain symptoms in the Asia-Pacific region (ASPECT): a prospective observational validation study. Lancet. Mar 26 2011;377(9771):1077-84. [Medline].

  27. [Guideline] Braunwald E, Antman EM, Beasley JW, Califf RM, Cheitlin MD, Hochman JS, et al. ACC/AHA guidelines for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina). J Am Coll Cardiol. Sep 2000;36(3):970-1062. [Medline].

  28. [Guideline] Braunwald E, Antman EM, Beasley JW, Califf RM, Cheitlin MD, Hochman JS, et al. ACC/AHA guidelines for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction: executive summary and recommendations. A report of the American College of Cardiology/American Heart Association task force on practice guidelines (committee on the management of patients with unstable angina). Circulation. Sep 5 2000;102(10):1193-209. [Medline].

  29. Reichlin T, Irfan A, Twerenbold R, et al. Utility of absolute and relative changes in cardiac troponin concentrations in the early diagnosis of acute myocardial infarction. Circulation. Jul 12 2011;124(2):136-45. [Medline].

  30. [Best Evidence] Reichlin T, Hochholzer W, Bassetti S, Steuer S, Stelzig C, Hartwiger S, et al. Early diagnosis of myocardial infarction with sensitive cardiac troponin assays. N Engl J Med. Aug 27 2009;361(9):858-67. [Medline].

  31. Keller T, Zeller T, Ojeda F, et al. Serial changes in highly sensitive troponin I assay and early diagnosis of myocardial infarction. JAMA. Dec 28 2011;306(24):2684-93. [Medline].

  32. Hubbard BL, Newton CR, Carter PM, Fowler JJ, Schaldenbrand J, Singal B, et al. The inability of B-type natriuretic protein to predict short-term risk of death or myocardial infarction in non-heart-failure patients with marginally increased troponin levels. Ann Emerg Med. Nov 2010;56(5):472-80. [Medline].

  33. Haaf P, Balmelli C, Reichlin T, et al. N-terminal Pro B-type Natriuretic Peptide in the Early Evaluation of Suspected Acute Myocardial Infarction. Am J Med. Aug 2011;124(8):731-9. [Medline].

  34. Fujita M, Nakae I, Kihara Y, Hasegawa K, Nohara R, Ueda K, et al. Determinants of collateral development in patients with acute myocardial infarction. Clin Cardiol. Sep 1999;22(9):595-9. [Medline].

  35. Vanoverschelde JL, Wijns W, Depré C, Essamri B, Heyndrickx GR, Borgers M. Mechanisms of chronic regional postischemic dysfunction in humans. New insights from the study of noninfarcted collateral-dependent myocardium. Circulation. May 1993;87(5):1513-23. [Medline].

  36. Terkelsen CJ, Sørensen JT, Maeng M, Jensen LO, Tilsted HH, Trautner S, et al. System delay and mortality among patients with STEMI treated with primary percutaneous coronary intervention. JAMA. Aug 18 2010;304(7):763-71. [Medline].

  37. Najjar SS, Rao SV, Melloni C, et al. Intravenous erythropoietin in patients with ST-segment elevation myocardial infarction: REVEAL: a randomized controlled trial. JAMA. May 11 2011;305(18):1863-72. [Medline].

  38. Shen YC, Hsia RY. Association between ambulance diversion and survival among patients with acute myocardial infarction. JAMA. Jun 15 2011;305(23):2440-7. [Medline].

  39. Modi KA, Nylk TM, Sheridan FM. Medical management of acute ST elevation myocardial infarction. J La State Med Soc. Jun 2001;153(6):284-90. [Medline].

  40. Ohman EM, Harrington RA, Cannon CP, Agnelli G, Cairns JA, Kennedy JW. Intravenous thrombolysis in acute myocardial infarction. Chest. Jan 2001;119(1 Suppl):253S-277S. [Medline].

  41. [Best Evidence] Rathore SS, Curtis JP, Chen J, Wang Y, Nallamothu BK, Epstein AJ, et al. Association of door-to-balloon time and mortality in patients admitted to hospital with ST elevation myocardial infarction: national cohort study. BMJ. May 19 2009;338:b1807. [Medline]. [Full Text].

  42. Sinert R, Newman DH, Brandler E, Paladino L. Immediate ß-blockade in patients with myocardial infarctions: is there evidence of benefit?. Ann Emerg Med. Nov 2010;56(5):571-7. [Medline].

  43. Brinkman WT, Herbert MA, Prince SL, et al. Preoperative Beta-blocker usage: is it really worthy of being a quality indicator?. Ann Thorac Surg. Sep 2011;92(3):788-96. [Medline].

  44. Venge P, Ohberg C, Flodin M, Lindahl B. Early and late outcome prediction of death in the emergency room setting by point-of-care and laboratory assays of cardiac troponin I. Am Heart J. Nov 2010;160(5):835-41. [Medline].

  45. Tsai CL, Magid DJ, Sullivan AF, Gordon JA, Kaushal R, Michael Ho P, et al. Quality of care for acute myocardial infarction in 58 U.S. emergency departments. Acad Emerg Med. Sep 2010;17(9):940-50. [Medline].

  46. Mascola A, Ko J, Bakhsheshi H, Budoff MJ. Electron beam tomography comparison of culprit and non-culprit coronary arteries in patients with acute myocardial infarction. Am J Cardiol. Jun 1 2000;85(11):1357-9. [Medline].

  47. Antman EM, Hand M, Armstrong PW, Bates ER, et al. 2007 Focused Update of the ACC/AHA 2004 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: developed in collaboration With the Canadian Cardiovascular Society endorsed by the American Academy of Family Physicians: 2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee. Circulation. Jan 15 2008;117(2):296-329. [Medline].

  48. Armstrong PW, Collen D. Fibrinolysis for acute myocardial infarction: current status and new horizons for pharmacological reperfusion, part 2. Circulation. Jun 19 2001;103(24):2987-92. [Medline].

  49. Topol EJ. Reperfusion therapy for acute myocardial infarction with fibrinolytic therapy or combination reduced fibrinolytic therapy and platelet glycoprotein IIb/IIIa inhibition: the GUSTO V randomised trial. Lancet. Jun 16 2001;357(9272):1905-14. [Medline].

  50. Topol EJ, Ohman EM, Armstrong PW, Wilcox R, Skene AM, Aylward P, et al. Survival outcomes 1 year after reperfusion therapy with either alteplase or reteplase for acute myocardial infarction: results from the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO) III Trial. Circulation. Oct 10 2000;102(15):1761-5. [Medline].

  51. Lundergan CF, Ross AM, McCarthy WF, Reiner JS, Boyle D, Fink C, et al. Predictors of left ventricular function after acute myocardial infarction: effects of time to treatment, patency, and body mass index: the GUSTO-I angiographic experience. Am Heart J. Jul 2001;142(1):43-50. [Medline].

  52. Budaj A, Eikelboom JW, Mehta SR, Afzal R, Chrolavicius S, Bassand JP, et al. Improving clinical outcomes by reducing bleeding in patients with non-ST-elevation acute coronary syndromes. Eur Heart J. Mar 2009;30(6):655-61. [Medline].

  53. Kushner FG, Hand M, Smith SC Jr, et al. 2009 Focused Updates: ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction (updating the 2004 Guideline and 2007 Focused Update) and ACC/AHA/SCAI Guidelines on Percutaneous Coronary Intervention (updating the 2005 Guideline and 2007 Focused Update): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. Dec 1 2009;120(22):2271-306. [Medline].

  54. Montalescot G, Zeymer U, Silvain J, et al. Intravenous enoxaparin or unfractionated heparin in primary percutaneous coronary intervention for ST-elevation myocardial infarction: the international randomised open-label ATOLL trial. Lancet. Aug 20 2011;378(9792):693-703. [Medline].

  55. Stone GW, Witzenbichler B, Guagliumi G, et al. Heparin plus a glycoprotein IIb/IIIa inhibitor versus bivalirudin monotherapy and paclitaxel-eluting stents versus bare-metal stents in acute myocardial infarction (HORIZONS-AMI): final 3-year results from a multicentre, randomised controlled trial. Lancet. Jun 25 2011;377(9784):2193-204. [Medline].

  56. Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, et al. 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). Circulation. Aug 3 2004;110(5):588-636. [Medline].

  57. Sabatine MS. Clopidogrel Shines in STEMI Reperfusion: CLARITY-TIMI 28. Paper presented at: American College of Cardiology Annual Scientific Session Late-Breaking Clinical Trials. March 9, 2005;. Orlando, FL..

  58. [Best Evidence] Chen ZM, Jiang LX, Chen YP, Xie JX, Pan HC, Peto R, et al. Addition of clopidogrel to aspirin in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. Lancet. Nov 5 2005;366(9497):1607-21. [Medline].

  59. Patti G, Barczi G, Orlic D, et al. Outcome Comparison of 600- and 300-mg Loading Doses of Clopidogrel in Patients Undergoing Primary Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction Results From the ARMYDA-6 MI (Antiplatelet therapy for Reduction of MYocardial Damage during Angioplasty-Myocardial Infarction) Randomized Study. J Am Coll Cardiol. Oct 4 2011;58(15):1592-9. [Medline].

  60. Bhatt DL, Cryer BL, Contant CF, Cohen M, Lanas A, Schnitzer TJ, et al. Clopidogrel with or without Omeprazole in Coronary Artery Disease. N Engl J Med. Nov 11 2010;363(20):1909-1917. [Medline].

  61. Charlot M, Grove EL, Hansen PR, et al. Proton pump inhibitor use and risk of adverse cardiovascular events in aspirin treated patients with first time myocardial infarction: nationwide propensity score matched study. BMJ. May 11 2011;342:d2690. [Medline]. [Full Text].

  62. Baigent C, Blackwell L, Collins R, Emberson J, Godwin J, Peto R, et al. Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomised trials. Lancet. May 30 2009;373(9678):1849-60. [Medline]. [Full Text].

  63. Antman EM, Giugliano RP, Gibson CM, McCabe CH, Coussement P, Kleiman NS. Abciximab facilitates the rate and extent of thrombolysis: results of the thrombolysis in myocardial infarction (TIMI) 14 trial. The TIMI 14 Investigators. Circulation. Jun 1 1999;99(21):2720-32. [Medline].

  64. Gibson CM, de Lemos JA, Murphy SA, Marble SJ, McCabe CH, Cannon CP, et al. Combination therapy with abciximab reduces angiographically evident thrombus in acute myocardial infarction: a TIMI 14 substudy. Circulation. May 29 2001;103(21):2550-4. [Medline].

  65. Schjerning Olsen AM, Fosbøl EL, Lindhardsen J, Folke F, Charlot M, Selmer C, et al. Duration of Treatment With Nonsteroidal Anti-Inflammatory Drugs and Impact on Risk of Death and Recurrent Myocardial Infarction in Patients With Prior Myocardial Infarction. Circulation. May 9 11;[Medline].

  66. Patel MR, Smalling RW, Thiele H, et al. Intra-aortic Balloon Counterpulsation and Infarct Size in Patients With Acute Anterior Myocardial Infarction Without Shock: The CRISP AMI Randomized Trial. JAMA. Aug 29 2011;[Medline].

  67. Zijlstra F, Patel A, Jones M, et al. Clinical characteristics and outcome of patients with early (< 2 h), intermediate (2-4 h) and late (>4 h) presentation treated by primary coronary angioplasty or thrombolytic therapy for acute myocardial infarction. Eur Heart J.; Apr 2002:23(7):550-7.

  68. Schömig A, Kastrati A, Dirschinger J, Mehilli J, Schricke U, Pache J, et al. Coronary stenting plus platelet glycoprotein IIb/IIIa blockade compared with tissue plasminogen activator in acute myocardial infarction. Stent versus Thrombolysis for Occluded Coronary Arteries in Patients with Acute Myocardial Infarction Study Investigators. N Engl J Med. Aug 10 2000;343(6):385-91. [Medline].

  69. Cantor WJ, Fitchett D, Borgundvaag B, Ducas J, Heffernan M, et al. Routine early angioplasty after fibrinolysis for acute myocardial infarction. N Engl J Med. Jun 25 2009;360(26):2705-18. [Medline].

  70. Vlaar PJ, Mahmoud KD, Holmes DR Jr, et al. Culprit Vessel Only Versus Multivessel and Staged Percutaneous Coronary Intervention for Multivessel Disease in Patients Presenting With ST-Segment Elevation Myocardial Infarction A Pairwise and Network Meta-Analysis. J Am Coll Cardiol. Aug 9 2011;58(7):692-703. [Medline].

  71. Hochman JS, Lamas GA, Buller CE, Dzavik V, Reynolds HR, Abramsky SJ, et al. Coronary intervention for persistent occlusion after myocardial infarction. N Engl J Med. Dec 7 2006;355(23):2395-407. [Medline]. [Full Text].

  72. Höfling B, von Pölnitz A. Invasive strategy for treatment of myocardial infarction. J Cardiovasc Pharmacol. 1990;16 Suppl 5:S120-2. [Medline].

  73. Celik T, Yuksel UC, Iyisoy A, Kilic S, Kardesoglu E, Bugan B, et al. The impact of preinfarction angina on electrocardiographic ischemia grades in patients with acute myocardial infarction treated with primary percutaneous coronary intervention. Ann Noninvasive Electrocardiol. Jul 2008;13(3):278-86. [Medline].

  74. Zhu MM, Feit A, Chadow H, Alam M, Kwan T, Clark LT. Primary stent implantation compared with primary balloon angioplasty for acute myocardial infarction: a meta-analysis of randomized clinical trials. Am J Cardiol. Aug 1 2001;88(3):297-301. [Medline].

  75. Hughes S,. REPAIR-AMI: Stem cells show benefit in MI patients. November 13, 2005;Accessed February 8, 2011. Available at http://www.theheart.org/article/597863.do.

  76. Traverse JH, Henry TD, Ellis SG, et al. Effect of intracoronary delivery of autologous bone marrow mononuclear cells 2 to 3 weeks following acute myocardial infarction on left ventricular function: the LateTIME randomized trial. JAMA. Nov 16 2011;306(19):2110-9. [Medline].

  77. David TE. Operative management of postinfarction ventricular septal defect. Semin Thorac Cardiovasc Surg. Oct 1995;7(4):208-13. [Medline].

  78. Gaudiani VA, Miller DG, Stinson EB, Oyer PE, Reitz BA, Moreno-Cabral RJ, et al. Postinfarction ventricular septal defect: an argument for early operation. Surgery. Jan 1981;89(1):48-55. [Medline].

  79. Daggett WM, Buckley MJ, Akins CW, Leinbach RC, Gold HK, Block PC, et al. Improved results of surgical management of postinfarction ventricular septal rupture. Ann Surg. Sep 1982;196(3):269-77. [Medline]. [Full Text].

  80. Singh S, Loke YK, Spangler JG, Furberg CD. Risk of serious adverse cardiovascular events associatedwith varenicline: a systematic review and meta-analysis. CMAJ. Available at http://www.cmaj.ca/content/early/2011/07/04/cmaj.110218.full.pdf+html.. Accessed July 5, 2011.

  81. García Rodríguez LA, Cea-Soriano L, Martín-Merino E, Johansson S. Discontinuation of low dose aspirin and risk of myocardial infarction: case-control study in UK primary care. BMJ. Jul 19 2011;343:d4094. [Medline].

  82. [Guideline] Goldstein LB, Bushnell CD, Adams RJ, Appel LJ, Braun LT, Chaturvedi S, et al. Guidelines for the Primary Prevention of Stroke. A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. Dec 6 2010;[Medline].

  83. [Best Evidence] Negassa A, Monrad ES, Bang JY, Srinivas VS. Tree-structured risk stratification of in-hospital mortality after percutaneous coronary intervention for acute myocardial infarction: a report from the New York State percutaneous coronary intervention database. Am Heart J. Aug 2007;154(2):322-9. [Medline]. [Full Text].

  84. Wang TY, Dai D, Hernandez AF, et al. The Importance of Consistent, High-Quality Acute Myocardial Infarction and Heart Failure Care Results From the American Heart Association's Get With The Guidelines Program. J Am Coll Cardiol. Aug 2 2011;58(6):637-44. [Medline].

  85. [Guideline] Wright RS, Anderson JL, Adams CD, et al. 2011 ACCF/AHA Focused Update of the Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction (Updating the 2007 Guideline): A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. Mar 28 2011;[Medline].

  86. Schwartz GG, Olsson AG, Ezekowitz MD, Ganz P, Oliver MF, Waters D, et al. Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes: the MIRACL study: a randomized controlled trial. JAMA. Apr 4 2001;285(13):1711-8. [Medline].

  87. Abbott BG, Abdel-Aziz I, Nagula S, Monico EP, Schriver JA, Wackers FJ. Selective use of single-photon emission computed tomography myocardial perfusion imaging in a chest pain center. Am J Cardiol. Jun 15 2001;87(12):1351-5. [Medline].

  88. Achenbach S, Ropers D, Regenfus M, Muschiol G, Daniel WG, Moshage W. Contrast enhanced electron beam computed tomography to analyse the coronary arteries in patients after acute myocardial infarction. Heart. Nov 2000;84(5):489-93. [Medline]. [Full Text].

  89. [Best Evidence] Chen ZM, Pan HC, Chen YP, Peto R, Collins R, Jiang LX, et al. Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. Lancet. Nov 5 2005;366(9497):1622-32. [Medline].

  90. Derumeaux G, Loufoua J, Pontier G, Cribier A, Ovize M. Tissue Doppler imaging differentiates transmural from nontransmural acute myocardial infarction after reperfusion therapy. Circulation. Jan 30 2001;103(4):589-96. [Medline].

  91. [Best Evidence] Dwivedi G, Janardhanan R, Hayat SA, Lim TK, Senior R. Comparison between myocardial contrast echocardiography and (99m)technetium sestamibi single photon emission computed tomography determined myocardial viability in predicting hard cardiac events following acute myocardial infarction. Am J Cardiol. Nov 1 2009;104(9):1184-8. [Medline].

  92. Galasko GI, Basu S, Lahiri A, Senior R. A prospective comparison of echocardiographic wall motion score index and radionuclide ejection fraction in predicting outcome following acute myocardial infarction. Heart. Sep 2001;86(3):271-6. [Medline]. [Full Text].

  93. Garg N, Agarwal AK. Role of echocardiography in acute myocardial infarction. J Assoc Physicians India. Jul 2000;48(7):719-23. [Medline].

  94. Hambÿe AS, Vervaet A, Dobbeleir A, Dendale P, Franken P. Prediction of functional outcome by quantification of sestamibi and BMIPP after acute myocardial infarction. Eur J Nucl Med. Oct 2000;27(10):1494-500. [Medline].

  95. Hillenbrand HB, Kim RJ, Parker MA, Fieno DS, Judd RM. Early assessment of myocardial salvage by contrast-enhanced magnetic resonance imaging. Circulation. Oct 3 2000;102(14):1678-83. [Medline].

  96. Knaapen P, de Mulder M, van der Zant FM, Peels HO, Twisk JW, van Rossum AC, et al. Infarct size in primary angioplasty without on-site cardiac surgical backup versus transferal to a tertiary center: a single photon emission computed tomography study. Eur J Nucl Med Mol Imaging. Feb 2009;36(2):237-43. [Medline].

  97. Kramer CM, Rogers WJ Jr, Pakstis DL. Absence of adverse outcomes after magnetic resonance imaging early after stent placement for acute myocardial infarction: a preliminary study. J Cardiovasc Magn Reson. 2000;2(4):257-61. [Medline].

  98. Kroll D, Farah W, McKendall GR, Reinert SE, Johnson LL. Prognostic value of stress-gated Tc-99m sestamibi SPECT after acute myocardial infarction. Am J Cardiol. Feb 15 2001;87(4):381-6. [Medline].

  99. Møller JE, Søndergaard E, Poulsen SH, Egstrup K. The Doppler echocardiographic myocardial performance index predicts left-ventricular dilation and cardiac death after myocardial infarction. Cardiology. 2001;95(2):105-11. [Medline].

  100. Pannu HK, Flohr TG, Corl FM, Fishman EK. Current concepts in multi-detector row CT evaluation of the coronary arteries: principles, techniques, and anatomy. Radiographics. Oct 2003;23 Spec No:S111-25. [Medline].

  101. Paventi S, Parafati MA, Di Luzio E, Pellegrino CA. Safety and feasibility of two-dimensional echocardiography and myocardial perfusion imaging in patients with chest pain. Angiology. May 2001;52(5):305-9. [Medline].

  102. Rathore SS, Curtis JP, Chen J, Wang Y, Nallamothu BK, Epstein AJ, et al. Association of door-to-balloon time and mortality in patients admitted to hospital with ST elevation myocardial infarction: national cohort study. BMJ. May 19 2009;338:b1807. [Medline]. [Full Text].

  103. Rocchi G, Kasprzak JD, Galema TW, de Jong N, Ten Cate FJ. Usefulness of power Doppler contrast echocardiography to identify reperfusion after acute myocardial infarction. Am J Cardiol. Feb 1 2001;87(3):278-82. [Medline].

  104. Tanaka R, Nakamura T. Time course evaluation of myocardial perfusion after reperfusion therapy by 99mTc-tetrofosmin SPECT in patients with acute myocardial infarction. J Nucl Med. Sep 2001;42(9):1351-8. [Medline].

  105. Vargas-Barrón J, Roldán FJ, Romero-Cárdenas A, Espinola-Zavaleta N, Keirns C, González-Pacheco H. Two- and three-dimensional transesophageal echocardiographic diagnosis of intramyocardial dissecting hematoma after myocardial infarction. J Am Soc Echocardiogr. Jun 2001;14(6):637-40. [Medline].

  106. Vasey CG, Usedom JE, Woodard SM, Bhapkar M, Schwartz T, Koch GG. Prediction of cardiac mortality after myocardial infarction: the role of maximal treadmill stress echocardiography. J Am Soc Echocardiogr. Jan 2001;14(1):38-43. [Medline].

  107. Zhang X, Liu XJ, Wu Q, Shi R, Gao R, Liu Y, et al. Clinical outcome of patients with previous myocardial infarction and left ventricular dysfunction assessed with myocardial (99m)Tc-MIBI SPECT and (18)F-FDG PET. J Nucl Med. Aug 2001;42(8):1166-73. [Medline].

 
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Acute anterior myocardial infarction.
Acute inferior myocardial infarction.
Posterolateral myocardial infarction.
A 53-year-old patient who had experienced 3 hours of chest pain had a 12-lead electrocardiogram performed, and the results are as shown. He was given sublingual nitroglycerin and developed severe symptomatic hypotension. His blood pressure normalized with volume resuscitation.
The right-sided leads indicate ST-segment elevations in RV4 and RV5, which are consistent with a right ventricular infarct.
The electrocardiogram shows lateral ST-segment elevation that is consistent with a lateral wall acute myocardial infarction.
This patient has a symptom duration of fewer than 12 hours. In the setting of active chest pain and electrocardiographic changes showing acute myocardial infarction, he would still benefit from thrombolysis. His history of surgery is not a contraindication and his blood pressure can be controlled with nitrates and beta-blockers.
This patient has an inferior wall myocardial infarction indicated on the ECG. Approximately 20% of inferior myocardial infarctions are right ventricular. Nitroglycerin will drop the preload; right ventricular (RV) output is very preload-dependent. Right-sided chest leads would be useful in demonstrating ST-segment elevations in RV4 and RV5.
Acute inferior myocardial infarction on an electrocardiogram.
After thrombolytic therapy, reperfusion arrhythmias, such as an accelerated idioventricular rhythm, may occur.
Hypokinesis of the anteroseptal wall observed during echocardiography in a patient presenting with an acute anteroseptal myocardial infarction.
Apical left ventricular dyskinesis (ventricular aneurysm) after an anterior myocardial infarction.
Image shows a scar in the anterior wall.
Graph
 
 
 
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