Diagnostic Considerations

Epigastric or chest symptoms from myocardial ischemia may incorrectly be attributed to a gastrointestinal (GI) source. Often, this occurs despite the presence of dyspnea or diaphoresis, symptoms that are difficult to attribute to the GI system. Additionally, patients with myocardial ischemia may report relief or improvement with GI remedies (eg, antacids).

The discomfort of myocardial ischemia may also erroneously be attributed to a musculoskeletal etiology. Tenderness of the chest wall is reported in as many as 5% of patients who are diagnosed with myocardial infarction (MI). If no injury or event is defined that could have led to a soft-tissue injury, the clinician should be reluctant to render a diagnosis of musculoskeletal chest pain.

Younger patients are overly represented in cases of missed MI. Most likely this is because of the inherent bias that MI is a disease of middle-aged and older individuals. Each patient with chest symptoms should be approached as an individual who could have the disease.

Unfortunately, in a series of missed MI, failure to recognize ischemic changes was 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 of the electrocardiographic (ECG) tracing. 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.

Differential Diagnoses

Abdominal Compartment Syndrome
Acute Aortic Dissection
Acute Cholecystitis and Biliary Colic
Acute Gastritis
Acute Mitral Regurgitation
Acute Pericarditis
Anxiety Disorders
Aortic Dissection
Aortic Regurgitation
Aortic Stenosis
Asthma
Biliary Disease
Cardiogenic Shock
Chronic Obstructive Pulmonary Disease (COPD) and Emphysema in Emergency Medicine
Depression
Dyspepsia
Esophageal Spasm
Esophagitis
Gallstones (Cholelithiasis)
Gastroesophageal Reflux Disease
Heart Rupture
Herpes Zoster
Infective Endocarditis
Mitral Valve Prolapse
Myocarditis
Myopericarditis
Pleurodynia
Pneumonia
Pneumothorax
Idiopathic Pulmonary Arterial Hypertension
Pulmonary Embolism (PE)

Workup

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Media Gallery

Acute anterior myocardial infarction.
Acute inferior myocardial infarction.
Acute 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 RV<inf>3</inf> to RV<inf>5</inf>, which are consistent with a right ventricular infarct.
Timing of release of various cardiac biomarker peaks after the onset of myocardial infarction
Modified 2-dimensional (top) echocardiogram and color flow Doppler image (bottom). Apical 4-chamber views show a breach in the interventricular septum and free communication between ventricles through a large apical septum ventricular septal defect in a patient who recently had an anterior myocardial infarction.
Apical 2-chamber view depicts a large left ventricular apical thrombus with mobile extensions.
Parasternal long-axis view of the left ventricle demonstrates a large inferobasal aneurysm. Note the wide neck and base of the aneurysm.
Acute myocardial infarct. At 3 days, there is a zone of yellow necrosis surrounded by darker hyperemic borders. The arrow points to a transmural infarct in the posterior wall of the left ventricle, in this short axis slice through the left and right ventricular chambers.
Acute myocardial infarction, reperfusion type. In this case, the infarct is diffusely hemorrhagic. There is a rupture track through the center of this posterior left ventricular transmural infarct. The mechanism of death was hemopericardium.
Healing myocardial infarction, lateral left ventricle. In this heart, there is a variegated or mottled appearance to the lateral left ventricle (left). This infarct began 19 days prior to death.
Early healed myocardial infarction, anterior septum. There is a glistening gelatinous appearance to this infarction, which occurred 6 weeks prior to death, from embolization during valve surgery.
Healed myocardial infarction, anterior left ventricle. There is diffuse scarring (white) with marked thinning of the ventricle (aneurysm).
Acute myocardial infarct. The earliest change is hypereosinophilia (above) with an intense pink cytoplasm. There is no inflammation at border between the necrotic myocardium and the viable myocardium (left and below), indicating that the necrosis is about 12-24 hours in age.
Acute myocardial infarct. After 24 hours, there is a neutrophilic infiltrate at the border of the infarct. Viable myocardium is at the left, and neutrophils with apoptosis (karyorrhexis) are seen infiltrating the necrotic muscle. This patient experienced abdominal pain 35 hours prior to death.
Healing myocardial infarct. This patient died 8 days after experiencing sudden chest pain at rest. There is a large area of necrosis with hypereosinophilia of myocytes, with a rim of viable myocardium at the very bottom. At the border, there is chronic inflammation with early granulation tissue, with ingrowth of endothelial cells.
Healing myocardial infarct. At 10 days to 2 weeks, there is chronic inflammation, hemosiderin-laden macrophages, and early fibroblasts without significant collagen deposition.
Healed myocardial infarct. At 3 months, there is dense scar, which is blue on this Masson trichrome stain. This infarct was subendocardial, in the posterior left ventricle near the ventricular septum.
This is a posteroanterior view of a right ventricular endocardial activation map during ventricular tachycardia in a patient with a previous septal myocardial infarction. Earliest activation is recorded in red; late activation shows as blue to magenta. Fragmented low-amplitude diastolic local electrocardiograms were recorded adjacent to the earliest (red) breakout area, and local ablation in this scarred zone (red dots) resulted in termination and noninducibility of this previously incessant arrhythmia.
A color-enhanced angiogram of the heart left shows a plaque-induced obstruction (top center) in a major artery, which can lead to myocardial infarction (MI). MIs can precipitate heart failure.

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Table 1. Absolute and Relative Contraindications to Fibrinolytic Therapy in Patients with STEMI

Absolute Contraindications

Relative Contraindications

Any prior intracranial hemorrhage
Known structural cerebral vascular lesion
Known intracranial neoplasm (primary or metastatic)
Ischemic stroke within the past 3 months (except for acute stroke within 4.5 hours)
Suspected aortic dissection
Active bleeding or bleeding diathesis (excluding menses)
Significant closed-head or facial trauma within 3 months
Intracranial or intraspinal surgery within 2 months
Severe uncontrolled hypertension (unresponsive to emergency therapy)
For streptokinase (no longer marketed in the US): Prior treatment within previous 6 months

History of chronic, severe, poorly controlled hypertension
Systolic pressure >180 mm Hg or diastolic pressure >110 mm Hg
History of prior ischemic stroke >3 months
Dementia
Known intracranial pathology not covered in absolute contraindications
Traumatic or prolonged CPR (>10 minutes)
Recent (within 2-4 weeks) internal bleeding
Noncompressible vascular punctures
Pregnancy
Active peptic ulcer disease
Current use of anticoagulants: The higher the INR, the higher the risk of bleeding
For streptokinase (no longer marketed in the US): Prior exposure (>5 days previously) or prior allergic reaction to these agents

CPR = cardiopulmonary resuscitation; INR = international normalized ratio; STEMI = ST-elevation myocardial infarction; US = United States of America.

Table modified from 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.^[2]

Table 2. Fibrinolytic Agents Used in Management of STEMI.

Fibrinolytic Agent	Dose	Fibrin Specificity	Antigenic	Patency Rate
Non-fibrin specific
Streptokinase (no longer marketed in the US)	1.5 million units IV given over 30–60 min	No	Yes	60%–68%
Fibrin specific
Tenecteplase (TNK-tPA)	30 mg for weight < 60 kg 35 mg for 60–69 kg 40 mg for 70–79 kg 45 mg for 80–89 kg 50 mg for >90 kg	++++	No	85%
Reteplase (rPA)	10-U IV boluses given 30 min apart	++	No	84%
Alteplase (tPA)	Bolus 15 mg followed by infusion 0.75 mg/kg for 30 min (maximum 50 mg), then 0.5 mg/kg (maximum 35 mg) over the next 60 min; total dose not to exceed 100 mg.	++	No	73%-84%
IV = intravenous; rPA = recombinant human tissue plasminogen activator; STEMI = ST-elevation myocardial infarction; tPA = tissue plasminogen activator; US = United States of America. Table modified from 2013 ACCF/AHA guidelines 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.^[2]

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Author

A Maziar Zafari, MD, PhD, FACC, FAHA Professor of Medicine, Emory University School of Medicine; Chief of Cardiology, Atlanta Veterans Affairs Health Care System; Adjunct Professor of Medicine, Morehouse School of Medicine

A Maziar Zafari, MD, PhD, FACC, FAHA is a member of the following medical societies: American College of Cardiology, American Heart Association

Disclosure: Nothing to disclose.

Coauthor(s)

Mahmoud H Abdou, MD Fellow, Division of Cardiology, Emory University School of Medicine

Mahmoud H Abdou, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, Libyan Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Yasmine S Ali, MD, MSCI, FACC, FACP Assistant Clinical Professor of Medicine, Vanderbilt University School of Medicine; President, LastSky Writing, LLC

Yasmine S Ali, MD, MSCI, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Medical Writers Association, National Lipid Association, Tennessee Medical Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: LastSky Writing;Philips Healthcare;M Health;Verywell Health; MedStudy;WellnessVerge;Prose Media; AKH, Inc.; LearnRoll, LLC; Eradigm; RxCe.com; M3 USA; M3 EU; Future US Inc.; Edanz Group; ChesterPA511<br/>Serve(d) as a speaker or a member of a speakers bureau for: RxCe.com.

Chief Editor

Eric H Yang, MD Associate Professor of Medicine, Director of Cardiac Catherization Laboratory and Interventional Cardiology, Mayo Clinic ArizonA

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

Disclosure: Nothing to disclose.

Additional Contributors

Samer M Garas, MD, FACC, FSCAI Interventional Cardiologist, President, St Vincent's Health System Cardiovascular Council

Samer M Garas, MD, FACC, FSCAI is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

Shilpa V Reddy, MD Fellow in Cardiovascular Disease, Division of Cardiology, Emory University School of Medicine

Shilpa V Reddy, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Acknowledgements

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.

Drew Evan Fenton, MD, FAAEM Private Practice

Disclosure: Nothing to disclose.

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

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

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.