Myocardial Infarction Clinical Presentation

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

History

The patient’s history is critical in diagnosing myocardial infarction and sometimes may provide the only clues that lead to the diagnosis in the initial phases of the patient presentation.

Patients with typical myocardial Infarction may have prodromal symptoms of fatigue, chest discomfort, or malaise in the days preceding the event; alternatively, typical STEMI may occur suddenly, without warning.

Myocardial infarction occurs most often in the early morning hours, perhaps partly because of the increase in catecholamine-induced platelet aggregation and increased serum concentrations of plasminogen activator inhibitor-1 (PAI-1) that occur after awakening. In general, the onset is not directly associated with severe exertion. Instead, it is concomitant with exertion. The immediate risk of myocardial infarction increases 6-fold on average and by as much as 30-fold in sedentary people.

A high index of suspicion should be maintained for myocardial infarction especially when evaluating women, patients with diabetes, older patients, patients with dementia, patients with a history of heart failure, cocaine users, patients with hypercholesterolemia, and patients with a positive family history for early coronary disease (See Etiology). A positive family history includes any first-degree male relative aged 45 years or younger or any first-degree female relative aged 55 years or younger who experienced a myocardial infarction.

Other symptoms of myocardial infarction include the following:

  • Anxiety
  • Light-headedness with or without syncope
  • Cough
  • Nausea with or without vomiting
  • Diaphoresis
  • Wheezing

The patient may recall only an episode of indigestion as an indication of myocardial infarction (see Physical Examination). In some cases, patients do not recognize chest pain, possibly because they have a stoic outlook, have an unusually high pain threshold, have a disorder that impairs function of the nervous system and that results in a defective anginal warning system (eg, diabetes mellitus), or have obtundation caused by medication or impaired cerebral perfusion. Elderly patients with preexisting altered mental status or dementia may have no recollection of recent symptoms and may have no complaints whatsoever.

Next

Physical Examination

For many patients, the first manifestation of coronary artery disease is sudden death likely from malignant ventricular dysrhythmia.

Physical examination findings for myocardial infarction can vary; one patient may be comfortable in bed, with normal examination results, while another may be in severe pain, with significant respiratory distress and a need for ventilatory support.

Patients with ongoing symptoms usually lie quietly in bed and appear pale and diaphoretic. Hypertension may precipitate myocardial infarction, or it may reflect elevated catecholamine levels due to anxiety, pain, or exogenous sympathomimetics. Hypotension may indicate ventricular dysfunction due to ischemia. Hypotension in the setting of myocardial infarction usually indicates a large infarct secondary to either decreased global cardiac contractility or a right ventricular infarct. Acute valvular dysfunction may be present. Valvular dysfunction usually results from infarction that involves the papillary muscle. Mitral regurgitation due to papillary muscle ischemia or necrosis may be present.

The typical chest pain of acute myocardial infarction is intense and unremitting for 30-60 minutes. It is retrosternal and often radiates up to the neck, shoulder, and jaw and down to the ulnar aspect of the left arm. Chest pain is usually described as a substernal pressure sensation that also may be described as squeezing, aching, burning, or even sharp. In some patients, the symptom is epigastric, with a feeling of indigestion or of fullness and gas.

Atypical presentations are common and frequently lead to misdiagnoses. Moreover, any patient may present with atypical symptoms, which are considered the anginal equivalent for that patient. A patient, for example, may present with abdominal discomfort or jaw pain as his or her anginal equivalent. An elderly patient may present with altered mental status. Atypical chest pain is common, especially in elderly patients and patients with diabetes. A low threshold should be maintained when evaluating high- and moderate-risk patients, as their anginal equivalents may mimic other presentations. Women tend to present more commonly with atypical symptoms such as sharp pain, fatigue, weakness, and other nonspecific complaints.

Diaphoresis, weakness, a sense of impending doom, profound restlessness, confusion, presyncope, hiccupping (which presumably reflects irritation of the phrenic nerve or diaphragm), nausea and vomiting, and palpitations may be present. (Nausea and/or abdominal pain often are present in infarcts involving the inferior or posterior wall.)

Decreased systolic ventricular performance may lead to impaired perfusion of vital organs and reflex-mediated compensatory responses, such as restlessness, impaired mentation, pallor, peripheral vasoconstriction and sweating, tachycardia, and prerenal failure.

By contrast, impaired left ventricular diastolic function leads to pulmonary vascular congestion with shortness of breath and tachypnea and, eventually, pulmonary edema with orthopnea. Shortness of breath may be the patient's anginal equivalent or a symptom of heart failure. In an elderly person or a patient with diabetes, shortness of breath may be the only complaint.

In patients with acute inferior-wall myocardial infarction with right ventricular involvement, distention of neck veins is commonly described as a sign of failure of the RV. (Central venous pressure is most properly estimated independently of venous distension on the basis of the height of the meniscus of venous pulsation above the mid atrium.) Impaired right ventricular diastolic function also leads to systemic venous hypertension, edema, and hepatomegaly with abdominojugular reflux, which may result in saline-response underfilling of the LV and a concomitant reduction in cardiac output.

Elderly patients and those with diabetes may have particularly subtle presentations and may complain of fatigue, syncope, or weakness. The elderly may also present with only altered mental status.

As many as half of myocardial infarctions are clinically silent in that they do not cause the classic symptoms described above and consequently go unrecognized by the patient. Myocardial infarction is clinically silent in as many as 25% of elderly patients, a population in whom 50% of myocardial infarctions occur; in such patients, the diagnosis is often established only retrospectively, by applying electrocardiographic criteria or by scanning the patients using 2-dimensional (2D) echocardiography or magnetic resonance imaging (MRI).

On clinical evaluation, ventricular aneurysms may be recognized late, with symptoms and signs of heart failure, recurrent ventricular arrhythmia, or recurrent embolization.

Vital signs

The patient's heart rate is often increased secondary to sympathoadrenal discharge. The pulse may be irregular because of ventricular ectopy, an accelerated idioventricular rhythm (demonstrated below), ventricular tachycardia, atrial fibrillation or flutter, or other supraventricular arrhythmias. Bradyarrhythmias may be present; bradyarrhythmias may be attributable to impaired function of the sinus node. An AV nodal block or infranodal block may be evident.

After thrombolytic therapy, reperfusion arrhythmiaAfter thrombolytic therapy, reperfusion arrhythmias, such as an accelerated idioventricular rhythm, may occur.

In general, the patient's blood pressure is initially elevated because of peripheral arterial vasoconstriction resulting from an adrenergic response to pain and ventricular dysfunction. However, with right ventricular myocardial infarction or severe left ventricular dysfunction, hypotension is seen.

The respiratory rate may be increased in response to pulmonary congestion or anxiety.

Coughing, wheezing, and the production of frothy sputum may occur.

Fever is usually present within 24-48 hours, with the temperature curve generally parallel to the time course of elevations of creatine kinase (CK) levels in the blood. Body temperature may occasionally exceed 102°F.

Funduscopic examination

Manifestations of atherosclerotic vascular disease include copper wiring, or narrowing, of arterioles. Hypertension may manifest with arteriovenous nicking, which is a pinching of the veins by small arteries where they cross. Extreme hypertension may cause cupping or loss of the margins of the optical disk. Antecedent long-standing hypertension may be reflected by arterial narrowing and hemorrhages.

Arterial pulsations

Arterial pulsations may exhibit pulsus alternans, which reflects impaired left ventricular function and is characterized by strong and weak alternating pulse waves (the variation in systolic pressure is >20 mm Hg). Carotid pulsation may be thin (pulsus parvus) because of decreased amplitude and length of the pulse secondary to decreased stroke volume.

Pulsus bisferiens consists of 2 systolic peaks; it may be palpated in association with hypertrophic obstructive cardiomyopathy (HOCM) or mixed aortic stenosis and regurgitation. A dicrotic pulse is encountered in cases involving hypovolemic shock, severe heart failure, or cardiac tamponade. It manifests as a double pulse, produced by a combination of the systolic wave followed by an exaggerated dicrotic (diastolic) wave.

A bigeminal pulse is observed in the presence of ectopic beats or Wenckebach heart block; it is characterized by regular coupling of 2 beats with the interval between a pair of beats greater than that between the coupled beats themselves.

Pulsus paradoxus is defined as a decline in systolic blood pressure of 10 mm Hg or more on inspiration; it is seen in cases involving cardiac tamponade, constrictive pericarditis, restrictive cardiomyopathy, hypotensive shock, severe chronic lung disease, or pulmonary embolism.

In patients with associated aortic regurgitation, a pulse with sharp descent, or a water-hammer pulse, may be observed.

Venous pulsations

Jugular venous distention may accompany right ventricular myocardial infarction or right ventricular failure secondary to profound left ventricular dysfunction and pulmonary hypertension. It may also be elevated as a result of an increase in right atrial pressure in patients with heart failure, decreased right ventricular compliance, pericardial disease, fluid overload, or tricuspid or superior vena cava obstruction. The Kussmaul sign, characterized by a paradoxical increase in jugular venous pressure during inspiration, may occur in patients with constrictive pericarditis, congestive HF (CHF), or tricuspid stenosis.

Chest

Rales or wheezes may be auscultated; these occur secondary to pulmonary venous hypertension, which is associated with extensive acute left ventricular myocardial infarction. Unilateral or bilateral pleural effusions may produce egophony at the lung bases. On chest radiographs, they are evidenced by blunted costophrenic angles; on MRI, they are evidenced by dependent fluid signal intensity; on echocardiography, they are evidenced by echolucent zones adjacent to the heart.

Heart

On palpation, lateral displacement of the apical impulse, dyskinesis (seen in the image below), a palpable S4 gallop, and a soft S1 sound may be found. These indicate diminished contractility of the compromised LV.

Apical left ventricular dyskinesis (ventricular anApical left ventricular dyskinesis (ventricular aneurysm) after an anterior myocardial infarction.

Paradoxical splitting of S2 may reflect the presence of left bundle-branch block or prolongation of the preejection period with delayed closure of the aortic valve, despite decreased stroke volume.

Increased S4 and S3 gallops may suggest increased LV stiffness; they represent the rapid filling phase (S3) or atrial contraction (S4).

A mitral regurgitation murmur (typically holosystolic near the apex) indicates papillary muscle dysfunction or rupture or mitral annular dilatation; it may be audible even when cardiac output is substantially decreased.

A holosystolic systolic murmur that radiates to the midsternal border and not to the back, possibly with a palpable thrill, suggests a ventricular septal rupture; such a rupture may occur as a complication in some patients with full-thickness (or Q-wave) myocardial infarctions. With resistive flow and an enlarged pressure difference, the ventricular septal defect murmur becomes harsher, louder, and higher in pitch than before.

A pericardial friction rub may be audible as a to-and-fro rasping sound with 1-3 components; it is produced through sliding contact of inflammation-roughened surfaces.

Neck vein and pulse patterns, splitting of S2, or ECG findings may suggest premature ventricular beats, brief runs of ventricular tachycardia, accelerated idioventricular rhythm, atrial flutter or atrial fibrillation, or conduction delays.

Abdomen

Patients frequently develop tricuspid incompetence; hepatojugular reflux may be elicited even when hepatomegaly is not marked.

Extremities

Peripheral cyanosis, edema, pallor, diminished pulse volume, delayed rise, and delayed capillary refill may indicate vasoconstriction, diminished cardiac output, and right ventricular dysfunction or failure. Pulse and neck-vein patterns may reveal other associated abnormalities, as previously discussed. Dependent edema may be graded 0-4 by assessing the depth of persistent pitting after thumb pressure is applied to the patient's inner shin for more than 10 seconds or by evaluating the lower back if the patient has had his or her legs elevated.

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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.

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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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