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.
Takotsubo cardiomyopathy (TTC) is an acute reversible cardiac condition often triggered by stressful events, which is often confused with acute coronary syndrome. In a 2012 report, TTC events occurred in a circadian pattern with a peak in the afternoon hours, as opposed to the the predilection of STEMI for occurring in the morning hours. This timing is consistent with mechanisms underlying stressful life events that usually trigger TTC. [31]
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:
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Anxiety
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Light-headedness with or without syncope
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Cough
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Nausea with or without vomiting
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Diaphoresis
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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.
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, 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.
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, a palpable S4 gallop, and a soft S1 sound may be found. These indicate diminished contractility of the compromised LV.
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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Acute anterior myocardial infarction.
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Acute inferior myocardial infarction.
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Acute posterolateral myocardial infarction.
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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.
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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.
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Timing of release of various cardiac biomarker peaks after the onset of myocardial infarction
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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.
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Apical 2-chamber view depicts a large left ventricular apical thrombus with mobile extensions.
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Parasternal long-axis view of the left ventricle demonstrates a large inferobasal aneurysm. Note the wide neck and base of the aneurysm.
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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.
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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.
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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.
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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.
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Healed myocardial infarction, anterior left ventricle. There is diffuse scarring (white) with marked thinning of the ventricle (aneurysm).
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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.
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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.
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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.
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Healing myocardial infarct. At 10 days to 2 weeks, there is chronic inflammation, hemosiderin-laden macrophages, and early fibroblasts without significant collagen deposition.
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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.
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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.
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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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- Overview
- Presentation
- DDx
- Workup
- Treatment
- Approach Considerations
- Prehospital Care
- Emergency Department Care
- In-Hospital Treatment
- Thrombolytic Therapy
- Antithrombotic Agents
- Aspirin and Antiplatelet Therapy
- Additional Medical Therapy
- Percutaneous Coronary Intervention
- Coronary Artery Bypass Graft Surgery
- No-Reflow Phenomenon
- New Treatment Strategies
- Special Concerns for Elderly Patients
- Diet
- Activity
- Complications
- Transfer
- Deterrence and Prevention
- Consultations
- Immediate and Short-Term Monitoring
- Long-Term Monitoring
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- Medication
- Media Gallery
- References
