Myocardial infarction arises when perfusion of cardiac muscle is inadequate, resulting in insufficient oxygen delivery to that portion of cardiac muscle from a complete occlusion of a major epicardial coronary vessel.
This causes the affected muscle to rely on anaerobic metabolism for its energy supply with concomitant production of lactic acid. Even transient ischemia can lead to changes in muscle tissue, but prolonged ischemia leads to breakdown of muscle cells and release of cellular proteins such as creatine kinase, lactic acid dehydrogenase, and troponin I.
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Severe loss of myocardial contractility occurs within 60 seconds of the onset of ischemia; loss of viability (irreversible injury) takes at least 20-40 minutes after total occlusion of blood flow.1
Anterior, apical, and septal infarcts of the left ventricle are usually due to thrombosis in the left anterior descending circulation; lateral and posterior left ventricular infarcts result from occlusions in the left circumflex system, whereas right ventricular and posterior-inferior left ventricular infarcts result from thrombosis in the right coronary artery.
In contrast, subendocardial (nontransmural, or “non-Q wave”) infarctions more often occurs in the setting of reduced myocardial perfusion due to hypotension or intimal hemorrhage, and less commonly follows coronary plaque rupture and thrombosis.
Most myocardial infarctions occur in patients with more than one severely narrowed (>75% narrowing of the cross-sectional area) coronary artery. A transmural infarction occurs in an area distal to a complete occlusion.
Coronary emboli or severe spasm is less commonly the cause.
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Ischemic symptoms frequently are first noted only with exercise or cardiac stress from cold exposure, meals, or a combination of factors and often resolve quickly once the inciting event is over.
Progressive symptoms or symptoms at rest may represent unstable angina due to coronary plaque rupture and thrombosis. Protracted episodes often represent myocardial infarction, although one-third of patients with acute myocardial infarction do not have chest pain. When present, the pain is commonly accompanied by a sense of anxiety or uneasiness. The location is usually retrosternal or left precordial. Because there are not the appropriate sensory nerves on the heart, the central nervous system interpretation of pain location often results in pressure or "heaviness" being referred to the throat, lower jaw, shoulders, inner arms, upper abdomen, or back. Ischemic pain is not related to position or respiration and is usually not elicited by chest palpation. One clue that the pain may be ischemic is the presence of other symptoms associated with the pain, such as shortness of breath, dizziness, a feeling of impending doom, and vagal symptoms, such as nausea and diaphoresis. Of importance, depression may mask symptoms, especially in women. When compared to men, women do appear to have a higher frequency of atypical angina (even with significant coronary disease) and, in some cases, evidence for microvascular coronary disease even when epicardial coronary disease is not evident at cardiac catheterization. A HEART score (History, ECG, Age, Risk factors and Troponin) has been proposed and validated to help distinguish coronary chest pain in the emergency department from noncoronary causes.
Hypertrophy of either ventricle, such as in aortic stenosis or hypertrophic cardiomyopathy, may result in subendocardial underperfusion during stress and may also give rise to atypical ischemic pain. Myocarditis, pulmonary hypertension, and mitral valve prolapse are also associated with chest pain atypical for angina pectoris. Pericarditis may produce pain that is greater supine than upright, and may increase with respiration, or swallowing. Pleuritic chest pain is not ischemic and characteristically increases with respiration; pain on palpation usually signals a musculoskeletal etiology. ]
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| Diagnosis | Risk Factors | Characteristic Findings | Diagnostic Testing |
|---|---|---|---|
| Age over 55, tobacco use, family history of coronary artery disease, diabetes, hypercholesterolemia, hypertension | S4 or S3 gallop, vomiting, diaphoresis, Levine sign (fist over center chest, low predictive value) | Electrocardiography, cardiac biomarkers | |
These patients will benefit from standard medical therapy as well as reperfusion. According to the 2007 ACC/AHA focused update on the management of patients with ST-elevation myocardial infarction, patients with acute STEMI will benefit from primary percutaneous intervention with a goal door-to-balloon time of <90 min. Fibrinolytic therapy within 30 min is preferred if transfer to a PCI-capable facility will make door-to-balloon time > 90 min. These guidelines are directed toward patients presenting to the hospital with STEMI, but may also help to decide when to transfer inpatients who develop STEMI during hospitalization. |
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Age over 55, tobacco use, family history of coronary artery disease, diabetes, hypercholesterolemia, hypertension
While preparing for percutaneous coronary intervention, the following are done.
Have patient chew aspirin (162–325 mg) and swallow at presentation
Oxygen
ESC: Give supplemental oxygen to treat hypoxia (SaO2 <95%), breathlessness, or acute heart failure
Patients with respiratory distress or O2 saturation of less than 90% should be started on oxygen to keep saturation within a normal range.
NOTE: Starting oxygen in patients with normal oxygen saturation possibly causes direct vasoconstriction on coronary arteries, so the routine use of oxygen in all patients is discouraged.
Primary PCI is preferable to fibrinolysis if performed by an experienced team within 120 minutes of first medical contact
If timely PCI is not available, give fibrinolytic therapy within 30 minutes of hospital arrival, unless contraindicated;
it is most useful if ischemic symptoms started within the past 12 hours, and is a reasonable choice between 12 and 24 hours if there is evidence of ongoing ischemia or a large area of myocardium at risk
Transfer to PCI-capable center
Primary PCI is indicated in all patients with STEMI and cardiogenic shock or severe acute heart failure
In PCI for STEMI, use either a bare-metal or drug-eluting stent; use a bare-metal stent in patients with high bleeding risk, inability to comply with 1 year of dual antiplatelet therapy, or upcoming invasive procedure
In comatose patients, use therapeutic hypothermia
Antiplatelet therapy (ACC/AHA 2016, ESC 2012)
Continue aspirin 81 mg indefinitely
After PCI for ACS, give dual antiplatelet therapy4 for 1 year
ESC: “Up to 12 months,” with strict minimum of 1 month for bare-metal stent and 6 months for drug-eluting stent
ACC/AHA: “Discontinuation after 6 months may be reasonable” if high bleeding risk; “>1 year may be reasonable” if low bleeding risk
After fibrinolytic therapy, continue dual antiplatelet therapy for at least 14 days and up to 1 year
ESC: If anticoagulation is otherwise indicated (i.e., for atrial fibrillation (AF)), give it in addition to antiplatelet therapy
Beta blockers (ACC/AHA 2013, ESC 2012)
Initiate oral beta blockers in the first 24 hours, unless heart failure, evidence of a low output state, or other contraindications
Renin-angiotensin-aldosterone system inhibitors (ACC/AHA 2013, ESC 2012)
Administer ACE inhibitor (or angiotensin receptor blocker, if intolerant of ACE) within the first 24 hours if anterior infarction, heart failure, or ejection fraction ≤40%
Give an aldosterone antagonist to patients who are already receiving an ACE inhibitor and beta blocker, and whose ejection fraction is ≤40% and either have symptomatic heart failure or diabetes mellitus, unless contraindicated
If patient did not undergo coronary angiography, or in patients with multi-vessel disease, perform noninvasive testing for ischemia before discharge
ACC/AHA 2013: O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction. J Am Coll Cardiol. 2013 Jan 29;61(4). [https://www.guideline.gov/summaries/summary/39429?]
ESC 2012: Steg PG, James SK, Atar D, et al. ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2012 Oct;33(20):2569–2619. [https://www.guideline.gov/summaries/summary/39353?]
NICE 2013: National Clinical Guideline Centre. Myocardial infarction with ST-segment elevation. The acute management of myocardial infarction with ST-segment elevation. National Institute for Health and Care Excellence (NICE); 2013 Jul. 28 p. [https://www.guideline.gov/summaries/summary/47019?]
ACC/AHA 2016: Levine GN, Bates ER, Bittl JA, et al. 2016 ACC/AHA guideline focused update on duration of dual antiplatelet therapy in patients with coronary artery disease. Am Coll Cardiol. 2016;68(10):1082–1115. [http://content.onlinejacc.org/article.aspx?articleid=2507082]
1Do not administer prasugrel to patients with a history of prior stroke or TIA.
2ESC guidelines favor prasugrel or ticagrelor over clopidogrel. ACC/AHA does not state a preference.
3ESC guidelines favor bivalirudin or enoxaparin to unfractionated heparin. ACC/AHA does not state a preference.
4ESC guidelines favor prasugrel or ticagrelor over clopidogrel for dual antiplatelet therapy. ACC/AHA lists three options: clopidogrel 75 mg daily, prasugrel 10 mg daily, or ticagrelor 90 mg BID.
Nitroglycerin (sublingual or spray)
Pain associated with ACS is usually severe and contributes to the ischemia by inducing further sympathetic output. Treating the pain should be started immediately. NTG 0.4 mg sublingual can be administered if the systolic blood pressure is more than 90 mm Hg. This usually works within a few minutes. The same dose can be repeated 2 more times in 5-minute intervals as needed. Make sure the patient has not received any phosphodiesterase inhibitor-5 during the last 24 hours before giving NTG. If pain persists, 2 to 4 mg of morphine sulfate should be tried. Sometimes, pain is refractory to sublingual NTG and morphine. In such circumstances, an intravenous NTG drip can be started if there is no concern about right ventricle infarction (to avoid excessive preload reduction and precipitating cardiac shock in these patients).
Morphine (2-4 mg intravenously every 5 min) until the pain is relieved.
Beta-blockers decrease early complications and improve long-term mortality in patients with ACS. If blood pressure allows, all patients should receive a beta-blocker as soon as possible. Cardioselective beta-blockers such as atenolol or metoprolol are preferred. Five milligrams of intravenous metoprolol every 2 minutes for a total of 3 doses, and then 50 mg orally 15 minutes after the last intravenous dose can be given. The patient should be on 50 mg every 6 hours for the first 48 hours, and then he or she can be switched to a maintenance twice-daily dose or a once-daily long-acting form. Even if the patient does not tolerate the intravenous dose, you can try a small dose of oral metoprolol (such as 12.5–25 mg) and follow the patient closely.
In addition to aspirin, a loading dose (300 mg) of clopidogrel is administered.
if >75 years of ag) with aspirin only(???)
If a patient has a history of gastrointestinal bleeding, a proton pump inhibitor can be added.
ACC/AHA: If hypertensive or having ongoing ischemia, give beta blocker at time of presentation, unless contraindicated
Analgesics
ESC: Give IV opioids to relieve pain
Anticoagulation (ACC/AHA 2013, ESC 2012, NICE 2013)
If patient will receive primary PCI, give anticoagulation with unfractionated heparin (UFH), enoxaparin, or bivalirudin3; a glycoprotein IIb/IIIa inhibitor (abciximab, eptifibatide, tirofiban) may be added to UFH
If patient will receive fibrinolytics, give anticoagulation until hospital discharge (minimum 48 hours, up to 8 days) or until revascularization is performed; options include UFH (titrated to a PTT of 1.5–2.0 times control), enoxaparin (IV bolus followed in 15 minutes by subcutaneous injection), or fondaparinux (initial IV dose followed in 24 hours by subcutaneous therapy)
Thrombosis from plaque disruption is one of the main causes of coronary artery obstruction. Thrombus-related events are preventable by anticoagulation. Heparins and direct thrombin inhibitors block the ongoing coagulation and reduce the death rate after MI.
Anticoagulation Medications Used in MI
| Anticoagulation Drug | Mechanism of Action |
|---|---|
| Unfractionated heparin | Activates antithrombin III that inactivates IIa and Xa |
| Enoxaparin | Activates antithrombin III that inactivates IIa and Xa |
| Fondaparinux | Antithrombin III–selective inhibition of Xa |
| Bivalirudin | Direct thrombin inhibitor |
Aortic counterpulsation
Initial workup plan:
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All patients with ACS should be moved to a telemetry bed for continuous monitoring and closer observation. Cardiac enzymes, complete blood count, coagulation profile, basic metabolic panel, and magnesium levels should be obtained stat. Platelet counts and the coagulation profile can affect the antiplatelet and anticoagulation choices. Creatinine level is important for adjustment of medication doses and allows for contrast nephropathy prophylaxis measures to be ordered if the patient has chronic kidney disease. Potassium and magnesium should be kept above 4.0 and 2.0 mEq/L, respectively, as this may decrease the risk of tachyarrhythmias.
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Draw serum markers routinely, but do not wait for results to initiate reperfusion therapy.
According to the 2007 ACC/AHA focused update on the management of patients with ST-elevation myocardial infarction, patients with acute STEMI will benefit from primary percutaneous intervention with a goal door-to-balloon time of <90 min.
Fibrinolytic therapy within 30 min is preferred if transfer to a PCI-capable facility will make door-to-balloon time > 90 min. These guidelines are directed toward patients presenting to the hospital with STEMI, but may also help to decide when to transfer inpatients who develop STEMI during hospitalization.
ACC/AHA GUIDELINES FOR THE MANAGEMENT OF PATIENTS WITH ST-ELEVATION MYOCARDIAL INFARCTION
Class 1 recommendations for the use of thrombolytics in myocardial infarction include any ONE of the following three ECG findings:
And
Class 2 recommendations for the use of thrombolytics in myocardial infarction include any ONE of the following:
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Reproduced from Antman EM, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction—executive summary. J Am Coll Cardiol. 2004;44(3): 671–719. Copyright 2004, with permission from Elsevier.
Reperfusion by thrombolytic treatment or mechanical means can restore oxygen levels and return the metabolic processes to aerobic metabolism.
A secondary consequence of reperfusion is reperfusion injury in which the highly reduced state of injured cells meets increased oxygen concentration and produces reactive oxygen radicals. Most notable of these is the hydroxyl radical (OHo), which attacks tissue components such as lipids and protein sulfhydryl groups.
Coronary artery bypass surgery
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A 59-year-old man complains of tight chest pressure and shortness of breath after lifting several boxes in his garage approximately 2 h ago. He perceives that his heart is skipping beats. His medical history is significant for hypertension and cigarette smoking. On examination, his heart rate is 55 beats/min and regular, and his lungs are clear to auscultation. An electrocardiogram shows bradycardia with an increased PR interval and ST-segment elevation in multiple leads including the anterior leads, V1 and V2.
Summary: A 59-year-old hypertensive male smoker has a 2-h history of tight chest pressure, shortness of breath, and palpitations after exertion. His heart rate is 55 beats/min and regular. The electrocardiogram (ECG) shows bradycardia, first-degree heart block, and ST-segment elevation in leads V1 and V2.
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A 51-year-old man presents to the emergency department with chest pain. He states that he has had chest discomfort or pressure intermittently over the last year especially with increased activity. He describes the chest pain as a pressure behind his breastbone that spreads to the left side of his neck. Unlike previous episodes, he was lying down, watching television. The chest pain lasted approximately 15 minutes then subsided on its own. He also noticed that he was nauseated and sweating during the pain episode. He has no medical problems that he is aware of and has not been to a physician for several years. On examination, he is in no acute distress with normal vital signs. His lungs were clear to auscultation bilaterally, and his heart had a regular rate and rhythm with no murmurs. Electrocardiography (ECG) revealed ST segment elevation and peaked T waves in leads II, III, and aVF. Serum troponin I and T levels are elevated.
Summary: A 51-year-old man with a history of chest pain with exertion presents with retrosternal chest pressure that radiates to the neck. He has nausea and diaphoresis while at rest. The patient has ST segment elevation and peaked T waves in the inferior ECG leads. The troponin I and T levels are elevated.
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Which of the following IS NOT necessary for a class 1 indication for tPA in a patient with an acute myocardial infarction?
The correct answer is B. You answered D.
The correct answer is "B." Class I indications for use of thrombolytics in MI include one of the following ECG findings: >1 mm of ST segment elevation in at least 2 contiguous limb leads, 1 to 2 mm of ST segment elevation in at least 2 contiguous precordial leads, new complete bundle branch block plus a history suggestive of MI AND presenting 12 hours since the onset of pain and age <75 years.
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Among the choices below, there is one incorrect answer. Identify which answer is incorrect.
An acute myocardial infarction is diagnosed when there is a rise or fall of a cardiac biomarker, preferably cardiac troponin, with at least one value above the 99th percentile upper reference limit and at least one of the following:
The correct answer is B.
The correct answer is B. The presence or absence of a pulmonary embolism is unrelated to establishing a diagnosis of myocardial infarction.