Myocardial Infarction, Acute Case File

Myocardial Infarction, Acute Case File

Eugene C. Toy, MD, Barry C. Simon, MD, Terrence H. Liu, MD, MHP, Katrin Y. Takenaka, MD, Adam J. Rosh, MD, MS

Case 2

A 58-year-old man arrives at the emergency department complaining of chest pain. The pain began 1 hour ago, during breakfast, and is described as severe, dull, and pressure-like. It is substernal in location, radiates to both shoulders, and is associated with shortness of breath. The patient vomited once. His wife adds that he was very sweaty when the pain began. The patient has diabetes and hypertension and takes hydrochlorothiazide and glyburide. His blood pressure is 150/100 mm Hg, pulse rate is 95 beats per minute, respiration is 20 breaths per minute, temperature 37.3°C (99.1°F), and oxygen saturation by pulse oximetry is 98%. The patient is diaphoretic and appears anxious. On auscultation, faint crackles are heard at both lung bases. The cardiac examination reveals an S4 gallop and is otherwise normal. The examination of the abdomen reveals no masses or tenderness. The ECG is shown in Figure 2–1.

⯈ What is the most likely diagnosis?

⯈ What are the next diagnostic steps?

⯈ What therapies should be instituted immediately?

Figure 2–1. 12-lead ECG.

ANSWERS TO CASE 2:

Myocardial Infarction, Acute

Summary: This is a 58-year-old man presenting with acute severe chest pain, diaphoresis, and dyspnea. The patient has a number of risk factors for underlying coronary heart disease and the history and physical examination are typical of an acute coronary syndrome (ACS).

• Most likely diagnosis: Acute myocardial infarction.
• Next diagnostic steps: Place the patient on a cardiac monitor, establish IV access, and obtain an electrocardiogram (ECG) immediately. A chest x-ray and serum levels of cardiac markers should be obtained as soon as possible.
• Immediate therapies: Aspirin is the most important immediate therapy. Oxygen and sublingual nitroglycerin are also standard early therapies. Depending on the result of the ECG, emergency reperfusion therapy, such as thrombolysis, may be indicated. Intravenous β-blockers, IV nitroglycerin, low-molecular-weight heparin, and additional antiplatelet agents, such as clopidogrel, might also be indicated.

ANALYSIS

Objectives

1. Recognize acute myocardial infarction (MI) and the spectrum of acute coronary syndromes (ACSs).
2. Know the appropriate diagnostic tests and their limitations.
3. Understand the therapeutic approach to ACS.

Considerations

Chest pain accounts for more than 6 million visits every year to emergency departments in the United States. Of these 6 million visits, nearly 800,000 will end with a diagnosis of MI and 1.5 million will be given the diagnoses of unstable angina (UA) or non–ST-elevation myocardial infarction (NSTEMI). Coronary heart disease (CHD) is the leading cause of death in adults in the United States. Furthermore, missed MI accounts for the most money paid in malpractice claims in emergency medicine. Because ACS is common, treatable, and potentially catastrophic both clinically and medicolegally, emergency physicians should be thoroughly familiar with this problem.

Our understanding of the pathophysiology behind cardiac ischemia has evolved from a model of progressive coronary artery narrowing to a current model of plaque rupture and thrombus formation. The concept of fixed narrowing explains only stable angina brought on by increased myocardial demand. In contrast, ACS, which encompasses the spectrum of UA, NSTEMI, and ST-elevation myocardial infarction (STEMI), involves a dynamic process of inflammation and intravascular thrombosis, beginning with coronary artery plaque rupture. The fate of this plaque, in terms of location and extent of subsequent thrombosis, determines the clinical presentation and seems to correlate with the subdivisions of ACS. STEMI occurs when total occlusion of an epicardial vessel causes transmural infarction, classically presenting as unremitting chest pain and ST-segment elevation on the electrocardiography (ECG). It is treated with immediate reperfusion therapy.

The clinical syndromes of NSTEMI and UA, in contrast, are caused by subendocardial infarction or ischemia, respectively, usually caused by microemboli arising from the ruptured plaque. Chest pain is often stuttering and ECG changes such as ST-segment depression may be transient. Although often indistinguishable upon initial presentation, elevation in cardiac markers is what eventually distinguishes NSTEMI from UA. Immediate therapy for both NSTEMI and UA focuses on halting ongoing thrombosis and reducing myocardial demand. Many patients go on to have percutaneous coronary intervention (PCI), such as stent placement, directed at the unstable plaque.

Approach To:

Suspected Myocardial Infarction

DEFINITIONS

MYOCARDIAL INFARCTION: Myocardial cell death caused by ischemia, as evidenced by a typical rise and fall in cardiac biomarkers.

ACUTE CORONARY SYNDROME: An ischemic chest pain syndrome, usually associated with coronary artery plaque rupture, encompassing STEMI, NSTEMI, and UA.

UNSTABLE ANGINA: An acute coronary syndrome, in which chest pain is of new onset, or increasing severity, or occurs at rest, and cardiac biomarkers are not elevated.

NON–ST-ELEVATION MYOCARDIAL INFARCTION: An acute coronary syndrome in which cardiac biomarkers are eventually elevated, but lacking new ST elevation on ECG.

ST-ELEVATION MYOCARDIAL INFARCTION: An acute coronary syndrome, in which significant ST elevation is found in two or more contiguous ECG leads, typically associated with epicardial coronary artery occlusion and transmural infarction, and resulting in Q waves if perfusion is not soon restored.

CLINICAL APPROACH

Evaluation

The cornerstone of diagnosis of acute coronary syndromes is the ECG. Because findings on the initial ECG form a critical branch point in therapy, patients presenting to the emergency department with chest pain suggestive of ACS should have an

Data from Hollander JE, Diercks DB. Intervention strategies for acute coronary syndromes. In: Tintinalli JE, Kelen GD,

Stapczynski JS, eds. Emergency Medicine. 6th ed. New York, NY: McGraw-Hill; 2004:108-124.

ECG within 10 minutes of arrival. Identifying STEMI by ECG as soon as possible is the first step toward rapidly establishing reperfusion and reducing mortality (the ECG criteria for reperfusion therapy are listed in Table 2–1). In contrast to STEMI, ECG findings may be subtle or absent in NSTEMI and UA, and are not required for diagnosis and initiation of therapy. However, certain findings, such as ST-segment depression or deep T-wave inversions, particularly those that change in accord with symptoms, can rapidly establish the diagnosis of UA and NSTEMI.

Unfortunately, the ECG is frequently nondiagnostic in ACS. Even in patients eventually diagnosed with MI, the initial ECG is nondiagnostic in about 50% and completely normal in up to 8%. Comparing the current ECG to old tracings is crucial, because subtle changes may be seen. Serial ECGs performed at 15- to 30-minute intervals, or continuous ST-segment monitoring, may reveal the subtle dynamic changes of UA, or those of an evolving MI (Table 2–2 lists the anatomical locations of MI).

In the face of a normal or nondiagnostic ECG, the decision whether to further evaluate for ACS depends on the likelihood that the pain is actually of cardiac

Abbreviations: LAD = left anterior descending artery; LCA = left circumfl ex artery; RCA = right circumfl ex artery; V4R =

right-sided lead which should be placed any time an inferior MI is suspected.

Data from Hollander JE, Diercks DB. Intervention strategies for acute coronary syndromes. In: Tintinalli JE, Kelen GD,

Stapczynski JS, eds. Emergency Medicine. 6th ed. New York, NY: McGraw-Hill; 2004:108-124.

Data from Hollander JE, Diercks DB. Intervention strategies for acute coronary syndromes. In: Tintinalli JE, Kelen GD,

Stapczynski JS, eds. Emergency Medicine. 6th ed. New York, NY: McGraw-Hill; 2004:108-124.

origin and on the patient’s overall risk profile. Inquiring about traditional risk factors for CHD remains a standard component of the chest pain evaluation. CHD risk factors are listed in Table 2–3. High risk is easily established if there is a prior history of definite CHD such as prior MI or abnormal coronary angiogram. Characteristics of the history and physical examination that alter the likelihood that the pain is of cardiac origin are listed in Table 2–4. Patients who are young, without a family history of premature CHD, and with an atypical history and a normal or nondiagnostic ECG can usually be safely discharged without further evaluation for ACS. Shortterm prognosis in those with known or suspected UA or NSTEMI can be calculated with the thrombolytics in myocardial infarction (TIMI) risk score (Table 2–5).

Serum cardiac markers are used to confirm or exclude myocardial cell death, and are considered the gold standard for the diagnosis of MI. There are a number of markers currently in wide use, including myoglobin, CKMB, and troponin. While algorithms vary, serum levels of 1 or more cardiac markers should be obtained initially and at 4 to 12 hours after presentation. Troponin I is extremely sensitive and specific for cardiac damage; thus an elevated level confirms infarction whereas a normal level at 8 to 12 hours after the onset of pain excludes infarction. Important limitations of cardiac markers are that levels remain normal in unstable angina and

Abbreviation: TIMI = thrombolysis in myocardial infarction.

^aOne point is assigned to each of the seven components. Risk of death, MI, or revascularization at 2 wk by score: 1, 5%; 2,

8%; 3, 13%; 4, 20%; 5, 26%; 6, 41%.

Data from Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for UA/NSTEMI. JAMA. 2000; 284(7):835-842.

serum elevations are delayed 4 to 12 hours after infarction. The trend and peak of positive biomarkers can indicate the dynamics of necrosis and infarct size.

Other studies that are routinely obtained in the workup of ACS include a chest radiograph (CXR), complete blood count, chemistries, coagulation studies, and blood type. The CXR serves to rule out other causes of chest pain, and to identify pulmonary edema. Although not a perfect test, a normal mediastinum on CXR makes aortic dissection least likely. For this reason, a chest radiograph should be performed prior to thrombolysis.

Treatment

When ACS is suspected based on history, treatment should be started immediately. The patient should be placed on a cardiac monitor, IV access established, and an ECG obtained. Unless allergic, affected patients should be immediately given aspirin to chew (162 mg dose is common). Aspirin is remarkably beneficial across the entire spectrum of ACS. For example, in the setting of STEMI, the survival benefit from a single dose of aspirin is roughly equal to that of thrombolytic therapy (but with

negligible risk or cost). Other mainstays of initial treatment are oxygen, sublingual nitroglycerin, which decreases wall tension and myocardial oxygen demand, and morphine sulfate. Together with aspirin these three therapies make up the mnemonic “MONA,” which is said to “greet chest pain patients at the door.” Based on results of the initial ECG, therapy then progresses in one of two directions.

ST-Elevation MI

When the ECG reveals STEMI and symptoms have been present for less than 12 hours, immediate reperfusion therapy is indicated. The saying “time is myocardium” is a reminder that myocardial salvage and clinical benefit are critically dependent on the time to restoration of flow in the infarct-related artery. Optimally, total ischemic time should be limited to less than 120 minutes. There are two ways to achieve reperfusion: primary PCI (angioplasty or stent placement) and thrombolysis. The choice is largely determined by the capabilities of the hospital.

Primary PCI is the treatment of choice when it can be performed rapidly by an experienced cardiologist. The standard “door-to-balloon time” goal is 90 minutes. Compared to thrombolysis, PCI leads to lower 30-day mortality (4.4% vs 6.5%), nonfatal reinfarction rate (7.2% vs 11.9%), and fewer hemorrhagic strokes. Recent studies suggest that if a patient presents to a hospital that does not offer PCI, transfer

to a neighboring facility for primary PCI is superior to thrombolysis if transfer can be accomplished within 90 minutes. PCI is also used for STEMI complicated by cardiogenic shock, when there is a contraindication to thrombolysis, and in cases where thrombolysis fails to restore perfusion (rescue PCI). Administration of lowmolecular- weight heparin and a glycoprotein IIB/IIIA inhibitor prior to PCI reduces the risk of reinfarction.

When PCI is not an option, intravenous thrombolytic agents may be used to achieve reperfusion. Studies of thrombolytic therapy versus placebo for STEMI show an absolute mortality reduction of roughly 3%. The benefit of thrombolysis is greatest when treatment is begun within 4 hours, and benefit approaches that of primary PCI when thrombolytics are begun within 30 minutes. However, benefit extends out to 12 hours. Adjunctive antithrombotic therapy with unfractionated or low-molecular-weight heparin is required with most thrombolytic agents. Table 2–6 lists other measures, in addition to aspirin and reperfusion therapy, that reduce mortality after MI.

Unstable Angina/Non-ST Elevation MI

Cases of ACS lacking ECG criteria for reperfusion fall into the UA/NSTEMI category. The approach to therapy for UA/NSTEMI tends to be graded, based on ECG findings, cardiac marker results, TIMI risk score, and whether the patient is likely to undergo early angiography and PCI. Aspirin and nitroglycerin constitute the minimum therapy. Morphine is added when chest discomfort continues despite nitroglycerin therapy. β-blockers, such as IV metoprolol, are usually added in cases presenting with hypertension or tachycardia. While the mortality benefit of chronic β-blocker therapy after MI is well established, in the acute setting, β-blockers should be used with caution because they can place certain patients at risk for cardiogenic shock, such as those presenting with signs of heart failure.

In high-risk patients, a more aggressive approach to halting the thrombotic process is taken, by adding low-molecular-weight heparin and oral clopidogrel, an antiplatelet agent. Patients are considered to be high risk if there are ischemic ECG

Data from American College of Cardiologists. Guidelines for managing patients with AMI, UA, and NSTEMI. J Am Coll

Cardiol. 2002;40:1366-1374.

changes, elevated cardiac markers, or if the TIMI risk score is 3 or greater. Intravenous glycoprotein IIB/IIIA inhibitors, an even more potent and expensive type of antiplatelet drug, are reserved for the subset of high-risk patients who will undergo early angiography and PCI, in whom these agents have been shown to reduce subsequent CHD morbidity.

In the past, angiography was often postponed for a number of days or weeks following an episode of ACS. However, recent studies have shown that an early invasive strategy, where high-risk patients with UA and NSTEMI are taken for angiography and PCI within 24 to 36 h, has slightly superior efficacy to medical therapy and delayed angiography. An early invasive strategy is indicated for any of the following: refractory angina, hemodynamic instability, signs of heart failure, ventricular tachycardia, ST depressions on ECG, or elevated cardiac enzymes. Like primary PCI for STEMI, whether an early invasive strategy is chosen often depends on hospital resources and cardiology expertise.

Complications

Several life-threatening complications of acute MI may arise at any time after presentation (Table 2–7). Serious complications occur most often in the setting of anterior STEMI. MI-associated ventricular tachycardia and ventricular fibrillation (sudden death) are the most frequently encountered complications in the ED and prehospital setting, occurring in approximately 10% of cases. Continuous cardiac monitoring and immediate cardioversion/defibrillation has been a mainstay of cardiac care since the 1960s, and has been shown to save lives on a large scale. Bradyarrhythmias may also complicate MI. Heart block that occurs in the setting of anterior MI generally implies irreversible damage to the His-Purkinje system and is an indication for transvenous pacing. Inferior MI, in contrast, frequently causes arteriovenous (AV) node dysfunction and second-degree block that is transient and may respond to atropine.

Data from Hollander JE, Diercks DB. Intervention strategies for acute coronary syndromes. In: Tintinalli JE, Kelen GD,

Stapczynski JS, eds. Emergency Medicine. 6th ed. New York, NY: McGraw-Hill; 2004:108-124.

Pump dysfunction, leading to pulmonary edema or cardiogenic shock, is an ominous complication of MI that implies a large area of myocardial injury. The left ventricular dysfunction that occurs with anterior MI usually causes recognizable pulmonary edema, with tachypnea, rales, and visible congestion on chest x-ray. A new systolic murmur may be heard when cardiogenic pulmonary edema is caused by papillary muscle dysfunction and acute mitral regurgitation. Signs of cardiogenic shock range from frank hypotension to subtle indicators of impaired perfusion such as oliguria, cool extremities, and confusion. Emergency PCI is the reperfusion strategy of choice for cardiogenic shock. Insertion of an aortic balloon pump may be indicated in addition to pressor agents. Right ventricular infarction, which complicates inferior MI, usually presents as hypotension without pulmonary congestion. The diagnosis is confirmed by ST elevation in lead V4 on a right-sided ECG, and the primary treatment is aggressive volume loading. Nitroglycerine and high-dose morphine should be avoided in these patients.

Late complications of MI that tend to occur in the intensive care unit several hours to days after presentation include left ventricular free wall rupture causing tamponade, ventricular septal defect, pericarditis, left ventricular aneurysm, and thromboembolism. Finally, iatrogenic complications of MI therapy can occur. Emergency physicians who administer thrombolytics for STEMI must consider the risk of serious hemorrhagic complications, particularly intracranial hemorrhage, which occurs in 0.5% to 0.7% of patients and is usually fatal. Heparin and antiplatelet therapy leads to significant bleeding in up to 10% of patients, depending on what agents are given, although life-threatening hemorrhage is rare.

COMPREHENSION QUESTIONS

2.1 A 48-year-old man is being seen for chest pain. In the initial evaluation of this patient, which of the following is the most important diagnostic test?

A. Chest x-ray

B. ECG

C. Serum cardiac markers

D. Computed tomography

E. Cholesterol levels

2.2 A 58-year-old man presents to his physician’s offi ce complaining of 2 hours of substernal chest pain and dyspnea. Which of the following is the most important next step in management?

A. Administration of propranolol

B. Aspirin to chew

C. Sublingual nitroglycerin

D. Administration of a diuretic agent

E. Chest radiograph

2.3 A 45-year-old man is seen in the emergency department with 3 hours of substernal chest pain radiating to his left arm. The ECG shows only nonspecifi c changes. Hearing that the ECG is normal, he requests to go home. Which of the following statements is most accurate?

A. The patient may be safely discharged home.

B. If a repeat ECG in 30 minutes is normal, myocardial infarction is essentially ruled out and the patient may be safely discharged.

C. The patient should be advised that half of heart attack patients have a nondiagnostic ECG and serial cardiac biomarkers levels should be assessed.

D. The patient should undergo an immediate thallium stress test to further assess for coronary artery disease to help clarify the management.

ANSWERS

2.1 B. The ECG is the crucial first diagnostic test in the evaluation of chest pain. Presence versus absence of ST elevation represents a major therapeutic branch point.

2.2 B. While all of these therapies are useful, aspirin significantly decreases mortality, with almost no downside in nonallergic patients, and should be given immediately.

2.3 C. Roughly half of patients with MI, as defined by a typical rise in cardiac biomarkers, will have a nondiagnostic ECG upon presentation. Risk stratifi cation by stress testing is sometimes ordered from the emergency department, but only after serial ECGs and cardiac biomarkers remain normal.

CLINICAL PEARLS

⯈ MONA greets chest pain at the door (morphine, oxygen, nitroglycerin, and, most importantly, aspirin).

⯈ An ECG should be performed immediately in all patients with chest pain concerning for ACS.

⯈ The ECG will dictate the next step in management: new ST elevation generally requires immediate reperfusion therapy. “Time is myocardium.”

References

Anderson J L, Adams C D, Antman E M, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. Circulation. 2007;116:e148-e304. 

Antman E M, Hand M, Armstrong P W, et al. 2007 focused update of the ACC/AHA 2004 guidelines for the management of patients with ST-elevation myocardial infarction. Circulation. 2008;117:296-329. 

Panju AA, Hemmelgarn BR. Is this patient having a myocardial infarction? JAMA. 1998;280:1256-1263.

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