Chapter 119: ST-Segment Elevation Myocardial Infarction

INTRODUCTION

Early recognition and immediate treatment of acute ST-segment elevation myocardial infarction (STEMI) are essential; diagnosis is based on characteristic history, ECG, and serum cardiac markers.

Symptoms

Chest pain similar to angina (Chap. 31) but more intense and persistent; not fully relieved by rest or nitroglycerin, often accompanied by nausea, sweating, apprehension. However, ~25% of MIs are clinically silent.

Physical Examination

Pallor, diaphoresis, tachycardia, S₄, dyskinetic cardiac impulse may be present. If CHF exists, rales and S₃ are present. Jugular venous distention is common in right ventricular infarction.

ECG

ST elevation, followed (if acute reperfusion is not achieved) by T-wave inversion, then Q-wave development over several hours.

Cardiac Biomarkers

Cardiac-specific troponins T and I are highly specific for myocardial injury and are the preferred biochemical markers for diagnosis of acute MI. They remain elevated for 7–10 days. Creatine phosphokinase (CK) level rises within 4–8 h, peaks at 24 h, and returns to normal by 48–72 h. CK-MB isoenzyme is more specific for MI but may also be elevated with myocarditis or after electrical cardioversion. Serum cardiac markers should be measured at presentation, 6–9 h later, and then at 12–24 h.

Noninvasive Imaging Techniques

Useful when diagnosis of MI is not clear. Echocardiography detects infarct-associated regional wall motion abnormalities (but cannot distinguish acute MI from a previous myocardial scar). Echo is also useful in detecting RV infarction, LV aneurysm, and LV thrombus. MRI with delayed gadolinium enhancement accurately indicates regions of infarction, but is technically difficult to obtain in acutely ill pts.

TREATMENT: STEMI INITIAL THERAPY

Initial goals are to (1) quickly identify if pt is candidate for reperfusion therapy, (2) relieve pain, and (3) prevent/treat arrhythmias and mechanical complications.

Aspirin should be administered immediately (162–325 mg chewed at presentation, then 75–162 mg PO qd), unless pt is aspirin-intolerant.
Perform targeted history, examination, and ECG to identify STEMI (>1 mm ST elevation in two contiguous limb leads, ≥2 mm ST elevation in two contiguous precordial leads, or new LBBB) and appropriateness of reperfusion therapy (percutaneous coronary intervention [PCI] or IV fibrinolytic agent), which reduces infarct size, LV dysfunction, and mortality.
Primary PCI is generally more effective than fibrinolysis and is preferred at experienced centers capable of performing the procedure rapidly (Fig. 119-1), especially when diagnosis is in doubt, cardiogenic shock is present, bleeding risk is increased, or symptoms have been present for >3 h.
Proceed with IV fibrinolysis if PCI is not available or if logistics would delay PCI >1 h longer than fibrinolysis could be initiated (Fig. 119-1). Door-to-needle time should be <30 min for maximum benefit. Ensure absence of contraindications (Fig. 119-2) before administering fibrinolytic agent. Those treated within 1–3 h benefit most; can still be useful up to 12 h if chest pain is persistent or ST remains elevated in leads that have not developed new Q waves. Complications include bleeding, reperfusion arrhythmias, and, in case of streptokinase (SK), allergic reactions. Enoxaparin or heparin (60 U/kg [maximum 4000 U], then 12 [U/kg]/h [maximum 1000 U/h]) should be initiated with fibrinolytic agents (Fig. 119-2); maintain activated partial thromboplastin time (aPTT) at 1.5–2.0 × control (~50–70 s).
If chest pain or ST elevation persists >90 min after fibrinolysis, consider referral for rescue PCI. Coronary angiography after fibrinolysis should also be considered for pts with recurrent angina or high-risk features (Fig. 119-2) including extensive ST elevation, signs of heart failure (rales, S₃, jugular venous distension, left ventricular ejection fraction [LVEF] ≤35%), or systolic bp <100 mmHg.

The initial management of NSTEMI (non-Q MI) is different (Chap. 120). In particular, fibrinolytic therapy should not be administered.

ADDITIONAL STANDARD TREATMENT

(Whether or not reperfusion therapy is undertaken):

Hospitalize in CCU with continuous ECG monitoring.
IV line for emergency arrhythmia treatment.
Pain control: (1) Morphine sulfate 2–4 mg IV q5–10 min until pain is relieved or side effects develop (nausea, vomiting, respiratory depression [treat with naloxone 0.4–1.2 mg IV], hypotension [if bradycardic, treat with atropine 0.5 mg IV; otherwise use careful volume infusion]); (2) nitroglycerin 0.3 mg SL if systolic bp >100 mmHg; for refractory pain: IV nitroglycerin (begin at 10 μg/min, titrate upward to maximum of 200 μg/min, monitoring bp closely); do not administer nitrates within 24 h of sildenafil or within 48 h of tadalafil (used for erectile dysfunction); (3) β-adrenergic antagonists (see below).
Oxygen: 2–4 L/min by nasal cannula (if needed to maintain O₂ saturation >90%).
Mild sedation (e.g., diazepam 5 mg, oxazepam 15–30 mg, or lorazepam 0.5–2 mg PO three to four times daily).
Soft diet and stool softeners (e.g., docusate sodium 100–200 mg/d).
β-Adrenergic blockers (Chap. 117) reduce myocardial O₂ consumption, limit infarct size, and reduce mortality. Especially useful in pts with hypertension, tachycardia, or persistent ischemic pain; contraindications include active CHF, systolic bp <95 mmHg, heart rate <50 beats/min, AV block, or history of bronchospasm. Consider IV (e.g., metoprolol 5 mg q2–5min to total dose of 15 mg) if pt is hypertensive. Otherwise, begin PO regimen (e.g., metoprolol tartrate 25–50 mg four times daily).
Anticoagulants: Most pts with STEMI should receive an anticoagulant (typically unfractionated heparin [UFH] or bivalirudin for those undergoing PCI [discontinued at end of procedure or shortly thereafter]; enoxaparin [for up to 8 days, or until discharge, whichever is earlier] or UFH [for ≥2 days] for those receiving fibrinolysis or no reperfusion therapy). Continued full-dose IV heparin (PTT 1.5–2 × control) or LMWH (e.g., enoxaparin 1 mg/kg SC q12h) followed by warfarin is recommended for pts with high risk of thromboembolism (severe LV dysfunction, presence of ventricular thrombus, large dyskinetic region in acute anterior MI, or pulmonary embolism). If used, warfarin is continued for 3–6 months.
Antiplatelet agents: Continue aspirin 162–325 md daily and an oral P2Y₁₂ platelet receptor antagonist after STEMI (e.g., ticagrelor, clopidogrel, or prasugrel [the latter only if PCI is undertaken]).
ACE inhibitors reduce mortality in pts following acute MI and should be prescribed within 24 h of hospitalization for pts with STEMI—e.g., captopril (6.25 mg PO test dose advanced to 50 mg PO tid). ACE inhibitors should be continued indefinitely after discharge in pts with heart failure or those with asymptomatic LV dysfunction (ejection fraction ≤40%); if pt is ACE inhibitor intolerant, use ARB (e.g., valsartan or candesartan).
Aldosterone antagonists (spironolactone or eplerenone 25–50 mg daily) further reduce mortality in pts with LVEF ≤40% and either symptomatic heart failure or diabetes; do not use in pts with advanced renal insufficiency (e.g., creatinine ≥2.5 mg/dL) or hyperkalemia.
Serum magnesium level should be measured and repleted if necessary to reduce risk of arrhythmias.

FIGURE 119-1

Reperfusion strategies in STEMI. DIDO, door-in-door-out; FMC, first medical contact; LOC, level of evidence. (Adapted from P O’Gara, et al: Circulation 127:e362, 2013.)

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FIGURE 119-2

Algorithm for fibrinolytic therapy of acute STEMI.

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COMPLICATIONS

Listen

(For arrhythmias, see also Chaps. 122 and 123)

Ventricular Arrhythmias

Isolated ventricular premature beats (VPBs) occur frequently. Precipitating factors should be corrected (hypoxemia, acidosis, hypokalemia, hypomagnesemia, CHF, arrhythmogenic drugs). Routine beta blocker administration (see above) diminishes ventricular ectopy. Other in-hospital antiarrhythmic therapy should be reserved for pts with sustained ventricular arrhythmias.

Ventricular Tachycardia

If hemodynamically unstable, perform immediate electrical countershock (unsynchronized discharge of 200–300 J or 50% less if using biphasic device). If hemodynamically tolerated, use IV amiodarone (bolus of 150 mg over 10 min, then infusion of 1.0 mg/min for 6 h, then 0.5 mg/min).

Ventricular Fibrillation

VF requires immediate defibrillation (200–400 J). If unsuccessful, initiate cardiopulmonary resuscitation (CPR) and standard resuscitative measures (Chap. 10). Ventricular arrhythmias that appear several days or weeks following MI often reflect pump failure and may warrant invasive electrophysiologic study and implantation of a cardioverter defibrillator (ICD).

Accelerated Idioventricular Rhythm

Wide QRS complex, regular rhythm, rate 60–100 beats/min, is common and usually benign; if it causes hypotension, treat with atropine 0.6 mg IV.

Supraventricular Arrhythmias

Sinus tachycardia may result from heart failure, hypoxemia, pain, fever, pericarditis, hypovolemia, administered drugs. If no cause is identified, suppressive beta blocker therapy may be beneficial to reduce myocardial oxygen demand. Other supraventricular arrhythmias (paroxysmal supraventricular tachycardia, atrial flutter, and fibrillation) are often secondary to heart failure. If hemodynamically unstable, proceed with electrical cardioversion. In absence of acute heart failure, suppressive alternatives include beta blockers, verapamil, or diltiazem (Chap. 123).

Bradyarrhythmias and AV Block

(See Chap. 122) In inferior MI, usually represent heightened vagal tone or discrete AV nodal ischemia. If hemodynamically compromised (CHF, hypotension, emergence of ventricular arrhythmias), treat with atropine 0.5 mg IV q5min (up to 2 mg). If no response, use temporary external or transvenous pacemaker. Isoproterenol should be avoided. In anterior MI, AV conduction defects usually reflect extensive tissue necrosis. Consider temporary external or transvenous pacemaker for (1) complete heart block, (2) Mobitz type II block (Chap. 122), (3) new bifascicular block (LBBB, RBBB + left anterior hemiblock, RBBB + left posterior hemiblock), (4) any bradyarrhythmia associated with hypotension or CHF.

Heart Failure

CHF may result from systolic “pump” dysfunction, increased LV diastolic “stiffness,” and/or acute mechanical complications.

Symptoms Dyspnea, orthopnea, tachycardia.

Examination Jugular venous distention, S₃ and S₄ gallop, pulmonary rales; systolic murmur if acute mitral regurgitation or ventricular septal defect (VSD) has developed.

TREATMENT: HEART FAILURE

Initial therapy includes diuretics (begin with furosemide 10–20 mg IV), inhaled O₂, and vasodilators, particularly nitrates (PO, topical, or IV [Chap. 124] unless pt is hypotensive [systolic bp <100 mmHg]); digitalis is usually of little benefit in acute MI (See Chaps. 13 and 124). Diuretic, vasodilator, and inotropic therapy (Table 119-1) may be guided by invasive hemodynamic monitoring (Swan-Ganz pulmonary artery catheter, arterial line), particularly in pts with accompanying hypotension (Table 119-2; Fig. 119-3). In acute MI, an acceptable pulmonary capillary wedge (PCW) pressure is 15–20 mmHg; in the absence of hypotension, PCW >20 mmHg is treated with diuretic plus vasodilator therapy (IV nitroglycerin [begin at 10 μg/min] or nitroprusside [begin at 0.5 μg/kg per min]) and titrated to optimize bp, PCW, and systemic vascular resistance (SVR).

Normal SVR = 900 − 1350 dyne • s/cm⁵. If PCW >20 mmHg and pt is hypotensive (Table 119-2 and Fig. 119-3), evaluate for VSD or acute mitral regurgitation, consider dobutamine (begin at 1–2 [μg/kg]/min), titrate upward to maximum of 10 (μg/kg)/min; beware of drug-induced tachycardia or ventricular ectopy.

After stabilization on parenteral vasodilator therapy, oral therapy follows with an ACE inhibitor or an ARB (Chap. 124). Consider addition of long-term aldosterone antagonist (spironolactone 25–50 mg daily or eplerenone 25–50 mg daily) to ACE inhibitor if LVEF ≤40% or symptomatic heart failure or diabetes are present—do not use if renal insufficiency or hyperkalemia are present.

TABLE 119-1IV VASODILATORS AND INOTROPIC DRUGS USED IN ACUTE MI

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TABLE 119-1IV VASODILATORS AND INOTROPIC DRUGS USED IN ACUTE MI

Drug

Usual Dosage Range

Comment

Nitroglycerin

5–100 μg/min

May improve coronary blood flow to ischemic myocardium

Nitroprusside

0.5–10 (μg/kg)/min

More potent vasodilator, but improves coronary blood flow less than nitroglycerin

With therapy >24 h or in renal failure, watch for thiocyanate toxicity (blurred vision, tinnitus, delirium)

Dobutamine

2–20 (μg/kg)/min

Results in ↑ cardiac output, ↓ PCW, but does not raise bp

Dopamine

2–20 (μg/kg)/min

More appropriate than dobutamine if hypotensive

Hemodynamic effect depends on dose: (μg/kg)/min

<5: ↑ renal blood flow

2.5–10: positive inotrope

>10: vasoconstriction

Norepinephrine

0.5–30 μg/min

Less likely than dopamine to cause arrhythmias in cardiogenic shock

TABLE 119-2HEMODYNAMIC COMPLICATIONS IN ACUTE MI

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TABLE 119-2HEMODYNAMIC COMPLICATIONS IN ACUTE MI

Condition

Cardiac Index, (L/min)/m²

PCW, mmHg

Systolic bp, mmHg

Treatment

Uncomplicated

>2.5

≤18

>100

—

Hypovolemia

<2.5

<15

<100

Successive boluses of normal saline

In setting of inferior wall MI, consider RV infarction (esp. if RA pressure >10)

Volume overload

>2.5

>20

>100

Diuretic (e.g., furosemide 10–20 mg IV)

Nitroglycerin, topical paste or IV (Table 119-1)

LV failure

<2.5

>20

>100

Diuretic (e.g., furosemide 10–20 mg IV)

IV nitroglycerin (or if hypertensive, use IV nitroprusside)

Severe LV failure

<2.5

>20

<100

If bp ≥90: IV dobutamine ± IV nitroglycerin or sodium nitroprusside

If bp <90: IV dopamine

If accompanied by pulmonary edema: attempt diuresis with IV furosemide; may be limited by hypotension

If new systolic murmur present, consider acute VSD or mitral regurgitation

Cardiogenic shock

<2.2

>20

<90 with oliguria and confusion

IV norepinephrine or dopamine

Intraaortic balloon pump

Reperfusion by PCI or CABG may be life-saving

Abbreviations: CABG, coronary artery bypass graft; PCI, percutaneous coronary intervention; PCW, pulmonary capillary wedge pressure; RA, right atrium; VSD, ventricular septal defect.

FIGURE 119-3

Emergency management of cardiogenic shock and pulmonary edema. (Modified from Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 7: The era of reperfusion: Section 1: Acute coronary syndromes [acute myocardial infarction]. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 102:1172, 2000.)

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Cardiogenic Shock

(See Chap. 11) Severe LV failure with hypotension (bp <90 mmHg), elevated PCW (>20 mmHg), cardiac index <2.2 L/min/m², accompanied by oliguria, peripheral vasoconstriction, dulled sensorium, and metabolic acidosis.

TREATMENT: CARDIOGENIC SHOCK

Swan-Ganz catheter and intraarterial bp monitoring are not always essential but may be helpful; aim for mean PCW of 18–20 mmHg with adjustment of volume (diuretics or infusion) as needed (Fig. 119-3). Vasopressors (e.g., norepinephrine or dopamine [Table 119-1]) and/or intraaortic balloon counterpulsation may be necessary to maintain systolic bp >90 mmHg and reduce PCW. Administer high concentration of O₂ by mask; if pulmonary edema coexists, consider bilateral positive airway pressure (BiPAP) or intubation and mechanical ventilation. Acute mechanical complications (see below) should be sought and promptly treated.

If cardiogenic shock develops within 36 h of acute STEMI, reperfusion by PCI or coronary artery bypass grafting (CABG) may markedly improve LV function.

Hypotension

May also result from right ventricular MI, which should be suspected in inferior or posterior MI, if jugular venous distention and elevation of right-heart pressures predominate (rales are typically absent and PCW may be normal); right-sided ECG leads typically show ST elevation, and echocardiography may confirm diagnosis. Treatment consists of volume infusion. Noncardiac causes of hypotension should be considered: hypovolemia, acute arrhythmia, or sepsis.

Acute Mechanical Complications

Ventricular septal rupture and acute mitral regurgitation due to papillary muscle ischemia/infarct develop during the first week following MI and are characterized by sudden onset of CHF and new systolic murmur. Echocardiography and Doppler interrogation can confirm presence of these complications. PCW tracings may show large v waves in either condition, but an oxygen “step-up” as the catheter is advanced from right atrium to right ventricle suggests septal rupture.

Acute medical therapy of these conditions includes vasodilator therapy (IV nitroprusside: begin at 10 μg/min and titrate to maintain systolic bp ~100 mmHg); intraaortic balloon pump may be required to maintain cardiac output. Mechanical correction is the definitive therapy. Acute ventricular free-wall rupture presents with sudden loss of bp, pulse, and consciousness, while ECG shows an intact rhythm (pulseless electrical activity); emergent surgical repair is crucial, and mortality is high.

Pericarditis

Characterized by pleuritic, positional pain, and pericardial rub (Chap. 116); atrial arrhythmias are common; must be distinguished from recurrent angina. Often responds to aspirin, 650 mg PO qid. Anticoagulants should be avoided when pericarditis is suspected to avoid development of pericardial bleeding/tamponade.

Ventricular Aneurysm

Localized “bulge” of LV chamber due to infarcted myocardium. True aneurysms consist of scar tissue and do not rupture. However, complications include CHF, ventricular arrhythmias, and thrombus formation. Typically an aneurysm is confirmed by echocardiography or by left ventriculography. The presence of thrombus within the aneurysm, or a large aneurysmal segment due to anterior MI, warrants consideration of oral anticoagulation with warfarin for 3–6 months.

Pseudoaneurysm is a form of cardiac rupture contained by a local area of pericardium and organized thrombus; direct communication with the LV cavity is present; surgical repair usually necessary to prevent rupture.

Recurrent Angina

Usually associated with transient ST-T wave changes; signals high incidence of reinfarction; when it occurs in early post-MI period, proceed directly to coronary arteriography, to identify those who would benefit from revascularization.

SECONDARY PREVENTION

Listen

For pts who have not already undergone coronary angiography and PCI, submaximal exercise testing should be performed prior to or soon after discharge. A positive test in certain subgroups (angina at a low workload, a large region of provocable ischemia, or provocable ischemia with a reduced LVEF) suggests need for cardiac catheterization to evaluate myocardium at risk of recurrent infarction. Beta blockers (e.g., metoprolol, 25–200 mg daily) should be prescribed routinely for at least 2 years following acute MI, unless contraindications present (asthma, active heart failure, bradycardia). Continue oral antiplatelet agents (e.g., aspirin 81–325 mg daily and a P2Y12 platelet receptor antagonist) to reduce incidence of reinfarction. If LVEF ≤40%, an ACE inhibitor or ARB (if ACE inhibitor is not tolerated) should be used indefinitely. Consider addition of aldosterone antagonist (see “Heart Failure,” above).

Modification of cardiac risk factors must be encouraged: discontinue smoking; control hypertension, diabetes, and serum lipids (typically atorvastatin 80 mg daily in immediate post-MI period—see Chap. 178); and pursue graduated exercise.

For a more detailed discussion, see Antman EM, Loscalzo J: ST-Segment Elevation Myocardial Infarction, Chap. 295, p. 1599; and Hochman JS, Ingbar DH: Cardiogenic Shock and Pulmonary Edema, Chap. 326, p. 1759, in HPIM-19.

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Chapter 119: ST-Segment Elevation Myocardial Infarction

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INTRODUCTION

Symptoms

Physical Examination

ECG

Cardiac Biomarkers

Noninvasive Imaging Techniques

FIGURE 119-1

FIGURE 119-2

COMPLICATIONS

Ventricular Arrhythmias

Ventricular Tachycardia

Ventricular Fibrillation

Accelerated Idioventricular Rhythm

Supraventricular Arrhythmias

Bradyarrhythmias and AV Block

Heart Failure

FIGURE 119-3

Cardiogenic Shock

Hypotension

Acute Mechanical Complications

Pericarditis

Ventricular Aneurysm

Recurrent Angina

SECONDARY PREVENTION

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