).Inotropes
Digitalis and intravenous inotropes can increase oxygen demand, provoke serious arrhythmias, and extend infarction. Current recommendations support the use of digoxin in selected patients recovering from acute MI who develop supraventricular tachyarrhythmias (e.g., AF) or heart failure refractory to ACE inhibitors and diuretics. Intravenous inotropes (e.g., dobutamine, dopamine, milrinone, and norepinephrine) are reserved for temporary support of patients with hypotension and circulatory failure that is unresponsive to volume replacement ( ). Other treatment measures for these patients (e.g., intra-aortic balloon pump, early revascularization) are discussed herein.Lipid-Lowering Therapy
Lipid lowering, particularly with hydroxymethylglutaryl-coenzyme A reductase inhibitors (statins), reduces event rates in patients with coronary disease, and a more aggressive approach appears to provide superior benefits[19] ( ). A fasting lipid profile should be obtained on admission, so a statin can be started promptly in the hospital with a low-density lipoprotein cholesterol goal of less than 70 mg/dL.Other Medical Therapies
Calcium channel blockers, although anti-ischemic, also are negatively inotropic and have not been shown to reduce mortality after ST segment elevation acute MI. With certain agents and in specific groups of patient, harm has been suggested. For example, short-acting nifedipine has been reported to cause reflex sympathetic activation, tachycardia, hypotension, and increased mortality. Verapamil or diltiazem (heart rate–slowing drugs) may be given to patients in whom β-blockers are ineffective or contraindicated for control of rapid ventricular response with AF or relief of ongoing ischemia in the absence of heart failure, LV dysfunction, or atrioventricular (AV) block. Magnesium is of no benefit in patients with acute MI who are treated with fibrinolysis. Supplementation is recommended if the magnesium level is lower than normal or in patients with torsades de pointes–type VT associated with a prolonged QT interval. Glucose-insulin-potassium affords no benefit on mortality, cardiac arrest, or cardiogenic shock when this combination is added to usual care in patients with acute ST segment elevation MI.[20] However, glucose control, using an insulin infusion to normalize high blood glucose, is recommended for patients in the acute phase of ST segment elevation MI, especially for those with a complicated course. After the acute phase, individualized treatment is indicated using agents or combinations of agents that best achieve glycemic control and are well tolerated ( C).Management of Complications
Recurrent Chest Pain
When chest pain recurs after acute MI, the diagnostic possibilities include post-infarction ischemia, pericarditis, infarct extension, and infarct expansion. Characterization of the pain, physical examination, ECG, echocardiography, and cardiac marker determinations assist in differential diagnosis. CK-MB often discriminates reinfarction better than cTnI or cTnT. Post-infarction angina developing spontaneously during hospitalization for acute MI despite medical therapy usually merits coronary angiography. β-blockers (IV, then orally) and nitroglycerin (IV, then orally or topically) are recommended medical therapies. Pain with recurrent ST segment elevation or recurrent elevation of cardiac markers may be treated with (re)administration of t-PA or, possibly, a GPIIb/IIIa inhibitor, together with nitroglycerin, β-blockade, and heparin. Streptokinase, which induces neutralizing antibodies, generally should not be reutilized after the first few days. If facilities for angiography, PCI, and surgery are available, an invasive approach is recommended to relieve discomfort occurring hours to days after an acute MI that is associated with objective signs of ischemia. Radionuclide testing (e.g., adenosine thallium) can be helpful in patients with discomfort that is transient or of uncertain ischemic origin. Infarct expansion implies circumferential slippage with thinning of the infarcted myocardium. Infarct expansion can be associated with chest pain but without recurrent elevation of cardiac markers. Expansive remodeling can lead to an LV aneurysm. The risk of remodeling is reduced with early recanalization therapy and administration of ACE inhibitors. Acute pericarditis most commonly manifests on days 2 to 4 in association with large, “transmural” infarctions causing pericardial inflammation. Occasionally, hemorrhagic effusion with tamponade develops; thus, excessive anticoagulation should be avoided. Pericarditis developing later (2 to 10 weeks) after acute MI could represent Dressler's syndrome, which is believed to be immune mediated. The incidence of this post-MI syndrome has decreased dramatically in the modern reperfusion era. Pericardial pain is treated with aspirin (preferred, especially in the acute setting) or other nonsteroidal agents (e.g., indomethacin); patients with severe symptoms could require corticosteroids.Rhythm Disturbances
Ventricular Arrhythmias
Acute MI is associated with a proarrhythmic environment that includes heterogeneous myocardial ischemia, heightened adrenergic tone, intracellular electrolyte disturbance, lipolysis and free fatty acid production, and oxygen free radical production on recanalization (). Arrhythmias thus are common early during acute MI. Micro-re-entry is likely the most common electrophysiologic mechanism of early phase arrhythmias, although enhanced automaticity and triggered activity also are observed in experimental models. Primary VF, the most serious MI-related arrhythmia, contributes importantly to mortality within the first 24 hours. It occurs with an incidence of 3 to 5% during the first 4 hours and then declines rapidly over 24 to 48 hours. Polymorphic VT and, less commonly, monomorphic VT are associated life-threatening arrhythmias that can occur in this setting. Clinical features (including warning arrhythmias) are not adequately specific or sensitive to identify patients at risk for sustained ventricular tachyarrhythmias, so all patients should be continuously monitored. Prophylactic lidocaine, which reduces primary VF but does not decrease (and may increase) mortality, is not recommended. Primary VF is associated with a higher rate of in-hospital mortality, but long-term prognosis is unaffected in survivors. Accelerated idioventricular rhythm (60 to 100 beats per minute) frequently occurs within the first 12 hours and is generally benign (i.e., is not a risk factor for VF). Indeed, accelerated idioventricular rhythm frequently heralds recanalization after fibrinolytic therapy. Antiarrhythmic therapy is not indicated except for sustained, hemodynamically compromising accelerated idioventricular rhythm. Late VF, which is defined as VF developing more than 48 hours after the onset of acute MI, often occurs in patients with larger MIs or heart failure, portends a worse prognosis for survival, and is an indication for aggressive measures (e.g., consideration of an ICD). Monomorphic VT resulting from re-entry in the context of a recent or old MI also can appear late after MI, and patients may require long-term therapy (e.g., an ICD). Electrical cardioversion is required for VF and sustained polymorphic VT (unsynchronized shock) and for sustained monomorphic VT that causes hemodynamic compromise (synchronized shock) ( ). Brief intravenous sedation is given to conscious, “stable” patients. For slower, stable VT and nonsustained VT requiring therapy, intravenous amiodarone or intravenous lidocaine is commonly recommended. After episodes of VT/VF, infusions of antiarrhythmic drugs may be given for 6 to 24 hours; the ongoing risk of arrhythmia then is reassessed. Electrolyte and acid-base imbalance and hypoxia should be corrected. β-Blockade is useful in patients with frequent polymorphic VT associated with adrenergic activation (“electrical storm”). Additional, aggressive measures should be considered to reduce cardiac ischemia (e.g., emergency PCI or CABG) and LV dysfunction (intra-aortic balloon pump) in patients with recurrent polymorphic VT despite the use of β-blockers and/or amiodarone. Patients with sustained VT or VF occurring late in the hospital course should be considered for long-term prevention and therapy. An ICD provides greater survival benefit than antiarrhythmic drugs in patients with ventricular arrhythmias and can improve survival after acute MI for patients with an ejection fraction of 30% or less, regardless of their rhythm status.[21]Atrial Fibrillation and other Supraventricular Tachyarrhythmias
AF occurs in up to 10 to 15% of patients after an acute MI, usually within the first 24 hours ( ). The incidence of atrial flutter or another supraventricular tachycardia is much lower. The risk of AF increases with age, larger MIs, heart failure, pericarditis, atrial infarction, hypokalemia, hypomagnesemia, hypoxia, pulmonary disease, and hyperadrenergic states. The incidence of AF is reduced by effective early recanalization. Hemodynamic compromise with rapid rates and systemic embolism (in ∼2%) are adverse consequences of AF. Systemic embolism can occur on the first day, so prompt anticoagulation with heparin is indicated. Recommendations for management of AF include the following: electrical cardioversion for patients with severe hemodynamic compromise or ischemia; rate control with intravenous digoxin for patients with ventricular dysfunction (i.e., give 1.0 mg, one half initially and one half in 4 hours), with an intravenous β-blocker (e.g., metoprolol, 5 mg over 2 minutes to a total of 15 mg over 10 to 15 minutes) in those without clinical ventricular dysfunction, or with intravenous diltiazem or verapamil in hemodynamically compensated patients with a contraindication to β-blockers; and anticoagulation with heparin (or LMWH). Amiodarone, which is generally reserved for patients with or at high risk for recurrence, may be continued for 6 weeks if sinus rhythm is restored and maintained.Bradycardias, Conduction Delays, and Heart Block
Sinus and AV nodal dysfunction are common during acute MI. Sinus bradycardia, a result of increased parasympathetic tone often in association with inferior acute MI, occurs in 30 to 40% of patients. Sinus bradycardia is particularly common during the first hour of acute MI and with recanalization of the right coronary artery (Bezold-Jarisch reflex). Vagally mediated AV block also can occur in this setting. Anticholinergic therapy (atropine, 0.5 to 1.5 mg IV) is indicated for symptomatic sinus bradycardia (heart rate generally <50 beats per minute associated with hypotension, ischemia, or escape ventricular arrhythmia), including ventricular asystole, and symptomatic second-degree (Wenckebach) or third-degree block at the AV nodal level (narrow QRS complex escape rhythm). Atropine is not indicated and can worsen infranodal AV block (anterior MI, wide complex escape rhythm). New-onset infranodal AV block and intraventricular conduction delays or BBBs predict substantially increased in-hospital mortality. Fortunately, their incidence has declined in the recanalization era (from 10 to 20% to ∼4%). Mortality is related more to extensive myocardial damage than to heart block itself, so cardiac pacing only modestly improves survival. Prophylactic placement of multifunctional patch electrodes, which allow for immediate transcutaneous pacing (and defibrillation) if needed, is indicated for symptomatic sinus bradycardia refractory to drug therapy, infranodal second-degree (Mobitz II) or third-degree AV block, and new or indeterminate-age bifascicular (LBBB; RBBB with left anterior or left posterior fascicular block) or trifascicular block (bilateral or alternating BBB [any age], BBB with first-degree AV block). Transcutaneous pacing is uncomfortable and is intended for prophylactic and temporary use only. In patients who require a pacemaker to maintain a rhythm or who are at very high risk (>30%) of requiring pacing (including patients with alternating, bilateral BBB, with new or indeterminate-age bifascicular block with first-degree AV block, and with infranodal second-degree AV block) should have a transvenous pacing electrode inserted as soon as possible. Indications for permanent pacing after acute MI depend on the prognosis of the AV block and not solely on symptoms. Class I indications include even transient second- or third-degree AV block in association with BBB and symptomatic AV block at any level. Advanced block at the AV nodal level (Wenckebach) rarely is persistent or symptomatic enough to warrant permanent pacing.Heart Failure and Other Low-Output States
Cardiac pump failure is the leading cause of circulatory failure and in-hospital death from acute MI. Manifestations of circulatory failure can include a weak pulse, low blood pressure, cool extremities, a third heart sound, pulmonary congestion, oliguria, and obtundation. However, several distinct mechanisms, hemodynamic patterns, and clinical syndromes characterize the spectrum of circulatory failure in acute MI. Each requires a specific approach to diagnosis, monitoring, and therapy (see Table 72-3 ).Left Ventricular Dysfunction
The degree of LV dysfunction correlates well with the extent of acute ischemia or infarction. Hemodynamic compromise becomes evident when impairment involves 20 to 25% of the left ventricle, and cardiogenic shock or death occurs with involvement of 40% or more ( Chapter 108 ). Pulmonary congestion and S3 and S4 gallops are the most common physical findings. Early recanalization (with fibrinolytic agents, PCI, or CABG) is the most effective therapy to reduce infarct size, ventricular dysfunction, and associated heart failure. Medical treatment of heart failure related to the ventricular dysfunction of acute MI is otherwise generally similar to that of heart failure in other settings ( Chapter 58 ) and includes adequate oxygenation and diuresis (begun early, blood pressure permitting, and continued on a long-term basis if needed). Morphine sulfate (i.e., 2 to 4 mg IV, with increments as needed after 5 to 15 minutes or more) is useful for patients with pulmonary congestion. Nitroglycerin also reduces preload and effectively relieves congestive symptoms. Titrated oral ACE inhibitor therapy (e.g., captopril, incremented from 3.125 to 6.25 mg three times daily to 50 mg twice daily as tolerated) also is indicated for heart failure and pulmonary edema unless excessive hypotension (systolic blood pressure <100 mm Hg) is present. Treatment can be begun sublingually (0.4 mg every 5 minutes three times), and then the transition can be made to intravenous therapy (initially 5 to 10 μg/minute, incrementing by 5 to 20 μg/minute until symptoms are relieved or until mean arterial pressure falls by 10% in normotensive or 30% in hypertensive patients but not <90 mm Hg or >30 mm Hg lower than baseline). Intravenous vasodilator therapy to reduce preload and afterload, inotropic support, and intra-aortic balloon counterpulsation (IABP), together with urgent recanalization, are indicated in cardiogenic shock ( Chapter 108 ).Volume Depletion
Relative or absolute hypovolemia is a frequent cause of hypotension and circulatory failure and is easily corrected if it is recognized and treated promptly. Poor hydration, vomiting, diuresis, and disease- or drug-induced peripheral vasodilation can contribute to this condition. Hypovolemia should be identified and corrected with intravenous fluids before more aggressive therapies are considered. An empirical fluid challenge may be tried in the appropriate clinical setting (e.g., for hypotension in the absence of congestion, for inferior or RV infarction, and for hypervagotonia). If filling pressures are measured, cautious fluid administration to a pulmonary capillary wedge pressure of up to about 18 mm Hg may optimize cardiac output and blood pressure without impairing oxygenation.Right Ventricular Infarction
RV ischemia and infarction occur with proximal occlusion of the right coronary artery (before the take-off of the RV branches). Ten to 15% of inferior acute ST segment elevation MIs show classic hemodynamic features, and these patients form the highest risk subgroup for morbidity and mortality (25 to 30% versus <6% hospital mortality). Improvement in RV function commonly occurs over time, a finding suggesting reversal of ischemic stunning and other favorable accommodations, if short-term management is successful. Hypotension in patients with clear lung fields and elevated jugular venous pressure in the setting of inferior or inferoposterior acute MI should raise the suspicion of RV infarction. Kussmaul's sign (distention of the jugular vein on inspiration) is relatively specific and sensitive in this setting. Right-sided ECG leads show ST segment elevation, particularly in V4R ( Chapter 52 ), in the first 24 hours of RV infarction. Echocardiography is helpful in confirming the diagnosis (RV dilation and dysfunction are observed). When right-sided heart pressures are measured, a right atrial pressure of 10 mm Hg or greater and 80% or more of the pulmonary capillary wedge pressure are relatively sensitive and specific for RV ischemic dysfunction. Management of RV infarction consists of early maintenance of RV preload with intravenous fluids, reduction of RV afterload (i.e., afterload-only reducing drugs as for LV dysfunction; consider intra-aortic balloon pump), early recanalization, short-term inotropic support if needed, and avoidance of venodilators (e.g., nitrates) and diuretics used for LV failure (they may cause marked hypotension). Volume loading with normal saline solution alone is often effective. If the cardiac output fails to improve after 0.5 to 1 L fluid, inotropic support with intravenous dobutamine (starting at 2 μg/kg/minute and titrating to hemodynamic effect or tolerance, up to 20 μg/kg/minute) is recommended. High-grade AV block is common, and restoration of AV synchrony with temporary AV sequential pacing can lead to substantial improvement in cardiac output. The onset of AF (in up to one third of RV infarcts) can cause severe hemodynamic compromise requiring prompt cardioversion. Early coronary recanalization with fibrinolysis or PCI markedly improves outcomes.Cardiogenic Shock
Cardiogenic shock ( Chapter 108 ) is a form of severe LV failure characterized by marked hypotension (systolic pressures <80 mm Hg) and reductions in cardiac index (to <1.8 L/minute/m2) despite high LV filling pressure (pulmonary capillary wedge pressure >18 mm Hg). The cause is loss of a critical functional mass (>40%) of the left ventricle. Cardiogenic shock is associated with mortality rates of more than 70 to 80% despite aggressive medical therapy. Risk factors include age, large (usually anterior) acute MI, previous MI, and diabetes. In patients with suspected shock, hemodynamic monitoring and IABP are indicated. Intubation often is necessary. Vasopressors are often needed. Early urgent mechanical revascularization (PCI or CABG), if feasible, affords the best chance for survival, especially in patients less than 75 years old[9] ( Chapter 108 ). IABP remains useful for patients with medically refractory unstable ischemic syndromes and for cardiogenic shock. The deflated balloon catheter is introduced into the femoral artery and is advanced into the aorta. The ECG triggers balloon inflation during early diastole, thereby augmenting coronary blood flow; deflation then occurs in early systole, thereby reducing LV afterload. Primary IABP therapy for cardiogenic shock associated with acute MI provides temporary stabilization but does not reduce mortality (>80%). IABP is currently recommended in the setting of acute MI as a stabilizing measure for patients undergoing angiography and subsequent PCI or surgery for (1) cardiogenic shock, (2) mechanical complications (acute mitral regurgitation, acute ventricular septal defect), (3) refractory post-MI ischemia, or (4) recurrent intractable VT or VF associated with hemodynamic instability. IABP is not useful in patients with significant aortic insufficiency or severe peripheral vascular disease.Mechanical Complications
Mechanical complications usually occur within the first weeks and account for approximately 15% of MI-related deaths. Such complications include acute mitral valve regurgitation, ventricular septal defect, free wall rupture, and LV aneurysm. Suspicion and investigation of a mechanical defect should be prompted by a new murmur and/or sudden, progressive hemodynamic deterioration with pulmonary edema and/or a low output state. Transthoracic or transesophageal Doppler echocardiography usually establishes the diagnosis. A balloon flotation catheter can be helpful in confirming the diagnosis. Arteriography to identify correctable coronary artery disease is warranted in most cases. Surgical consultation should be requested promptly, and urgent repair is usually indicated. Acute mitral valve regurgitation ( Chapter 75 ) results from infarct-related rupture or dysfunction of a papillary muscle. Total rupture leads to death in 75% of patients within 24 hours. Medical therapy is initiated with nitroprusside (beginning with 0.1 μg/kg/minute and titrating upward every 3 to 5 minutes to the desired effect, as tolerated by blood pressure response, up to 5 μg/kg/minute), to lower preload and to improve peripheral perfusion, and inotropic support (e.g., dobutamine, titrated from 2 up to 20 μg/kg/minute in normotensive patients; dopamine, titrated from 2 up to 20 μg/kg/minute in hypotensive patients; or combined dobutamine and dopamine). An IABP is used to maintain hemodynamic stability. Emergency surgical repair (if possible) or replacement is then undertaken. Surgery is associated with high mortality (≥25 to 50%), but it leads to better functional and survival outcomes than medical therapy alone. Post-infarction septal rupture with ventricular septal defect, which occurs with increased frequency in elderly patients, in patients with hypertension, and possibly after fibrinolysis, also warrants urgent surgical repair. Because a small post-MI ventricular septal defect can suddenly enlarge and cause rapid hemodynamic collapse, all septal perforations should be repaired. On diagnosis, invasive monitoring is recommended, together with vasodilators (e.g., nitroprusside, initially 0.1 μg/kg/minute, titrated upward every 3 to 5 minutes to desired effect, as tolerated by blood pressure response, up to 5 μg/kg/minute) and, if needed, judicious use of inotropic agents (e.g., dobutamine, titrated from 2 up to 20 μg/kg/minute in normotensive patients; dopamine, titrated from 2 up to 20 μg/kg/minute in hypotensive patients; or combined dobutamine and dopamine). An IABP should be inserted, a surgical consultation promptly obtained, and surgical repair undertaken as soon as feasible. LV free wall rupture usually causes acute cardiac tamponade with sudden death. In a small percentage of cases, however, resealing or localized containment (“pseudoaneurysm”) can allow medical stabilization, usually with inotropic support and/or an IABP, followed by emergency surgical repair. An LV aneurysm can develop after a large, usually anterior, acute MI. If refractory heart failure, VT, or systemic embolization occurs despite medical therapy and PCI, aneurysmectomy with CABG is indicated.Thromboembolic Complications
Thromboembolism has been described in approximately 10% of clinical series and 20% of autopsy series, a finding suggesting a high rate of undiagnosed events. Thromboembolism contributed to up to 25% of hospital deaths from acute MI in the past, but the incidence has declined in the recanalization era in association with greater use of antithrombotics, reductions of infarct size, and earlier ambulation. Systemic arterial emboli (including cerebrovascular emboli) typically arise from an LV mural thrombus, whereas pulmonary emboli commonly arise from thrombi in leg veins. Arterial embolism can cause dramatic clinical events, such as hemiparesis, loss of a pulse, ischemic bowel, or sudden hypertension, depending on the regional circulation involved. Mural thrombosis with embolism typically occurs in the setting of a large (especially anterior) ST segment elevation acute MI and heart failure. The risk of embolism is particularly high when a mural thrombus is detected by echocardiography. Thus, in patients with anterior ST segment elevation acute MI and in other high-risk patients, echocardiography should be performed during hospitalization; if results are positive, anticoagulation should be started (with an antithrombin), if not already initiated, and continued (with warfarin) for 6 months. Deep vein thrombosis can be prevented by lower extremity compression therapy, by limiting the duration of bedrest, and by the use of subcutaneous unfractionated heparin or LMWH (in patients at risk not receiving intravenous heparin) until patients are fully ambulatory ( Chapter 81 ). Patients with pulmonary embolism are treated with intravenous heparin, then oral anticoagulation for 6 months ( Chapter 99 ).Risk Stratification after Myocardial Infarction
The goal of risk stratification before and early after discharge for acute MI is to assess ventricular and clinical function, latent ischemia, and arrhythmic risk, to use this information for patient education and prognostic assessment, and to guide therapeutic strategies (see Fig. 72-3 ).Cardiac Catheterization and Noninvasive Stress Testing
Risk stratification generally involves functional assessment by one of three strategies: cardiac catheterization, submaximal exercise stress ECG before discharge (at 4 to 6 days), or symptom-limited stress testing at 2 to 6 weeks after discharge. Many or most patients with ST segment elevation acute MI undergo invasive evaluation for primary PCI or after fibrinolytic therapy. Catheterization generally is performed during hospitalization for patients at high risk. In others, predischarge submaximal exercise testing (to peak heart rate of 120 to 130 beats per minute or 70% of the predicted maximum) appears safe when it is performed in patients who are ambulating without symptoms; it should be avoided within 2 to 3 days of acute MI and in patients with unstable post-MI angina, uncompensated heart failure, or serious cardiac arrhythmias. Alternatively or in addition, patients may undergo symptom-limited stress testing at 2 to 6 weeks before they return to work or resume other increased physical activities. Abnormal test results include not only ST segment depression but also low functional capacity, exertional hypotension, and serious arrhythmias. Patients with positive test results should be considered for coronary angiography. The sensitivity of stress testing can be augmented with radionuclide perfusion imaging (thallium-201 and/or technetium-99m-sestamibi; Chapter 54 ) or echocardiography ( Chapter 53 ). Supplemental imaging also can quantify the LV ejection fraction and size the area of infarction and/or ischemia (e.g., by cardiac magnetic resonance imaging; Chapter 55 ). For patients taking digoxin or for those with ST segment changes that preclude accurate ECG interpretation (e.g., baseline LBBB or LV hypertrophy), an imaging study is recommended with initial stress testing. In others, an imaging study may be performed selectively for those in whom the exercise ECG test result is positive or equivocal. For patients unable to exercise, pharmacologic stress testing can be performed using adenosine or dipyridamole scintigraphy or dobutamine echocardiography.Electrocardiographic Monitoring
Modern telemetry systems capture complete rhythm information during hospital observations and allow for identification of patients with serious arrhythmias, so routine 24- to 48-hour ambulatory ECG (Holter) monitoring before or after hospital discharge is not recommended. Sustained VT or VF occurring late during hospitalization or provoked during electrophysiologic study in patients with nonsustained VT on monitoring are candidates for an ICD, especially if the ejection fraction is less than 40% ( Fig. 72-4 ) ( Chapters 64 and 65 ). Prophylactic ICD placement prevents sudden death after acute MI for patients with severely depressed function (ejection fraction ≤0.30) regardless of the rhythm status.[21]Secondary Prevention, Patient Education, and Rehabilitation
Secondary Prevention
Advances in secondary prevention have resulted in increasingly effective measures to reduce recurrent MI and cardiovascular death. Secondary prevention should be conscientiously applied after acute MI ( Table 72-8 ). A fasting lipid profile is recommended on admission, and lipid-lowering therapy, typically with a statin, is begun in the hospital, generally with an LDL cholesterol goal of less than 70 mg/dL ( Chapter 217 ). Continued smoking doubles the subsequent mortality risk after acute MI, and smoking cessation reduces the risk of reinfarction and death within 1 year ( Chapter 30 ). An individualized smoking cessation plan should be formulated, including pharmacologic aids (nicotine gum and patches, bupropion). Antiplatelet therapy ( Chapter 35 ; Fig. 72-5 ) should consist of aspirin, given on a long-term basis to all patients without contraindications (maintenance dose, 75 to 162 mg/day). Clopidogrel (75 mg/day) is given to patients who received PCI with stenting and is also appropriate for others at higher risk for recurrent vascular events. Therapy is recommended for a minimum of 1 month after a bare metal stent, for at least 3 months for sirolimus-eluting stents, and for at least 6 months for paclitaxel-eluting stents. If patients are not at high risk of bleeding, therapy is continued for up to 1 year or more. Anticoagulant therapy (i.e., warfarin, with an international normalized ratio goal of 2.0 to 3.0) is indicated after acute MI for patients unable to take antiplatelet therapy (aspirin or clopidogrel), for those with persistent or paroxysmal AF, for those with LV thrombus, and for those who have suffered a systemic or pulmonary embolism. Anticoagulants also may be considered for patients with extensive wall motion abnormalities and markedly depressed ejection fraction with or without heart failure. Data on the benefit of warfarin instead of or in addition to aspirin are inconclusive. ACE inhibitor therapy can prevent adverse myocardial remodeling after acute MI and can reduce heart failure and death; it is clearly indicated for long-term use in patients with anterior acute MI or an LV ejection fraction less than 40%. ACE inhibitors also reduce recurrent MI in higher-risk patients with an ejection fraction greater than 40%. In contrast, ACE inhibition, when added to other contemporary therapies, provides little additional benefit in reducing cardiovascular events in patients who have stable coronary disease and a low risk (<5%/year) of a coronary event. These data suggest a rationale for the long-term use of ACE inhibitors (e.g., ramipril, 2.5 mg titrated to 10 mg/day, or lisinopril, 2.5 to 5 mg titrated to 10 mg/day) in all patients after MI, except perhaps those at lowest risk (i.e., without heart failure, hypertension, glucose intolerance, or reduced ejection fraction). An ARB (e.g., valsartan, 80 to 160 mg twice daily, or losartan, 50 to 100 mg/day) should be substituted in patients who cannot tolerate an ACE inhibitor; in patients with advanced heart failure, both an ACE inhibitor and an ARB may be complementary ( Chapter 58 ). An aldosterone receptor blocker (e.g., eplerenone, 25 mg/day orally, increased to 50 mg/day after 4 weeks if tolerated, with monitoring of serum potassium levels) also should be added to the ACE inhibitor or ARB (but not both) regimen on a long-term basis in patients with depressed ejection fraction (≤0.40) and clinical heart failure or diabetes, unless this approach is contraindicated. Long-term β-blocker therapy is strongly recommended for all MI survivors without uncompensated heart failure or other contraindications. Long-term therapy in patients at low risk (normal ventricular function, successful recanalization, absence of arrhythmias) is reasonable but not mandatory. Nitroglycerin (0.4 mg) is prescribed routinely for sublingual or buccal administration for acute anginal attacks. Longer-acting oral therapy (isosorbide mononitrate, 30 to 60 mg orally every morning, or dinitrate, 10 to 40 mg orally two to three times daily) or topical nitroglycerin (e.g., start 0.5 inch, can titrate up to 2 inches, every 6 hours for 2 days) may be added to treatment regimens for angina or heart failure in selected patients. Calcium-channel blockers are negatively inotropic and are not routinely given on a long-term basis; however, they may be given to selected patients without LV dysfunction (ejection fraction >0.40) who are intolerant of β-blockers and who require these drugs for antianginal therapy (e.g., amlodipine, 5 to 10 mg/day orally, or diltiazem, 120 to 480 mg/day orally as sustained release or divided doses) or for control of heart rate in AF (e.g., diltiazem, 120 to 480 mg/day orally, or verapamil, 180 to 480 mg/day orally, as sustained release or in divided doses). Short-acting nifedipine should be avoided. Hormone therapy with estrogen with or without progestin is not begun after an acute MI because it increases thromboembolic risk and does not prevent reinfarction. For women already receiving hormone replacement, therapy should be discontinued unless it is being given for another compelling indication. Hypertension ( Chapter 66 ) and diabetes mellitus ( Chapter 247 ) must be assessed and tightly controlled in patients after acute MI. ACE inhibitors or β-blockers as described earlier are usually the first-choice therapies for hypertension, with ARBs indicated when ACE inhibitors are not tolerated. ACE inhibitors and ARBs also can reduce the long-term complications of diabetes. Antioxidant supplementation (e.g., vitamin E, vitamin C) does not benefit patients after acute MI and is not recommended. Folate therapy reduces homocyst(e)ine levels, but it has not been effective in reducing clinical events in large secondary prevention trials. Evidence regarding fish oil supplements is insufficient to make recommendations for or against them. Antiarrhythmic drugs are not generally recommended after acute MI, and class I antiarrhythmic agents can increase the risk of sudden death. Class III drugs (amiodarone, sotalol, dofetilide) may be used as part of the management strategy for specific arrhythmias (e.g., AF, VT) ( Chapters 63 and 64 ).Patient Education and Rehabilitation
The hospital stay provides an important opportunity to educate patients about their MI and its treatment, coronary risk factors, and behavioral modification. Education should begin on admission and should continue after discharge. However, the time before hospital discharge is particularly opportune. Many hospitals use case managers and prevention specialists to augment physicians and nurses, to provide educational materials, to review important concepts, to assist in formulating and actualizing individual risk-reduction plans, and to ensure proper and timely outpatient follow-up. This follow-up should include early return appointments with the patient's physician (within a few weeks). Instructions on activities also should be given before discharge. Many hospitals have cardiac rehabilitation programs that provide supervised, progressive exercise. |
