Published: August 2010
Acute myocardial infarction (MI) remains a leading cause of morbidity and mortality worldwide. Myocardial infarction occurs when myocardial ischemia, a diminished blood supply to the heart, exceeds a critical threshold and overwhelms myocardial cellular repair mechanisms designed to maintain normal operating function and homeostasis. Ischemia at this critical threshold level for an extended period results in irreversible myocardial cell damage or death.
Critical myocardial ischemia can occur as a result of increased myocardial metabolic demand, decreased delivery of oxygen and nutrients to the myocardium via the coronary circulation, or both. An interruption in the supply of myocardial oxygen and nutrients occurs when a thrombus is superimposed on an ulcerated or unstable atherosclerotic plaque and results in coronary occlusion.1 A high-grade (>75%) fixed coronary artery stenosis caused by atherosclerosis or a dynamic stenosis associated with coronary vasospasm can also limit the supply of oxygen and nutrients and precipitate an MI. Conditions associated with increased myocardial metabolic demand include extremes of physical exertion, severe hypertension (including forms of hypertrophic obstructive cardiomyopathy), and severe aortic valve stenosis. Other cardiac valvular pathologies and low cardiac output states associated with a decreased mean aortic pressure, which is the prime component of coronary perfusion pressure, can also precipitate MI.
Myocardial infarction can be subcategorized on the basis of anatomic, morphologic, and diagnostic clinical information. From an anatomic or morphologic standpoint, the two types of MI are transmural and nontransmural. A transmural MI is characterized by ischemic necrosis of the full thickness of the affected muscle segment(s), extending from the endocardium through the myocardium to the epicardium. A nontransmural MI is defined as an area of ischemic necrosis that does not extend through the full thickness of myocardial wall segment(s). In a nontransmural MI, the area of ischemic necrosis is limited to the endocardium or to the endocardium and myocardium. It is the endocardial and subendocardial zones of the myocardial wall segment that are the least perfused regions of the heart and the most vulnerable to conditions of ischemia. An older subclassification of MI, based on clinical diagnostic criteria, is determined by the presence or absence of Q waves on an electrocardiogram (ECG). However, the presence or absence of Q waves does not distinguish a transmural from a nontransmural MI as determined by pathology.2
A consensus statement was published to give a universal definition of the term myocardial infarction. The authors stated that MI should be used when there is evidence of myocardial necrosis in a clinical setting consistent with MI. Myocardial infarction was then classified by the clinical scenario into various subtypes. Type 1 is a spontaneous MI related to ischemia from a primary coronary event (e.g., plaque rupture, thrombotic occlusion). Type 2 is secondary to ischemia from a supply-and-demand mismatch. Type 3 is an MI resulting in sudden cardiac death. Type 4a is an MI associated with percutaneous coronary intervention, and 4b is associated with in-stent thrombosis. Type 5 is an MI associated with coronary artery bypass surgery.3
A more common clinical diagnostic classification scheme is also based on electrocardiographic findings as a means of distinguishing between two types of MI, one that is marked by ST elevation (STEMI) and one that is not (NSTEMI). Management practice guidelines often distinguish between STEMI and non-STEMI, as do many of the studies on which recommendations are based. The distinction between STEMI and NSTEMI also does not distinguish a transmural from a nontransmural MI. The presence of Q waves or ST-segment elevation is associated with higher early mortality and morbidity; however, the absence of these two findings does not confer better long-term mortality and morbidity.4
Myocardial infarction is the leading cause of death in the United States and in most industrialized nations throughout the world. Approximately 450, 000 people in the United States die from coronary disease per year.5 The survival rate for U.S. patients hospitalized with MI is approximately 95%. This represents a significant improvement in survival and is related to improvements in emergency medical response and treatment strategies.
The incidence of MI increases with age; however, the actual incidence is dependent on predisposing risk factors for atherosclerosis. Approximately 50% of all MIs in the United States occur in people younger than 65 years. However, in the future, as demographics shift and the mean age of the population increases, a larger percentage of patients presenting with MI will be older than 65 years.
Six primary risk factors have been identified with the development of atherosclerotic coronary artery disease and MI: hyperlipidemia, diabetes mellitus, hypertension, tobacco use, male gender, and family history of atherosclerotic arterial disease. The presence of any risk factor is associated with doubling the relative risk of developing atherosclerotic coronary artery disease.1
Elevated levels of total cholesterol, LDL, or triglycerides are associated with an increased risk of coronary atherosclerosis and MI. Levels of HDL less than 40 mg/dL also portend an increased risk. A full summary of the National Heart, Lung, and Blood Institute's cholesterol guidelines is available online.6
Patients with diabetes have a substantially greater risk of atherosclerotic vascular disease in the heart as well as in other vascular beds. Diabetes increases the risk of MI because it increases the rate of atherosclerotic progression and adversely affects the lipid profile. This accelerated form of atherosclerosis occurs regardless of whether a patient has insulin-dependent or non–insulin-dependent diabetes.
High blood pressure (BP) has consistently been associated with an increased risk of MI. This risk is associated with systolic and diastolic hypertension. The control of hypertension with appropriate medication has been shown to reduce the risk of MI significantly. A full summary of the National Heart, Lung, and Blood Institute's JNC 7 guidelines published in 2003 is available online.7
Certain components of tobacco and tobacco combustion gases are known to damage blood vessel walls. The body's response to this type of injury elicits the formation of atherosclerosis and its progression, thereby increasing the risk of MI. A small study in a group of volunteers showed that smoking acutely increases platelet thrombus formation. This appears to target areas of high shear forces, such as stenotic vessels, independent of aspirin use.8 The American Lung Association maintains a website with updates on the public health initiative to reduce tobacco use and is a resource for smoking-cessation strategies for patients and health care providers.
The incidence of atherosclerotic vascular disease and MI is higher in men than women in all age groups. This gender difference in MI, however, narrows with increasing age.
A family history of premature coronary disease increases an individual's risk of atherosclerosis and MI. The cause of familial coronary events is multifactorial and includes other elements, such as genetic components and acquired general health practices (e.g. smoking, high-fat diet).
Most myocardial infarctions are caused by a disruption in the vascular endothelium associated with an unstable atherosclerotic plaque that stimulates the formation of an intracoronary thrombus, which results in coronary artery blood flow occlusion. If such an occlusion persists for more than 20 minutes, irreversible myocardial cell damage and cell death will occur.
The development of atherosclerotic plaque occurs over a period of years to decades. The two primary characteristics of the clinically symptomatic atherosclerotic plaque are a fibromuscular cap and an underlying lipid-rich core. Plaque erosion can occur because of the actions of matrix metalloproteases and the release of other collagenases and proteases in the plaque, which result in thinning of the overlying fibromuscular cap. The action of proteases, in addition to hemodynamic forces applied to the arterial segment, can lead to a disruption of the endothelium and fissuring or rupture of the fibromuscular cap. The loss of structural stability of a plaque often occurs at the juncture of the fibromuscular cap and the vessel wall, a site otherwise known as the shoulder region. Disruption of the endothelial surface can cause the formation of thrombus via platelet-mediated activation of the coagulation cascade. If a thrombus is large enough to occlude coronary blood flow, an MI can result.
The death of myocardial cells first occurs in the area of myocardium most distal to the arterial blood supply: the endocardium. As the duration of the occlusion increases, the area of myocardial cell death enlarges, extending from the endocardium to the myocardium and ultimately to the epicardium. The area of myocardial cell death then spreads laterally to areas of watershed or collateral perfusion. Generally, after a 6- to 8-hour period of coronary occlusion, most of the distal myocardium has died. The extent of myocardial cell death defines the magnitude of the MI. If blood flow can be restored to at-risk myocardium, more heart muscle can be saved from irreversible damage or death.
The severity of an MI depends on three factors: the level of the occlusion in the coronary artery, the length of time of the occlusion, and the presence or absence of collateral circulation. Generally, the more proximal the coronary occlusion, the more extensive the amount of myocardium that will be at risk of necrosis. The larger the myocardial infarction, the greater the chance of death because of a mechanical complication or pump failure. The longer the period of vessel occlusion, the greater the chances of irreversible myocardial damage distal to the occlusion.
STEMI is usually the result of complete coronary occlusion after plaque rupture. This arises most often from a plaque that previously caused less than 50% occlusion of the lumen. NSTEMI is usually associated with greater plaque burden without complete occlusion. This difference contributes to the increased early mortality seen in STEMI and the eventual equalization of mortality between STEMI and NSTEMI after 1 year.
Acute MI can have unique manifestations in individual patients. The degree of symptoms ranges from none at all to sudden cardiac death. An asymptomatic MI is not necessarily less severe than a symptomatic event, but patients who experience asymptomatic MIs are more likely to be diabetic. Despite the diversity of manifesting symptoms of MI, there are some characteristic symptoms.
An MI can occur at any time of the day, but most appear to be clustered around the early hours of the morning or are associated with demanding physical activity, or both. Approximately 50% of patients have some warning symptoms (angina pectoris or an anginal equivalent) before the infarct.
Identifying a patient who is currently experiencing an MI can be straightforward, difficult, or somewhere in between. A straightforward diagnosis of MI can usually be made in patients who have a number of atherosclerotic risk factors along with the presence of symptoms consistent with a lack of blood flow to the heart. Patients who suspect that they are having an MI usually present to an emergency department. Once a patient's clinical picture raises a suspicion of MI, several confirmatory tests can be performed rapidly. These tests include electrocardiography, blood testing, and echocardiography.
The first diagnostic test is electrocardiography (ECG), which may demonstrate that a MI is in progress or has already occurred. Interpretation of an ECG is beyond the scope of this chapter; however, one feature of the ECG in a patient with an MI should be noted because it has a bearing on management. Practice guidelines on MI management consider patients whose ECG does or does not show ST-segment elevation separately. As noted earlier, the former is referred to as ST elevation MI (Fig. 1) and the latter as non-ST elevation MI (Fig. 2). In addition to ST-segment elevation, 81% of electrocardiograms during STEMI demonstrate reciprocal ST-segment depression as well.
Living myocardial cells contain enzymes and proteins (e.g., creatine kinase, troponin I and T, myoglobin) associated with specialized cellular functions. When a myocardial cell dies, cellular membranes lose integrity, and intracellular enzymes and proteins slowly leak into the blood stream. These enzymes and proteins can be detected by a blood sample analysis. These values vary depending on the assay used in each laboratory. Given the acuity of a STEMI and the need for urgent intervention, the laboratory tests are usually not available at the time of diagnosis. Thus, good history taking and an ECG are used to initiate therapy in the appropriate situations. The real value of biomarkers such as troponin lies in the diagnosis and prognosis of NSTEMI (Fig. 3).
An echocardiogram may be performed to compare areas of the left ventricle that are contracting normally with those that are not. One of the earliest protective actions of myocardial cells used during limited blood flow is to turn off the energy-requiring mechanism for contraction; this mechanism begins almost immediately after normal blood flow is interrupted. The echocardiogram may be helpful in identifying which portion of the heart is affected by an MI and which of the coronary arteries is most likely to be occluded. Unfortunately, the presence of wall motion abnormalities on the echocardiogram may be the result of an acute MI or previous (old) MI or other myopathic processes, limiting its overall diagnostic utility.
The goals of therapy in acute MI are the expedient restoration of normal coronary blood flow and the maximum salvage of functional myocardium. These goals can be met by a number of medical interventions and adjunctive therapies. The primary obstacles to achieving these goals are the patient's failure to recognize MI symptoms quickly and the delay in seeking medical attention. When patients present to a hospital, there are a variety of interventions to achieve treatment goals. “Time is muscle” guides the management decisions in acute STEMI, and an early invasive approach is the standard of care for acute NSTEMI.4
The use of aspirin has been shown to reduce mortality from MI. Aspirin in a dose of 325 mg should be administered immediately on recognition of MI signs and symptoms.4, 9 The nidus of an occlusive coronary thrombus is the adhesion of a small collection of activated platelets at the site of intimal disruption in an unstable atherosclerotic plaque. Aspirin irreversibly interferes with function of cyclooxygenase and inhibits the formation of thromboxane A2. Within minutes, aspirin prevents additional platelet activation and interferes with platelet adhesion and cohesion. This effect benefits all patients with acute coronary syndromes, including those with amyocardial infarction. Aspirin alone has one of the greatest impacts on the reduction of MI mortality. Its beneficial effect is observed early in therapy and persists for years with continued use. The long-term benefit is sustained, even at doses as low as 75 mg/day.
The Clopidogrel and Metoprolol in Myocardial Infarction Trial/Second Chinese Cardiac Study (COMMIT-CCS 2) trial evaluated the use of clopidogrel versus placebo in patients who were taking aspirin but not undergoing reperfusion therapy. It demonstrated a benefit in favor of clopidogrel when used with aspirin.10 The Clopidogrel as Adjunctive Reperfusion Therapy—Thrombolysis in Myocardial Infarction 28 (CLARITY-TIMI 28) study compared clopidogrel versus placebo in patients receiving fibrinolytics within 12 hours of STEMI and showed a benefit in favor of clopidogrel as well.11 The current recommendations for antiplatelet agents is summarized in Table 1.
|Medical management||75-162 mg/day indefinitely||Optional: 75 mg/day × 1 month|
|Bare Metal stent||162-325 mg/day × 1 month, then 75-162 mg/day indefinitely||300 mg loading dose,* then
75 mg/day × 1 month
|Sirolimus eluting stent
|162-325 mg/day × 3 months, then 75-162 mg/day indefinitely||300 mg loading dose,* then
75 mg/day × 1 year
|Paclitaxel eluting stent
|162-325 mg/day × 6 months, then 75-162 mg/day indefinitely||300 mg loading dose,* then
75 mg/day × 1 year
* Note: No loading dose in patients older than 75 years.
Oxygen should be administered to patients with symptoms or signs of pulmonary edema or with pulse oximetry less than 90% saturation.4 The rationale for using oxygen is the assurance that erythrocytes will be saturated to maximum carrying capacity. Because MI impairs the circulatory function of the heart, oxygen extraction by the heart and by other tissues may be diminished. In some cases, elevated pulmonary capillary pressure and pulmonary edema can decrease oxygen uptake as a result of impaired pulmonary alveolar-capillary diffusion. Supplemental oxygen increases the driving gradient for oxygen uptake.1
Arterial blood that is at its maximum oxygen-carrying capacity can potentially deliver oxygen to myocardium in jeopardy during an MI via collateral coronary circulation. The recommended duration of supplemental oxygen administration in a MI is 2 to 6 hours, longer if congestive heart failure occurs or arterial oxygen saturation is less than 90%. However, there are no published studies demonstrating that oxygen therapy reduces the mortality or morbidity of an MI.
Intravenous nitrates should be administered to patients with MI and congestive heart failure, persistent ischemia, hypertension, or large anterior wall MI.4, 9 The primary benefit of nitrates is derived from its vasodilator effect. Nitrates are metabolized to nitric oxide in the vascular endothelium. Nitric oxide relaxes vascular smooth muscle and dilates the blood vessel lumen. Vasodilatation reduces cardiac preload and afterload and decreases the myocardial oxygen requirements needed for circulation at a fixed flow rate. Vasodilatation of the coronary arteries improves blood flow through the partially obstructed vessels as well as through collateral vessels. Nitrates can reverse the vasoconstriction associated with thrombosis and coronary occlusion.
When administered sublingually or intravenously, nitroglycerin has a rapid onset of action. Clinical trial data have supported the initial use of nitroglycerin for up to 48 hours in MI. There is little evidence that nitroglycerin provides substantive benefit as long-term post-MI therapy, except when severe pump dysfunction or residual ischemia is present.4 Low BP, headache, and tachyphylaxis limit the use of nitroglycerin. Nitrate tolerance can be overcome by increasing the dose or by providing a daily nitrate-free interval of 8 to 12 hours. Nitrates must be avoided in patients who have taken a phosphodiesterase inhibitor within the previous 24 hours.4
Pain from MI is often intense and requires prompt and adequate analgesia. The agent of choice is morphine sulfate, given initially IV at 5 to 15 minute intervals at typical doses of 2 to 4 mg.4 Reduction in myocardial ischemia also serves to reduce pain, so oxygen therapy, nitrates, and beta blockers remain the mainstay of therapy. Because morphine can mask ongoing ischemic symptoms, it should be reserved for patients being sent for coronary angiography. This was downgraded to a IIa recommendation in the latest STEMI guidelines.
Beta blocker therapy is recommended within 12 hours of MI symptoms and is continued indefinitely.4, 9 Treatment with a beta blocker decreases the incidence of ventricular arrhythmias, recurrent ischemia, reinfarction, and, if given early enough, infarct size and short-term mortality. Beta blockade decreases the rate and force of myocardial contraction and decreases overall myocardial oxygen demand. In the setting of reduced oxygen supply in MI, the reduction in oxygen demand provided by beta blockade can minimize myocardial injury and death (Table 2).
|Metoprolol||15 mg IV × 1 then 200 mg/day PO in divided doses||MIAMI19|
|Atenolol||5-10 mg IV × 1, then 100 mg/day PO||ISIS-120|
|Carvedilol||6.25 mg bid titrated to 25 mg BID||CAPRICORN21|
ISIS-1, International Studies of Infarct Survival-1; MIAMI, Metoprolol in Acute Myocardial Infarction.
The use of a beta blocker has a number of recognized adverse effects. The most serious are heart failure, bradycardia, and bronchospasm. During the acute phase of an MI, beta blocker therapy may be initiated intravenously; later, patients can switch to oral therapy for long-term treatment. The COMMIT-CCS 2 trial raised safety concerns about the use of early intravenous beta blockers in high-risk patients.10 In some patients who are considered high risk due to age or hemodynamic instability, it may be reasonable to hold off on early intravenous therapy.
According to the 2007 guideline updates, anticoagulation should be added to standard medical therapy for most patients after myocardial infarction.4
Unfractionated heparin is beneficial until the inciting thrombotic cause (ruptured plaque) has completely resolved or healed. Unfractionated heparin has been shown to be effective when administered intravenously or subcutaneously according to specific guidelines. The minimum duration of heparin therapy after MI is generally 48 hours, but it may be longer, depending on the individual clinical scenario. Heparin has the added benefit of preventing thrombus through a different mechanism than aspirin (Box 1).
|Box 1: Unfractionated Heparin Dosing
PTT, prothrombin time.
Low-molecular-weight heparin (LMWH) can be administered to MI patients who are not treated with fibrinolytic therapy and who have no contraindications to heparin. The LMWH class of drugs includes several agents that have distinctly different anticoagulant effects. LMWHs are proved to be effective for treating acute coronary syndromes characterized by unstable angina and NSTEMI.4 Their fixed doses are easy to administer, and laboratory testing to measure their therapeutic effect is usually not necessary (Table 3).
(after SC dosing)
|Dosing in ACS||FDA Approved Indications|
|Dalteparin||3-5 hr||120 U/kg SC bid||Prevention of ischemic complications in UA and NSTEMI|
|Enoxaparin||4.5 hr||100 U/kg (1 mg/kg) SC q12h||Prophylaxis of ischemic complications of UA and NSTEMI when administered with aspirin|
UA, unstable angina; NSTEMI, non−ST segment elevation myocardial infarction.
Warfarin is not routinely used after MI, but it does have a role in selected clinical settings. The latest guidelines recommend the use of warfarin for at least 3 months in patients with left ventricular aneurysm or thrombus, a left ventricular ejection fraction less than 30%, or chronic atrial fibrillation.
Restoration of coronary blood flow in MI patients can be accomplished pharmacologically with the use of a fibrinolytic agent. Fibrinolytic therapy is indicated for patients who present with a STEMI within 12 hours of symptom onset without a contraindication. Absolute contraindications to fibrinolytic therapy include history of intracranial hemorrhage, ischemic stroke or closed head injury within the past 3 months, presence of an intracranial malignancy, signs of an aortic dissection, or active bleeding. Fibrinolytic therapy is primarily used at facilities without access to an experienced interventionalist within 90 minutes of presentation.9
As a class, the plasminogen activators have been shown to restore normal coronary blood flow in 50% to 60% of STEMI patients. The successful use of fibrinolytic agents provides a definite survival benefit that is maintained for years. The most critical variable in achieving successful fibrinolysis is time from symptom onset to drug administration. A fibrinolytic is most effective within the first hour of symptom onset and when the door-to-needle time is 30 minutes or less.9
Angiotensin-converting enzyme (ACE) inhibitors should be used in all patients with a STEMI without contraindications. ACE inhibitors are also recommended in patients with NSTEMI who have diabetes, heart failure, hypertension, or an ejection fraction less than 40%. In such patients, an ACE inhibitor should be administered within 24 hours of admission and continued indefinitely. Further evidence has shown that the benefit of ACE inhibitor therapy can likely be extended to all patients with an MI and should be started before discharge.4, 9 Contraindications to ACE inhibitor use include hypotension and declining renal function. The most commonly used ACE inhibitors are summarized in Table 4.
|Agent||Dosing (PO)||Original Trial|
|Captopril||6.25 mg tid titrated to 50 mg tid||SAVE: 3-16 days post-MI in asymptomatic patients with EF <40%22|
|Ramipril||1.25 mg bid titrated to 5 mg bid||AIRE: 3-10 days post-MI with symptoms of heart failure23|
|Captopril||6.25 mg bid titrated to 50 mg bid||ISIS-4: started within 24 hr of MI24|
|Lisinopril||5 mg/day titrated to 10 mg/day||GISSI-3: started within 24 hr of MI25|
AIRE, Acute Infarction Ramipril Efficacy; EF, ejection fraction; GISSI-3, Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico; ISIS-4, International Studies of Infarct Survival-1; MI, myocardial infarction; SAVE, Survival and Ventricular Enlargemen.
ACE inhibitors decrease myocardial afterload through vasodilatation. One effective strategy for instituting an ACE inhibitor is to start with a low-dose, short-acting agent and titrate the dose upward toward a stable target maintenance dose at 24 to 48 hours after symptom onset. Once a stable maintenance dose has been achieved, the short-acting agent can be continued or converted to an equivalent-dose long-acting agent to simplify dosing and encourage patient compliance. For patients intolerant of ACE inhibitors, angiotensin receptor blocker (ARB) therapy may be considered.
Glycoprotein IIb/IIIa receptors on platelets bind to fibrinogen in the final common pathway of platelet aggregation. Antagonists to glycoprotein IIb/IIIa receptors are potent inhibitors of platelet aggregation. The use of glycoprotein IIb/IIIa inhibitors during percutaneous coronary intervention (PCI) and in patients with MI and acute coronary syndromes has been shown to reduce the composite end point of death, reinfarction, and the need to revascularize the target lesion at follow-up. The current guidelines recommend the use of a IIb/IIIa inhibitor for patients in whom PCI is planned. For high-risk patients with NSTEMI who do not undergo PCI, a IIb/IIIa inhibitor may be used for 48 to 72 hours (Table 5).4
|Agent||Loading Dose (IV)||Maintenance Dose (IV)||Duration of Infusion||FDA Approved Indications|
|Abciximab||0.25 mg/kg||0.125 µg/kg/min
max 10 µg/min
|12-24 hr||Coronary intervention|
|Eptifibatide||180 µg/kg||2 µg/kg/min||Up to 72 hr||Acute coronary syndrome
|Tirofiban||0.4 µg/kg/min for 30 min||0.1 µg/kg/min||12-24 hr||Acute coronary syndrome
Evidence is less well established for the direct thrombin inhibitor, bivalirudin. The 2007 American College of Cardiology (ACC) and the American Heart Association (AHA) guidelines recommend bivalirudin as an alternative to heparin therapy for patients who cannot receive heparin for a variety of reasons (e.g., heparin-induced thrombocytopenia).4, 9
A statin should be started in all patients with a myocardial infarction without known intolerance or adverse reaction prior to hospital discharge. Preferably, a statin would be started as soon as a patient is stabilized after presentation. The Pravastatin or Atorvastatin Evaluation and Infection—Thrombolysis in Myocardial Infarction 22 (PROVE IT-TIMI 22) trial suggested a benefit of starting patients on high-dose therapy from the start (e.g., atorvastatin 80 mg/day).12
In the Epleronone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) trial, a mortality benefit was seen with eplerenone administration in all post-MI patients, provided multiple criteria were met. The criteria included concomitant use of an ACE inhibitor, ejection fraction less than 40%, symptomatic heart failure or diabetes, a creatinine clearance greater than 30 mL/min, and a potassium level less than 5 mEq/dL.13 In patients that meet these criteria, the use of eplerenone has a Class I indication.
Patients with STEMI or MI with new left bundle branch block should have PCI within 90 minutes of arrival at the hospital if skilled cardiac catheterization services are available.9 Patients with NSTEMI and high-risk features such as elevated cardiac enzymes, ST-segment depression, recurrent angina, hemodynamic instability, sustained ventricular tachycardia, diabetes, prior PCI, or bypass surgery are recommended to undergo early PCI (<48 hours). PCI consists of diagnostic angiography combined with angioplasty and, usually, stenting. It is well established that emergency PCI is more effective than fibrinolytic therapy in centers in which PCI can be performed by experienced personnel in a timely fashion.14 An operator is considered experienced with more than 75 interventional procedures per year. A well-equipped catheterization laboratory with experienced personnel performs more than 200 interventional procedures per year and has surgical backup available. Centers that are unable to provide such support should consider administering fibrinolytic therapy as their primary MI treatment.
Restoration of coronary blood flow in a MI can be accomplished mechanically by PCI. PCI can successfully restore coronary blood flow in 90% to 95% of MI patients. Several studies have demonstrated that PCI has an advantage over fibrinolysis with respect to short-term mortality, bleeding rates, and reinfarction rates. However, the short-term mortality advantage is not durable, and PCI and fibrinolysis appear to yield similar survival rates over the long term. PCI provides a definite survival advantage over fibrinolysis for MI patients who are in cardiogenic shock. The use of stents with PCI for MI is superior to the use of PCI without stents, primarily because stenting reduces the need for subsequent target vessel revascularization.15
Emergent or urgent coronary artery bypass grafting (CABG) is warranted in the setting of failed PCI in patients with hemodynamic instability and coronary anatomy amenable to surgical grafting.9 Surgical revascularization is also indicated in the setting of mechanical complications of MI, such as ventricular septal defect, free wall rupture, or acute mitral regurgitation. Restoration of coronary blood flow with emergency CABG can limit myocardial injury and cell death if performed within 2 or 3 hours of symptom onset. Emergency CABG carries a higher risk of perioperative morbidity (bleeding and MI extension) and mortality than elective CABG. Elective CABG improves survival in post-MI patients who have left main artery disease, three-vessel disease, or two-vessel disease not amenable to PCI.
The results of a multicenter automatic defibrillator implantation trial have expanded the indications for automatic implantable cardioverter-defibrillators (ICDs) in post-MI patients. The trial demonstrated a 31% relative risk reduction in all-cause mortality with the prophylactic use of an ICD in post-MI patients with depressed ejection fractions.16 The current guidelines recommend waiting 40 days after an MI to evaluate the need for ICD implantation. ICD implantation is appropriate for patients in NYHA functional class II or III with an ejection fraction less than 35%. For patients in NYHA functional class I, the ejection fraction should be less than 30% before considering ICD placement. ICDs are not recommended while patients are in NYHA functional class IV.17
An individual patient's long-term outcome following an MI depends on numerous variables, some of which are not modifiable from a clinical standpoint. However, patients can modify other variables by complying with prescribed therapy and adopting lifestyle changes.
Cardiac stress testing after MI has established value in risk stratification and assessment of functional capacity.4 The timing of performing cardiac stress testing remains debatable. The degree of allowable physiologic stress during testing depends on the length of time from MI presentation. Stress testing is not recommended within several days after a myocardial infarction. Only submaximal stress tests should be performed in stable patients 4 to 7 days after an MI. Symptom-limited stress tests are recommended 14 to 21 days after an MI. Imaging modalities can be added to stress testing in patients whose electrocardiographic response to exercise is inadequate to confidently assess for ischemia (e.g., complete left bundle branch block, paced rhythm, accessory pathway, left ventricular hypertrophy, digitalis use, and resting ST-segment abnormalities).4
From a prognostic standpoint, an inability to exercise and exercise-induced ST-segment depression are associated with higher cardiac morbidity and mortality compared with patients able to exercise and without ST-segment depression.4 Exercise testing identifies patients with residual ischemia for additional efforts at revascularization. Exercise testing also provides prognostic information and acts as a guide for post-MI exercise prescription and cardiac rehabilitation.
Smoking is a major risk factor for coronary artery disease and MI. For patients who have undergone an MI, smoking cessation is essential to recovery, long-term health, and prevention of reinfarction. In one study, the risk of recurrent MI decreased by 50% after 1 year of smoking cessation.18 All STEMI and NSTEMI patients with a history of smoking should be advised to quit and offered smoking cessation resources, including nicotine replacement therapy, pharmacologic therapy, and referral to behavioral counseling or support groups.4, 9 Smoking cessation counselling should begin in the hospital, at discharge, and during follow-up. The American Lung Association maintains a website (http://www.lungusa.org) with updates on public health initiatives to reduce tobacco use; it is a resource for smoking cessation strategies for patients and health care providers. Other public and private sources of smoking cessation information are available online as well.
Most oral medications instituted in the hospital at the time of MI will be continued long term. Therapy with aspirin and beta blockade is continued indefinitely in all patients. ACE inhibitors are continued indefinitely in patients with congestive heart failure, left ventricular dysfunction, hypertension, or diabetes.4, 9 A lipid-lowering agent, specifically a statin, in addition to diet modification, is continued indefinitely as well. Post-MI patients with diabetes should have tight glycemic control according to earlier studies. The latest ACC/AHA guidelines recommend a goal HbA1c of less than 7%.
Cardiac rehabilitation provides a venue for continued education, reinforcement of lifestyle modification, and adherence to a comprehensive prescription of therapies for recovery from MI including exercise training. Participation in cardiac rehabilitation programs after MI is associated with decreases in subsequent cardiac morbidity and mortality. Other benefits include improvements in quality of life, functional capacity, and social support. However, only a minority of post-MI patients actually participate in formal cardiac rehabilitation programs because of several factors, including lack of structured programs, physician referrals, low patient motivation, noncompliance, and financial constraints.