Advanced coronary atherosclerosis and even complete occultion may remain clinically silent. there is only a modest correlaation between the clinical symptoms and the anatomic extent of disease. at present, the only means of determinig the location and extent of narrowing is coronary arteriography, although ischemia can be recogniszed by other less invasive studies.
Myocardial ischemia may be provoked by either increased myocardial oxygen requirements(exercise, mental stress, and blood pressure) or by decrease oxygen supply (caused by coronary vasospasm, platelet plugging or partial thrombosis).
The term "myocardial infarction" focuses on the heart muscle, which is called the myocardium,and the changes that occur in it due to the sudden deprivation of circulating blood. This is usually caused by arteriosclerosis with narrowing of the coronary arteries, the culminating event being a thrombosis (clot). The main change is death (necrosis) of myocardial tissue.
The word "infarction" comes from the Latin "infarcire" meaning "to plug up or cram." It refers to the clogging of the artery, which is frequently initiated by cholesterol piling up on the inner wall of the blood vessels that distribute blood to the heart muscle.
Definition and causes
Acute myocardial infarction (MI) is defined as death or necrosis of myocardial cells.. Myocardial infarction occurs when myocardial ischemia exceeds a critical threshold and overwhelms myocardial cellular repair mechanisms designed to maintain normal operating function and hemostasis. It is a diagnosis at the end of the spectrum of myocardial ischemia or acute coronary syndromes
Ischemia at this critical threshold level for an extended period results in irreversible myocardial cell damage or death.Critical myocardial ischemia may 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. A high-grade (more than 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 aortic diastolic 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 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.
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 an 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.
Risk factors
Six primary risk factors have been identified with the development of atherosclerotic coronary artery disease and MI—hyperlipidemia, diabetes mellitus, hypertension, smoking, 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.Hypertension.
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 VI guidelines is available online.
2.High Blood Cholesterol Level.
An elevated level of total cholesterol is associated with an increased risk of coronary atherosclerosis and MI. Laboratory testing provides a measure of certain types of circulating fat particles. Elevated levels of low-density lipoprotein (LDL) cholesterol are associated with an increased incidence of atherosclerosis and MI. A full summary of the National Heart, Lung, and Blood Institute's cholesterol guidelines is available online and includes a free Palm OS software download for point of care use.
3.Diabetes Mellitus.
Diabetics have a substantially greater risk of atherosclerotic vascular disease in the heart as well as in other areas of their vasculature. Diabetes increases the risk of MI because it increases the rate of atherosclerotic progression and adversely affects blood cholesterol levels. This accelerated form of atherosclerosis occurs regardless of whether a patient has insulin- or noninsulin-dependent diabetes.
4.Family History.
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).
5.Male Gender.
The incidence of atherosclerotic vascular disease and MI is higher in men than women in all age groups. This gender difference in MI incidence, however, narrows with increasing age.
6.Tobacco Use.
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. 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. Other public and private sources of smoking cessation information are also available online.
Pathophysiology
Signs and Symptoms of a Myocardial Infarction
Acute MI may 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.there are some chareacteristic symptoms of MI:
- Chest pain described as a pressure sensation, fullness, or squeezing in the midportion of the thorax
- Syncope or near-syncope without other cause
- Impairment of cognitive function without other cause
- Radiation of chest pain into the jaw or teeth, shoulder, arm, and/or back
- Associated dyspnea or shortness of breath
- Associated epigastric discomfort with or without nausea and vomiting
- Associated diaphoresis or sweating
Mechanisms of Myocardial Damage
The severity of an MI is dependent on three factors: (1) the level of the occlusion in the coronary artery; (2) the length of time of the occlusion; and (3) the presence or absence of collateral circulation. Generally, the more proximal the coronary occlusion, the more extensive the amount of myocardium at risk of necrosis. The larger the MI, 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.
Mechanisms of Occlusion
Most MIs 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 long enough (20 to 40 minutes), irreversible myocardial cell damage and cell death will occur.
The development of atherosclerotic plaque occurs over a period of years to decades. The initial vascular lesion leading to the development of atherosclerotic plaque is not known with certainty. The two primary characteristics of the clinically symptomatic atherosclerotic plaque are a fibromuscular cap and an underlying lipid-rich core. Plaque erosion may occur because of the actions of 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 degree of disruption of the overlying endothelium can range from minor erosion to extensive fissuring, which results in an ulceration of the plaque. 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 plaque's “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 completely for a sufficient period, MI can result.
The death of myocardial cells first occurs in the area of myocardium most distal to the arterial blood supply—that is, 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.
An MI may occur at any time of the day, but most appear to be clustered around the early hours of the morning, 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.
Diagnosis
Identifying a patient who is currently experiencing a MI can be extremely 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 a MI usually present to an emergency department. Once a patient's clinical picture raises a suspicion of a MI, several confirmatory tests can be performed rapidly. These tests include electrocardiography, blood testing, and echocardiography.
- Electrocardiography
12-lead electrocardiogram showing ST-segment (V1 to V4) elevation myocardial infarction (STEMI)
2.Blood Tests
Living heart cells contain enzymes and proteins (e.g., creatine phosphokinase, troponin, myoglobin) within cell membranes associated with specialized cellular functions such as contraction. When a heart muscle dies, cellular membranes lose integrity and intracellular enzymes and proteins slowly leak into the bloodstream. These enzymes and proteins can be detected by a blood sample analysis. The concentration of enzymes in a blood sample—and more importantly, the changes in concentration found in samples taken over time—correlate with the amount of heart muscle that has died
Normal Values of Blood Tests to Detect Myocardial Infarction
Analyte Normal Range
Total creatinine phosphokinase (CPK) 30-200 U/L
CK, MB fraction 0.0-8.8 ng/mL
CK, MB fraction (% of total CPK) 0-4%
CK, MB2 fraction <1 U/L Troponin I 0.0-0.4 ng/mL Troponin T 0.0-0.1 ng/mL
3.Echocardiography
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 within minutes after normal blood flow is interrupted. The echocardiogram can be helpful in identifying which portion of the heart is affected by a 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. Thus, the usefulness of echocardiography for the diagnosis of MI is limited. Back to Top Treatment The goals of therapy in AMI 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 MI.
Management Goals for ST-Elevation Myocardial Infarction (STEMI) and Non–ST-Elevation Myocardial Infarction (NSTEMI) Intervention Timing Acute MI STEMI Acute MI NSTEMI Comments Aspirin * At or before arrival Beta blocker † At arrival Some contraindications Fibrinolytic therapy Also for LBBB Fibrinolytic therapy At arrival, within 30 min Also for LBBB Coronary angiography, angioplasty Within 90 min after arrival Also for LBBB (in facilities so equipped) Reperfusion Within 12 hr of onset of symptoms LDL cholesterol assessment During hospital stay Unless recently done Aspirin * Prescribe at discharge Beta blocker Prescribed at discharge Lipid-lowering agent Prescribe at discharge ACEI or ARB Prescribe at discharge Smoking cessation counseling During hospitalization * For medications, only use if no contraindication or sensitivity. †Consider risks and benefits of beta blockers if patient has beta blocker allergy, bradycardia at admission or within 24 hours, heart failure at admission or within 24 hours; second- or third-degree heart block; shock at admission or within 24 hours. ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; LBBB, left bundle branch block; LDL, low-density lipoprotein. Medical Treatment Aspirin The use of aspirin has been shown to reduce mortality from MI. Aspirin in a dose of at least 160 mg and up to 325 mg should be administered immediately on recognition of MI signs and symptoms and continued daily indefinitely. 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 interferes with function of the enzyme 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 an MI. 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. Other antiplatelet agents, including clopidogrel, ticlopidine, and dipyridamole, have not been shown in any large-scale trial to be superior to aspirin for MI. These other antiplatelet agents, specifically clopidogrel, may be useful for patients who have a true allergy to aspirin and for patients with known resistance to aspirin's effects. Supplemental Oxygen Supplemental oxygen should be administered to patients with symptoms and/or signs of pulmonary edema or pulse oximetry, less than 90% blood oxygen saturation. The rationale for use 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. Arterial blood that is at its maximum oxygen-carrying capacity can potentially deliver oxygen to myocardium in jeopardy during an MI via the 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%. Despite this, however, there are no published studies demonstrating that oxygen therapy reduces the mortality or morbidity of an MI. Nitrates Intravenous nitrates should be administered to patients with MI and congestive heart failure, persistent ischemia, hypertension, or large anterior wall MI. 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. Vasodilation reduces cardiac preload and afterload and decreases the myocardial oxygen requirements needed for circulation at a fixed flow rate. Vasodilation 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. 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
Nitroglycerin Dosage Schedule in Myocardial Infarction Nitroglycerin Formulation Dosage Sublingual tablet 0.2-0.6 mg every 5 min Spray 0.4 mg every 5 min Transdermal or paste 0.2-0.8 mg/hr Intravenous 5.0-200 mcg/min Pain Control Agents 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. Typical doses are 2 to 4 mg, with increments of 2 to 8 mg. 1 Reduction in myocardial ischemia also serves to reduce pain, so oxygen therapy, nitrates, and β-blocker therapy complement morphine. Beta Blockers Beta blocker therapy is recommended within 12 hours of MI symptoms and is continued indefinitely. 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 minimizes myocardial injury and death. The use of a beta blocker has a number of recognized adverse effects. The most serious are heart failure, bradycardia, and bronchospasm. Even so, the benefits in reducing both mortality and the risk of reinfarction are so great that there are no absolute contraindications to beta blocker use in MI. 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
Selective Beta1 Blockers Beta1 Blocker Dosage Metoprolol 25-200 mg every 12 hr Atenolol 25-200 mg every 24 hr Esmolol 50-300 μg/kg/min IV Betaxolol 5-20 mg every 24 hr Bisoprolol 5-20 mg every 24 hr Acebutolol 200-600 mg every 12 hr Heparin Unfractionated Heparin. This is not used routinely for MI—for example, for uncomplicated NSTEMI. IV unfractionated heparin is recommended for patients with an MI who undergo percutaneous revascularization or fibrinolytic therapy with alteplase. IV unfractionated heparin is also recommended for patients with an MI who receive fibrinolytic therapy with a nonselective fibrinolytic agent (e.g., urokinase, streptokinase, anistreplase) and are at increased risk for systemic emboli because of a prior embolic event, large or anterior wall infarction, known left ventricular thrombus, or atrial fibrillation. 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 post-MI generally is 48 hours, but may be longer, depending on the individual clinical scenario. Low-Molecular-Weight Heparin. Low-molecular-weight heparin (LMWH) can be administered to MI patients not treated with fibrinolytic therapy who have no contraindications to heparin. The LMWH class of drugs includes several agents that have distinctly different anticoagulant effects. LMWHs have been proved to be effective for treating acute coronary syndromes characterized by unstable angina and non–Q wave MI. Their fixed doses are easy to administer, and laboratory testing to measure their therapeutic effect is not necessary. On the other hand, the absence of monitoring currently remains an obstacle to the more widespread use of LMWHs in MI patients who might require percutaneous or surgical revascularization
Heparin Dosage Type of Heparin Dosage Unfractionated heparin 60-70 U/kg IV load (max, 5000 U); 12-15 U/kg/hr IV maintenance drip; nomogram—titrate to maintain aPTT 1.5-2.5 × control Enoxaparin 1 mg/kg subcutaneously every 12 hr Dalteparin 120 IU/kg subcutaneously every 12 hr (max, 10,000IU in 24hr) aPTT, activated partial thromboplastin time.
Fibrinolytic therapy is indicated for patients with a suspected MI, especially for STEMI or NSTEMI with left bundle branch block. 5 Therapy should be started within 30 minutes of hospital arrival. 1,5 Fibrinolytic therapy is especially important in health care facilities that cannot mount a rapid coronary catheterization intervention. Restoration of coronary blood flow in MI patients can be accomplished pharmacologically with the use of a fibrinolytic agent. As a class, the plasminogen activators have been shown to restore coronary blood flow in 50% to 80% of MI patients. The successful use of fibrinolytic agents provides a definite survival benefit that is maintained for years. A randomized controlled trial has established that an accelerated alteplase-heparin regimen is superior to two streptokinase-heparin regimens. Reteplase has been shown to produce slightly higher 60- and 90-minute angiographic patency rates than accelerated alteplase, although adverse event rates were equal. However, the better early patency rate did not translate into any survival advantage at 30 days follow-up. The most critical variable in achieving successful fibrinolysis is time from symptom onset to drug administration. A fibrinolytic is most effective when the door to needle time is 30 minutes or less
Fibrinolytic Therapy for Myocardial Infarction Agent Dosage Patency at 90 minutes Alteplase (Activase) Body weight > 67 kg: 15-mg loading dose + 50 mg/30 min + 35 mg/60 min IV 75%
Body weight < 67 kg: 15-mg loading dose + 0.75 mg/kg/30 min (<50 mg total) + 0.5 mg/kg/60 min (<35 mg total)
Reteplase (Retavase) 10 U over 2 min; wait 30 min; 10 U/2 min IV 75%
Streptokinase (Streptase) 1,500,000 U over 60 min IV 50%
Glycoprotein IIb/IIIa Antagonists
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 IV 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 for target lesion revascularization at follow-up.
Glycoprotein Ilb/IIa Inhibitors
Agent Use(s) Dosage
Abciximab Coronary intervention 0.25 mg/kg IV loading dose; 0.125 mcg/kg/min IV maintenance (max, 10 mcg/min); duration of infusion, 12-24 hr
Eptifibatide Acute coronary syndrome; coronary intervention 180 mcg/kg IV loading dose; 2.0 mcg/kg/min IV maintenance; duration of infusion, up to 72 hr
Tirofiban Acute coronary syndrome; coronary intervention 0.4 mcg/kg/min x 30 min IV loading dose; 0.1 mcg/kg/min IV maintenance; duration of infusion, 12-24 hr
Other Treatment Option
Patients with STEMI or MI with left bundle branch block should have PCI within 90 minutes of arrival at the hospital if skilled cardiac catheterization services are available. 1,5 PCI consists of diagnostic angiography combined with angioplasty and, frequently, 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. An operator is considered experienced with more than 75 interventional procedures per year. 1,5 A well-equipped catheterization laboratory with experienced personnel performs more than 200 interventional procedures per year and has surgical backup available. As noted earlier, 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. Mechanical revascularization by PCI is used as a primary therapy in many well-equipped medical centers and as an alternative to fibrinolysis when fibrinolysis is not clearly indicated or contraindicated. 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. Any advantage that PCI has over fibrinolytic therapy is predicated on a rapid restoration (less than 90 minutes) of coronary blood flow. PCI re-establishes brisk flow in more than 90% of patients.
Surgical Revascularization
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. 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. The risk of operative mortality during emergency CABG is increased in patients who are in cardiogenic shock, those with previous CABG surgery, and those with multivessel disease. On the other hand, urgent CABG confers a survival benefit for patients with recurrent ischemia post-MI whose coronary anatomy is unsuitable for complete revascularization with PCI. 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 timing of elective CABG post-MI is controversial, but retrospective studies have indicated that when CABG is performed as early as 3 to 7 days post-MI, operative mortality is equivalent to CABG performed on non-MI patients
Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers
Drugs of the angiotensin-converting enzyme inhibitors (ACEI) class have been shown to decrease mortality rates for patients with both STEMI and NSTEMI who have impaired left ventricular ejection fraction (lower than 40%). Benefit has also been shown for diabetic patients with left ventricular dysfunction. In such patients, an ACEI or angiotensin receptor blocker (ARB) should be administered within 24 hours of admission and continued indefinitely
Oral ACEI therapy is recommended for MI patients within the first 24 hours of symptom onset, if no contraindications exist. Contraindications to ACEI use include hypotension and declining renal function. The use of an ACEI 4 to 6 weeks after presentation of an MI is recommended for patients with congestive heart failure, left ventricular dysfunction (ejection fraction less than 40%), hypertension, or diabetes. ACEIs decrease myocardial afterload through vasodilation. One effective strategy for instituting an ACEI 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 ACEIs, blockade with angiotensin receptor blocker (ARB) therapy may be considered. The use of ARBs post-STEMI remains somewhat controversial, although valsartan monotherapy (target dose, 160 mg twice daily) is recommended for STEMI patients intolerant of ACEIs who have evidence of left ventricular dysfunction. 6
Angiotension-Converting Enzyme Inhibitors
Agent Divided Doses Dosage
Captopril Three times daily 12.5-450 mg/day
Enalapril Twice daily 2.5-40 mg/day
Moexipril Once or twice daily 7.5-30 mg/day
Benazepril Once or twice daily 5-40 mg/day
Quinapril Once or twice daily 5-80 mg/day
Ramipril Once or twice daily 2.5-20 mg/day
Perindopril Once or twice daily 4-16 mg/day
Trandolapril Once daily 1-4 mg/day
Fosinopril Once daily 10-40 mg/day
Lisinopril Once daily 2.5-40 mg/day
Smoking Cessation
As noted earlier (“Risk Factors”), 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. 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 (bupropion), and referral to behavioral counseling or support groups. 6 Smoking cessation counseling should begin in the hospital, at discharge, and during follow-up.
Outcomes
An individual patient's long-term outcome following a MI is dependent on numerous variables, some of which are not modifiable from a clinical standpoint. However, patients can modify other variables by complying with prescribed therapy, adopting lifestyle changes, or both.
Cardiac Stress Testing
Cardiac stress testing post-MI has established value in risk stratification and assessment of functional capacity. 1The timing of performing cardiac stress testing remains debatable. The degree of allowable physiologic stress during testing is dependent on the length of time from MI presentation. Stress testing is not recommended within several days post-MI. 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 assess for ischemia confidently (e.g., complete left bundle branch block, paced rhythm, accessory atrioventricular pathway, left ventricular hypertrophy, digitalis use, and resting ST-segment abnormalities).
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.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.
Lipid Management
All post-MI patients should be on an American Heart Association step II diet (less than 200 mg cholesterol/day, less than 7% of total calories from saturated fats). Post-MI patients with LDL cholesterol levels higher than 100 mg/dL on a step II diet are recommended to be on drug therapy to lower LDL cholesterol levels to less than 100 mg/dL. Post-MI patients with high-density lipoprotein (HDL) cholesterol levels lower than 35 mg/dL on a step II diet are recommended to participate in a regular exercise program and on drug therapy designed to increase HDL cholesterol levels. Recent data have indicated that all MI patients should be on statin therapy, regardless of lipid levels or diet.
Long-term Medications
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. ACEIs are continued indefinitely in patients with congestive heart failure, left ventricular dysfunction (ejection fraction less than 0.40), hypertension, or diabetes. A lipid-lowering agent, specifically a statin, in addition to dietary modification, is continued indefinitely.
Implantable Cardiac Defibrillators
The results of a multicenter automatic defibrillator implantation trial have expanded the indications for automatic implantable cardioverter-defibrillators (AICDs) in patients post-MI. The trial demonstrated a 31% relative risk reduction in all-cause mortality with the prophylactic use of an AICD in patients post-MI with ejection fractions of less than 30%. 4 This trial, which broadens the indications for AICD, will have to address the high costs of device therapy.
Cardiac Rehabilitation
Cardiac rehabilitation provides a venue for continued education, reinforcement of lifestyle modification, and adherence to a comprehensive prescription of therapies for recovery from MI, which includes exercise training. Participation in cardiac rehabilitation programs post-MI is associated with decreases in subsequent cardiac morbidity and mortality. 1 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 constraint
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