Acute myocardial infarction

Acute myocardial infarction


Acute myocardial infarction (MI) is defined as death or necrosis of myocardial cells. It is a diagnosis at the end of the spectrum of myocardial ischemia or acute coronary syndromes. Myocardial infarction occurs when myocardial ischemia exceeds a critical threshold and overwhelms myocardial cellular repair mechanisms that are designed to maintain normal operating function and hemostasis. Ischemia at this critical threshold level for an extended time period results in irreversible myocardial cell damage or death.1-3
Critical myocardial ischemia may occur as a result of increased myocardial metabolic demand and/or decreased delivery of oxygen and nutrients to the myocardium via the coronary circulation. 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 (> 75%) fixed coronary artery stenosis due to 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.1-3
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 either the endocardium or 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 are 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 non-transmural MI as determined by pathology.4
A more common clinical diagnostic classification scheme is also based on ECG findings as a means of distinguishing between two types of MI—one that is marked by ST elevation and one that is not. The distinction between an ST-elevation MI and a non-ST-elevation MI also does not distinguish a transmural from a non-transmural 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
The most common etiology of MI is a thrombus superimposed on a ruptured or unstable atherosclerotic plaque.5

PREVALENCE

Myocardial infarction is the leading cause of death in the United States (US) as well as in most industrialized nations throughout the world. Approximately 800,000 people in the US are affected and in spite of a better awareness of presenting symptoms, 250,000 die prior to presentation to a hospital.4 The survival rate for US patients hospitalized with MI is approximately 90% to 95%. This represents a significant improvement in survival and is related to improvements in emergency medical response and treatment strategies.
In general, MI can occur at any age, but its incidence rises with age. The actual incidence is dependent upon predisposing risk factors for atherosclerosis, which are discussed below. Approximately 50% of all MI's in the US occur in people younger than 65 years of age. 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.4,1,2

PATHOPHYSIOLOGY

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 min), irreversible myocardial cell damage and cell death will occur.5
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 due to 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 that 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." Any amount of 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 completely occlude coronary blood flow for a sufficient time period, MI can result.
Mechanisms of Myocardial Damage:
The severity of an MI is dependent 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 speaking, the more proximal the coronary occlusion, the more extensive is the amount of myocardium at risk of necrosis. The larger the MI, the greater is the chance of death due to a mechanical complication or pump failure. The longer the time period of vessel occlusion, the greater the chances of irreversible myocardial damage distal to the occlusion.
The death of myocardial cells first occurs in the area of myocardium that 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.
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.4,1,2
High Blood Cholesterol
Cholesterol is a major component of the atherosclerotic plaque that is associated with MI. 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 cholesterol are associated with an increased incidence of both atherosclerosis and MI. A full summary of the National Heart, Lung, and Blood Institutes' cholesterol guidelines is available online and includes a free Palm OS software download for point of care utilization.6
Diabetes Mellitus
Patients who are diabetic have a substantially greater risk of atherosclerotic vascular disease in the heart as well as in other areas of the 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-dependent or noninsulin-dependent diabetes. Resources for health care professionals on the diagnosis and management of diabetes and its role in atherosclerotic vascular disease and MI can be found online.
Hypertension
High blood pressure (BP) has consistently been associated with an increased risk of MI. This risk is associated with both systolic and diastolic hypertension. The control of hypertension with appropriate medication has been shown to significantly reduce the risk of MI. A full summary of the National Heart, Lung, and Blood Institutes' JNC VI guidelines is available online.7
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 on-line.
The Community Guide to Preventive Services
Tobacco Cessation Guideline
Quitnet
To Change or Not to Change: "Sounds Like You Have a Dilemma," Annals of Internal Medicine
With Smoking Cessation Drugs, Dosing Is Key8
The Journal of the American Medical Association
(This reference requires a user ID and password)
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.
Family History
A family history of premature coronary disease increases an individual's risk of atherosclerosis and MI. The etiology of familial coronary events is multifactorial, and includes other elements such as genetic components and acquired general health practices (eg, smoking and high-fat diets).

SIGNS AND SYMPTOMS

Acute MI may have unique presentations 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 MI's are more likely to be diabetic. Despite the diversity of presenting symptoms of MI, there are some characteristic symptoms (Table 1):
Table 1:

Signs and Symptoms of a Myocardial Infarction

Chest pain described as a pressure sensation, fullness, or squeezing in the midportion of the thorax
Radiation of chest pain into the jaw/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
Syncope or near-syncope without other cause
Impairment of cognitive function without other cause



A MI may occur at any time of the day, but most appear to be clustered around the early hours of the morning and/or are associated with demanding physical activity. Approximately 50% of patients have some warning symptoms (angina pectoris or an anginal equivalent) prior to the infarct.4

DIAGNOSIS

Identifying a patient who is currently experiencing a MI can be extremely straightforward, very 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 ECG, blood testing, and echocardiography.
Electrocardiography:
The first test is the ECG, which may demonstrate that a MI is in progress or has already occurred (Figure 1).
Blood Tests:
Blood tests can be performed to detect evidence of myocardial cell death. Living heart cells contain certain enzymes and proteins (eg, creatine phosphokinase, troponin, and 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—correlates with the amount of heart muscle that has died (Table 2).9
Table 2:

Normal Values of Blood Tests to
Detect Myocardial Infarction

Analysis
Normal Range

Total creatinine
phosphokinase (CPK)
30-200 U/L

CPK, MB fraction
0.0-8.8 ng/mL

CPK, MB fraction percent of total CPK
0-4%

CPK, MB2 fraction
< 1 U/L

Troponin I
0.0-0.4 ng/mL

Troponin T
0.0-0.1 ng/mL



Echocardiography:
An echocardiogram may be performed in order to compare areas of the left ventricle that are contracting normally with those that are not. One of the earliest protective mechanisms of myocardial cells utilized during limited blood flow is to "turn off" the energy requiring "machinery" 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 due to an acute MI or previous (old) MI or other myopathic processes. Thus, the usefulness of echocardiography in the diagnosis of MI is limited.

THERAPY

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 quickly recognize MI symptoms and the delay in seeking medical attention. When patients present to a hospital, there are a variety of interventions to achieve treatment goals.
Antiplatelet Agents:
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.4 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 cyclo-oxygenase 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 a 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.4,10
Other antiplatelet agents—including clopidogrel, ticlopidine, and dipyridamole-have not been shown in any large-scale trial to be superior to aspirin in 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.11-13
Supplemental Oxygen:
Supplemental oxygen should be administered to patients with symptoms and/or signs of pulmonary edema or pulse oximetry reading less than 90% blood oxygen saturation.4 In practice, supplemental oxygen is one of the three most frequently administered agents used in the treatment of MI. 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 a 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 or arterial oxygen saturation is less than 90%. Yet despite this, there are no published studies demonstrating that oxygen therapy reduces mortality or morbidity of a MI.
Nitrates:
Intravenous nitrates should be administered to patients with MI and congestive heart failure, persistent ischemia, hypertension, or large anterior wall MI.4 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 both 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.4,14
When administered sublingually or intravenously, nitroglycerin has a rapid onset of action. Clinical trial data support the initial use of nitroglycerin for up to 48 hours in MI. There is little evidence that nitroglycerin provides substantive benefit as a 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 either by increasing the dose or by providing a daily nitrate-free interval of 8-12 hours (Table 3).4,14
Table 3:

Nitroglycerine Dosing Schedule
in Myocardial Infarction

Nitroglycerine Formulation
Dosing

Sublingual tablet
0.2-0.6 mg every 5 minutes

Spray
0.4 mg every 5 minutes

Transdermal or paste
0.2-0.8 mg/hour

Intravenous
5.0-200 mcg/minute



Beta-blockers:
Beta-blocker therapy is recommended within 12 hours of MI symptoms and is continued indefinitely. Treatment with a beta-blocker reduces MI mortality—presumably by decreasing the incidence of arrhythmogenic death. 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 a MI, beta-blocker therapy may be initiated intravenously; later patients can switch to oral therapy for long-term treatment (Table 4).
Table 4:

Selective Beta-1-blockers

Beta-1-blocker
Dosing

Metoprolol
25-200 mg every 12 hours

Atenolol
25-200 mg every 24 hours

Esmolol
50-300 mcg/kg/minute intravenously

Betaxolol
5-20 mg every 24 hours

Bisoprolol
5-20 mg every 24 hours

Acebutolol
200-600 mg every 12 hours



Heparin:
Unfractionated Heparin
Intravenous unfractionated heparin is recommended in patients with a MI who undergo percutaneous revascularization or fibrinolytic therapy with alteplase. Intravenous unfractionated heparin is also recommended in patients with a MI who receive fibrinolytic therapy with a non-selective fibrinolytic agent (urokinase, streptokinase, anistreplase) and are at increased risk for systemic emboli (prior embolic event, large or anterior wall infarction, known left ventricular thrombus, or atrial fibrillation).4
Unfractionated heparin forms a chemical complex with antithrombin III. This complex inactivates both free thrombin and factor Xa. The desired clinical effect of heparin is the inhibition of additional formation and propagation of thrombi. 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 either 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 (LMWH)
LMWH can be administered to MI patients not treated with fibrinolytic therapy that have no contra-indication to heparin.4 The LMWH class of drugs includes several agents that have distinctly different anticoagulant effects. These effects can be characterized by a given agent's ratio of activity against factors Xa and IIa. LMWHs have been proven to be effective in treating acute coronary syndromes that are 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 remains an obstacle at present to the more widespread use of LMWHs in MI patients who might require percutaneous or surgical revascularization (Table 5).4
Fibrinolytics:
Fibrinolytic therapy is indicated for patients with a presentation compatible with MI and ST segment elevation greater than 0.1 mV in 2 contiguous EKG leads, or new onset of a bundle branch block, who present less than 12 hours but not more than 24 hours after symptom onset.4 Restoration of coronary blood flow in MI can also be accomplished pharmacologically with the use of a fibrinolytic agent.15-17 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. The GUSTO trial established that an accelerated alteplase/heparin regimen was superior to two streptokinase/heparin regimens.18 Reteplase has been shown to produce slightly higher 60- and 90-minute angiographic patency rates than accelerated alteplase, while adverse-event rates were equal.19 However, the better early patency rate did not translate into any survival advantage at 30 days followup. 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 (Table 6).4
Percutaneous Coronary Intervention:
Percutaneous coronary intervention is an alternative therapy to fibrinolysis if performed by a skilled operator supported by experienced personnel performed in a well-equipped catheterization laboratory.4 An operator is considered experienced with > 75 interventional procedures per year.4,20 A well-equipped catheterization laboratory with experienced personnel performs > 200 interventional procedures per year and has surgical backup available.4 Although controversial, opinion leaders have stated that centers that are unable to provide such support should consider administering fibrinolytic therapy as their primary MI treatment.12,13,20 The performance standard for primary percutaneous intervention as a MI therapy is a "door-to-balloon" time of 90 minutes (± 30 minutes).4 Restoration of coronary blood flow in a MI can be accomplished mechanically by percutaneous coronary intervention (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 a MI patients.12 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.4
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.12 Any advantage that PCI has over fibrinolytic therapy is predicated on a rapid (< 90 min) restoration of coronary blood flow. PCI re-establishes brisk (TIMI grade II or III) flow in more than 90% of patients.4,12
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 intravenous glycoprotein IIb/IIIa inhibitors during PCI and in patients with MI and acute coronary syndromes have been shown to reduce the composite endpoint of death, reinfarction, and the need for target-lesion revascularization at followup (Table 7).21
Surgical Revascularization:
Emergent or urgent coronary artery bypass graft surgery is warranted in the setting of failed percutaneous intervention 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.4 Restoration of coronary blood flow with emergency coronary artery bypass grafting (CABG) can limit myocardial injury and cell death if it is 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 with multi-vessel disease. On the other hand, urgent CABG confers a survival benefit in 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 that is not amenable to PCI. The timing of elective CABG post-MI is controversial, but retrospective studies indicate 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.4
Angiotensin Converting Enzyme
Inhibitors (ACEI):
Oral angiotensin converting enzyme inhibitors are recommended in MI patients within the first 24 hours of symptom onset, if no contra-indications exist.4 Contra-indications to ACEI use include hypotension and declining renal function with ACEI use. The use of an ACEI 4 to 6 weeks after presentation of MI is recommended for patients with congestive heart failure, left ventricular dysfunction (ejection fraction < 0.40), hypertension, or diabetes.4,22 ACEI decrease myocardial afterload through vasodilatation. One effective strategy for instituting ACEI is to start with a low dose, short acting agent and titrate the dose upward towards a stable target maintenance dose at 24 to 48 hours after symptom onset. Once a stable maintenance dose is achieved, the short acting agent can be continued or converted to an equivalent dose long-acting agent to simplify dosing and encourage patient compliance (Table 8).

OUTCOMES

An individual patient's long-term outcome following a MI is dependent upon numerous variables, some of which are not modifiable from a clinical standpoint. However, patients can modify other variables by complying with prescribed therapy and/or adopting lifestyle changes.
Cardiac Stress Testing:
Cardiac stress testing post-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 is dependent upon the length of time from MI presentation. Stress testing is not recommended within several days post-MI. Only sub-maximal stress tests should be performed in stable patients 4 to 7 days after MI. Symptom-limited stress tests are recommended 14 to 21 days after MI. Imaging modalities can be added to stress testing in patients whose electrocardiographic response to exercise is inadequate to confidently assess for ischemia (i.e. complete left bundle branch block, paced rhythm, accessory A-V pathway, left ventricular hypertrophy, digitalis use, and resting ST-segment abnormalities).4 From a prognostic stand-point, an inability to exercise and exercise induced ST-segment depression are associated with higher cardiac morbidity and mortality compared to 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.4
Lipid Management:
All post-MI patients should be on an American Heart Association Step II diet (< 200 mg cholesterol/day, < 7% of total calories from saturated fats). Post-MI patients with LDL-cholesterol levels > 100 mg/dL on a Step II diet are recommended to be on drug therapy to lower LDL-cholesterol levels < 100 mg/dL. Post-MI patients with HDL-cholesterol levels < 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.4 Recent data indicate the all MI patients should be on statin therapy, regardless of lipid levels or diet (Table 9).
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. ACEI is continued indefinitely in patients with congestive heart failure, left ventricular dysfunction (ejection fraction < 0.40), hypertension, or diabetes.4 A lipid-lowering agent, specifically a statin, in addition to dietary modification is continued indefinitely.
Implantable Cardiac Defibrillators:
The results of the multi-center automatic defibrillator implantation trial II (MADIT II) have expanded the indications for automatic implantable cardiac defibrillators (AICD) 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 less than 30%.23 The implication of the results of this trial, expanded indication for treatment with an AICD, is likely to be tempered initially by the cost for therapy on a local, regional and national level.
Cardiac Rehabilitation:
Cardiac rehabilitation provides a venue for continued education, re-enforcement 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 a decrease in subsequent cardiac morbidity and mortality.4 Other benefits include improvement in quality of life, functional capacity and social support. A minority of post-MI patients actually participate in formal cardiac rehabilitation programs due to either lack of structured programs, physician referrals, low patient motivation, non-compliance, or financial constraints.4

Acute myocardial infarction

thanks