• Patients with definite acute coronary syndrome should be evaluated for immediate reperfusion therapy (ACC/AHA guidelines; SOR: A).
Acute coronary syndromes (ACS) occur as a result of sudden atheromatous plaque rupture. Plaques with heightened inflammation, irrespective of severity, can rupture leading to overlying platelet and fibrin mesh formation, resulting in abrupt cessation of coronary blood flow. Patients might experience unstable angina or myocardial infarction (MI), depending on whether myocardial necrosis occurs. In the United States, 2.3 million people suffer an ACS annually.
Several crucial facts need to be considered by the practicing family physician. First, a large percentage of angiographically "normal" coronary arteries have significant plaque burden by intravascular ultrasound or magnetic resonance imaging (MRI), particularly in patients older than 40 years. Second, more than 60% of MIs are induced by culprit lesions that initially obstruct less than 50% of the arterial lumen. These lesions are generally not detected by stress testing. Third, when an ACS occurs, multiple vulnerable plaques generally coexist at the same time throughout the vascular tree. In an inadequately managed patient, any one of these lesions could suddenly rupture and precipitate an ACS. Therefore, a normal stress test does not necessarily exclude the possibility of CAD and risk for MI. The prevention of MI should focus on reducing the chance of plaque rupture by controlling and normalizing, as much as possible, multiple cardiac risk factors, including hypertension, uncontrolled diabetes, dyslipidemia, obesity, lack of routine exercise, a heightened inflammatory state, and smoking.
Unstable Angina/Non-ST Segment Myocardial Infarction
Patients with unstable angina or a non-ST segment MI experience a partial occlusion to coronary flow as a result of plaque rupture and thrombus formation, microembo-lization, or the release of vasoactive substances leading to localized spasm. Patients typically have severe chest pain, with rest or minimal activity, which can be of sudden onset and with no preceding warnings and likely to last for more than 20 minutes unless treated with anti-ischemic agents. These patients are at high risk of ST-segment elevation MI and sudden death. Data from the Thrombolysis in Myocardial Infarction III (TIMI-III) registry indicated that death and MI could occur in these patients at a rate of 7.3% to 18.5%, depending on the severity of their symptoms, with postin-farction angina carrying the highest risk (Sharis et al., 2002). Patients might have electrocardiographic changes to indicate ischemia, mostly ST-segment depression in contiguous leads, T-wave inversion, or pseudonormalization of T waves. However, the electrocardiogram (ECG) could also be silent. Comparing the ECG to a previous one can be very helpful for detecting subtle but significant new changes.
Patients with suspected unstable angina should be referred to the emergency department (ED) or a specialized chest pain unit as soon as possible. They should be encouraged to call 9-1-1 and not drive themselves to the ED. A complete evaluation of their chest pain, including a comprehensive physical examination and history, obtaining an ECG within 10 minutes of arrival, chest radiograph and cardiac enzymes (e.g., troponin I, creatinine kinase MB), needs to be performed. Patients should be admitted to the hospital if they have ischemia on the ECG (ST-segment deviation or new T-wave abnormalities or new left BBB), ongoing chest pain, abnormal cardiac bio-markers, or develop CHF or hemodynamic instability.
Abnormal cardiac enzymes allow a definite diagnosis of MI. The most frequently used cardiac markers are myoglobin, creatinine kinase (CK) and CK-MB fractions, troponins T (TT) and I (TI). Myoglobin becomes abnormal in the first 1 to 2 hours following myocardial necrosis and remains abnormal for at least 7 to 12 hours. Its sensitivity is high for myocardial injury (83% within 6 hours of symptom onset), but it has a lower specificity. A positive myoglobin can result from muscle trauma, muscle disorders, rigorous exercise, and certain drugs such as statins. A more sensitive and specific marker than myoglobin is CK and its cardiac isoform CK-MB. This marker is 90% accurate for the diagnosis of MI at 6 hours from symptom onset. CK reaches its peak at about 24 hours of symptom onset and returns to normal or near normal by 72 hours. Troponin I is a very sensitive test for the diagnosis of MI at about 10 to 14 hours after onset of chest pain. Its sensitivity and specificity at 6 hours are approximately 58% and 94%, respectively, and 92% and 95% at 10 hours. TI levels remain abnormal for several days after myocardial injury.
Box 27-4 High-Risk Indicators in Patients with Unstable Angina*
1. New or presumably new ST-segment depression
2. Elevated troponin T or troponin I
3. Recurrent angina at rest or low level despite intense medical therapy
4. Reduced left ventricular function (ejection fraction <40%)
5. Recurrent angina or ischemia with congestive heart failure symptoms
6. Sustained ventricular arrhythmias
7. Hemodynamic instability
8. Recent history of coronary angioplasty or bypass surgery (past 6 months)
9. High risk based on noninvasive stress testing
*Level of evidence A, ACC/AHA guidelines (Braunwald, 2002).
Depending on the time of onset of chest pain, these markers have different levels of utility in the diagnosis of MI. For example, the diagnosis of MI in a patient who had chest pain more than 48 hours after presentation is best made with TI, whereas a recent onset MI of less than 6 hours' duration can best be made with myoglobin, CK and CK-MB. A negative TI after 12 hours of chest pain indicates a low risk for a cardiac event in the immediate future (<1 month). Therefore, patients who present with chest pain and have a negative TI at 12 hours after onset of chest pain can undergo a stress test either in the ED or as an outpatient, as long as the test has been scheduled within a few days of discharge.
Patients with suspected unstable angina/non-ST segment MI benefit significantly from an early aggressive therapy with angiography and revascularization, particularly when early high-risk indicators exist (Box 27-4).
The Treat Angina with Aggrastat and Determine Cost of Therapy with an Invasive or Conservative Strategy (TACTICS TIMI-18) study randomized unstable angina/non-ST elevation MI patients to an early aggressive therapy with revascu-larization (within 48 hours of presentation) versus an early conservative therapy in which patients were treated medically and then risk-stratified with exercise stress testing (Cannon et al., 2001). A significant reduction in the primary combined end point of death, MI, and rehospitalization for ACS was noted at 6 months (odds ratio [OR] 0.78, 95% CI [0.62, 0.97], p = 0.025). Other high-risk features include advanced age (>70), history of vascular disease, diabetes, and elevated hsCRP, WBC count, and B-type natriuretic peptide (BNP). Furthermore, based on data for the TIMI11B trial (1999), Antman and co-workers (2000) predicted that the risk of death, reinfarction, or recurrent severe ischemia requiring revascularization increased from 5% to 41% depending on the sum of the following individual prognostic variables: age greater than 65 years, more than three coronary risk factors, prior angiographic coronary obstruction, ST-segment deviation, more than two angina events within 24 hours, use of aspirin within 7 days, and elevated cardiac markers.
Although most unstable coronary syndromes are caused by plaque rupture, thrombosis, and superimposed spasm, rapidly progressive plaques can infrequently lead to an unstable syndrome. In addition, unstable angina can be precipitated by secondary causes such as thyrotoxicosis, severe
Box 27-5 Acute Pharmacologic Therapy of Unstable Angina/ Non-ST Elevation Myocardial Infarction*
1. Aspirin (or clopidogrel in patients who cannot take aspirin) should be administered as soon as possible after onset of symptoms and continued indefinitely.
2. Clopidogrel should be added to aspirin in the hospitalized patient and continued for a least 1 month whether patient will be undergoing percutaneous intervention or treated conservatively. Continuing clopidogrel and aspirin for up to 9 months is based on Level B evidence.
3. Antithrombin therapy with unfractionated heparin or low-molecular-weight heparin (preferred over unfractionated heparin unless bypass surgery is planned within 24 hours) should be started with clopidogrel and aspirin.
4. Gpllb/IIIa inhibitors should be added to aspirin, clopidogrel, and antithrombin in patients with planned revascularization, or those with no planned revascularization but who are undergoing ischemia or having abnormal cardiac biomarkers. However, abciximab should be avoided in patients with no planned revascularization.
5. Fibrinolytics are contraindicated in patients with unstable angina or non-ST segment elevation myocardial infarction.
*Level of evidence A, ACC/AHA guidelines (Braunwald, 2002)
hypertension or valvular stenosis, tachycardia, anemia, hypotension, and hypoxia.
Pharmacologic management of the patient with unstable angina or non-ST segment MI can be divided into acute and chronic therapy. In the acute phase (Box 27-5), patients are typically treated with an antithrombin drug (unfractionated heparin or low-molecular-weight heparin), upstream use of intravenous (IV) GP2b/3a inhibitors such as tirofiban (Aggrastat) or eptifibatide (Integrilin) (upstream use of the monoclonal antibody abciximab should be discouraged unless patients are brought to the cardiac catheterization laboratory within few hours of starting this drug, because the resurfacing of GP2b/3a receptors occurs with prolonged infusion of abciximab leading to partial loss of its antiplatelet effect), aspirin, clopidogrel, beta blockers, statins, IV nitrate therapy, ACE inhibitors (in patients with left ventricular dysfunction and continued hypertension or in diabetic patients) and supplemental oxygen therapy (in patients with respiratory distress and hypoxemia).
Low-molecular-weight heparin (LMWH; e.g., enoxapa-rin or Lovenox) has been shown to have some advantages over unfractionated heparin (UFH). These include more reliable anticoagulation with predictable pharmacokinetics, resistance to inhibition by platelet factor 4, a lower risk of causing heparin-induced thrombocytopenia (HIT), greater anti-Xa activity, and possibly greater efficacy in reducing risk for ACS. In the Efficacy and Safety of Subcutaneous Enoxapa-rin in Non-Q-Wave Coronary Events (ESSENCE) trial, enoxa-parin plus aspirin was more effective than UFH plus aspirin in reducing the incidence of the combined end points of death, myocardial infarction, and recurrent angina (19.8% vs. 23.3%, respectively; p = 0.016) in patients with unstable angina or non-Q-wave MI at 1 month of follow-up (Cohen et al., 1997). A recent meta-analysis of 22,000 patients also demonstrated that enoxaparin is more effective than UFH in preventing the combined end point of death or MI (Petersen et al., 2004). Currently, enoxaparin, 1 mg/kg subcutane-ously twice daily, is preferred over UFH (70 U/kg bolus IV, then 1000 U/hr adjusted every 6 hours with PTT checks) in patients who present with unstable angina or non-ST segment elevation MI.
Continued chest pain in patients with unstable angina despite optimal medical therapy indicates that the patient should be brought to the cardiac catheterization laboratory for immediate angiography and revascularization to minimize the chance of irreversible myocardial damage and loss of function. As previously noted, even in the pain-free patient with high-risk features, an aggressive approach to therapy is indicated and needs to be implemented within 48 hours of symptom onset. Morphine sulfate can be used to treat the acute pain unresponsive to anti-ischemic therapy.
Optimal antiplatelet treatment is needed with antithrom-bin drugs in the management of the patient with an ACS. Vascular injury leads to platelet activation and aggregation with subsequent fibrin deposition and thrombosis. Anti-thrombin therapy alone without optimal platelet inhibition leads to an inferior outcome during percutaneous coronary intervention (PCI). Early experience with PCI was performed with UFH in patients pretreated with aspirin. Aspirin is only partially effective as an antiplatelet drug by inhibiting cyclo-oxygenase and therefore partially blocking thromboxane A2 and collagen-mediated platelet activation and aggregation (Shammas et al., 2005). Platelet inhibition with clopi-dogrel (Plavix) is dose and time dependent. After a single 400-mg dose of clopidogrel, maximum platelet inhibition is achieved in 2 to 5 hours. In contrast, clopidogrel at 75 mg daily requires 3 to 7 days to reach the same level of inhibition. Blocking the ADP receptor irreversibly with clopidogrel has become an important step before PCI to reduce intermediate and long-term cardiac events. In the Clopidogrel for the Reduction of Events during Observation (CREDO) study, pretreatment of patients with clopidogrel (300 mg) at least 15 hours preintervention reduced long-term adverse events (Steinhubl et al., 2002). In the ISAR-REACT trial, pretreatment with clopidogrel (600 mg) provided similar outcomes in low-risk to intermediate-risk patients, regardless of assignment to abciximab or placebo, with maximum antiplatelet effect seen within 2 to 3 hours of treatment before intervention (Kandzari et al., 2004). In the Antiplatelet Therapy for Reduction of Myocardial Damage during Angioplasty (ARMYDA-2) study, clopidogrel at 600 mg was more effective in reducing cardiac events than clopidogrel at 300 mg when given at a mean of 6 hours before PCI in both arms (Patti et al., 2005). ARMYDA-2 also did not exclude patients from receiving GPIIb/IIIa inhibitors, thereby also supporting the hypothesis that optimal ADP receptor antagonism before PCI might be essential even when intraprocedural inhibition of platelet aggregation is achieved with GpIIb/IIIa inhibitors.
Currently, clopidogrel is given to all patients with an ACS immediately on presentation at an oral loading dose of 300 mg, then 75 mg daily. If a patient is proceeding to the cardiac catheterization laboratory and has not been receiving clopidogrel, a total of 600 mg as a loading dose should be administered.
In the chronic phase, typically following a revascularization procedure, the mainstay of therapy is aspirin, clopidogrel for 9 to 12 months, statins, ACE inhibitors, and beta blockade.
The Heart Outcomes Prevention Evaluation (HOPE) trial showed that ramipril (10 mg daily) reduced cardiovascular events significantly, including cardiovascular and total mortality and strokes (Yusuf et al., 2000). Patients were 55 years or older, and the majority had a history of vascular disease (80% history of CAD and 42% with PAD). Similar data were seen in the European Trial on Reduction of Cardiac Events with Perindopril in Stable CAD (EUROPA), which included 13655 patients with previous MI (64%), angiographic evidence of CAD (61%), coronary revascularization (55%), or a positive stress test only (5%). The mean age was 60 years, and patients had no CHF and stable CAD (Fox, 2003). In this study, 10% of placebo and 8% of perindopril (8 mg once daily) patients experienced the combined primary end point of cardiovascular death, MI, or cardiac arrest (20% RR reduction; p = 0.0003; favoring perindopril therapy) at a mean follow-up of 4.2 years.
Patients will also need to quit smoking, exercise, adhere to a low-fat, low-carbohydrate diet, lose weight if obese, and if diabetic, achieve aggressive control of their blood sugar to keep their HbA1c less than 7% and preferably less than 6.5%.
Aspirin (75-324 mg daily) or clopidogrel (75 mg daily, in patients with intolerance or hypersensitivity to aspirin), lipid-lowering drugs, and diet are recommended in patients with low-density lipoprotein greater than 130 mg/dL (or LDL >100 mg/dL) (ACC/ AHA guidelines) (SOR: B).
ACE inhibitors in patients with left ventricular dysfunction (ejection fraction <40%), congestive heart failure, hypertension, or diabetes should be initiated in those with unstable coronary syndromes (ACC/AHA guidelines) (SOR: A).
ST-segment elevation MI (STEMI) occurs secondary to a sudden interruption of coronary blood supply to a part of the myocardium as a result of a complete thrombotic occlusion of a coronary artery (DeWood et al., 1980). Plaque rupture is the predominant mechanism of STEMI with subsequent platelet and fibrin deposition. It is estimated that half a million STEMIs occur in the United States every year (Fig. 27-10).
Emergent and complete revascularization is the most important goal in the acute STEMI therapy. Current guidelines indicate that a patient with symptoms and signs of STEMI should receive either thrombolytics within 30 minutes or angioplasty within 90 minutes of arrival to the ED (Antman et al., 2004). Based on a hospital multidisciplinary protocol preapproved by the cardiologists, ED physicians, primary care physicians, and allied health care professionals, the ED physician generally decides on the choice of therapy. Currently, angioplasty is considered the first choice because it leads to overall superior results (Magid et al., 2000), primarily reducing the rate of nonfatal MI, and fewer intracra-nial bleeds compared to thrombolysis. Stronger evidence exists for primary angioplasty in STEMI as the risk of fibrinolysis increases (Kent et al., 2002). Patients with cardiogenic shock or severe CHF benefit more from primary angioplasty (Hochman, 2001; Wu et al., 2002). To be effective, however, angioplasty should be performed in intermediate- and
high-volume centers with an experienced catheterization team and interventional cardiologists on call and an multi-disciplinary-approved hospital process (Canto et al., 2000). This MI "alert system" should be capable of effectively mobilizing all resources available to stay within the 90-minute period to first balloon inflation from arrival to the ED. Centers that do not have primary angioplasty capabilities should use fibrinolytic therapy as first-line therapy in STEMI. Box 27-6 lists contraindications to fibrinolysis.
Thrombolytic therapy has been shown to reduce mortality in patients with STEMI. Thrombolytics are contraindicated in patients with non-ST elevation MI because no clinical benefit has been shown and unwarranted risks exist. Thrombolysis enhances the bod/ s fibrinolytic system by accelerating the formation of plasmin from plasminogen (Shammas, 1993). Plasmin degrades fibrin and several plasma proteins, including fibrinogen, prothrombin, and factors V and VIII, leading to a defective hemostasis. Thrombolytic agents are classified as clot-specific (alteplase [tPA], reteplase [recombinant-PA], and tenecteplase [TNK-tPA]) or non-clot-specific (streptokinase [SK], urokinase [UK], and anisoylated plasminogen activator complex [APSAC]). Clot-specific thrombolytics activate plasminogen at the site of the clot, whereas non-clot-specific ones act by generalized systemic lysis. In the United States, clot-specific thrombolytics are most often used (Table 27-8).
On arrival to the ED, patients with chest pain should have an ECG done within 10 minutes. If the ECG does not show ST-segment elevation, it is strongly advised that it be repeated within 5 to 10 minutes in patients with continued chest pain to rule out late appearance STEMI. It should be noted that ST-segment depression in the anterior leads with early precordial transition could indicate ST elevation posterior wall MI, particularly if associated with ST elevation in the inferior leads (inferoposterior MI). Right-sided precordial leads can be helpful in patients with acute inferior wall MI to
Box 27-6 Contraindication to Fibrinolytic Therapy*
1. History of intracranial hemorrhage
2. Known intracranial neoplasm or vascular lesions
3. Active bleeding or known bleeding disorder (exclude menses)
4. Embolic stroke within 3 months (exception: embolic stroke within 3 hours)
5. Suspected aortic dissection
6. Significant facial or head trauma within 3 months
1. Uncontrolled severe hypertension (> 180 systolic, > 110 diastolic)
2. Prolonged CPR (> 10 minutes) or recent surgery (<3 weeks) or noncompressible vascular puncture
3. Recent internal bleeding or active peptic ulcer disease
5. Currently anticoagulated with high INR
6. For streptokinase; prior exposure to the drug or history of allergic reaction
*ACC/AHA guidelines (Antman, 2004).
CPR, Cardiopulmonary resuscitation; INR, international normalized ratio.
determine right ventricular involvement (ST elevation will be seen in the right precordial leads) (Fig. 27-11).
Patients with STEMI should receive supplemental oxygen therapy, morphine sulfate for pain control, IV nitrate therapy if they are not hypotensive and have not ingested a phosphodiesterase inhibitor for erectile dysfunction, 162 mg of chew-able aspirin, statins, ACE inhibitors (particularly in patients with CHF, reduced left ventricular function, hypertension, or diabetes), and clopidogrel (Box 27-7).
Hemodynamic instability should be aggressively treated with pressor agents, typically dopamine started at 5 \ig/kg/ min and titrated every 5 minutes to keep the systolic pressure above 90 mm Hg. Normal saline fluid boluses can be helpful, particularly in the inferoposterior MI patient with right-sided involvement. In these patients, bradycardia also needs to be aggressively treated if associated with hypotension,
1.5 million IU
Watch for hypotension,
Give infusion over
bleeding, and stroke.
Give second dose of 10 U IV 30 minutes after first dose if no complications.
Watch for intracranial hemorrhage, arrhythmia, and hemorrhage.
Activase 15-mg bolus IV, then 0.75 mg/Kg (max 50 mg) over 30 minutes, then 0.5 mg/Kg (max 35 mg) over 60 minutes; give with heparin.
Watch for intracranial hemorrhage, arrhythmia, severe bleeding, and anaphylaxis.
Activase 15-mg bolus IV, then 0.75 mg/Kg (max 50 mg) over 30 minutes, then 0.5 mg/Kg (max 35 mg) over 60 minutes; give with heparin.
Tenecteplase Weight <60 kg: 30 Watch for intracranial mg IV, max 50 mg bleeding, anaphylaxis, and
Wt 60-69 kg: 35 mg reperfusion arrhythmias.
IV, max 50 mg using either atropine (1 mg IV, can repeat twice) or a temporary pacemaker if there is inadequate response to atropine. Patients with right ventricular involvement usually respond well to a fluid challenge, correcting the bradycardia, administering dopamine, and maintaining sinus rhythm as they rely on a normal atrial kick for increasing their end-diastolic volume and cardiac output. If hypotension does not respond well to these conservative measures, patients need to have an intra-aortic balloon pump inserted. Typically, these patients should be brought emergently to the cardiac catheterization laboratory for more definitive management because their mortality is excessively high without immediate revascular-ization (Hochman et al., 2001).
The long-term management of these patients is similar to the unstable angina/non-ST elevation MI, with aggressive preventive measures and continued long-term aspirin, beta blockers, ACE inhibitors, statins, exercise, and low-fat diet. Smoking cessation, control of hypertension and diabetes, and achieving ideal body weight are paramount to prevent further progression of disease and MI. Preferably, clopidogrel needs to be continued for 12 months irrespective of whether the patient received a revascularization procedure with drug-eluting stents or was conservatively managed.
Prasugrel (Effient) is a new ADP-receptor antagonist, recently approved by the U.S. Food and Drug Administration (FDA) to treat ACS patients after coronary angioplasty. In the landmark Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel (TRITON-TIMI-38), in patients with acute coronary syndrome (unstable angina, non-ST elevation MI, and STEMI), prasugrel reduced the combined end point of death from cardiovascular causes, nonfatal MI, or nonfatal stroke at 450 days by 19% compared to clopidogrel (12.1% vs. 9.9%, p <0.001). Acute stent thrombosis was also reduced by 52% using prasugrel compared to clopidogrel (p <0.001) during the same time frame. Major bleeding, however, was increased with prasugrel (2.4% vs. 1.8%, p = 0.03) compared to clopidogrel, including life-threatening bleed (1.4% vs. 0.9%, p = 0.01) and fatal bleed (0.4% vs. 0.1%, p = 0.002). The net clinical benefit, however, favored prasugrel over clopidogrel for the combined end point of all-cause death, nonfatal MI,
Watch for intracranial hemorrhage, arrhythmia, severe bleeding, and anaphylaxis.
Box 27-7 Acute and Secondary Pharmacologic Therapy of ST Elevation Myocardial Infarction (STEMI)*
Acute Pharmacologic Therapy
1. Chewable aspirin (162 mg) in patients not previously taking aspirin.
2. Intravenous (IV) beta blockers should not be administered to STEMI patients who have (a) signs of heart failure, (b) evidence of a low-output state, (c) increased risk for cardiogenic shock, or (d) other relative contraindications to beta blockade (P-R interval >0.24 second; second-degree or third-degree heart block; active asthma; or reactive airway disease).
3. STEMI patients presenting to a hospital with percutaneous coronary intervention (PCI) capability should be treated with primary PCI within 90 minutes of first medical contact as a systems goal.
4. STEMI patients presenting to a hospital without PCI capability and who cannot be transferred to a PCI center and undergo PCI within 90 minutes of first medical contact should be treated with fibrinolytic therapy within 30 minutes of hospital presentation as a systems goal unless fibrinolytic therapy is contraindicated (Level B).
5. In the absence of arrhythmias, IV magnesium should not be administered.
6. For patients with BP of 140/90 mm Hg or greater (or >130/80 mm Hg for patients with diabetes or chronic kidney disease), it is useful as tolerated, to add BP medication, treating initially with beta blockers and/or ACE inhibitors, with the addition of other drugs such as thiazides as needed to achieve goal BP.
7. A fasting lipid profile should be assessed in all patients and within 24 hours of hospitalization for those with an acute cardiovascular or coronary event. For hospitalized patients, initiation of lipid-low-ering medication is indicated as recommended before discharge. LDL-C should be less than 100 mg/dL.
8. If baseline LDL-C is 100 mg/dL or greater, LDL-lowering drug therapy should be initiated.
9. If on-treatment LDL-C is 100 mg/dL or greater, intensifying LDL-lowering drug therapy (may require LDL-lowering drug combination) is recommended.
10. Managing warfarin to INR of 2.0 to 3.0 for paroxysmal or chronic atrial fibrillation or flutter is recommended, and in post-MI patients when clinically indicated (e.g., atrial fibrillation, left ventricular thrombus).
11. ACE inhibitors should be started and continued indefinitely in all patients recovering from STEMI with left ventricular ejection fraction (LVEF) of 40% or less and for those with hypertension, diabetes, or chronic kidney disease, unless contraindicated.
12. Use of angiotensin receptor blockers (ARBs) is recommended in patients who are intolerant of ACE inhibitors and have heart failure (HF) or have had an MI (LVEF <40%).
13. It is beneficial to start and continue beta-blocker therapy indefinitely in all patients who have had MI, acute coronary syndrome (ACS), or LV dysfunction with or without HF symptoms, unless contraindicated.
*Level of evidence A. From Antman EM, Anbe DT, Armstrong PW, et al. ACC/ AHA guidelines for the management of patients with ST-elevation myocardial infarction—executive summary: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1999 guidelines for the management of patients with acute myocardial infarction). J Am Coll Cardiol 2004;44:671-719. Focused Update 2007. J Am Coll Cardiol 2008;51:210-247.
nonfatal stroke, and non-CABG TIMI major bleed (12.2% vs. 13.9%, p = 0.004). Physicians using prasugrel need to weigh its risks and benefits as they decide which drug to use when treating patients (Wiviott et al., 2007).
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