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Medication

Medication Summary

Medications that provide symptomatic relief but have not been found to have an effect on long-term major events include nitrates, diltiazem or verapamil, and heparin. Medications that have been convincingly shown to reduce short- or long-term adverse events are as follows:

Aspirin
Clopidogrel
P2Y12 inhibitors
Lipid-lowering agents (statins)
Glycoprotein (GP) IIb/IIIa antagonists
Beta-adrenergic blocking agents
Angiotensin-converting enzyme (ACE) inhibitors
Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors

Class Summary

Antiplatelet agents prevent the formation of thrombi associated with myocardial infarction (MI) and inhibit platelet function by blocking aggregation. Antiplatelet therapy has been shown to reduce mortality by reducing the risk of fatal MIs, fatal strokes, and vascular death.

Aspirin (Anacin, Bayer Buffered Aspirin, Ecotrin)

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Aspirin prevents the formation of thrombi associated with MI and inhibits platelet function by blocking aggregation. Antiplatelet therapy has been shown to reduce mortality by reducing the risk of fatal MIs, fatal strokes, and vascular death.

Clopidogrel (Plavix)

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Clopidogrel selectively inhibits adenosine diphosphate (ADP) binding to platelet receptors and subsequent ADP-mediated activation of GP llb/llla complex, thereby inhibiting platelet aggregation. This agent is used as an alternative to aspirin or in addition to aspirin after coronary stenting.

Ticagrelor (Brilinta)

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Ticagrelor and its major metabolite reversibly interact with the platelet P2Y12 ADP-receptor to prevent signal transduction and platelet activation. This agent is indicated to reduce the rate of thrombotic cardiovascular events in patients with acute coronary syndrome (ACS)—that is, unstable angina, non-ST elevation MI (NSTEMI), or ST-elevation MI (STEMI). It also reduces the rate of stent thrombosis in patients who have undergone stent placement for treatment of ACS, and is indicated in patients with a history of MI more than 1 year previously. Patients can be transitioned from clopidogrel to ticagrelor without interruption of the antiplatelet effect.

Class Summary

Lipid lowering agents, specifically the HMG-CoA reductase inhibitors, also known as the statins, are used to treat hypercholesterolemia; they are highly efficacious and very well tolerated. The statins are highly effective in reducing low-density lipoprotein cholesterol (LDL-C), total cholesterol, and triglycerides, and they also increase high-density lipoprotein cholesterol (HDL-C) levels.

Simvastatin (Zocor)

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Simvastatin inhibits HMG-CoA reductase, and this, in turn, inhibits cholesterol synthesis and increases cholesterol metabolism. This agent is used to decrease increased cholesterol levels associated with nephrotic syndrome.

Atorvastatin (Lipitor)

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Atorvastatin can provide up to 60% reduction in LDL-C. It inhibits HMG-CoA reductase, thereby inhibiting cholesterol synthesis and increasing cholesterol metabolism. The half-life of atorvastatin and its active metabolites is longer than those of all the other statins (ie, approximately 48 hours, as opposed to 3-4 hours). Atorvastatin is one of the most extensively studied statins, and many long term evidence-based medicine trials support its benefits.

Pitavastatin (Livalo)

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Pitavastatin is an HMG-CoA reductase inhibitor (statin) indicated for primary or mixed hyperlipidemia. In clinical trials, pitavastatin 2 mg/day achieved reductions in total cholesterol and LDL-C similar to those seen with atorvastatin 10 mg/day and simvastatin 20 mg/day.

Pravastatin (Pravachol)

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Pravastatin competitively inhibits HMG-CoA reductase, which catalyzes the rate-limiting step in cholesterol synthesis. This agent is a good alternative if other statins are not tolerated.

Class Summary

Over the last decade, inhibition of proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a promising target to reduce residual cardiovascular disease risk. PCSK9 is a protein that binds to low-density lipoprotein (LDL) receptors (LDLR) to promote their degradation. Monoclonal antibodies inhibit PCSK9 and thus prevent LDLR degradation. This action will increase the number of LDLRs and subsequently increase the clearance of LDL, ultimately lowering LDL-C levels.

In December 2017, the FDA approved the first PCSK9 inhibitor, evolocumab (Repatha), for the prevention of strokes, heart attacks, and coronary revascularizations.^[88]The approval was based on data from the evolocumab cardiovascular outcomes study (FOURIER). In the FOURIER clinical trial, evolocumab demonstrated significant benefits for 27,564 patients with established cardiovascular disease. The study revealed that when used in addition to optimized statin therapy, evolocumab reduced the risk of heart attack by 27%, the risk of stroke by 21%, and the risk of coronary revascularization by 22%. In addition, evolocumab showed a statistically significant 15% reduction in the risk of the primary composite endpoint, which included hospitalization for unstable angina, coronary revascularization, heart attack, stroke, or cardiovascular death.^[81]

In April 2019, the FDA expanded the indication for alirocumab (Praluent) to include risk reduction of MI, stroke, and unstable angina requiring hospitalization in adults with established cardiovascular disease.^[89]Approval was based on the ODYSSEY OUTCOMES trial (N=18,924) in patients with elevated LDL-C despite treatment with maximally tolerated statins. Patients who received injections of alirocumab 75 mg or 150 mg every other week achieved reduction in the risk for major cardiovascular events by 15% and all-cause death by 15% at a median follow-up of 2.8 years compared with those who received placebo.^[82]

Evolocumab (Repatha)

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Human monoclonal IgG2 directed against PCSK9. Evolocumab binds to PCSK9 and inhibits circulating PCSK9 from binding to the LDLR, preventing PCSK9-mediated LDLR degradation and permitting LDLR to recycle back to the liver cell surface. By inhibiting the binding of PCSK9 to LDLR, evolocumab increases the number of LDLRs available to clear LDL from the blood, thereby lowering LDL-C levels.

Alirocumab (Praluent)

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Monoclonal antibody that binds to PCSK9. LDL-C is cleared from the circulation preferentially through the LDL receptor (LDLR) pathway. PCSK9 is a serine protease that destroys LDLR in the liver, resulting in decreased LDL-C clearance and increased plasma LDL-C.

Class Summary

Specific cardiovascular antiplatelet agents work via GP IIb/IIIa receptor antagonists to reversibly prevent fibrinogen, von Willebrand factor (vWF), and other adhesion ligands from binding to the GP IIb/IIIa receptor, thereby inhibiting platelet aggregation. Up to 80,000 copies of these integrins on the platelet cell surface serve as ligands for fibrinogen cross-linkage, the final common pathway for platelet aggregation and thrombus formation, even under arterial shear stress conditions.

Tirofiban (Aggrastat)

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Tirofiban is a nonpeptide antagonist of the platelet GP IIb/IIIa receptor; it reversibly prevents vWF, fibrinogen, and other adhesion ligands from binding to the receptor, thus inhibiting platelet aggregation. Effects persist over the duration of maintenance infusion and are reversed after the infusion ends. Tirofiban is approved by the US Food and Drug Administration (FDA) to reduce the rate of thrombotic cardiovascular events (combined endpoint of death, myocardial infarction, or refractory ischemia/repeat cardiac procedure) in patients with non-ST elevation acute coronary syndrome (NSTE-ACS).

Eptifibatide (Integrilin)

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Eptifibatide is a cyclic heptapeptide antagonist of the platelet GP IIb/IIIa receptor; its effects are the same as those of tirofiban. This agent has been approved by the FDA for use in combination with heparin for patients with ACS, patients who are being managed medically, and patients undergoing PCI.

Abciximab (ReoPro)

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Abciximab is a chimeric human-murine monoclonal antibody approved for use in elective, urgent, and emergency PCI. Abciximab binds to receptors with high affinity and reduces platelet aggregation by 80% for up to 48 hours following infusion.

Class Summary

Selective beta1-adrenergic blocking agents limit heart rate, reduce blood pressure, and exert antiarrhythmic effects by targeting beta1 receptor sites. All beta-adrenergic blocking agents thus decrease myocardial oxygen demand and oppose the effects of elevated catecholamines. Infrequent situations in which beta-blocker therapy should be avoided in patients with unstable angina include nonischemic exacerbation of heart failure, cocaine-induced coronary vasoconstriction, and vasospastic angina.

Atenolol (Tenormin)

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Atenolol (Tenormin)

Atenolol blocks beta1 receptors but has little or no effect on beta2 types. Beta blockers affect blood pressure via multiple mechanisms, including a negative chronotropic effect that decreases heart rate at rest and after exercise, a negative inotropic effect that decreases cardiac output, reduction of sympathetic outflow from the central nervous system (CNS), and suppression of renin release. Atenolol improves and preserves hemodynamic status by acting on myocardial contractility, reducing congestion, and decreasing myocardial energy expenditure.

Metoprolol (Lopressor, Toprol XL)

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Metoprolol is a selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions. During intravenous (IV) administration, carefully monitor blood pressure, heart rate, and the electrocardiogram (ECG).

Class Summary

Esmolol acts as a beta-adrenergic blocking agent to limit heart rate and reduces blood pressure by selectively targeting beta1 receptor sites; this drug also has class II antiarrhythmic properties. All beta-adrenergic blocking agents decrease myocardial oxygen demand and oppose the effects of elevated catecholamines. Infrequent situations in which beta-blocker therapy should be avoided in patients with unstable angina include nonischemic exacerbation of heart failure, cocaine-induced coronary vasoconstriction, and vasospastic angina.

Esmolol (Brevibloc)

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Esmolol has been shown to reduce episodes of chest pain and clinical cardiac events. Its very short half-life (8 minutes) allows a large degree of dosing flexibility, so that its cardiovascular benefits are comparable to those of oral propranolol, yet its adverse effects can be managed promptly. Esmolol is particularly useful for patients at risk for complications with beta blockade (eg, reactive airway disease or chronic obstructive pulmonary disease [COPD], severe bradycardia, or poor left ventricular function).

Class Summary

Nadolol is a nonselective beta-adrenergic blocking agent that limits heart rate, reduces blood pressure, and have antiarrhythmic properties. All beta-adrenergic blocking agents thus decrease myocardial oxygen demand and oppose the effects of elevated catecholamines. Infrequent situations in which beta-blocker therapy should be avoided in patients with unstable angina include nonischemic exacerbation of heart failure, cocaine-induced coronary vasoconstriction, and vasospastic angina.

Nadolol (Corgard)

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Nadolol competitively blocks beta1 and beta2 receptors. It does not exhibit membrane-stabilizing activity or intrinsic sympathomimetic activity.

Class Summary

Propranolol is a beta blocker that limits heart rate and reduces blood pressure by nonselectively targeting beta receptor sites; it also has class II antiarrhythmic properties. All beta-adrenergic blocking agents thus decrease myocardial oxygen demand and oppose the effects of elevated catecholamines. Infrequent situations in which beta-blocker therapy should be avoided in patients with unstable angina include nonischemic exacerbation of heart failure, cocaine-induced coronary vasoconstriction, and vasospastic angina.

Propranolol (Inderal)

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Propranolol is a nonselective beta blocker that is lipophilic (ie, penetrates the CNS). Although it is generally a short-acting agent, long-acting preparations are also available.

Class Summary

Thrombin, the end product of the coagulation mechanism, initiates transformation of fibrinogen to a fibrin clot and activates platelets. Its antagonist, antithrombin III, is the major endogenous inhibitor of the coagulation cascade and is the essential cofactor for heparin.

Heparin

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Heparin catalyzes the effect of antithrombin III on coagulative proteinases (eg, factors II, XII, XI, IX, and X, along with tissue factor VIIa). It prevents clot reaccumulation after endogenous fibrinolysis. When unfractionated heparin (UFH) is used, the activated partial thromboplastin time (aPTT) should not be checked until 6 hours after the initial heparin bolus.

Class Summary

Low-molecular-weight heparin (LMWH) represents an anticoagulation option for unstable angina. The many potential benefits of using LMWH include lower rates of bleeding, cost savings, and reduced incidence of heparin-induced thrombocytopenia (HIT). LMWH is prepared by selectively treating UFH to isolate the low-molecular-weight (< 9 kDa) fragments. Its activity is measured in units of factor X inactivation; monitoring of aPTT is not required, and the dose is weight-adjusted.

Enoxaparin (Lovenox)

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Enoxaparin (Lovenox)

Enoxaparin is the only LMWH now approved by the FDA for treatment of and prophylaxis for deep venous thrombosis and pulmonary embolism. LMWH has been widely used in pregnancy, although clinical trials are not yet available to demonstrate that it is as safe as UFH. Except in overdoses, checking the prothrombin time (PT) or aPTT is not useful, because aPTT does not correlate with the anticoagulant effect of fractionated LMWH.

Dalteparin (Fragmin)

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Dalteparin enhances inhibition of factor Xa and thrombin by increasing antithrombin III activity. In addition, it preferentially increases inhibition of factor Xa. Except in overdoses, checking PT or aPTT is not useful, because aPTT does not correlate with the anticoagulant effect of fractionated LMWH. The average duration of treatment is 7-14 days.

Tinzaparin (Innohep)

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Tinzaparin enhances inhibition of factor Xa and thrombin by increasing antithrombin III activity. In addition, it preferentially increases inhibition of factor Xa. Average duration of treatment is 7-14 days.

Class Summary

Angiotensin-converting enzyme (ACE) inhibitors reduce angiotensin II levels, thus decreasing aldosterone secretion. They are of particular benefit in patients with large anterior infarctions, especially those with compromised left ventricular function (eg, from STEMI) but without hypotension. The benefit in patients with unstable angina is less clear. Currently, ACE inhibitors are recommended in patients with left ventricular dysfunction or congestive heart failure, diabetes, and hypertension.

Captopril (Capoten)

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Captopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

Lisinopril (Zestril)

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Lisinopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Enalapril (Vasotec)

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Enalapril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. This agent helps to control blood pressure and proteinuria.

Enalapril decreases pulmonary-to-systemic flow ratio in the catheterization laboratory and increases systemic blood flow in patients with relatively low pulmonary vascular resistance. It has a favorable clinical effect when administered over a long period. Enalapril helps to prevent potassium loss in the distal tubules. The body conserves potassium; thus, less oral potassium supplementation is needed.

Ramipril (Altace)

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Ramipril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Class Summary

Direct thrombin inhibitors, such as hirudin, lepirudin (recombinant hirudin), and bivalirudin, are potential alternatives to heparin. Their advantages over heparin are efficacy against clot-bound thrombin, resistance to inactivation by platelet factor 4 and thrombospondin, and nondependence on antithrombin III pathways. Although direct thrombin inhibitors should not be routinely used in the treatment of unstable angina, they may be of clinical benefit in special circumstances, such as HIT.

Bivalirudin (Angiomax)

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Bivalirudin is a synthetic analogue of recombinant hirudin. It is used for anticoagulation in patients with unstable angina undergoing percutaneous transluminal coronary angioplasty (PTCA).

With provisional use of an GP IIb/IIIa inhibitor, bivalirudin is indicated for use as an anticoagulant in patients undergoing PCI. Its potential advantages over conventional heparin therapy include more predictable and precise levels of anticoagulation, activity against clot-bound thrombin, absence of natural inhibitors (eg, platelet factor 4 and heparinase), and continued efficacy after clearance from plasma (because of binding to thrombin).

Lepirudin (Refludan)

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Lepirudin is recombinant hirudin derived from yeast cells; it is a highly specific direct inhibitor of thrombin. Natural hirudin is produced in trace amounts as a family of highly homologous isopolypeptides by the leech Hirudo medicinalis. Biosynthetic lepirudin is identical to natural hirudin except for the substitution of leucine for isoleucine at the N-terminal end of the molecule and the absence of a sulfate group on the tyrosine at position 63. Lepirudin has been approved by the FDA for use in patients with HIT and associated thrombotic disease.

Desirudin (Iprivask)

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Desirudin is a selective inhibitor of free circulating and clot-bound human thrombin, with protein structures similar to those of naturally occurring hirudin (an anticoagulant present in medicinal leeches). It prolongs thrombin-dependent coagulation assays (eg, activated partial thromboplastin time [aPTT] and thrombin time [TT]).

Argatroban

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Argatroban is used as an anticoagulant for prophylaxis or treatment of thrombosis in HIT. This agent inhibits fibrin formation, platelet aggregation, and activation of coagulation factors V, VIII, and XIII, as well as protein C.

Class Summary

Nitrates are vasodilators that relieve chest discomfort (angina) by improving myocardial oxygen supply, thereby, in turn, dilating epicardial and collateral vessels and thus improving blood supply to the ischemic myocardium. Vasodilators oppose coronary artery spasm, which augments coronary blood flow and reduces cardiac work by decreasing preload and afterload.

These drugs are effective in the management of symptoms in acute MI but may reduce mortality only slightly. Nitroglycerin can be administered sublingually by tablet or spray, topically, or intravenously (IV). In acute MI, topical administration is a less desirable route because of unpredictable absorption and the onset of clinical effects.

Nitroglycerin IV

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Nitroglycerin causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. Whether administered topically, sublingually, orally, or IV, nitrates ameliorate several pathways of unstable angina and reduce the incidence of symptomatic ischemia. Nitrates lower systemic arterial pressure and decrease venous return to the heart, both of which reduce myocardial wall stress. Similarly, nitrates are excellent coronary vasodilators.

Other possible beneficial effects include a transient inhibition of platelet aggregation, an increase in coronary collateral blood flow, and a favorable redistribution of regional flow. Notably, induction of heparin resistance has been reported.

Questions

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Media Gallery

Unstable Angina. Pathogenesis of acute coronary syndromes.
Unstable Angina. Thrombolysis in Myocardial Infarction (TIMI) Risk Score correlates with major adverse outcome and effect of therapy with low-molecular-weight heparin. ARD = absolute risk difference; ESSENCE = Efficacy and Safety of Subcutaneous Enoxaparin in Non–Q-wave Coronary Events; No. = number; NNT = number needed to treat.
Unstable Angina. Algorithm for initial invasive strategy. ASA = acetylsalicylic acid (aspirin); GP IIb/IIIa= glycoprotein IIb/IIIa; IV = intravenous; LOE = level of evidence; UA/NSTEMI = unstable angina/non–ST-segment elevation myocardial infarction; UFH = unfractionated heparin. (Adapted from 2007 ACC/AHA UA/NSTEMI Guidelines.)
Unstable Angina. Algorithm for initial conservative strategy. ASA = acetylsalicylic acid (aspirin); EF = ejection fraction; GP IIb/IIIa= glycoprotein IIb/IIIa; IV = intravenous; LOE = level of evidence; LVEF = left ventricular ejection fraction; UA/NSTEMI = unstable angina/non–ST-segment elevation myocardial infarction. (Adapted from 2007 ACC/AHA UA/NSTEMI Guidelines.)
Unstable Angina. Rate and timing of revascularization for patients with unstable angina using invasive versus conservative approach (FRagmin during InStability in Coronary artery disease [FRISC] II).
Unstable Angina. Time course of elevations of serum markers after acute myocardial infarction. CK = creatine kinase; CK-MB = creatine kinase MB fraction; LDH = lactate dehydrogenase.

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Table 1. Patient Characteristics, GUARANTEE Versus CRUSADE Trials

Characteristics	GUARANTEE, 1995-96 ^[12]	CRUSADE, 2001-06 ^[13]
Mean age (y)	62	69
Patients >65 y (%)	44	–
Female (%)	39	40
Hypertension (%)	60	73
Diabetes mellitus (%)	26	33
Current smoker (%)	25	–
Hypercholesterolemia (%)	43	50
Previous stroke (%)	9	–
Previous MI (%)	36	30
Previous angina (%)	66	–
CHF (%)	14	18
Previous coronary intervention (%)	23	21
Previous coronary bypass surgery (%)	25	19
CHF = congestive heart failure; CRUSADE = Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the American College of Cardiology/American Heart Association guidelines; GUARANTEE = Global Unstable Angina Registry and Treatment Evaluation; MI = myocardial infarction.

Table 2. Demographic Characteristics of Patients in International OASIS-2 Registry

Characteristics ^[15]		Australia	Brazil	Canada	Hungary	Poland	United States
General	Number of patients	1899	1478	1626	931	1135	918
	Mean age (y)	65	62	66	65	63	66
	Women (%)	37	42	37	45	40	37
Clinical	NQMI presentation (%)	7	7	14	22	17	16
Clinical	Abnormal ECG (%)	74	91	82	95	97	87
Select treatments	Beta blocker (%)	67	53	73	67	59	57
Select treatments	Calcium blocker (%)	59	51	53	52	43	59
Invasive procedures (index hospitalization)	Cardiac catheterization (%)	24	69	43	20	7	58
	PCI (%)	7	19	16	5	0.4	24
	CABG (%)	4	20	10	7	0.4	17
CABG = coronary artery bypass grafting; ECG = electrocardiographic; NQMI = non-Q wave myocardial infarction; OASIS = Organization to Assess Strategies for Ischemic Syndromes; PCI = percutaneous coronary intervention.

Table 3. Thirty-Day Clinical Outcome in Patients With Acute Coronary Syndromes in Clinical Trials

Study	Year	Number of Patients	Death (%)	Myocardial Infarction (%)	Major Bleed (%)
TIMI-3	1994	1,473	2.5	9.0	0.3
GUSTO-IIb	1997	8,011	3.8	6.0	1.0
ESSENCE	1998	3,171	3.3	4.5	1.1
PARAGON-A	1998	2,282	3.2	10.3	4.0
PRISM	1998	3,232	3.0	4.2	0.4
PRISM-PLUS	1998	1,915	4.4	8.1	1.1
PURSUIT	1998	10,948	3.6	12.9	2.1
TIMI-11B	1999	3,910	3.9	6.0	1.3
PARAGON-B	2000	5,225	3.1	9.3	1.1
Pooled		40,167	3.5	8.5	1.5
ESSENCE = Efficacy and Safety of Subcutaneous Enoxaparin in Non–Q-wave Coronary Events; GUSTO-IIb = Global Utilization of Streptokinase and TPA (tissue plasminogen activator) for Occluded Coronary Arteries; PARAGON-A = Platelet IIb/IIIa Antagonism (lamifiban) for the Reduction of Acute Coronary Syndrome Events in a Global Organization Network; PARAGON-B = Platelet IIb/IIIa Antagonism (lamifiban) for the Reduction of Acute Coronary Syndrome Events in a Global Organization Network; PRISM = Platelet Receptor Inhibition in Ischemic Syndrome Management; PRISM-PLUS = Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Angina Signs and Symptoms; PURSUIT = Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy; TIMI-11B = Thrombolysis in Myocardial Infarction Clinical Trial 11B; TIMI-3 = Thrombolysis in Myocardial Infarction Clinical Trial 3.

Table 4. Braunwald Classification of Unstable Angina

Characteristic	Class/Category	Details
Severity	I	Symptoms with exertion
	II	Subacute symptoms at rest (2-30 days prior)
	III	Acute symptoms at rest (within prior 48 hr)
Clinical precipitating factor	A	Secondary
	B	Primary
	C	Postinfarction
Therapy during symptoms	1	No treatment
	2	Usual angina therapy
	3	Maximal therapy

Table 5. Recommendations for Selection of Preferred Management Strategy

Preferred Strategy	Patient Characteristic/Clinical Risk
Immediate Invasive Strategy (< 2 hours)	Refractory angina
	Signs/symptoms of heart failure or new or worsening mitral regurgitation
	Hemodynamic instability or cardiogenic shock
	Recurrent angina/ischemia at rest or with low-level activities despite intensive medical therapy
	Sustained ventricular tachycardia or ventricular fibrillation
Ischemia-Guided Strategy	Low-risk score (eg, TIMI 0 or 1, GRACE < 109)
	Low-risk Tn-negative female
	Patient or physician preference in the absence of high-risk features
Early Invasive Strategy (< 24 hours)	GRACE score >140
	Rise or fall in Tn compatible with myocardial infarction
	New or presumably new ST-segment depression
Delayed Invasive Strategy (24-72 hours)	Diabetes mellitus
	Renal insufficiency (GFR < 60 mL/min/1.73m²)
	Reduced LV systolic function (LVEF < 40%)
	Early postinfarction angina
	PCI within 6 months
	Prior CABG
	GRACE score 109-140; TIMI Score ≥2
ACC/AHA = American College of Cardiology/American Heart Association; CABG = coronary artery bypass grafting; GFR = glomerular filtration rate; GRACE = Global Registry of Acute Coronary Events; LV = left ventricle; LVEF = left ventricular ejection fraction; PCI = percutaneous coronary intervention; TIMI = Thrombolysis in Myocardial Infarction Clinical Trial; Tn = troponin.

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Author

Walter Tan, MD, MS Associate Professor of Medicine, Wake Forest University School of Medicine; Director of Cardiac Cath Labs, Wake Forest Baptist Medical Center

Walter Tan, MD, MS is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American Heart Association, American Stroke Association, National Stroke Association, Society for Vascular Medicine, Society of Interventional Radiology

Disclosure: Nothing to disclose.

Coauthor(s)

David J Moliterno, MD Professor of Medicine, Jefferson Morris Gill Professor of Cardiology, Chief, Division of Cardiovascular Medicine, University of Kentucky; Vice Chairman of Internal Medicine, Chandler Medical Center; Medical Director, Gill Heart Institute

David J Moliterno, MD is a member of the following medical societies: American College of Cardiology, European Society of Cardiology, Association of Professors of Cardiology, American College of Physicians, American Heart Association, American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Richard A Lange, MD, MBA President, Texas Tech University Health Sciences Center, Dean, Paul L Foster School of Medicine

Richard A Lange, MD, MBA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Association of Subspecialty Professors

Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD Associate Professor of Medicine, Director of Cardiac Catherization Laboratory and Interventional Cardiology, Mayo Clinic ArizonA

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Acknowledgements

Steven James Filby, MD Fellow in Interventional Cardiology, The Cleveland Clinic Foundation

Disclosure: Nothing to disclose.

Justin D Pearlman, MD, ME, PhD, FACC, MA Chief, Division of Cardiology, Director of Cardiology Consultative Service, Director of Cardiology Clinic Service, Director of Cardiology Non-Invasive Laboratory, Director of Cardiology Quality Program KMC, Dartmouth-Hitchcock Medical Center, Dartmouth Medical School

Justin D Pearlman, MD, ME, PhD, FACC, MA is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, International Society for Magnetic Resonance in Medicine, and Radiological Society of North America

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Unstable Angina Medication

Medication Summary

Antiplatelet agents

Class Summary

Aspirin (Anacin, Bayer Buffered Aspirin, Ecotrin)

Clopidogrel (Plavix)

Ticagrelor (Brilinta)

Lipid-Lowering Agents, Statins

Class Summary

Simvastatin (Zocor)

Atorvastatin (Lipitor)

Pitavastatin (Livalo)

Pravastatin (Pravachol)

PCSK9 Inhibitors

Class Summary

Evolocumab (Repatha)

Alirocumab (Praluent)

Antiplatelet Agent, Cardiovascular

Class Summary

Tirofiban (Aggrastat)

Eptifibatide (Integrilin)

Abciximab (ReoPro)

Beta-Blockers, Beta-1 Selective

Class Summary

Atenolol (Tenormin)

Metoprolol (Lopressor, Toprol XL)

Beta-Blockers, Beta-1 Selective; Antidysrhythmics, II

Class Summary

Esmolol (Brevibloc)

Beta-Blockers, Nonselective

Class Summary

Nadolol (Corgard)

Beta-Blockers, Nonselective; Antidysrhythmics, II

Class Summary

Propranolol (Inderal)

Anticoagulant

Class Summary

Heparin

Low Molecular Weight Heparins

Class Summary

Enoxaparin (Lovenox)

Dalteparin (Fragmin)

Tinzaparin (Innohep)

ACE Inhibitors

Class Summary

Captopril (Capoten)

Lisinopril (Zestril)

Enalapril (Vasotec)

Ramipril (Altace)

Thrombin inhibitors

Class Summary

Bivalirudin (Angiomax)

Lepirudin (Refludan)

Desirudin (Iprivask)

Argatroban

Nitrates, Angina

Class Summary

Nitroglycerin IV

References

Tables

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