Treatment of acute coronary syndromes (ACS) is designed to relieve distress, interrupt thrombosis, reverse ischemia, limit infarct size, reduce cardiac workload, and prevent and treat complications. An ACS is a medical emergency; outcome is greatly influenced by rapid diagnosis and treatment. Treatment occurs simultaneously with diagnosis. Treatment includes revascularization (with percutaneous coronary intervention, coronary artery bypass grafting, or fibrinolytic therapy) and pharmacologic therapy to treat ACS and underlying coronary artery disease.
Medications used depend on the type of ACS and include
clopidogrel if fibrinolytic therapy has not been given)
Beta-blocker
Glycoprotein IIb/IIIa inhibitor for certain patients undergoing percutaneous coronary intervention (PCI) and high-risk lesions (eg, high thrombus burden, no reflow)
heparinST-segment elevation myocardial infarction [STEMI] who are at high risk of bleeding)
Fibrinolytics for select patients with STEMI when timely PCI unavailable
Angiotensin-converting enzyme (ACE) inhibitor (as early as possible)
Statins
Medications for Coronary Artery Disease).
Fibrinolyticsshould be used if not contraindicated for STEMI if primary PCI is not immediately available but worsen outcome for unstable angina and non-ST elevation myocardial infarction (NSTEMI).
Nitroglycerin is preferable to morphine, which should be used judiciously (eg, if a patient has a contraindication to nitroglycerin or is in pain despite nitroglycerin therapy). is initially given sublingually, followed by continuous IV drip if needed. Morphine 2 to 4 mg IV, repeated every 15 minutes as needed, is highly effective but can depress respiration, can reduce myocardial contractility, and is a potent venous vasodilator. Evidence also suggests that morphine interferes with some P2Y12 receptor inhibitors. A large retrospective trial showed that morphine may increase mortality in patients with acute myocardial infarction (1, 2). Hypotension and bradycardia secondary to morphine can usually be overcome by prompt elevation of the lower extremities.
shock are ominous and must be treated aggressively with IV fluids and sometimes vasopressors.
References
1. Meine TJ, Roe MT, Chen AY, et al: Association of intravenous morphine use and outcomes in acute coronary syndromes: results from the CRUSADE Quality Improvement Initiative. Am Heart J 149(6):1043-1049, 2005. doi 10.1016/j.ahj.2005.02.010
2. Kubica J, Adamski P, Ostrowska M, et al: Morphine delays and attenuates ticagrelor exposure and action in patients with myocardial infarction: the randomized, double-blind, placebo-controlled IMPRESSION trial. Eur Heart J 37(3):245–252, 2016. doi: 10.1093/eurheartj/ehv547
Antiplatelet Agents
aspirin 160 to 325 mg (not enteric-coated), if not contraindicated (eg, life-threatening active bleeding), at presentation and 81 mg once a day indefinitely thereafter. Chewing the first dose before swallowing quickens absorption. Aspirin reduces short- and long-term mortality risk (1).
If aspirinClopidogrel has largely replaced ticlopidine for routine use because neutropenia is a risk with ticlopidine, and the white blood cell count must be monitored regularly if patients are taking ticlopidine.
Patients not undergoing revascularization
Patients with acute coronary syndrome
Patients undergoing revascularization
Antiplatelet agent reference
1. Lawton JS, Tamis-Holland JE, Bangalore S, et al: 2021 ACC/AHA/SCAI guideline for coronary artery revascularization: a report of the ACC/AHA Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol 79(2):e21–e129, 2022. doi: 10.1016/j.jacc.2021.09.006
Anticoagulant Agents
Either a low molecular weight heparin (LMWH), unfractionated heparin
Patients at high risk of systemic emboli (eg, atrial fibrillation with CHA2DS2VASc score
Unfractionated heparin
heparin are shorter and can be reversed (by promptly stopping the heparin
Low molecular weight heparin
The LMWHs have better bioavailability, are given by simple weight-based dosing without monitoring aPTT and dose titration, and have lower risk of heparin-induced thrombocytopenia. They also may produce an incremental benefit in outcomes relative to unfractionated heparinenoxaparin may pose a higher bleeding risk in patients with STEMI who are >
Choice of heparin
heparin in patients with unstable angina or NSTEMI and in patients < age 75 years with STEMI who are not undergoing PCI.
< 30 mL/minute (0.5 mL/second).
heparin is continued for 48 hours (or longer if symptoms persist).
Heparin alternatives
The difficulties with the heparins (including bleeding complications, the possibility of , and, with unfractionated heparin, the need for dosing adjustments) have led to the search for alternative anticoagulants.
The direct thrombinthrombinheparin for patients undergoing PCI who are at high risk of bleeding. The factor Xaheparin in patients with STEMI (1). Although routine use of these alternative anticoagulants is thus not currently recommended, they should be used in place of unfractionated heparin or LMWH in patients with a known or suspected history of heparin-induced thrombocytopenia.
For patients who require anticoagulation for another reason (eg, atrial fibrillation
Anticoagulants reference
1. Yusuf S, Mehta SR, Chrolavicius S, et al. Effects of fondaparinux on mortality and reinfarction in patients with acute ST-segment elevation myocardial infarction: the OASIS-6 randomized trial. JAMA 2006;295(13):1519-1530. doi:10.1001/jama.295.13.joc60038
Beta-Blockers
Beta-blockers are recommended unless contraindicated (eg, by bradycardia, heart block, hypotension, or asthma), especially for high-risk patients. Beta-blockers reduce heart rate, arterial pressure, and contractility, thereby reducing cardiac workload and oxygen demand. Infarct size largely determines cardiac performance after recovery. Oral beta-blockers given within the first few hours improve prognosis by reducing infarct size, recurrence rate, incidence of ventricular fibrillation, and mortality risk (1).
Beta-blocker reference
1. Chen ZM, Pan HC, Chen YP, et al. Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomised placebo controlled trial. Lancet 366:1622–1632, 2005.
Nitrates
Nitroglycerin dilates veins, arteries, and arterioles, reducing left ventricular preload and afterload. As a result, myocardial oxygen demand is reduced, lessening ischemia.
heart failure, large anterior myocardial infarction, persistent chest discomfort, or hypertension. BP should not be reduced to < 110 to 120 mm Hg systolic; patients who remain symptomatic at that BP should have emergency PCI rather than further BP reduction.
Nitroglycerin is not routinely given to low-risk patients with uncomplicated myocardial infarction.
Fibrinolytics
plasminogen activator complex—APSAC), all given IV, are plasminogen activators. They convert single-chain plasminogen to double-chain plasminogen, which has fibrinolytic activity. They have different characteristics and dosing regimens (see table IV Fibrinolytic Therapies) and are appropriate only for selected patients with STEMI).
tenecteplaseTenecteplaseReteplase has the highest risk of intracranial hemorrhage and a recanalization rate similar to that of tenecteplase, and it is expensive.
Streptokinase (not available in the United States) may induce allergic reactions, especially if it has been used previously, and must be given by infusion over 30 to 60 minutes; however, it has a low incidence of intracerebral hemorrhage and is relatively inexpensive. Anistreplase, related to streptokinaseplasminogen activators. Because of the possibility of allergic reactions, patients who previously received streptokinase or anistreplase are not given that drug again.
Alteplase
Contraindications to fibrinolytic therapy
There are many absolute and relative contraindications to fibrinolytic therapy. In general, the presence of active bleeding or a condition where bleeding would be life-threatening is an absolute contraindication. The contraindications to fibrinolytic therapy are listed in the table Contraindications to Fibrinolytic Therapy.
Other Medications for Acute Coronary Syndromes
Angiotensin-converting enzyme (ACE) inhibitors reduce mortality risk in patients with myocardial infarction, especially in those with anterior infarction, heart failure, or tachycardia. The greatest benefit occurs in the highest-risk patients early during convalescence. ACE inhibitors are given > 24 hours after thrombolysis stabilization and, because of continued beneficial effect, may be prescribed long-term.
Angiotensin II receptor blockers (ARBs) may be an effective alternative for patients who cannot tolerate ACE inhibitors (eg, because of cough). They are not first-line treatment after myocardial infarction. Contraindications include hypotension, kidney failure, bilateral renal artery stenosis, and known allergy.
Statins (HMG-CoA reductase inhibitors) have long been used for prevention of coronary artery disease and acute coronary syndromes, but there is now increasing evidence that they also have short-term benefits, such as stabilizing plaque, reversing endothelial dysfunction, decreasing thrombogenicity, and reducing inflammation. Thus, all patients without contraindications (eg, statin-induced myopathy, liver dysfunction) to therapy should receive a statin at the maximally tolerated dose as early as possible following ACS regardless of their serum lipid levels (1).
PCSK-9 inhibitors
2).
Other medications references
1. Wang WT, Hellkamp A, Doll JA, et al. Lipid Testing and Statin Dosing After Acute Myocardial Infarction. J Am Heart Assoc 2018;7(3):e006460. Published 2018 Jan 25. doi:10.1161/JAHA.117.006460
2. Gaba P, Bhatt DL, Steg PG, et al. Prevention of Cardiovascular Events and Mortality With Icosapent Ethyl in Patients With Prior Myocardial Infarction. J Am Coll Cardiol 2022;79(17):1660-1671. doi:10.1016/j.jacc.2022.02.035
