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Antithrombotic Therapy in Patients with Acute Coronary Syndromes

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Antithrombotic Therapy in Patients with Acute Coronary Syndromes REVIEW ARTICLE Antithrombotic Therapy in Patients With Acute Coronary Syndromes Glenn N. Levine, MD; M. Nadir Ali, MD; Andrew I. Schafer, MD he potential armamentarium of agents used in the treatment of acute coronary syn- dromes continues to expand, including such well-tested agents as aspirin, unfraction- ated heparin, and earlier-generation fibrinolytic agents, and newer agents such as low- molecular-weight heparins, direct thrombin inhibitors, thienopyridines, platelet Tglycoprotein IIb/IIIa receptor inhibitors, and bolus-administration fibrinolytic agents. Older and newer antithrombotic agents have undergone and continue to undergo intensive clinical investi- gation in patients with the clinical spectrum of acute coronary syndromes, which includes un- stable angina, non–Q-wave (non–ST-segment elevation) myocardial infarction, and ST-segment elevation myocardial infarction. These studies, often conducted on an international scope and in- volving thousands of patients, provide data allowing practitioners to optimize the care of patients with acute coronary syndromes. In this article, studies of these established and newer agents in the treatment of patients with acute coronary syndromes are reviewed critically and summarized. Recommendations regarding use of antithrombotic agents in patients with acute coronary syn- dromes are then given. Arch Intern Med. 2001;161:937-948 UNDERSTANDING THE is the fact that Q waves may not develop NOMENCLATURE USED in some patients who present with ST- IN CLINICAL TRIALS segment elevation (probably as a result of early spontaneous, pharmacological, or Although older studies of antithrombotic mechanical reperfusion) and are later therapy have addressed unstable angina as termed to have non–Q-wave MI. Also, Q- a distinct condition, more recent studies wave MI may develop in a small propor- have recognized that unstable angina and tion of patients who present without ST- non–Q-wave myocardial infarction (MI) segment elevation. are part of a continuum of coronary throm- For the purposes of clarity in this re- botic disorders termed acute coronary syn- view, in studies in which patients labeled dromes and have assessed antithrombotic as presenting with unstable angina or non– therapy in these patients as a group (and Q-wave MI were enrolled and studied, the used acute coronary syndrome to refer to term non–ST-segment elevation acute coro- this group of patients). Acute coronary syn- nary syndromes will be used. The term dromes has also been used variably in the acute coronary syndrome will be reserved literature to also include those patients only for describing the broad spectrum of who present with ST-segment elevation patients that includes unstable angina, MI. Further confusing the nomenclature non–Q-wave MI, and ST-segment eleva- tion MI. From the Department of Medicine, Baylor College of Medicine (Drs Levine, Ali, and ANTIPLATELET AGENTS Schafer), the Section of Cardiology, Houston Veterans Administration Medical Center (Drs Levine and Ali), and Methodist Hospital (Dr Schafer), Houston, Tex. Dr Levine has received monetary compensation for speaking engagements on behalf of several Aspirin pharmaceutical companies, including Cor/Key, which markets eptifibatide (Integrilin), and Aventis, which markets enoxaparin sodium (Lovenox). Dr Ali has received Aspirin has been used medicinally since monetary compensation for speaking engagements on behalf of several pharmaceutical antiquity. Its antithrombotic action is due companies, including Merck & Co, Inc, which markets tirofiban hydrochloride to irreversible blockade of the formation (Aggrastat), and Aventis. of thromboxane A2, a potent mediator of (REPRINTED) ARCH INTERN MED/ VOL 161, APR 9, 2001 WWW.ARCHINTERNMED.COM 937 ©2001 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 35 Ticlopidine and Clopidogrel Neither Aspirin 30 Heparin The thienopyridines ticlopidine hy- Aspirin + Heparin drochloride and clopidogrel block 25 adenosine diphosphate (ADP)– 20 mediated platelet activation and lead to irreversible inhibition of platelet 15 aggregation.7 The inhibitory effects % of Patients of the thienopyridines on platelet ag- 10 gregation may be synergistic to those 7 5 achieved with aspirin therapy. Like aspirin, the thienopyridines are rela- 0 tively weak inhibitors of platelet ac- Refractory MI Death Any Event Angina tivation compared with the platelet glycoprotein IIb/IIIa (GpIIb-IIIa) in- Figure 1. Results of the Montreal Heart Institute study of patients with unstable angina, showing the reduction in adverse events in patients treated with aspirin, heparin sodium, or both, compared with hibitors. those treated with neither agent. MI indicates myocardial infarction. Adapted from data in Theroux et al.4 Although the thienopyridines have become an integral part of phar- 600 fer a nonfatal or fatal MI (absolute Placebo macological therapy in patients un- rates, approximately 12% vs 3%, dergoing coronary stent implanta- 500 respectively). In the larger Re- tion, there remain only scant data on Aspirin search Group on Instability in Coro- the role of these agents in patients 400 Streptokinase nary Artery Disease (RISC) study of with acute coronary syndromes. In patients with unstable angina or an Italian study, 652 patients with 300 Aspirin + Streptokinase non–Q-wave MI, the risk for subse- unstable angina were treated with quent MI or death was reduced by ticlopidine hydrochloride (Ticlid), 200 aspirin therapy (75 mg/d) at 5-day 250 mg twice daily, plus conven- No. of Vascular Deaths No. of Vascular follow-up by 57% (from 5.8% to tional therapy or with conven- 100 2.5%).5 tional therapy alone during hospi- In the ISIS-2 (Second Interna- talization, with continued therapy 0 7 14 21 28 35 tional Study of Infarct Survival) trial, for approximately 6 months after Days From Randomization more than 17000 patients with sus- discharge.8 Treatment with ticlopi- Figure 2. Results of the Second International pected MI were randomized to aspi- dine decreased the incidences of Study of Infarct Survival (ISIS-2) in which rin therapy (160 mg/d), streptoki- nonfatal MI and vascular death by patients with suspected myocardial infarction nase, both therapies, or neither.6 The 46%. However, the conventional were treated with aspirin, streptokinase, both, or study included patients with ST- therapy arm did not include aspi- placebo. Aspirin or streptokinase therapy alone reduced vascular mortality by 23% to 25% segment elevation, ST-segment de- rin or heparin, and most of the re- compared with placebo therapy; treatment with pression, bundle-branch block, or duction in events with ticlopidine both agents reduced vascular mortality by 42%. other electrocardiographic (ECG) ab- therapy occurred not during the ini- Adapted with permission from the ISIS-2 Collaborative Group.6 normalities. Treatment with aspirin tial hospitalization but in the months decreased vascular mortality by 23%, after discharge. a reduction comparable to the 25% re- The relatively short onset of ac- platelet aggregation. The inhibi- duction achieved with streptokinase tion (in terms of platelet inhibi- tory effects of aspirin on platelet ag- therapy. Patients in the ISIS-2 trial tion) provided by a loading dose of gregation are rapid, with maximal ef- treated with streptokinase derived ad- clopidogrel (Plavix), the once- fects achieved within 15 to 30 ditional benefit from concomitant daily dosing schedule, and the minutes of oral administration of a therapy with aspirin. In those treated moderate degree of platelet inhibi- dose as low as 81 mg.1 with both agents, vascular mortality tion achieved might make this The beneficial effects of aspi- was decreased by 42%. The addi- agent a possible alternate therapy rin in patients with unstable an- tional beneficial effect of aspirin in in patients with acute coronary gina were demonstrated in several those receiving thrombolytic therapy syndromes who have true aspirin studies conducted in the 1980s,2-5 in- is believed to be due at least in part allergies. However, such a role has cluding a study conducted at the to aspirin’s decreasing the rates of ves- not been established or, at least in Montreal Heart Institute.4 In that sel reocclusion and thus of myocar- terms of published studies, evalu- study, 479 patients with unstable an- dial reinfarction. The result of these ated. Nevertheless, given the rec- gina were randomized to treatment treatment regimens on vascular mor- ognized importance of antiplatelet with aspirin (325 mg twice daily), tality in the ISIS-2 trial are shown in therapy in acute MI in patients intravenous heparin sodium, both, Figure 2. These trials thus firmly es- with true aspirin allergies, it has or neither (Figure 1). Compared tablished the clinically relevant ben- been recommended that other with patients who received neither eficial effect of aspirin therapy for the antiplatelet agents such as clopido- therapy, those who were treated with broad range of patients with acute grel or ticlopidine be considered as aspirin were 71% less likely to suf- coronary syndromes. alternate therapies.9 (REPRINTED) ARCH INTERN MED/ VOL 161, APR 9, 2001 WWW.ARCHINTERNMED.COM 938 ©2001 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 Platelet GpIIb-IIIa Inhibitors Each platelet contains approxi- mately 60000 to 80000 GpIIb-IIIa receptors for fibrinogen on its mem- brane. When platelets are acti- vated, these GpIIb-IIIa complexes
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