Myocardial Infarction Medication
- Author: A Maziar Zafari, MD, PhD; Chief Editor: Eric H Yang, MD more...
The goals of pharmacotherapy for myocardial infarction are to reduce morbidity and to prevent complications. The main goals of emergency department medical therapy are rapid intravenous thrombolysis and/or rapid referral for percutaneous coronary intervention (PCI), optimization of oxygenation, reduction of cardiac workload, and pain control.
Antiplatelet agents have a strong mortality benefit. There is an increased risk of bleeding in cases of emergency coronary artery bypass graft (CABG).
Early administration of aspirin in patients with acute myocardial infarction has been shown to reduce cardiac mortality rate by 23% in the first month.
Clopidogrel selectively inhibits adenosine diphosphate (ADP) binding to platelet receptors and subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.
Clopidogrel may have a positive influence on several hemorrhagic parameters and may exert protection against atherosclerosis, not only through inhibition of platelet function but also through changes in the hemorrhagic profile.
This agent has been shown to decrease cardiovascular death, myocardial infarction, and stroke in patients with acute coronary syndrome (ie, unstable angina, non-ST elevation MI (NSTEMI), or ST-elevation MI (STEMI)).
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). Ticagrelor also reduces the rate of stent thrombosis in patients who have undergone stent placement for treatment of ACS, and it 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 antiplatelet effect.
Prasugrel is a prodrug, a thienopyridine that inhibits platelet activation and aggregation through irreversible binding of active metabolite to adenosine phosphate (ADP) platelet receptors (specifically, P2Y12 receptor)
It is indicated for reduction of thrombotic cardiovascular events (including stent thrombosis) in patients with acute coronary syndrome (ACS) managed by means of percutaneous coronary intervention (PCI) who have either (a) unstable angina or non-ST-elevation MI (NSTEMI) or (b) ST-elevation MI (STEMI) when managed with primary or delayed PCI.
The use of prasugrel is not recommended for patients with a history of stroke or transient ischemic attack (TIA).
Vorapaxar reversibly inhibits protease-activated receptor 1 (PAR-1) which is expressed on platelets, but its long half-life makes it effectively irreversible. It is indicated to reduce thrombotic cardiovascular events in patients with a history of MI or with peripheral arterial disease. It is not used as monotherapy, but added to aspirin and/or clopidogrel.
Antithrombotic agents, which include heparin, bivalirudin, and enoxaparin, prevent the formation of thrombi associated with myocardial infarction and inhibit platelet function by blocking cyclooxygenase and subsequent platelet aggregation. Antiplatelet therapy has been shown to reduce mortality rates by reducing the risk of fatal myocardial infarctions, fatal strokes, and vascular death. Unfractionated intravenous heparin and fractionated low-molecular-weight subcutaneous heparins are the 2 choices for initial anticoagulation therapy.
Bivalirudin, a synthetic analogue of recombinant hirudin, inhibits thrombin; it is used for anticoagulation in patients with unstable angina who are undergoing PCI. With provisional use of glycoprotein IIb/IIIa inhibitor (GP IIb/IIIa inhibitor), bivalirudin is indicated for use as an anticoagulant in patients undergoing PCI. 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, heparinase), and continued efficacy following clearance from plasma (because of binding to thrombin).
Heparin augments the activity of antithrombin III and prevents the conversion of fibrinogen to fibrin. Heparin does not actively lyse, but it is able to inhibit further thrombus formation and prevents reaccumulation of a clot after spontaneous fibrinolysis.
Enoxaparin enhances the inhibition of factor Xa and thrombin by increasing antithrombin III activity. In addition, it preferentially increases the inhibition of factor Xa. Enoxaparin is indicated for the treatment of acute STEMI managed medically or with subsequent PCI. It is also indicated for prophylaxis of ischemic complications caused by unstable angina and non-Q-wave myocardial infarction.
Enhances inhibition of factor Xa and thrombin by increasing antithrombin III activity. In addition, preferentially increases inhibition of factor Xa.
Except in overdoses, no utility exists in checking PT or aPTT, because aPTT does not correlate with anticoagulant effect of fractionated LMWH.
Average duration of treatment is 7-14 d.
Glycoprotein IIb/IIIa Inhibitors
Glycoprotein IIb/IIIa inhibitors prevent acute cardiac ischemic complications in unstable angina that is unresponsive to conventional therapy.
Abciximab is a chimeric human-murine monoclonal antibody. It binds to the platelet surface glycoprotein IIb/IIIa (GPIIb/IIIa) receptor with high affinity, preventing the binding of fibrinogen and reducing platelet aggregation by 80%. Inhibition of platelet aggregation persists for as long as 48 hours after infusion stops.
Tirofiban is a nonpeptide antagonist of the glycoprotein IIb/IIIa receptor. It is a reversible antagonist of fibrinogen binding, and when administered intravenously, it inhibits platelet aggregation by more than 90%.
Eptifibatide is a cyclic peptide that also reversibly inhibits platelet aggregation by binding to the glycoprotein IIb/IIIa receptor. Blocks platelet aggregation and prevents thrombosis.
Vasodilators relieve chest discomfort by improving myocardial oxygen supply, which in turn dilates epicardial and collateral vessels, improving blood supply to the ischemic myocardium.
Nitroglycerin relaxes vascular smooth muscle via stimulation of intracellular cyclic guanosine monophosphate production, causing a decrease in blood pressure. Nitrates are useful for preload reduction and symptomatic relief but have no apparent impact on mortality rate in myocardial infarction.
This category of drugs has the potential to suppress ventricular ectopy due to ischemia or excess catecholamines. In the setting of myocardial ischemia, beta-blockers have antiarrhythmic properties and reduce myocardial oxygen demand secondary to elevations in heart rate and inotropy.
This category of drugs, which includes metoprolol (Lopressor) and esmolol (Brevibloc), has the potential to suppress ventricular ectopy due to ischemia or excess catecholamines. In the setting of myocardial ischemia, beta-blockers have antiarrhythmic properties and reduce myocardial oxygen demand secondary to elevations in heart rate and inotropy.
Esmolol is a useful drug for patients at risk of experiencing complications from beta-blockers, particularly reactive airway disease, mild-to-moderate left ventricular dysfunction, and peripheral vascular disease. Its short half-life of 8 minutes allows for titration to desired effect, with the ability to stop quickly if necessary.
Used to treat hypertension. Selectively blocks beta1-receptors with little or no effect on beta 2 types. Beta-adrenergic blocking agents affect blood pressure via multiple mechanisms. Actions include negative chronotropic effect that decreases heart rate at rest and after exercise, negative inotropic effect that decreases cardiac output, reduction of sympathetic outflow from the CNS, and suppression of renin release from the kidneys. Used to improve and preserve hemodynamic status by acting on myocardial contractility, reducing congestion, and decreasing myocardial energy expenditure.
Beta-adrenergic blockers reduce inotropic state of left ventricle, decrease diastolic dysfunction, and increase LV compliance, thereby reducing pressure gradient across LV outflow tract. Decreases myocardial oxygen consumption, thereby reducing myocardial ischemia potential. Decreases heart rate, thus reducing myocardial oxygen consumption and reducing myocardial ischemia potential.
During IV administration, carefully monitor blood pressure, heart rate, and ECG.
Angiotensin-Converting Enzyme Inhibitors
ACE inhibitors may prevent the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. ACE inhibitors reduce mortality rates after myocardial infarction. Administer ACE inhibitors as soon as possible as long as the patient has no contraindications and remains in stable condition. ACE inhibitors have the greatest benefit in patients with ventricular dysfunction.
Captopril has a short half-life, which makes it an important drug for initiation of ACE inhibitor therapy. It can be started at a low dose and titrated upward as needed and as the patient tolerates.
Enalapril prevents conversion of angiotensin I to angiotensin II, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. Has a favorable clinical effect when administered over a long period of time.
Quinapril prevents conversion of angiotensin I to angiotensin II, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.
Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.
Angiotensin-receptor blockers may be used as an alternative to ACE inhibitors in patients who develop adverse effects, such as a persistent cough, although initial trials need to be confirmed. An angiotensin-receptor blocker should be administered to patients with STEMI who are intolerant of ACE inhibitors and who have either clinical or radiologic signs of heart failure or an LVEF of less than 40%.
Blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II at tissue receptor site. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors and does not affect response to bradykinin (less likely to be associated with cough and angioedema).
Candesartan blocks vasoconstriction and aldosterone-secreting effects of angiotensin II. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. Use in patients unable to tolerate ACE inhibitors.
Produces direct antagonism of angiotensin II receptors. Displaces angiotensin II from AT1 receptor and may lower blood pressure by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses. Use in patients unable to tolerate ACE inhibitors.
Angiotensin II blocker; displaces angiotensin II from AT1 receptor and may lower blood pressure by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water absorption, and hypertrophic responses
May induce more complete inhibition of renin-angiotensin system compared with ACE inhibitors; does not affect response to bradykinin
Inhibits the pressor effects of an angiotensin II infusion in a dose-related manner
Nonpeptide angiotensin II receptor antagonist that blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors and does not affect response to bradykinin and is less likely to be associated with cough and angioedema.
For patients unable to tolerate ACE inhibitors.
Angiotensin II receptor blockers reduce blood pressure and proteinuria, protecting renal function, and delaying onset of end-stage renal disease.
Angiotensin II receptor antagonist that blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. May induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors, does not affect the response to bradykinin, and is less likely to be associated with cough and angioedema. For patients unable to tolerate ACE inhibitors.
The main objective of thrombolysis is to restore circulation through a previously occluded vessel by the rapid and complete removal of a pathologic intraluminal thrombus or embolus that has not been dissolved by the endogenous fibrinolytic system.
The first generation of fibrinolytic drugs (eg, streptokinase, urokinase, acetylated plasminogen streptokinase activator complexes [APSACs], reteplase, and novel plasminogen activator [nPA]) indiscriminately induced activation of circulating plasminogen and clot-associated plasminogen. First-generation drugs invariably elicited a systemic lytic state characterized by depletion of circulating fibrinogen, plasminogen, and hemostatic proteins and by marked elevation of concentrations of fibrinogen degradation products in plasma.
Second-generation drugs (eg, alteplase [t-PA], single-chain urokinase plasminogen activator), such as tenecteplase, preferentially activate plasminogen in the fibrin domain, rather than in the circulation, as with free plasminogen. Therefore, they have clot selectivity. Tenecteplase should be initiated as soon as possible in STEMI patients; tenecteplase is administered as a single bolus exhibiting a biphasic disposition from the plasma.
In optimal regimens, these agents induce clot lysis without inducing a systemic lytic state, they are less prone than nonselective agents to predispose the patient to hemorrhage necessitating transfusion, and they are effective in inducing recanalization in 80-90% of infarct-related arteries within 90 minutes. Therefore, t-PA recanalizes 75-80% of infarct-related arteries.
Alteplase (t-PA) is a fibrin-specific agent with a brief half-life of 5 minutes. Adjunctive therapy with IV heparin is necessary to maintain the patency of arteries recanalized by t-PA, especially during the first 24-48 hours.
Tenecteplase is a modified version of alteplase (t-PA) made by substituting 3 amino acids of alteplase. It can be given as a single bolus over a 5-second infusion, instead of 90 minutes with alteplase. Tenecteplase appears to cause less nonintracranial bleeding, but the risk of intracranial bleeding and stroke is similar to that of alteplase. Base the dose using patient weight. Initiate treatment as soon as possible after the onset of acute STEMI symptoms. Because tenecteplase contains no antibacterial preservatives, reconstitute immediately before use.
Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who experience pain.
Morphine sulfate is the drug of choice for narcotic analgesia due to its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Morphine sulfate is administered intravenously, may be dosed in a number of ways, and commonly is titrated until the desired effect is achieved.
Antiplatelet Agents, Cardiovascular
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|Absolute Contraindications||Relative Contraindications|
|CPR = cardiopulmonary resuscitation; INR = international normalized ratio; STEMI = ST-elevation myocardial infarction; US = United States of America.
Table modified from 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.
|Fibrinolytic Agent||Dose||Fibrin Specificity||Antigenic||Patency Rate|
|Streptokinase (no longer marketed in the US)||1.5 million units IV given over 30–60 min||No||Yes||60%–68%|
|30 mg for weight <60 kg
35 mg for 60–69 kg
40 mg for 70–79 kg
45 mg for 80–89 kg
50 mg for >90 kg
|Reteplase (rPA)||10-U IV boluses given 30 min apart||++||No||84%|
|Alteplase (tPA)||Bolus 15 mg followed by infusion 0.75 mg/kg for 30 min (maximum 50 mg), then 0.5 mg/kg (maximum 35 mg) over the next 60 min; total dose not to exceed 100 mg.||++||No||73%-84%|
|IV = intravenous; rPA = recombinant human tissue plasminogen activator; STEMI = ST-elevation myocardial infarction; tPA = tissue plasminogen activator; US = United States of America.
Table modified from 2013 ACCF/AHA guidelines for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.