Wellens Syndrome Medication
- Author: Benjamin B Mattingly, MD; Chief Editor: Erik D Schraga, MD more...
The goals of pharmacotherapy are to reduce morbidity and prevent complications. Agents used in the management of Wellens syndrome include salicylates, antihypertensive drugs, antianginal drugs, antiplatelet drugs, analgesics, low-molecular-weight heparins (LMWHs), antiarrhythmic drugs, and anticoagulants.
Salicylates have antiplatelet properties.
Aspirin is an odorless white powdery substance that is available in 81-mg, 325-mg, and 500-mg tablets for oral use. When exposed to moisture, it hydrolyzes into salicylic acid and acetic acids. Aspirin is a stronger inhibitor of both prostaglandin synthesis and platelet aggregation than other salicylic acid derivatives are. Its acetyl group is responsible for inactivation of cyclooxygenase via acetylation. Aspirin is hydrolyzed rapidly in plasma, and elimination follows zero-order pharmacokinetics.
Aspirin irreversibly inhibits platelet aggregation by inhibiting platelet cyclooxygenase. This, in turn, inhibits conversion of arachidonic acid to prostaglandin I2 (PGI2, a potent vasodilator and inhibitor of platelet activation) and thromboxane A2 (TXA2, a potent vasoconstrictor and platelet aggregator). Platelet inhibition lasts for the life of cell (approximately 10 days).
Aspirin may be used in low doses to inhibit platelet aggregation and improve complications of venous stasis and thrombosis. It reduces the likelihood of myocardial infarction (MI) and is also very effective in lowering the risk of stroke. Early administration of aspirin in patients with acute MI may reduce cardiac mortality in the first month.
These agents reduce high blood pressure.
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 electrocardiography (ECG). The goal of treatment is to reduce the heart rate to 60-90 beats/min.
Antianginal agents can reduce blood pressure.
Sublingual nitroglycerin causes relaxation of the vascular smooth muscle via stimulation of intracellular cyclic guanosine monophosphate production, causing a decrease in blood pressure.
Antiplatelet agents inhibit platelet aggregation.
Abciximab is a chimeric human-murine monoclonal antibody approved for use in elective, urgent, or emergency percutaneous coronary intervention (PCI). It binds to the receptor with high affinity and reduces platelet aggregation by 80% for as long as 48 hours after infusion.
Clopidogrel selectively inhibits adenosine diphosphate (ADP) binding to platelet receptors and subsequent ADP-mediated activation of the glycoprotein (GP) IIb/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. It has been shown to lower the rates of cardiovascular death, MI, and stroke in patients with acute coronary syndrome (ie, unstable angina and non-Q-wave MI).
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 because of its reliable and predictable effects, good safety profile, and easy reversibility with naloxone. IV morphine sulfate may be dosed in a number of ways and is commonly titrated until the desired effect is obtained.
LMWHs inhibit thrombogenesis. LMWH differs from unfractionated heparin (UFH) in that it has a higher ratio of anti–factor Xa to anti–factor IIa. It binds to antithrombin III, enhancing its therapeutic effect. The heparin-antithrombin III complex binds to and inactivates activated factor X (Xa) and factor II (thrombin). It does not actively lyse but is able to inhibit further thrombogenesis. It prevents reaccumulation of clot after spontaneous fibrinolysis.
Enoxaparin is an LMWH produced by partial chemical or enzymatic depolymerization of UFH. Its advantages include intermittent dosing and a decreased requirement for monitoring. Heparin anti-Xa levels may be obtained if needed to establish adequate dosing. There is no utility in checking the activated partial thromboplastin time (aPTT), because the drug has a wide therapeutic window and aPTT does not correlate with anticoagulant effect. Maximal anti-Xa and antithrombin activities occur 3-5 hours after administration.
Enoxaparin is indicated for treatment of acute ST-segment elevation MI (STEMI) managed either medically or with subsequent PCI. It is also indicated for prophylaxis of ischemic complications caused by unstable angina and non-Q-wave MI.
Antiarrhythmic agents reduce episodes of chest pain and clinical cardiac events.
Esmolol is an ultra–short-acting agent that selectively blocks beta1-receptors with little or no effect on beta2-receptor types. It is particularly useful in patients with elevated arterial pressure, especially if surgery is planned. Esmolol has been shown to reduce episodes of chest pain and clinical cardiac events in comparison with placebo. It can be discontinued abruptly if necessary.
Esmolol is useful in patients at risk for complications from beta blockade, particularly those with reactive airway disease, mild-to-moderate left ventricular dysfunction, or peripheral vascular disease. Its short half-life (8 min) allows titration to the desired effect and quick discontinuance if necessary.
Propranolol has membrane-stabilizing activity and decreases the automaticity of contractions. It is not suitable for emergency treatment of hypertension. Do not administer it intravenously in hypertensive emergencies.
This class II antiarrhythmic agent blocks K+ channels, increases sinus cycle length, slows the heart rate, increases AV nodal refractoriness, and decreases AV nodal conduction. It has been shown to be effective in the maintenance of sinus rhythm, even in patients with underlying structural heart disease. It is a non–cardiac selective beta-adrenergic blocker. It has both beta1 and beta2 receptor blocking activity.
Acebutolol selectively blocks beta1-adrenergic receptors. It has intrinsic activity and membrane stabilizing activity.
Anticoagulants are used for anticoagulation in patients with unstable angina.
Lepirudin is a recombinant hirudin derived from yeast cells. When compared with UFH in unstable angina trials, hirudin demonstrated a modest short-term reduction in the composite endpoint of death or nonfatal MI. The risk of bleeding is modestly increased. Currently, hirudin is indicated only in patients who are unable to receive heparin because of heparin-induced thrombocytopenia.
Bivalirudin is a synthetic analogue of recombinant hirudin. It inhibits thrombin and is used for anticoagulation in patients with unstable angina who are undergoing percutaneous transluminal coronary angioplasty (PTCA). With provisional use of a GPIIb/IIIa inhibitor, it is indicated for anticoagulation in patients undergoing PCI.
The potential advantages of bivalirudin therapy 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).
Argatroban is a selective thrombin inhibitor that inhibits thrombin formation by binding to the active thrombin site of free and fibrin-bound thrombin. It inhibits thrombin-induced platelet aggregation.
Dabigatran etexilate is a selective thrombin inhibitor that inhibits thrombin formation by binding to the active thrombin site of free and fibrin-bound thrombin. It inhibits thrombin-induced platelet aggregation.
de Zwaan C, Bar FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr. 103(4 Pt 2):730-6. [Medline].
Nisbet BC, Zlupko G. Repeat Wellens' Syndrome: Case Report of Critical Proximal Left Anterior Descending Artery Restenosis. J Emerg Med. 2008 Apr 2. [Medline].
Patel K, Alattar F, Koneru J, Shamoon F. ST-Elevation Myocardial Infarction after Pharmacologic Persantine Stress Test in a Patient with Wellens' Syndrome. Case Rep Emerg Med. 2014. 2014:530451. [Medline]. [Full Text].
Moore KL, Dalley AF. Thorax. Clinically Oriented Anatomy. 4th ed. Baltimore, Maryland: Lippincott Williams & Wilkins; 1999. 135.
de Zwaan C, Bar FW, Janssen JH, et al. Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. Am Heart J. 1989 Mar. 117(3):657-65. [Medline].
Tandy TK, Bottomy DP, Lewis JG. Wellens' syndrome. Ann Emerg Med. 1999 Mar. 33(3):347-51. [Medline].
Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens' syndrome. Am J Emerg Med. 2002 Nov. 20(7):638-43. [Medline].
Tatli E, Aktoz M, Buyuklu M, Altun A. Wellens' syndrome: the electrocardiographic finding that is seen as unimportant. Cardiol J. 2009. 16(1):73-5. [Medline].
Narasimhan S, Robinson GM. Wellens syndrome: a combined variant. J Postgrad Med. 2004 Jan-Mar. 50(1):73-4. [Medline].
Singh B, Singh Y, Singla V, Nanjappa MC. Wellens' syndrome: a classical electrocardiographic sign of impending myocardial infarction. BMJ Case Rep. 2013 Feb 18. 2013:[Medline].
Movahed MR. Wellens' syndrome or inverted U-waves?. Clin Cardiol. 2008 Mar. 31(3):133-4. [Medline].