Takotsubo (Stress) Cardiomyopathy (Broken Heart Syndrome) Medication

Updated: Jul 31, 2019
  • Author: Eric B Tomich, DO; Chief Editor: Erik D Schraga, MD  more...
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Medication

Medication Summary

Currently, no randomized controlled trials have been performed to evaluate medical therapies for takotsubo (stress) cardiomyopathy (broken heart syndrome); however, it is common practice to prescribe angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs), at least until left ventricular (LV) function is restored. Beta blockers are also indicated and may be useful in the long term. However, a review study and meta-analysis by Singh et al suggested that while ACEIs and ARBs may reduce the recurrence rate of takotsubo cardiomyopathy, beta blockers may not. [28]

Other standard outpatient post-ST-segment elevation myocardial infarction (STEMI) medications, such as statins, aspirin, and clopidogrel, are of unknown benefit.

Patients with a known LV thrombus should be anticoagulated until LV function normalizes and the thrombus is no longer present on echocardiogram. [43] Chronic beta-blocker therapy may reduce the likelihood of recurrent episodes. [27]

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Salicylates

Class Summary

These agents inhibit platelet aggregation.

Aspirin (Ascriptin, Bayer Aspirin, Bayer Buffered Aspirin, Ecotrin)

Aspirin is an odorless, white, powdery substance available in 81 mg, 325 mg, and 500 mg for oral use. When exposed to moisture, aspirin hydrolyzes into salicylic acid and acetic acid. It is a stronger inhibitor of prostaglandin synthesis and platelet aggregation than are other salicylic acid derivatives. The acetyl group is responsible for the inactivation of cyclooxygenase via acetylation.

Aspirin is hydrolyzed rapidly in plasma, and elimination follows zero-order pharmacokinetics. It irreversibly inhibits platelet aggregation by inhibiting platelet cyclooxygenase. This, in turn, inhibits the conversion of arachidonic acid to PGI2 (a potent vasodilator and an inhibitor of platelet activation) and thromboxane A2 (a potent vasoconstrictor and platelet aggregate). Platelet inhibition lasts for life of cell (approximately 10 d).

Aspirin may be used in low dose to inhibit platelet aggregation and improve the complications of venous stases and thrombosis. It reduces the likelihood of myocardial infarction and is also very effective in reducing the risk of stroke. Early administration of aspirin in patients with acute myocardial infarction may reduce cardiac mortality in the first month.

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Antianginal Agents

Class Summary

These agents reduce blood pressure.

Nitroglycerin topical (Nitro-Bid, Nitrolingual pumpspray, Nitrostat, Nitro-Dur)

Nitroglycerin causes relaxation of the vascular smooth muscle via stimulation of intracellular cyclic guanosine monophosphate production, causing a decrease in blood pressure.

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Analgesics

Class Summary

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 (Astramorph, Duramorph, MS Contin, Oramorph SR, Avinza)

This is the drug of choice for narcotic analgesia because of its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Morphine sulfate administered intravenously may be dosed in a number of ways and is commonly titrated until the desired effect is obtained.

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Anticoagulants

Class Summary

Anticoagulants inhibit thrombogenesis.

Heparin

Heparin augments the activity of antithrombin III and prevents the conversion of fibrinogen to fibrin. It does not actively lyse but is able to inhibit further thrombogenesis. Heparin prevents the recurrence of a clot after spontaneous fibrinolysis.

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Low Molecular Weight Heparins

Class Summary

Low ̶ molecular weight heparins (LMWHs) inhibit thrombogenesis.

Enoxaparin (Lovenox)

Enoxaparin is produced by the partial chemical or enzymatic depolymerization of unfractionated heparin (UFH). LMWH differs from UFH by having a higher ratio of antifactor Xa to antifactor IIa.

Enoxaparin 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, preventing clot reaccumulation after spontaneous fibrinolysis.

The advantages of enoxaparin include intermittent dosing and a decreased requirement for monitoring. Heparin anti–factor Xa levels may be obtained if needed to establish adequate dosing. There is no utility in checking activated partial thromboplastin time (aPTT); the drug has a wide therapeutic window, and aPTT does not correlate with the anticoagulant effect. The maximum antifactor Xa and antithrombin activities occur 3-5 hours after administration.

Enoxaparin is indicated for the treatment of acute STEMI managed medically or with subsequent percutaneous coronary intervention (PCI). It is also indicated as prophylaxis for ischemic complications caused by unstable angina and non-Q-wave myocardial infarction.

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Antiarrhythmic Agents

Class Summary

Antiarrhythmic agents reduce episodes of chest pain.

Esmolol (Brevibloc)

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 compared with placebo. It can be discontinued abruptly if necessary.

Esmolol is useful in patients at risk of experiencing complications from beta blockade, particularly those with reactive airway disease, mild-moderate left ventricular dysfunction, and/or peripheral vascular disease. The drug's short, 8-minute half-life allows for titration to the desired effect and for quick discontinuation if needed.

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Platelet Aggregation Inhibitors

Class Summary

These agents reduce platelet aggregation.

Abciximab (ReoPro)

Abciximab is a chimeric human-murine monoclonal antibody that has been approved for use in elective/urgent/emergent PCI. It binds to the receptor with high affinity and reduces platelet aggregation by 80% for up to 48 hours following infusion.

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Loop Diuretics

Class Summary

Loop diuretics reduce blood pressure.

Furosemide (Lasix)

Furosemide increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. It increases renal blood flow without increasing the filtration rate. The onset of action generally is within 1 hour. Furosemide increases potassium, sodium, calcium, and magnesium excretion.

The dose must be individualized to the patient. Depending on the response, administer furosemide at increments of 20-40 mg, until the desired diuresis occurs. When treating infants, titrate with 1-mg/kg/dose increments until a satisfactory effect is achieved.

Diuretics have major clinical uses in managing disorders involving abnormal fluid retention (edema) or in treating hypertension, in which their diuretic action causes decreased blood volume.

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Thiazide Diuretics

Class Summary

These agents reduce blood pressure.

Hydrochlorothiazide (Microzide)

Hydrochlorothiazide inhibits the reabsorption of sodium in distal tubules, causing the increased excretion of sodium and water, as well as of potassium and hydrogen ions.

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Antihypertensive Agents

Class Summary

Antihypertensive agents reduce blood pressure.

Spironolactone (Aldactone)

Spironolactone is used for the management of edema resulting from excessive aldosterone excretion. It competes with aldosterone for receptor sites in the distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions.

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Antiplatelet Agents

Class Summary

These agents inhibit platelet aggregation.

Eptifibatide (Integrilin)

Eptifibatide is an antagonist of the GP IIb/IIIa receptor; it reversibly prevents von Willebrand factor, fibrinogen, and other adhesion ligands from binding to the GP IIb/IIIa receptor. Eptifibatide inhibits platelet aggregation. Its effects persist over the duration of maintenance infusion and are reversed when infusion ends.

Tirofiban (Aggrastat)

Tirofiban is a nonpeptide antagonist of the GP IIb/IIIa receptor. It is a reversible antagonist of fibrinogen binding. When tirofiban is administered intravenously, more than 90% of platelet aggregation is inhibited. The drug is approved for use in combination with heparin for patients with unstable angina who are being treated medically and for those undergoing PCI.

Clopidogrel (Plavix)

Clopidogrel selectively inhibits adenosine diphosphate (ADP) binding to the platelet receptor and the subsequent ADP-mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. The drug may have a positive influence on several hemorrhagic parameters and may exert protection against atherosclerosis not only through the inhibition of platelet function but also through changes in the hemorrhagic profile.

Clopidogrel has been shown to decrease cardiovascular death, myocardial infarction, and stroke in patients with acute coronary syndrome (ie, unstable angina, non-Q-wave myocardial infarction).

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Angiotensin-converting Enzyme (ACE) Inhibitors

Class Summary

ACE inhibitors help to control blood pressure.

Lisinopril (Prinivil, Zestril)

Lisinopril prevents the 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)

Enalapril also prevents the conversion of angiotensin I to angiotensin II, leading to increased levels of plasma renin and reduced aldosterone secretion. The drug helps to control blood pressure and proteinuria. Enalapril decreases the pulmonary-to-systemic flow ratio in the catheterization laboratory and increases the systemic blood flow in patients with relatively low pulmonary vascular resistance.

The drug has a favorable clinical effect when it is administered over a long period. It helps to prevent potassium loss in the distal tubules; the body conserves potassium, and thus, less oral potassium supplementation is needed.

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Beta-adrenergic Blockers

Class Summary

These agents are used to reduce blood pressure.

Atenolol (Tenormin)

Atenolol is used to treat hypertension. It selectively blocks beta1 receptors, with little or no affect on beta2 types. Beta-adrenergic blocking agents affect blood pressure via multiple mechanisms; actions include a negative chronotropic effect that decreases the heart rate at rest and after exercise, a negative inotropic effect that decreases cardiac output, a reduction of sympathetic outflow from the central nervous system (CNS), and a suppression of renin release from the kidneys.

Atenolol is used to improve and preserve hemodynamic status by acting on myocardial contractility, reducing congestion, and decreasing myocardial energy expenditure.

Beta-adrenergic blockers reduce the inotropic state of the left ventricle, decrease diastolic dysfunction, and increase left ventricular compliance, thereby reducing the pressure gradient across the left ventricular outflow tract.

Atenolol reduces the heart rate, thus lowering myocardial oxygen consumption and reducing the potential for myocardial ischemia. During intravenous administration, carefully monitor the patient's blood pressure, heart rate, and ECG.

Metoprolol (Lopressor, Toprol XL)

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

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Calcium Channel Blockers

Class Summary

Calcium channel blockers improve oxygen delivery to myocardial tissue.

Verapamil (Calan, Calan SR, Covera-HS, Verelan)

During depolarization, verapamil inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.

Diltiazem (Cardizem CD, Cardizem LA, Dilacor XR, Diltzac, Tiazac)

During depolarization, diltiazem inhibits the influx of extracellular calcium across the myocardial and vascular smooth muscle cell membranes. Serum calcium levels remain unchanged. The resultant decrease in intracellular calcium inhibits the contractile processes of myocardial smooth muscle cells, resulting in dilation of the coronary and systemic arteries and improved oxygen delivery to the myocardial tissue.

Diltiazem decreases the conduction velocity in the atrioventricular (AV) node. It also increases the refractory period, via the blockade of calcium influx. This, in turn, stops reentrant phenomenon.

Diltiazem decreases myocardial oxygen demand by reducing peripheral vascular resistance, reducing the heart rate by slowing conduction through the sinoatrial (SA) and AV nodes, and reducing LV inotropy. The drug slows AV nodal conduction time and prolongs AV nodal refractory period, which may convert supraventricular tachycardia or slow the rate in atrial fibrillation. It also has vasodilator activity but may be less potent than other agents. Total peripheral resistance, systemic blood pressure, and afterload are decreased.

Calcium channel blockers provide control of hypertension associated with less impairment of function of the ischemic kidney. They may have beneficial long-term effects, but this remains uncertain.

Amlodipine (Norvasc)

Amlodipine is generally regarded as a dihydropyridine, although experimental evidence suggests that it also may bind to the nondihydropyridine binding sites. The drug is appropriate for the prophylaxis of variant angina.

Amlodipine has antianginal and antihypertensive effects. It blocks the postexcitation release of calcium ions into cardiac and vascular smooth muscle, thereby inhibiting the activation of adenosine triphosphatase (ATPase) on myofibril contraction. The overall effect is reduced intracellular calcium levels in cardiac and smooth muscle cells of the coronary and peripheral vasculature, resulting in dilatation of coronary and peripheral arteries.

Amlodipine also increases myocardial oxygen delivery in patients with vasospastic angina. In addition, it may potentiate ACE inhibitor effects. During depolarization, amlodipine inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.

The drug benefits nonpregnant patients with systolic dysfunction, hypertension, or arrhythmias and can be used during pregnancy if clinically indicated. Amlodipine has a substantially longer half-life than nifedipine and diltiazem and is administered daily.

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