Hypertrophic Cardiomyopathy Medication

  • Author: Sandy N Shah, DO, MBA, FACC, FACOI; Chief Editor: Henry H Ooi, MBBCh   more...
 
Updated: Apr 11, 2012
 

Medication Summary

The purpose of pharmacologic therapy is to reduce the pressure gradient across the LV outflow tract by reducing the inotropic state of the left ventricle, improving compliance of the left ventricle, and reducing diastolic dysfunction. To date, only 1 pharmacologic agent, amiodarone (Cordarone), has been shown to reduce the incidence of arrhythmogenic sudden cardiac death.[31, 32]

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Beta-Adrenergic Blocking Agents

Class Summary

These reduce the inotropic state of the left ventricle. They decrease diastolic dysfunction and increase LV compliance, thereby reducing the pressure gradient across LV outflow tract. Beta-adrenergic blocking agents decrease heart rate, thus lowering myocardial oxygen consumption and reducing the potential for myocardial ischemia.

Metoprolol (Lopressor, Toprol XL)

 

This is a first-line therapy in the treatment of obstructive and nonobstructive hypertrophic cardiomyopathy (HCM). Rarely, patients may require up to 200 mg orally twice daily to achieve the desired effect. The dose is titrated to a heart rate of between 50 and 60 bpm.

Atenolol (Tenormin)

 

Atenolol selectively blocks beta1 receptors, with little or no effect on beta2 types.

Sotalol (Betapace, Sorine)

 

This is a class III antiarrhythmic agent that blocks K+ channels, prolongs action potential duration, and lengthens the QT interval. Sotalol is a noncardiac selective beta-adrenergic blocker that may be helpful in the conversion of atrial fibrillation and flutter to normal rhythm. It may also suppress the recurrence of atrial fibrillation and flutter.

Propranolol (Inderal LA, InnoPran XL)

 

Propranolol is a class II antiarrhythmic nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases the automaticity of contractions. The

dose is titrated to a heart rate of between 50 and 60 bpm.

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Antiarrhythmics

Class Summary

These agents alter the electrophysiologic mechanisms responsible for arrhythmia.

Disopyramide (Norpace, Norpace CR)

 

Disopyramide decreases the inotropic state of the left ventricle. It decreases ventricular and supraventricular arrhythmias. The drug decreases diastolic dysfunction and increases LV compliance, thereby reducing the pressure gradient across the LV outflow tract. Disopyramide raises the threshold for atrial and ventricular ectopy.

Amiodarone (Cordarone, Pacerone)

 

Amiodarone is the only agent proven to reduce the incidence and risk of cardiac sudden death, with or without obstruction to LV outflow. It is very effective at converting atrial fibrillation and flutter to sinus rhythm and at suppressing the recurrence of these arrhythmias.

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Calcium Channel Blockers

Class Summary

An alternative to beta blockers, calcium channel blockers decrease the inotropic state of the left ventricle, decrease the gradient across the LV outflow tract, decrease diastolic dysfunction, and increase diastolic filling of the left ventricle by improving LV diastolic relaxation. These agents may have a better effect on exercise performance.

Verapamil (Calan, Isoptin, Verelan)

 

During depolarization, verapamil inhibits calcium ions from entering slow channels or voltage-sensitive areas of the vascular smooth muscle and myocardium. The drug provides an alternative to beta-blocker therapy. It is useful in patients with moderate to severe chronic obstructive pulmonary disease (COPD).

The use of short-acting calcium channel blockers is being discouraged because of numerous reports of adverse cardiac and hemodynamic events associated with their use, particularly in patients with known coronary artery disease.

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Anticoagulants, Cardiovascular

Class Summary

Anticoagulants are used to prevent thromboembolic complications.

Warfarin (Coumadin, Jantoven)

 

Warfarin is a competitive, direct thrombin inhibitor. Thrombin enables fibrinogen conversion to fibrin during the coagulation cascade, thereby preventing thrombus development. It inhibits both free and clot-bound thrombin and thrombin-induced platelet aggregation. Warfarin is indicated for the prevention of stroke and thromboembolism associated with nonvalvular atrial fibrillation.

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Contributor Information and Disclosures
Author

Sandy N Shah, DO, MBA, FACC, FACOI  Cardiologist

Sandy N Shah, DO, MBA, FACC, FACOI is a member of the following medical societies: American College of Cardiology, American College of Osteopathic Internists, and American Osteopathic Association

Disclosure: Nothing to disclose.

Chief Editor

Henry H Ooi, MBBCh  Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Gary Edward Sander, MD, PhD, FACC, FAHA, FACP, FASH Professor of Medicine, Director of CME Programs, Team Leader, Root Cause Analysis, Tulane University Heart and Vascular Institute; Director of In-Patient Cardiology, Tulane Service, University Hospital; Visiting Physician, Medical Center of Louisiana at New Orleans; Faculty, Pennington Biomedical Research Institute, Louisiana State University; Professor, Tulane University School of Medicine

Gary Edward Sander, MD, PhD, FACC, FAHA, FACP, FASH is a member of the following medical societies: Alpha Omega Alpha, American Chemical Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Society for Pharmacology and Experimental Therapeutics, American Society of Hypertension,American Thoracic Society, Heart Failure Society of America, Louisiana State Medical Society, National Lipid Association, and Southern Society for Clinical Investigation

Disclosure: Forest Labs Honoraria Speaking and teaching

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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