Aortic Regurgitation Medication

  • Author: Stanley S Wang, MD, JD, MPH; Chief Editor: Richard A Lange, MD   more...
 
Updated: Apr 2, 2012
 

Medication Summary

Vasodilator therapy may be considered under the conditions described above. Many classes of vasodilators have been studied, with long-term hydralazine or nifedipine therapy being associated with higher EF and less LV dilation in smaller trials, but a less consistent association has been found for enalapril and quinapril.[5]

Historically, beta-blocker therapy has been discouraged in patients with severe AR because heart rate reduction could prolong diastole, thus worsening AR. However, beta-blockers have been shown to produce beneficial neuroendocrine alterations in patients with heart failure. A recent observational study has suggested that beta-blocker therapy is associated with a significant survival benefit in patients with severe AR[25] , spurring hope that further investigation may confirm this finding and allow its translation into a clinically meaningful recommendation.

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Angiotensin-converting enzyme inhibitors

Class Summary

Competitive inhibitors of angiotensin-converting enzyme (ACE). Reduce angiotensin II levels, decreasing aldosterone secretion.

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Enalapril (Vasotec)

 

ACE-I produces a small increase in EF and significant decrease in LV volume and mass. Effective vasodilator therapy requires adjustment of dosage to achieve a decrease in arterial pressure.

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Calcium channel blockers

Class Summary

Inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.

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Nifedipine (Procardia)

 

Produces significant fall in arterial pressure, reduces LV volume and mass, increases EF, and delays need for AVR in asymptomatic patients with severe AR and normal LV systolic function. Effective vasodilator therapy requires adjustment of dosage to decrease arterial pressure.

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Cardiac glycosides

Class Summary

Inhibit sodium-potassium ATPase. Inhibition of the enzyme leads to an increase in the intracellular concentration of sodium and calcium. Vagomimetic action leads to reduced activity of sympathetic nervous system.

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Digoxin (Lanoxin)

 

Pharmacologic consequences include an increase in the force and velocity of myocardial systolic contraction (positive inotropic action) and slowing of the heart rate and decreased conduction velocity through the AV node (vagomimetic effect). Use in patients with heart failure is associated with 25% reduction in the frequency of hospitalization for heart failure. Use is not associated with mortality benefit.

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Diuretics

Class Summary

Increase urine flow. These agents are ion transport inhibitors that decrease the reabsorption of sodium at different sites in the nephron. 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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Furosemide (Lasix)

 

Like torsemide and bumetanide, is a potent loop diuretic. Compared to all other classes of diuretics, these drugs have the highest efficacy in mobilizing sodium and chloride from the body. Loop diuretics inhibit the Na+, K+, and Cl- cotransport in the ascending limb of the loop of Henle. Furosemide and other loop diuretics are indicated in treatment of edema associated with CHF, cirrhosis of the liver, and renal disease, including nephrotic syndrome. May be used to treat hypertension alone or in combination with other antihypertensive agents.

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Direct-acting adrenergic agonists

Class Summary

Act directly on alpha- and beta-receptors, producing effects similar to those that occur following stimulation of sympathetic nerves or release of the hormone epinephrine from the adrenal medulla.

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Dobutamine (Dobutrex)

 

Synthetic direct-acting catecholamine and beta-receptor agonist. Increases cardiac contractility and output in CHF. At therapeutic dose, mainly an inotropic agent, while producing comparatively mild chronotropic and vasodilative effects. As compared to other sympathomimetic drugs, does not significantly increase myocardial oxygen demands, which is its major advantage compared to other direct-acting catecholamines.

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Contributor Information and Disclosures
Author

Stanley S Wang, MD, JD, MPH  Clinical Cardiologist, Austin Heart South; Director of Legislative Affairs, Austin Heart; Director, Sleep Disorders Center at Heart Hospital of Austin; Assistant Professor of Medicine (Adjunct), University of North Carolina School of Medicine

Stanley S Wang, MD, JD, MPH is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, American Society of Echocardiography, American Society of Nuclear Cardiology, American Stroke Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Martin Gerard Keane, MD, FACC, FAHA  Associate Professor, Cardiovascular Medicine Division, Department of Medicine, University of Pennsylvania School of Medicine

Martin Gerard Keane, MD, FACC, FAHA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Heart Association, American Society of Echocardiography, Pennsylvania Medical Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

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

Steven J Compton, MD, FACC, FACP  Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Amer Suleman, MD  Private Practice

Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Chief Editor

Richard A Lange, MD  Professor and Executive Vice Chairman, Department of Medicine, Director, Office of Educational Programs, University of Texas Health Science Center at San Antonio

Richard A Lange, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, and Association of Subspecialty Professors

Disclosure: Nothing to disclose.

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