eMedicine Specialties > Cardiology > Valvular Heart Disease
Aortic Regurgitation: Treatment & Medication
Updated: Jun 26, 2007
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
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Treatment
Medical Care
Medical versus surgical treatment
Medical therapy is appropriate for many patients with mild to moderate chronic AR. The appropriate use of vasodilators is associated with improvement in symptoms and is thought to slow the development of LV enlargement and dysfunction and the need for surgery. That said, physicians treating patients with chronic AR must be attentive to any changes that suggest worsening LV function and the need for surgery. Annual echocardiography to assess LV size and function is useful.
Patients with acute, significant AR represent an entirely different group. Surgical treatment is almost always indicated and medical therapy (typically using intravenous medications titrated to blood pressure, as described below) is recommended only as an interim measure.
Medical treatment with vasodilators
Vasodilator therapy is designed to optimize LV loading conditions and achieve a favorable remodeling process through systolic unloading and reduction in regurgitant volume. Treat asymptomatic patients with chronic severe AR and dilated but normal LV systolic function medically, and monitor their cases for development of indications for aortic valve surgery. Patients with mild AR and normal LV size require no therapy other than endocarditis prophylaxis.
- Earlier studies revealed that long-term vasodilator therapy with nifedipine reduces or delays the need for AVR in asymptomatic patients with severe AR and normal LV function. Nifedipine was also shown to reduce LV size and mass significantly. However, use of nifedipine in patients with LV dysfunction should be cautioned because calcium channel blockers are generally contraindicated in patients with CHF.
- Enalapril therapy achieves significant LV mass regression, LV end-diastolic and end-systolic volume index reduction, and renin-angiotensin system suppression. Enalapril may have favorable influence on the natural history of chronic AR by delaying the need for aortic valve surgery.
- Recent publications have yielded conflicting results on the use of vasodilators. One recent follow-up study confirmed the positive effects of using nifedipine in severe asymptomatic AR; nifedipine delayed the onset of LV dysfunction, prolonged survival and protected the myocardium after AVR, even if stopped at surgery. Patients in this study had moderate to severe hypertension at entry into the study. A separate study comparing the use of nifedipine, enalapril, and placebo was unable to show a benefit to vasodilator therapy in a cohort of normotensive patients. In this study, vasodilator therapy with nifedipine or enalapril did not delay the need for AVR or improve parameters such as regurgitant volume, LV size, or LV systolic function.
- The main goal of medical therapy is to significantly reduce the systolic hypertension associated with chronic severe AR.
- Digoxin and diuretics can be used to relieve symptoms of congestion.
- Antibiotic prophylaxis for endocarditis is discussed as follows:
- AR leads to damaged endothelial lining of the valve and predisposes the valve to platelet and fibrin deposition.
- In the presence of bacteremia, colonization of platelets and/or fibrin deposition can lead to bacterial endocarditis; thus, antibiotic prophylaxis is important for preventing this serious complication.
- Acute AR usually is severe and rapidly leads to LV decompensation, failure, and cardiogenic shock. The treatment of choice for acute AR is AVR. Medical therapy can be used as a bridge to surgery but should not replace it.
- Dobutamine reduces afterload and assists with forward outflow. It also has a positive inotropic effect.
- Vasodilators achieve significant LV mass regression, LV end-diastolic and end-systolic volume index reduction, and renin-angiotensin system suppression.
- Intra-aortic balloon pump is contraindicated in AR.
- Percutaneous transcatheter implantation of a heart valve prosthesis may be available in the future, but these techniques are investigational at this time.
Surgical Care
Surgical treatment of AR usually requires replacement of the diseased valve with a prosthetic valve. However, valve repair is now an option for many individuals because of recent improvements in valve sparing surgical techniques. The surgical mortality rate for AVR is probably 3%, although the mortality rate may be higher if patients also need coronary artery bypass grafts. In addition, the long-term complications of prosthetic valves need to be considered.
- Aortic valve surgery is indicated in patients with normal systolic function (defined as EF >0.50 at rest) who have New York Heart Association (NYHA) functional class III or IV symptoms. Also consider patients with Canadian Heart Association functional class II-IV angina pectoris for surgery. In many patients with NYHA functional class II dyspnea, the etiology of symptoms is often unclear and clinical judgment is required.
- Patients with NYHA functional class II, III, or IV symptoms and with mild-to-moderate LV systolic dysfunction (EF 0.25-0.49) should undergo aortic valve surgery. Patients with functional class IV symptoms have worse postoperative survival rates and a lower likelihood of recovery of systolic function when compared with patients with less severe symptoms, but aortic valve surgery improves ventricular loading conditions and expedites subsequent management of LV dysfunction.
- Symptomatic patients with severe LV dysfunction (EF <0.25) pose difficult management issues. Most patients develop irreversible myocardial damage and may not show improved LV function or NYHA functional class after aortic valve surgery; however, some patients may gain meaningful recovery of LV function. Surgery carries an operative mortality rate of approximately 10%, but medical therapy alone carries a mortality rate of higher than 20% per year; thus, high-risk aortic valve surgery may be a viable option when compared with the even worse prognosis associated with medical therapy alone.
- Asymptomatic patients with evidence of LV systolic dysfunction (EF <0.50) should undergo aortic valve surgery. The postoperative recovery of LV function and survival is strongly associated with preoperative LV function; thus, do not delay aortic valve surgery for patients with evidence of LV dysfunction.
- Asymptomatic patients with severe AR and normal LV function but with severe LV dilatation (end-diastolic dimension >75 mm or end-systolic dimension >55 mm) should undergo aortic valve surgery. These patients tend to progress to symptomatic or LV dysfunction rapidly. Postoperative survival and reduction of LV dimension in this subgroup of patients are excellent.
- Preoperative predictors of poor postoperative survival and LV function include the following:
- LVESD greater than 55 mm
- LVEF less than 0.50
- NYHA CHF class III, IV
- Duration of CHF symptoms longer than 12 months
Consultations
- Cardiologist
- Cardiothoracic surgeon
Diet
Place patients on a low-sodium diet with fluid restriction when CHF symptoms appear.
Activity
Asymptomatic patients with normal LV systolic function may participate in all forms of normal daily physical activity, including mild forms of exercise and, in some cases, competitive athletics; however, isometric exercise (eg, weight lifting) should be avoided. Patients with evidence of LV dysfunction or low cardiac reserve should not engage in vigorous sports or heavy exertion.
Medication
Vasodilator therapy has reduced severity of AR and LV volume and mass successfully, postponing the need for surgical intervention.
Angiotensin-converting enzyme inhibitors
Competitive inhibitors of angiotensin-converting enzyme (ACE). Reduce angiotensin II levels, decreasing aldosterone secretion.
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.
Adult
5 mg PO bid for 2 wk initially; if hemodynamically stable, increase to 10 mg PO bid for 2 wk, then to 20 mg PO bid maintenance
Pediatric
Not established
NSAIDs may reduce hypotensive effects; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects of ACE inhibitors may be enhanced when administered concurrently with diuretics
Documented hypersensitivity; second or third trimester pregnancy, breastfeeding, history of angioneurotic edema, significant renal artery stenosis
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Pregnancy category D in second and third trimester of pregnancy; caution in renal impairment, valvular stenosis, severe CHF, or angioedema; oliguria, seizures, and unpredictable effects on BP may occur in children
Calcium channel blockers
Inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.
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.
Adult
10 mg PO bid initially, then titrate to 20 mg PO bid
Pediatric
Not established
Alcohol, cimetidine, and ranitidine increase bioavailability and effect; antihypertensive medications produce an additive effect; may decrease quinidine levels; may increase digoxin levels; rifampin, phenobarbital, and phenytoin decrease effects
Documented hypersensitivity; CHF, cardiogenic shock, acute MI
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Renal or hepatic dysfunction; breastfeeding; may cause lower extremity edema; allergic hepatitis is rare
Cardiac glycosides
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.
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.
Adult
<70 years and good renal function: 0.25 mg PO qd general initial dose
>70 years or impaired renal function: 0.125 mg PO qd general initial dose
Marked renal impairment: 0.0625 mg general initial dose
0.4-0.6 mg if rapid digitalization with IV loading is needed; produces detectable effect in 5-30 min; 0.1- to 0.3-mg additional doses may be administered cautiously at 6- to 8-h intervals until clinical evidence of an adequate effect
Pediatric
Adjust loading and daily maintenance dose by body weight
Digitalization in infants and children not generally recommended; suggested doses are as follows:
TDD
Premature infants: 0.02-0.03 mg/kg if tab; 0.015-0.025 mg/kg if cap, IV, or IM in divided doses
Full-term infants: 0.025-0.035 mg/kg if tab; 0.02-0.03 if cap, IV, or IM in divided doses
1-24 months: 0.035-0.06 mg/kg if tab; 0.03-0.05 mg/kg if cap, IV, or IM in divided doses
2-5 years: 0.03-0.04 mg/kg if tab; 0.025-0.035 mg/kg if cap, IV, or IM in divided doses
5-10 years: 0.02-0.035 mg/kg if tab; 0.015-0.030 mg/kg if cap, IV, or IM in divided doses
>10 years: 0.01-0.015 mg/kg if tab; 0.008-0.012 if cap, IV, or IM in divided doses
May accomplish digitalization by giving half TDD in first dose followed by 2 doses that are one fourth TDD given at 8- to 12-h intervals
Maintenance dose
Premature infants: 0.005-0.0075 mg/kg if tab; 0.004-0.006 mg/kg if cap, IV, or IM divided q12h
Full-term infants: 0.006-0.01 mg/kg if tab; 0.005-0.008 if cap, IV, or IM divided q12h
1-24 months: 0.010-0.015 mg/kg if tab; 0.0075-0.012 mg/kg if cap, IV, or IM divided q12h
2-5 years: 0.0075-0.01 mg/kg if tab; 0.006-0.009 mg/kg if cap, IV, or IM divided q12h
5-10 years: 0.005-0.01 mg/kg if tab; 0.004-0.008 mg/kg if cap, IV, or IM divided q12h
>10 years: 0.0025-0.005 mg/kg if tab; 0.002-0.003 if cap, IV, or IM qd or divided q12h
See prescribing information in PDR for more detailed information
Potassium-depleting diuretics are a major contributing factor to digitalis toxicity; quinidine, verapamil, amiodarone, propafenone, indomethacin, itraconazole, alprazolam, and spironolactone raise serum digoxin concentrations because of a reduction in clearance and/or in volume of distribution of drug, digitalis intoxication may result
Documented hypersensitivity (hypersensitivity reaction to other digitalis preparations usually constitutes a contraindication to digoxin), ventricular fibrillation
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Because digoxin slows sinoatrial and AV conduction, drug commonly prolongs PR interval; may cause severe sinus bradycardia or sinoatrial block in preexisting sinus node disease, and may cause advanced or complete heart block in preexisting incomplete AV block; patients with paroxysmal atrial fibrillation or flutter and a coexisting accessory AV pathway have developed increased antegrade conduction across the accessory pathway bypassing the AV node, leading to a very rapid ventricular response or ventricular fibrillation after use; unless conduction down the accessory pathway has been blocked (either pharmacologically or by surgery), do not prescribe digoxin to such patients
Diuretics
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.
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.
Adult
Individualize according to patient response to gain maximal therapeutic response and to determine the minimal dose needed to maintain that response
20-80 mg PO administered as a single dose is usual initial dose; repeat or increase 6-8 h later if needed; dose may be titrated carefully up to 600 mg/d in patients with clinically severe edematous states; at higher doses, careful clinical observation and close laboratory monitoring are particularly important
Pediatric
2 mg/kg PO administered as a single dose is usual dose in infants and children; dosage may be increased by 1-2 mg/kg no sooner than 6-8 h after previous dose if needed; not to exceed 6 mg/kg
May increase ototoxic potential of aminoglycoside antibiotics, especially in impaired renal function
Documented hypersensitivity; anuria
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Excessive diuresis may cause dehydration and blood volume reduction with circulatory collapse; observe all patients receiving furosemide therapy for signs or symptoms of fluid or electrolyte imbalance; asymptomatic hyperuricemia can occur, and gout may be precipitated
Direct-acting adrenergic agonists
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.
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.
Adult
Start at low rate (1 mcg/kg/min IV infusion) titrated at intervals of few minutes guided by the patient's response, including systemic blood pressure, urine flow, frequency of ectopic activity, heart rate, and, if possible, measurement of cardiac output, central venous pressure, and/or pulmonary capillary wedge pressure
2-20 mcg/kg/min IV usual range, but clinical response dictates optimal infusion rate
Pediatric
Not established
Animal studies indicate that may be ineffective if patient recently received a beta-blocking drug; in this case, peripheral vascular resistance may increase
Documented hypersensitivity, idiopathic hypertrophic subaortic stenosis
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
During administration, monitor ECG and blood pressure continuously; monitor pulmonary wedge pressure and cardiac output whenever possible to aid in safety and efficacy of infusion
More on Aortic Regurgitation |
| Overview: Aortic Regurgitation |
| Differential Diagnoses & Workup: Aortic Regurgitation |
 Treatment & Medication: Aortic Regurgitation |
| Follow-up: Aortic Regurgitation |
| Multimedia: Aortic Regurgitation |
| References |
| « Previous Page | Next Page » |
References
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Further Reading
Keywords
aortic regurgitation, AR, aortic insufficiency, aortic disease, syphilitic aortitis, rheumatic valvulitis, aortic root disorders, Marfan disease, Marfan syndrome, degeneration of bicuspid aortic valves, bicuspid aortic valve degeneration, regurgitant aortic flow
