eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology
Mitral Valve Insufficiency: Treatment & Medication
Updated: Apr 28, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
In children, mitral regurgitation (MR) tends to progress with age. MR fosters MR because of the repeating cycle described earlier. As a result of this tendency, these patients must be examined regularly even though the MR may be mild. Early treatment of infants and children with MR is primarily medical. Guidelines for treating children are not well defined and are based largely on information derived from adults.- Depending on the cause of MR, a patient may require medications such as anti-inflammatory agents for rheumatic fever or Kawasaki disease and antibiotics for infective processes. Baseline information, such as a chest radiography, ECG, and echocardiography, should be obtained. Patients with mild MR should have follow-up monitoring at regular intervals. Little change may occur in asymptomatic patients as they age. Primary medical intervention is bacterial endocarditis prophylaxis. For more information, see Antibiotic Prophylactic Regimens for Endocarditis.
- Optimal medical therapy is aimed at increasing systemic cardiac output and decreasing regurgitant flow. No clear guidelines are available regarding when to initiate medical management; however, treatment probably is indicated when the left ventricle (LV) begins to dilate.
- Afterload reduction may be the most beneficial therapy because it reduces work on the heart by decreasing systemic arteriolar resistance, thereby decreasing the regurgitant volume. However, no studies have demonstrated that afterload reduction actually delays (or eliminates) the need for surgery.
- If the patient develops symptoms, such as dyspnea and exercise intolerance, anticongestive medications (digoxin, diuretics) should be added. By decreasing LV end-diastolic volume, the diameter of the mitral annulus also is decreased, thereby decreasing the regurgitant orifice.
- Diuretics are also helpful in decreasing the total volume and may alleviate the pulmonary edema and congestion that may be present.
- Digoxin is useful in patients with left heart failure because it allows the heart to pump more efficiently.
- Acute MR causes a sudden decrease in cardiac output and an increase in left atrial pressure, resulting in pulmonary congestion. Severity of the MR depends on the size of the orifice and the time period over which the MR develops. If the orifice is large, a sudden decrease in systemic blood flow and pressure occurs, and pulmonary edema develops. Decreasing afterload may temporarily relieve these symptoms.
- Vasodilators, such as nitroprusside, are very effective; however, preexisting hypotension may be exacerbated.
- Inotropic agents may improve systolic blood pressure. Intra-aortic balloon counterpulsation or immediate surgical intervention (valvuloplasty) may be necessary in severe cases.
- In patients who stabilize but remain symptomatic, early semielective surgery should be considered to reduce the risk of irreversible ventricular dysfunction.
- Patients who become asymptomatic with medical therapy can be treated in the same manner as those with chronic MR.
- Patients with chronic MR should receive maintenance doses of afterload agents such as ACE inhibitors, hydralazine, or calcium channel blockers. Diuretics and digoxin also are useful.
Surgical Care
When a patient becomes severely symptomatic (New York Heart Association class III or IV) because of LV failure, the patient should be encouraged to undergo cardiac surgery. Surgical replacement versus repair may be an issue at this time. For children, reconstruction is preferable to avoid the need for anticoagulation therapy. Because the valve is more compliant and pliable in children than in adults, repair is often feasible. By repairing the valve instead of replacing it, the subvalvular apparatus remains intact, helping to preserve LV function. In general, patients should undergo surgery before severe symptoms develop. Operating earlier and repairing the valve improves the chance of normal postoperative function without the associated risks of prosthesis placement. On the other hand, pediatric patients often have associated congenital abnormalities that may dictate the need for valve replacement.
Surgical repair of the regurgitant mitral valve can be classified into 3 major groups depending on the leaflet motion, namely, normal, prolapsing, and restricted. Repair of these conditions can proceed in several ways, depending on the specific abnormality involved.
- If the mitral annulus is dilated, an annuloplasty may be successful in alleviating the degree of regurgitation.
- The annuloplasty may involve the use of a ring prosthesis.
- In younger patients (in whom restriction of valve growth is undesirable), resection of a portion of the leaflet and annular plication may be performed.
- Shortening of the chordae and/or papillary muscles may repair prolapsed leaflets.
- MR with restricted leaflet motion is observed in parachute and hammock valves and, along with a valvuloplasty, can be improved by incising the valve leaflets at an appropriate location.
- Mitral valve replacement is the final option in the treatment of MR.7 The choice of which valve to use (mechanical vs bioprosthesis) can be difficult.
- A mechanical prosthesis has good longevity and performance, but the size of the valve is problematic in neonates and infants.8 Low-profile valves occupy less space and cause less distortion to the LV outflow tract. The major drawback to mechanical prosthesis is the need for anticoagulation therapy. Since flow through the mitral valve position is at a low velocity, anticoagulation with warfarin is the only long-term option. Warfarin must be administered daily, and the prothrombin time and international normalized ratio (INR) must be monitored closely, at least until a steady state is reached. Even then, regular monitoring of prothrombin time and INR is desirable. Too much warfarin may result in excessive bleeding, while insufficient anticoagulation may lead to thromboembolism. For the older child, contact sports usually are contraindicated because of anticoagulation therapy.
- Bioprosthetic valves resolve the anticoagulation issue but raise problems of their own. Bioprostheses may degenerate rapidly and may become calcified and dysfunctional as early as 6 months after insertion. Because the anticipated lifespan of a bioprosthetic valve in infants and children is shortened, bioprosthetic valves are less desirable because of the need for early repeat surgery. A bioprosthetic valve may be more desirable for women of childbearing age in view of the teratogenic potential of warfarin in the first trimester of pregnancy and the potential dangers of anticoagulation therapy during delivery.
- Definitive long-term surgical treatment of the child with mitral valve regurgitation continues to be an area that needs further study. Impairment of annular growth and the need for repeated surgical intervention as the child ages continue to be of concern despite current advancements in technology.
Activity
- Contact sports are contraindicated in children taking warfarin.
Medication
ACE inhibitors and diuretics are the mainstay of medical therapy for patients with mitral regurgitation (MR).
Afterload reducers
These agents are used to improve preoperative or postoperative cardiac output. They reduce systemic vascular resistance and increase systemic blood flow resulting from myocardial dysfunction, significant mitral valve insufficiency, or both.
Captopril (Capoten)
Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.
By decreasing the systemic blood pressure, ACE inhibitors decrease the amount of work placed on the heart. The regurgitant fraction also is decreased because of the lower systemic blood pressure.
Adult
6.25-12.5 mg PO tid 1 h ac; not to exceed 150 mg tid
Pediatric
Neonates: 0.05-0.1 mg/kg/dose PO q8h 1 h ac
Children: 0.3-0.5 mg/kg/dose PO q8h 1 h ac; may titrate upward; not to exceed 6 mg/kg/d
NSAIDs may reduce hypotensive effects of captopril; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases captopril levels; probenecid may increase captopril levels; hypotensive effects of ACE inhibitors may be enhanced when administered concurrently with diuretics
Documented hypersensitivity; renal impairment
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
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Category D in second and third trimester of pregnancy; caution in renal impairment, valvular stenosis, or severe congestive heart failure
Hydralazine (Apresoline)
Decreases systemic resistance through direct vasodilation of arterioles.
Adult
10 mg PO qid initially; may increase by 10-25 mg/d q3d; not to exceed 300 mg/d
Pediatric
1 mg/kg/d PO divided bid/qid initially; may gradually increase over 1 mo; not to exceed 5-7.5 mg/kg/d
MAOIs or beta-blockers may increase hydralazine toxicity; pharmacologic effects of hydralazine may be decreased by indomethacin
Documented hypersensitivity; mitral valve rheumatic heart disease
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Hydralazine has been implicated in myocardial infarction; caution in suspected coronary artery disease
Nifedipine (Procardia, Adalat)
Relaxes coronary smooth muscle and produces coronary vasodilation, which in turn improves myocardial oxygen delivery.
Adult
10-30 mg IR cap tid; not to exceed 120-180 mg/d
30-60 mg/d SR tab; not to exceed 90-120 mg/d
Pediatric
0.6-0.9 mg/kg/d PO divided tid/qid
Caution with coadministration of any agent that can lower BP including beta-blockers and opioids; H2 blockers (eg, cimetidine) may increase toxicity
Documented hypersensitivity
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
May cause lower extremity edema; allergic hepatitis has occurred but is rare
Nitroprusside (Nitropress)
Afterload-reducing agent used for acute MR. Produces vasodilation and increases inotropic activity of the heart. At higher doses, may exacerbate myocardial ischemia by increasing the heart rate.
Adult
0.3-0.5 mcg/kg/min IV initially; titrate to desired effect by increasing by increments of 0.5 mcg/kg/min; average dose is 1-6 mcg/kg/min Infusion rates >10 mcg/kg/min may lead to cyanide toxicity
Pediatric
Administer as in adults
Effects are additive when administered with other hypotensive agents
Documented hypersensitivity; subaortic stenosis, decreased cerebral perfusion, arteriovenous shunt, coarctation of aorta (eg, compensatory hypertension), and atrial fibrillation or flutter
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
Caution in increased intracranial pressure, hepatic failure, severe renal impairment, and hypothyroidism; in renal or hepatic insufficiency, nitroprusside levels may increase and can cause cyanide toxicity; sodium nitroprusside can lower blood pressure, thus, should be used only in patients with mean arterial pressures >70 mm Hg
Diuretic agents
These agents promote excretion of water and electrolytes by the kidneys. They are used to treat heart failure or hepatic, renal, or pulmonary disease when sodium and water retention have resulted in edema or ascites.
Furosemide (Lasix)
Increases excretion of water by interfering with chloride-binding cotransport system, which in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Dose must be individualized. Depending on response, administer at increments of 20-40 mg, no sooner than 6-8 h after the previous dose, until desired diuresis occurs. When treating infants, titrate using increments of 1 mg/kg/dose until a satisfactory effect is achieved.
Adult
20-80 mg/d PO/IV/IM; titrate up to 600 mg/d for severe edematous states
Pediatric
1-2 mg/kg/dose PO; not to exceed 6 mg/kg/dose; do not administer more frequently than q6h
Alternatively, 1 mg/kg IV/IM slowly under close supervision; not to exceed 6 mg/kg
Metformin decreases furosemide concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when administered concurrently; increased plasma lithium levels and toxicity are possible when administered concurrently
Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion
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
Perform frequent serum electrolyte, CO2, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter
Spironolactone (Aldactone)
For management of edema resulting from excessive aldosterone excretion. Competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions.
Adult
25-200 mg/d PO qd or divided bid
Pediatric
1.5-3.5 mg/kg/d PO divided q6-24h
May decrease effect of anticoagulants; potassium and potassium-sparing diuretics may increase toxicity of spironolactone
Documented hypersensitivity; anuria, renal failure, or hyperkalemia
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in renal and hepatic impairment
Ethacrynic acid (Edecrin)
Use as a second-line IV diuretic for those with congestive heart failure. Inhibits loop of Henle and proximal and distal convoluted tubule sodium and chloride resorption.
Adult
0.5-1 mg/kg/dose IV; may repeat q8-12h as warranted; not to exceed 100 mg/dose
Pediatric
1 mg/kg IV q8-12h
May cause additive ototoxicity with aminoglycosides or cisplatin; additive hypotensive effects with coadministration of other diuretics or antihypertensives; may cause hypokalemia and increase toxicity of digoxin; may increase anticoagulant effect of warfarin; increases lithium serum levels
Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution with blood dyscrasias and liver or kidney disease; monitor electrolyte, calcium, glucose, uric acid, CO2, creatinine, and BUN levels
Inotropic agents
These are effective medications when cardiac function is slightly decreased or compromised by the amount of MR. Positive inotropic agents increase the force of contraction of the myocardium and are used to treat acute and chronic congestive heart failure (CHF). Some agents may also increase or decrease the heart rate (ie, positive or negative chronotropic agents), provide vasodilatation, or improve myocardial relaxation. These additional properties influence the choice of drug for specific circumstances. Cardiac glycosides are used predominantly for their inotropic effects.
Digoxin (Lanoxin)
Cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system. Acts directly on cardiac muscle, increasing myocardial systolic contractions. Its indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.
Adult
0.125-0.375 mg/d PO
Pediatric
Total digitalizing dose (TDD):
5-10 years: 20-35 mcg/kg PO
>10 years: 10-15 mcg/kg PO
May accomplish digitalization by administering one half of TDD in first dose, followed by 2 doses that are one fourth of TDD administered at 8- to 12-h intervals
Maintenance dose:
Use 25-35% of TDD
Neonates and infants: 5-10 mcg/kg/d PO
Medications that may increase digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, PO amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil
Medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, PO colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid
Documented hypersensitivity; beriberi heart disease, idiopathic hypertrophic subaortic stenosis, constrictive pericarditis, and carotid sinus syndrome
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
Hypokalemia may reduce positive inotropic effect of digitalis; IV calcium may produce arrhythmias in patients taking digitalis; hypercalcemia predisposes patients to digitalis toxicity; hypocalcemia can make digoxin ineffective until serum calcium levels are in reference range; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients diagnosed with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis
Milrinone (Primacor)
Bipyridine-positive inotropic agent and vasodilator with little chronotropic activity. Different in mode of action from both digitalis glycosides and catecholamines.
Adult
50 mcg/kg IV loading dose over 10 min, followed by continuous IV infusion at 0.375-0.75 mcg/kg/min
Pediatric
Administer as in adults
Although used as DOC in many pediatric ICUs, safety and efficacy are not well established
Milrinone precipitates in presence of furosemide
Documented hypersensitivity
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
Monitor fluids, electrolyte changes, and renal function during therapy; excessive diuresis may increase potassium loss and predispose patients taking digitalis to arrhythmias; important to correct hypokalemia with potassium supplementation prior to treatment; patients showing excessive decreases in blood pressure should have infusion rates slowed or stopped; previous vigorous diuretic therapy has caused significant decreases in cardiac filling pressure (cautiously administer milrinone and monitor blood pressure, heart rate, and clinical symptomatology)
Anticoagulants
These agents prevent recurrent or ongoing thromboembolic occlusion of the vertebrobasilar circulation. Lifelong anticoagulation therapy is needed in patients with mechanical valves.
Warfarin (Coumadin)
Interferes with hepatic synthesis of vitamin K–dependent coagulation factors. Used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. Tailor dose to maintain an INR in the range of 2-3.
Adult
5-15 mg/d PO for 2-5 d; adjust dose according to desired INR
Pediatric
Administer weight-based dose of 0.05-0.34 mg/kg/d PO; adjust dose according to desired INR
Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, or sucralfate
Medications that may increase anticoagulant effects of warfarin include PO antibiotics, capecitabine, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, or sulindac
Documented hypersensitivity; severe liver or kidney disease; open wounds; GI tract ulcers
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
Do not switch brands after achieving therapeutic response; caution in active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis
More on Mitral Valve Insufficiency |
| Overview: Mitral Valve Insufficiency |
| Differential Diagnoses & Workup: Mitral Valve Insufficiency |
 Treatment & Medication: Mitral Valve Insufficiency |
| Follow-up: Mitral Valve Insufficiency |
| Multimedia: Mitral Valve Insufficiency |
| References |
| Further Reading |
| « Previous Page | Next Page » |
References
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Further Reading
- Relevant clinical guidelines include the following:
- Guidelines on the management of valvular heart disease
- American College of Cardiology Foundation/American Heart Association 2005 guideline update for the diagnosis and management of chronic heart failure in the adult
- American College of Cardiology/American Heart Association 2006 guidelines for the management of patients with valvular heart disease
- Relevant clinical trials include the following:
- Pivotal Study of a Percutaneous Mitral Valve Repair System
- Comparing the Effectiveness of Repairing Versus Replacing the Heart's Mitral Valve in People With Severe Chronic Ischemic Mitral Regurgitation
- Comparing the Effectiveness of a Mitral Valve Repair Procedure in Combination With Coronary Artery Bypass Grafting (CABG) Versus CABG Alone in People With Moderate Ischemic Mitral Regurgitation
- Related eMedicine topics include the following:
Keywords
mitral valve insufficiency, mitral valve regurgitation, mitral regurgitation, MR, heart defect, congential heart defect, acquired heart defect, mitral valve defect, cardiomyopathy, cardiac disease, cardiac defect, left-sided heart disease, heart failure, pulmonary edema, pulmonary congestion, pulmonary hypertension, failure to thrive, endocarditis, myocarditis, rheumatic heart disease, systemic lupus erythematosus, SLE, ischemic, mitral valve prolapse, Marfan syndrome, Ehlers-Danlos syndrome, coronary artery disease, amyloidosis, sarcoidosis, cardiomyopathy, transposition of the great arteries, anomalous origin of the left coronary artery, scleroderma, hypertrophic cardiomyopathy, treatment, diagnosis
