Pediatric Aortic Valve Insufficiency Medication
- Author: Mohsen Saidinejad, MD, MPH, MBA; Chief Editor: Stuart Berger, MD more...
The goal of drug therapy is to stop or slow the progression of left ventricle (LV) systolic dysfunction. For chronic severe aortic valve insufficiency, vasodilators, ACE inhibitors, and digoxin may be useful. Please refer to the list of medications below.
Antibiotics to prevent bacterial endocarditis for aortic valve insufficiency are no longer recommended, according to the latest American Heart Association (AHA) guidelines. This is a significant change in the position of the AHA and was made based on the fact that infective endocarditis can only be prevented with antibiotic prophylaxis in a very small number of cases. Over the past 50 years, the AHA has been revising its recommendation based on accumulating information from expert studies. The recent revision in this recommendation was based on several factors. These include the following:
Infective endocarditis is much more likely to result from frequent exposure to random bacteremias associated with daily activities than from bacteremia caused by a dental, GI tract, or GU tract procedure.
Prophylaxis may prevent an exceedingly small number of cases of infectious endocarditis, if any, in individuals who undergo a dental, GI tract, or GU tract procedure.
The risk of antibiotic-associated adverse events exceeds the benefit, if any, from prophylactic antibiotic therapy.
Maintenance of optimal oral health and hygiene may reduce the incidence of bacteremia from daily activities and is more important than prophylactic antibiotics for a dental procedure to reduce the risk of infective endocarditis.
The mainstay of management for chronic aortic valve insufficiency is vasodilator therapy and observation. Vasodilators reduce systemic vascular resistance (SVR), allowing more forward flow to occur and, thus, improving cardiac output. In cases of acute mitral or aortic valve failure, a significant portion of the cardiac output is regurgitated through an incompetent valve. Catecholamines can worsen this effect by increasing peripheral vascular resistance. Oral hydralazine was found to reduce end-diastolic volume and increase ejection fraction when observed in clinical trials that lasted 1-2 years.
Dihydropyridine calcium channel blockers (eg, nifedipine) cause acute reduction in peripheral vascular resistance. Other physiologic effects include an immediate increase in cardiac output, decreased regurgitant volume, reduction in end-diastolic volume, increased ejection fraction, and reduction of LV dilation. Alpha-blockers (eg, prazosin) or direct vasodilators (eg, nitroprusside) are also effective.
Decreases systemic resistance through direct vasodilation of arterioles.
Produces vasodilation and increases inotropic activity of the heart. At higher dosages, may exacerbate myocardial ischemia by increasing heart rate.
Relaxes coronary smooth muscle and produces coronary vasodilation, which in turn improves myocardial oxygen delivery. For this indication, SL administration is generally safe, despite theoretical concerns.
Alpha1-adrenergic agonist. When increasing dosages, administer first dose of each increment hs to reduce syncopal episodes.
Angiotensin-converting enzyme (ACE) inhibitors
These agents are typically less effective than calcium channel blockers but are tolerated better by most patients. Pharmacologic effects result in a decrease in SVR, reducing blood pressure, preload, and afterload.
Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.
These agents are used to treat edema associated with congestive heart failure.
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 to patient circumstances.
These agents are used to treat acute aortic valve insufficiency. They are not to be used for long-term situations because of their potential to decrease LV function.
Beta1-blockade produces decreased heart rate and myocardial contractility, resulting in a decrease in cardiac output. Blockade of beta-receptors in cardiac conduction tissue results in slowing of AV conduction and suppression of automaticity.
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