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Antibiotics Aortic Insufficiency


Aortic Insufficiency and Antibiotics - Aortic Insufficiency Treatment - Aortic valve prolapse - Aortic regurgitation

The aortic valve is between the heart's left ventricle (lower chamber that pumps blood to the body) and the aorta (the large artery that receives blood from the heart's left ventricle and distributes it to the body). Regurgitation means the valve doesn't close properly, and blood can leak backward through it. This means the left ventricle must pump more blood than normal, and will gradually get bigger because of the extra workload. Aortic regurgitation can range from mild to severe.

This is a condition in which the aortic valve has become disfigured to such an extent that its leaflets no longer are able to completely oppose each other during diastole

This condition allows blood to flow back into the left ventricle from the ascending aorta during diastole. Normally, there is no leakage of blood from the ascending aorta back into the left ventricle after systole.

Some people may have no symptoms for years. But as the condition worsens, symptoms will appear. These can include:

  • fatigue (especially during times of increased activity)
  • shortness of breath
  • edema (retention of fluid) in certain parts of the body such as the ankles
  • heart arrhythmias (abnormal heartbeats)
  • angina pectoris (chest pain or discomfort caused by reduced blood supply to the heart muscle)

Causes of Aortic Regurgitation

Aortic regurgitation can be caused by several things. It may be due to a bicuspid aortic valve. This is a congenital (existing at birth) deformity of the valve. In it, the valve has two cusps (flaps) rather than the normal three cusps. It can also be found in other kinds of congenital heart disease. Aortic regurgitation can also be caused by infections of the heart, such as rheumatic fever or infective endocarditis. Diseases that can cause the aortic root (the part of the aorta attached to the ventricle) to widen, such as the Marfan syndrome or high blood pressure, are other causes.

Aortic valve regurgitation can be caused by infection of the aortic valve due to syphilis via unprotected coitus and bacteria, which have gained access to the blood stream and the aortic valve through the use of illicit drugs intravenously.

Treatment of Aortic Regurgitation

All patients with AR need antibiotic prophylaxis to prevent infective endocarditis. Patients with AR of a rheumatic origin need antibiotic prophylaxis to prevent recurrences of rheumatic carditis. Patients with syphilitic AR need a course of antibiotics to treat syphilis. Patients with mild AR need no specific therapy. They do not need to restrict their activities and can lead a normal life. Patients with moderate AR also usually need no specific therapy. These patients, however, should avoid heavy physical exertion, competitive sports, and isometric exercise.

Patients with mild aortic regurgitation who have few or no symptoms need to see their physician regularly. As conditions worsen, medications may be used. These drugs can help regulate the heart rhythm, rid the body of fluids to control edema, and/or help the left ventricle pump better.

Serious cases may require surgical treatment. This involves replacing the diseased valve with an artificial one.

People with aortic regurgitation are at increased risk for developing an infection of the heart valve or lining of the heart (endocarditis). In the past, the American Heart Association has recommended that patients with aortic regurgitation take a dose of antibiotics before certain dental or surgical procedures. However, our association no longer recommends antibiotics before dental procedures except for patients at the highest level of risk for bad outcomes from endocarditis, such as:

  • patients with a prosthetic cardiac valve,
  • patients who have had endocarditis before,
  • patients with certain kinds of congenital heart disease, or
  • heart transplant patients who develop a problem with a heart valve.

Symptomatic patients with severe AR need medical and surgical treatment. Medical treatment consists of the administration of digitalis, diuretics, and vasodilators. Digitalis acts by increasing myocardial contractility, often reducing LV end-diastolic volume while increasing the LV ejection fraction and also the cardiac output if it is reduced in the resting state. Digitalis is clearly indicated in patients with symptoms.

Medical Treatment of Patients with Aortic Regurgitation

The need for and benefits of this therapy in asymptomatic patients have not been well documented. Diuretics are of value when the left atrial pressure is elevated and in the presence of heart failure.

Vasodilators are either arterial, venous, or both. Vasodilators act by reducing the peripheral arterial resistance, which favors forward cardiac output and reduces regurgitant volume; initially, the total LV stroke volume remains unchanged. If the left atrial pressure is elevated and LV ejection fraction reduced, vasodilators frequently result in an improvement in both. Long-term hydralazine therapy in symptomatic patients resuits in significant benefit in only 20 to 35 percent of patients.Those who are likely to benefit cannot be predicted. Vasodilators are indicated in patients who refuse surgery or are not operative candidates for any reason.

Vasodilators are also indicated for short-term therapy in patients awaiting valve replacement to optimize their hemodynamics (reduce filling pressures and increase cardiac output) and thus reduce their operative risks. If LV systolic function is normal, they can be given long-acting nifedipine. if they have abnormal LV systolic function, they should be treated with digitalis and ACE inhibitors; diuretics and hydralazine, with or without nitrates, can be used if needed. Small doses of hydralazine (50 mg) are without therapeutic effect in AR, and larger doses (approximately 100 mg) need to be given only twice daily; the twice-daily regimen reduces the incidence of side effects. Hydralazine should be started in small doses and gradually increased, depending on patient tolerance of the drug.

Vasodilators are of considerable short-term benefit in patients in functional classes III and IV or heart failure. All such patients need digitalis, diuretics, and ACE inhibitors. In patients in functional class IV with heart failure, vasodilators should ideally be started after the institution of beside henmodynamic monitoring-that is measuring of pulmonary artery wedge pressure and cardiac output with the use of ballon flotation catheters. Hemodynamic monitoring accurately identifies patients who need the therapy, since clinical judgments can be wrong. It establishes whether arterial dilators alone will suffice or whether additional venodilators are needed. Finally, it provides information on the optimum dosage of vasodilator therapy. After the initial hemodynamic measurements are made, arterial dilators are given in progressively increasing dosage until an optimum effect on cardiac output has been obtained. If cardiac output does not show any further increase but left atrial pressure is still very high, additional venodilator therapy should be given. If the patient is very ill or the hemodynamic abnormalities are marked, intravenous therapy (e.g., sodium nitroprusside) is the vasodilator of first choice. In this situation, intravenous vasodilator therapy should be used only with bedside hemodynamic monitoring. Inotropic agents, such as dobutamine, may be needed to improve LV function and increase cardiac output. Low-dose dopamine may be of value to increase urinary output.

Patients with severe chronic AR need valve surgery. The correct timing of surgical therapy is now better defined but is not fully clarified. Valve replacement should be performed before irreversible LV dysfunction occurs. The major problem, however, is identifying the precise point at which LV dysfunction will occur. Here, two major difficulties are encountered: (1) patients may already have impaired LV systolic pump function at rest when they firstpresent or at the time of the first symptom and
(2) patients with severe symptoms may have normal LV systolic pump function. Patients may be in NYHA functional class III (symptoms with less than ordinary activity), with a normal LV ejection fraction, or they may be in functional class I (asymptomatic), with a reduced LV ejection fraction. A reduced LV ejection fraction demonstrated by two-dimensional echocardiography and/or radionuclide ventriculography is the best noninvasive indicator of depressed LV systolic function.

Aortic Regurgitation
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