I have aortic valve insufficiency, do I need heart surgery (valve replacement) and when?

Answer 1

You can have a minimal amount of AOV insufficiency and never need open heart. It all depends on how much that valve leaks and how fast it gets worse.

If you had an Echocardiogram then they are aware of how much it leaks. If they didn't mentions valve replacement then I would just ask to have an Echo done yearly so you stay on top of the problem.
I know that it is hard, but try not to stress over it too much.

Nobody can predict if or when you will need surgery.

Best of luck

Answer 2

Will you need heart surgery? Yes.

When is a more complex question and answer.
It depends on :
1. The current function of the heart.
2. The degree of insufficiency.
3. The health of the person.
4. Other medical problems.

When the insufficiency begins to affect the pumping function of the heart to the point that exercise or daily life is affected it is time to have an artificial valve. This is not an easy decision to make as the new valve can also cause problems and new valves may need to be replaced eventially.

This is something to discuss with a cardiologist as each person is different.

Answer 3

The aortic valve is a semilunar valve that controls blood flow from the left ventricle to the systemic system of the body.. Its only job is to close so that backflow of blood back to the left ventricle will not be attained.. If the valve is not functioning properly the person's diastolic pressure will increase which will ultimately cause a cardiac infarction. The actual replacement can be achieved, but it is a very delicate surgery because the aorta is the biggest blood vessel in the body. Usually an aortic bypass is performed.

Answer 4

Your cardiologist should be in a good position to provide you with an answer to your question.

Answer 5

can email dr ng http://www.emedihub.com/profile.php?pid=217

Answer 6

what did your cardiologist say when you asked him this question?

Answer 7

Background: Aortic valve insufficiency (AI) results from leakage and backflow of blood that is ejected from the left ventricle (LV) into the ascending aorta back into the left ventricle.

Many mechanisms contribute to AI. These include abnormalities of the aortic valve leaflets and pathologies of the proximal aortic root. This article primarily focuses on AI caused by abnormalities in the aortic valve leaflets.

Anatomy of the aortic valve

The aortic valve is composed of 3 thin leaflets (ie, cusps) that project from the wall of the proximal ascending aorta. These leaflets and their respective sinuses of Valsalva are called left, right, and noncoronary.

Embryologic development of the aorta

In the embryonic stage, the truncus arteriosus connects to the dorsal aspect of the aorta via 6 pairs of aortic arches. The separation of truncus arteriosus into 2 great arteries results from the fusion of the aorticopulmonary septum and the truncus septum. The semilunar valves and their related sinuses are created by absorption and the hollowing out of tissue at the distal side of the truncus ridges.

Many mouse single-gene-knockout models of truncus arteriosus have been reported (eg, Sox4 null, Tbx1 null, pax3Splotch), although only NFATc1 null and Sox4 null display absent semilunar cusps. Ablation of a particular region in the cranial neural crest also results in truncus arteriosus, at least in the chick.

AI can be due to, or associated with, congenital heart disease.


Ventricular septal defect of the membranous (conoventricular) or conal septal (infundibuloventricular) types

Bicuspid (ie, bicommissural) aortic valve

Subvalvular aortic stenosis

Dysplasia of valve cusps, without fusion of commissures

Absence of 2 or 3 aortic valve leaflets
Acquired valvular aortic insufficiency

Causes of acquired AI include endocarditis, trauma, systemic diseases, and connective tissue syndromes. Systemic diseases causing AI include the following:


Rheumatic fever

Systemic lupus erythematosus
Syndromes leading to AI include the following:


Marfan syndrome

Ehlers-Danlos syndrome, type IV

Turner syndrome
In recent years, the percentage of individuals with AI caused by aortic root disease has been steadily increasing compared with the percentage of those with valvular disease. In fact, more than half of patients presenting with pure aortic regurgitation (AR) without any associated cardiac anomalies have AI caused by aortic root disease.



Pathophysiology: Regardless of etiology, AI results in volume overload on the LV because the LV is forced to pump the entire diastolic volume received from the left atrium and the regurgitant volume from the aorta through an incompetent aortic valve. Over time, such volume overload (ie, increased preload) causes eccentric hypertrophy of the LV. (Compare this to the concentric hypertrophy observed in aortic stenosis.)

Chronic aortic insufficiency

In long-standing AR, this compensatory mechanism begins to deteriorate. When LV function cannot continue to compensate for volume overload, the LV dilates and LV end-diastolic volume increases, even without further increase in AR volume. The LV thickness–to–chamber size ratio decreases. This causes an increase in systolic wall tension and a decrease in ejection fraction, stroke volume, and ventricular emptying. This larger end-systolic volume leads to progressively larger end-diastolic volume.

With progressive increases in wall tension, a mismatch occurs between oxygen demand and supply. Supply, which is always abnormally tenuous because of the lower-than-normal coronary driving pressure (difference in aortic diastolic pressure and ventricular diastolic pressure), cannot keep up with the increased demand. Interstitial fibrosis begins to occur, reducing wall compliance and further increasing end-diastolic LV pressure. If untreated, this interstitial fibrosis leads to elevated left atrial pressure and pulmonary venous congestion, especially during exercise. Ventricular ectopy is another manifestation of the oxygen supply-demand mismatch.

Acute severe aortic insufficiency

In acute severe AI due to endocarditis or sudden trauma, the LV cannot immediately respond with increased stroke volume to facilitate proper emptying because the element of eccentric hypertrophy is missing. As a result, LV diastolic pressure suddenly rises. Volume overload in the LV results in an early closure of the mitral valve during diastole. This occurs as a natural defense mechanism to protect the pulmonary venous system from the high-pressure regurgitant backflow coming from the high-pressure LV chamber.

Systolic pressures remain effectively unchanged in the aorta and the LV. Because of the increase in LV diastolic pressure, the pulse pressure may not significantly widen in acute severe AI. Tachycardia and early closure of the mitral valve are the compensatory mechanisms here.

Natural history

The natural history of AI after diagnosis is as follows:


Asymptomatic patients with normal LV systolic function

The 5-year survival rate is approximately 75%.

The 10-year survival rate is approximately 50%.

Progression to symptoms and/or LV dysfunction occurs in fewer than 6% of patients per year.

Progression to asymptomatic LV dysfunction occurs in fewer than 3.5% of patients per year.

Sudden death occurs in fewer than 0.2% of patients per year.

Asymptomatic patients with LV systolic dysfunction: Progression to cardiac symptoms occurs in more than 25% of patients per year.

Symptomatic patients: The mortality rate is higher than 10% per year.
Most findings in patients with AI are related to LV volume overload and eventual myocardial dysfunction.

Individuals with chronic AI may be asymptomatic for several years. This is because of adaptation of the LV to the pressure dynamics generated from long-standing volume overload. Many patients with chronic AI are no longer in the pediatric age group by the time signs and symptoms appear.

However, in acute severe AI, the LV does not have the ability to adapt to sudden volume overload resulting from AI. In this setting, LV failure and cardiac collapse occur. They are manifested as chest discomfort, dyspnea, and hypotension.

Answer 8

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