Aortic stenosis

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Aortic stenosis ( AS or AoS ) is the narrowing of the left ventricle exit of the heart (where the aorta begins), resulting in trouble. This can occur in the aortic valve and also above and below this level. This usually worsens over time. Symptoms often appear gradually with a decrease in the ability to exercise that often occurs first. If heart failure, loss of consciousness, or heart-related chest pain occur because the result is worse. Loss of consciousness usually occurs by standing or exercising. Signs of heart failure include shortness of breath especially when lying down, at night, or with exercise, and swelling of the feet. Unconstricted valve thickening is known as aortic sclerosis.

Causes include birth with a bicuspid aortic valve, and rheumatic fever. The bicuspid aortic valve affects about one to two percent of the population. Currently, rheumatic heart disease occurs in many developing countries. Normal valves may also harden for decades. Risk factors are similar to coronary artery disease and include smoking, high blood pressure, high cholesterol, diabetes, and being male. The aortic valve usually has three leaflets and is located between the left ventricle of the heart and the aorta. The US usually produces a heart murmur. The severity can be divided into mild, moderate, severe, and very severe, distinguishable from cardiac ultrasound.

Aortic stenosis is usually followed by recurrent ultrasound. After becoming severe, treatment primarily involves valve replacement surgery, with replacement of the transkatheter aortic valve (TAVR) being an option in some people at high risk of surgery. Valves can be either mechanical or bioprosthetic, with each having risks and benefits. Another less invasive procedure, aortic valvuloplasty balloon (BAV), can yield benefits, but only for a few months. Complications such as heart failure can be treated in the same way as those with mild to moderate AS. In those with severe disease, a number of drugs should be avoided, including ACE inhibitors, nitroglycerin, and some beta blockers. Nitroprusside or phenylephrine may be used in those with decompensated heart failure depending on blood pressure.

Aortic stenosis is the most common heart valve disease in developed countries. It affects about 2% of people over the age of 65 years. Price estimates are unknown in most developing countries by 2014. In those with symptoms, without improving the likelihood of death at five years around 50% and at 10 years about 90%. Aortic stenosis was first described by the French physician Lazare RiviÃÆ'¨re in 1663.

Video Aortic stenosis

Signs and symptoms

Symptoms associated with aortic stenosis depend on the degree of stenosis. Most people with mild to moderate aortic stenosis have no symptoms. Symptoms are usually present in individuals with severe aortic stenosis, although they may occur in those with mild to moderate aortic stenosis as well. The three main symptoms of aortic stenosis are loss of consciousness, angina chest pain and shortness of breath with other activities or symptoms of heart failure such as shortness of breath when lying flat, night breathless episodes, or swollen feet and legs. It may also be accompanied by the characteristic "Dresden china" pale appearance with flush light.

Angina

Angina in the regulation of heart failure also increases the risk of death. In people with angina, the 5-year mortality rate is 50% if the aortic valve is not replaced.

Angina in the US setting occurs due to left ventricular hypertrophy (LVH) caused by constant production of the increased pressure required to overcome the pressure gradient caused by the US. While the left ventricular muscle layer thickens, the arteries supplying the muscles do not increase significantly longer or larger, so the muscles may not receive enough blood supply to meet their oxygen requirements. This ischemia may be first proven during exercise when the heart muscle needs an increase in blood supply to compensate for the increase in workload. Individuals may complain of angina chest pain with exertion. At this stage, a heart stress test with imaging may be suggestive of ischemia.

However, in the end, the heart muscle will require more blood supply at rest than can be given by the branches of the coronary arteries. At this point there may be signs of ventricular strain pattern (ST segment depression and T wave inversion) on the ECG, indicating subendocardial ischemia. Subendocardium is the region most susceptible to ischemia because it is the most distant from the epicardial coronary artery.

Sync

The syncope (fainting spell) of aortic valve stenosis is usually eksertional. In the setting of heart failure increases the risk of death. In people with syncope, the three-year mortality rate is 50% if the aortic valve is not replaced.

It is not clear why aortic stenosis causes syncope. One of the popular theories is that the heavy US produces an almost fixed heart output. When a person with aortic stenosis exercise, their peripheral vascular resistance will decrease as the blood vessels of skeletal muscle enlarge to allow the muscles to receive more blood to enable them to do more work. This decrease in peripheral vascular resistance is usually compensated by an increase in cardiac output. Because people with severe AS can not increase their cardiac output, blood pressure decreases and people will pass out due to decreased blood perfusion to the brain.

The second theory of why syncope can occur in the US is that during exercise, the high pressure produced in the left ventricle that develops hypertrophy leads to a vasodepressor response, which causes secondary peripheral vasodilation which, in turn, causes a decrease in blood flow to the brain resulting in loss of consciousness. Indeed, in aortic stenosis, because obstruction remains to the outflow of blood from the heart, it may not be possible for the heart to increase its output to compensate for peripheral vasodilation.

The third mechanism can sometimes work. Due to left ventricular hypertrophy in aortic stenosis, including the inability of the coronary arteries to supply sufficient blood to the myocardium (see "Angina" below), abnormal heart rhythms may occur. This can cause syncope.

Finally, in calcified aortic stenosis at least, calcification in and around the aortic valve can develop and extend to involve the electrical conduction system of the heart. If that happens, the result may be a heart block - potentially deadly syncope conditions that may be a symptom.

Congestive congestive heart failure

Congestive heart failure (CHF) carries the prognosis of graves in people with AS. People with CHF are due to the US having a 2% death rate of 50% if the aortic valve is not replaced. CHF in the US setting is due to a combination of left ventricular hypertrophy with fibrosis, systolic dysfunction (decrease in ejection fraction) and diastolic dysfunction (high fill pressure of LV).

Related symptoms

In Heyde syndrome, aortic stenosis is associated with gastrointestinal bleeding due to colonic angiodysplasia. Recent research has shown that stenosis causes the form of von Willebrand disease by breaking down the associated coagulation factor (factor VIII-related antigen, also called von Willebrand factor), due to increased turbulence around the valve stenosis.

Complications

Nevertheless, the American Heart Association recently changed its recommendations on prophylactic antibiotics for endocarditis. In particular, in 2007 it was recommended that such prophylaxis should be limited only to those who had prosthetic heart valves, those with previous episodes of endocarditis, and those with certain types of congenital heart disease.

Because stenosed aortic valves can limit cardiac output, people with aortic stenosis are at risk of syncope and dangerous low blood pressure should they use one of a number of drugs for cardiovascular disease that often coexist with aortic stenosis. Examples include nitroglycerin, nitrates, ACE inhibitors, terazosin (Hytrin), and hydralazine. Note that all of these substances cause peripheral vasodilation. Under normal circumstances, in the absence of aortic stenosis, the heart is able to increase its output and thus compensate for the effect of enlarged blood vessels. In some cases of aortic stenosis, however, due to obstruction of blood flow out of the heart caused by a stenosed aortic valve, cardiac output can not be increased. Low blood pressure or syncope can occur.

Maps Aortic stenosis

Cause

Aortic stenosis is most often caused by age-related progressive calcifications (& gt; 50% of cases), with an average age of 65 to 70 years. Another major cause of aortic stenosis is calcification of the congenital bicuspid aortic valve (30-40% of cases), usually earlier in those aged 40 to 50.

Post-inflammatory acute rheumatic fever is the cause of less than 10% of cases. The rare causes of aortic stenosis include Fabry's disease, systemic lupus erythematosus, Paget's disease, high blood uric acid levels, and infections.

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Pathophysiology

Human aortic valves typically consist of three leaves or leaflets and have an opening of 3.0-4.0 square centimeters. When the left ventricle contracts, it forces blood through the valve into the aorta and then throughout the body. When the left ventricle inflates, the aortic valve closes and prevents blood in the aorta from flowing backwards (regurgitation) into the left ventricle. In aortic stenosis, the opening of the aortic valve becomes narrowed or narrowed (stenotik) (eg due to calcification). Degenerative (the most common variation), and bicuspid aortic stenosis, both begin with damage to endothelial cells from increased mechanical stress. Inflammation is thought to be involved in the early stages of US pathogenesis and associated risk factors are known to promote the precipitation of LDL cholesterol and lipoproteins (a), highly destructive substances, into the aortic valve, causing significant damage and stenosis. overtime.

As a consequence of this stenosis, the left ventricle must produce a higher pressure with each contraction to effectively move the blood forward to the aorta. Initially, LV produces an increase in this pressure by thickening the muscle wall (myocardial hypertrophy). The type of hypertrophy most commonly seen in the US is known as concentric hypertrophy, where the LV wall is (approximately) as thickened.

In the later stages, the left ventricle widened, the walls thinned, and systolic function worsened (resulting in impaired ability to pump blood forward). Morris and Innasimuthu et al. shows that different coronary anatomy is associated with different valve disease. Research is underway to see if different coronary anatomies can cause turbulent flow at the valve level causing inflammation and degeneration.

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Diagnosis

Aortic stenosis is most often diagnosed when asymptomatic and can sometimes be detected during a routine examination of the heart and circulatory system. Good evidence exists to show that certain characteristics of the peripheral pulse may rule in diagnosis. In particular, there may be slow and/or sustained pulse arteries, and the pulse may have low volume. This is sometimes referred to as pulsus parvus et tardus . There may also be a marked delay between the first heart sound (on auscultation) and the corresponding pulse of the carotid artery (so-called 'apical-carotid delay'). In the same way, there may be a delay between the appearance of each pulse in the brachial artery (in the arm) and the radial artery (at the wrist).

The first heart sound may be followed by a sharp ejection sound ("ejection click") sounds best in the lower left and sternal bounds of the sternum, and, thus, appears "split". The ejection noise, caused by the impact of left ventricular outflow on partially fused aortic valves, is more often associated with a mobile bicuspid aortic valve than a stationary calcific aortic valve. This sound intensity does not vary with respiration, which helps distinguish it from ejection clicks generated by the pulmonary valve stenosis, which will decrease slightly in intensity during inspiration.

A systolic, crescendo-decrescendo (ie, 'ejection') murmur is heard loudest in the upper right sternal border, in the right 2nd intercostal space, and radiates into the carotid artery bilaterally. The murmur increases with squatting and decreases with standing and contraction of isometric muscles such as Valsalva maneuver, which helps to distinguish it from obstructive hypertrophic cardiomyopathy (HOCM). Murmurs sound louder during expiration but are also easy to hear during inspiration. The more severe the degree of stenosis, then the peak occurs in the crescendo-decrescendo of the murmur.

The second heart sound (A ₂ ) tends to be decreased and softer as aortic stenosis becomes more severe. This is the result of an increase in valve calcification that prevents it from "snapping" closing and producing a sharp and loud sound. Due to the increase in left ventricular pressure from the stenotic aortic valve, over time the ventricles may develop hypertrophy, resulting in diastolic dysfunction. As a result, there may be a fourth heart sound because the ventricles are stiff. With increasing ventricular pressure, ventricular dilatation will occur, and a third heart sound may manifest.

Finally, aortic stenosis often coincides with some degree of aortic insufficiency (aortic regurgitation). Therefore, physical examination of aortic stenosis may also reveal the latter signs, for example, early decrescendo diastolic murmur. Indeed, when both valve abnormalities are present, the expected findings can be modified or even absent. In contrast, new signs reflecting the presence of simultaneous aortic stenosis and insufficiency, for example, pulsus bisferiens, appear.

According to meta-analysis, the most useful findings for reigning in aortic stenosis in clinical settings is the slow rate of increase in carotid pulse (a positive likelihood ratio ranging from 2.8 to 130 in all studies), mid to final intensity of the murmur (positive possibility ratio , 8.0-101), and a decrease in the intensity of the second heart sound (positive possibility ratio, 3.1-50).

Other peripheral signs include:

• sustained, rising apex beat, which is not displaced unless systolic dysfunction of the left ventricle has grown
• Precordial Sensation
• narrow pulse pressure

Electrocardiogram

Although aortic stenosis does not lead to specific findings in electrocardiogram (EKG), it still often causes a number of electrocardiographic disorders. EKG manifestations of left ventricular hypertrophy (LVH) are common in aortic stenosis and arise as a result of stenosis after placing a high chronic stress load on the left ventricle (with LVH being the expected response to chronic pressure burden on the left ventricle no matter what the cause).

As mentioned above, the calcification process that occurs in aortic stenosis can progress beyond the aortic valve and into the heart's electrical conduction system. Evidence of this phenomenon may rarely include characteristic ECG patterns of certain types of heart block such as left bundle branch block.

Cardiac catheterization

Cardiac catheterization provides a definitive diagnosis, indicating severe stenosis in the valve area & lt; 1.0 cm ² (normally about 3 cm ² ). It can directly measure the pressure on both sides of the aortic valve. The pressure gradient can be used as a decision point for treatment. This is useful in symptomatic people before surgery. The standard for the diagnosis of aortic stenosis is a noninvasive test with echocardiography. Cardiac catheterization is provided for cases where there is a difference between clinical features and non-invasive testing, because of the inherent risk of aortic valve crossing, such as stroke.

Echocardiogram

Echocardiogram (cardiac ultrasound) is the best noninvasive way to evaluate the anatomy and function of the aortic valve.

The aortic valve area can be calculated non-invasively using echocardiographic flow rates. By using the velocity of blood through the valve, the pressure gradient in the valve can be calculated by a continuity equation or using a modified Bernoulli equation:

Gradient = 4 (speed) Ã,² mmHg

Normal aortic valve has a gradient of only a few mmHg. The reduced valve area causes an increase in pressure gradient, and this parameter is used to classify and assess aortic stenosis as mild, moderate or severe. The pressure gradient can be very low in the presence of mitral stenosis, heart failure, joint aortic regurgitation and also ischemic heart disease (diseases associated with decreased blood supply and oxygen causing ischemia).

Echocardiogram may also show left ventricular hypertrophy, a thickened and immobile aortic valve and aortic root dilatation. However, it may seem normal in acute cases.

Chest Rontgen

Chest X-rays can also assist in the diagnosis and provide clues about the severity of the disease, indicating valve calcification levels, and in chronic conditions, the left ventricle and the enlarged atrium.

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Management

Treatment is generally not necessary in asymptomatic individuals. In moderate cases, echocardiography is performed every 1-2 years to monitor progress, possibly complemented by a cardiac stress test. In severe cases, echocardiography is performed every 3-6 months. In mild and moderate cases, the person should immediately re-visit or be admitted for hospitalization if any new symptoms are present. There is no therapeutic option available today to treat people with aortic valve stenosis; However, studies have shown that the disease occurs as a result of active cellular processes, suggesting that targeting this process may lead to a viable therapeutic approach.

Medication

The effect of statins on US development is unclear. Recent trials do not show any benefit in slowing US progression, but show a decrease in ischemic cardiovascular events.

In general, medical therapy has relatively poor efficacy in treating aortic stenosis. However, it may be useful to manage common living conditions that are generally correlated with aortic stenosis:

• Every angina is commonly treated with beta-blockers and/or calcium blockers. Nitrate is contraindicated because of its potential to cause great hypotension in aortic stenosis.
• Any hypertension is treated aggressively, but caution should be done in managing beta-blockers.
• Every heart failure is generally treated with digoxin and diuretics, and, if not contraindicated, careful administration of ACE inhibitors.

While observational studies have shown an association between lowering cholesterol with statins and decreased progression, randomized clinical trials published in 2005 failed to find any effect on calcified aortic stenosis. A 2007 study showed slowing of aortic stenosis with statin rosuvastatin.

Repair of aortic valve

Aortic valve repair or aortic valve reconstruction illustrates the reconstruction of both the shape and function of the original aortic valve and dysfunction. Most often it is applied to the treatment of aortic regurgitation. It may also be necessary for the treatment of aortic aneurysm, less commonly for congenital aortic stenosis.

Aortic valve replacement

In adults, severe aortic stenosis of symptoms usually requires the replacement of the aortic valve (AVR). While AVR has been the standard treatment for aortic stenosis for decades, current aortic valve replacement approaches include open heart surgery, minimally invasive cardiac surgery (MICS) and minimally invasive catheter-aortic valve replacement valves. However, surgical aortic valve replacement is well studied and generally has a good long-term and established long-term prognosis.

The aortic valve pain is most often replaced using a surgical procedure with a mechanical or tissue valve. This procedure is performed either in open heart surgery procedures or, in a smaller but growing number of cases, a minimally invasive cardiac surgical procedure (MICS).

Transfrom aortic valve replacement

Globally more than 250,000 people have received aortic transcatheter valve replacement (TAVR). For non-candidates for surgical valve replacement and most patients older than 75, TAVR may be a suitable alternative.

Balloon valvuloplasty

For infants and children, balloon valvuloplasty, in which the balloon is inflated to stretch the valve and allow for greater flow, may also be effective. In adults, however, it is generally ineffective, because the valves tend to return to a state of stenosis. The surgeon will make a small incision at the top of the person's foot and proceed to insert the balloon into the artery. The balloon then rises to the valve and is pumped to stretch the open valve.

Heart failure

Acute decompensated heart failure because the US can be temporarily administered by intra-aortic balloon pumps while waiting for surgery. In those with nitroprusside high blood pressure can be used with caution. Phenylephrine can be used on those with very low blood pressure.

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Prognosis

If left untreated, severe symptomatic aortic stenosis carries a poor prognosis with a 2-year mortality rate of 50-60% and a 3-year survival rate of less than 30%. The prognosis after aortic valve replacement for people younger than 65 is about five years less than the general population; for people older than 65 it's almost the same.

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Epidemiology

Approximately 2% of people over age 65, 3% of people over age 75, and 4% percent of people over the age of 85 have aortic valve stenosis. Prevalence increases with aging populations in North America and Europe.

Risk factors are known to influence the development of US diseases including lifestyle habits that are similar to coronary artery disease such as hypertension, old age, being male, hyperlipidemia, diabetes mellitus, smoking, metabolic syndrome, and end-stage renal disease.

src: circinterventions.ahajournals.org

History

Aortic stenosis was first described by the French physician Lazare RiviÃÆ'¨re in 1663.

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Research

People with bisphosphonates have little development of aortic stenosis and some have regressed. This finding led to some ongoing experiments. Subsequent studies failed to confirm initial positive results.

src: circinterventions.ahajournals.org

References

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External links

• Aortic stenosis in Curlie (based on DMOZ)
• Aortic stenosis in children
• Bonow, Robert O.; Brown, Alan S.; Gillam, Linda D.; Kapadia, Samir R.; Kavinsky, Clifford J.; Lindman, Brian R.; Mack, Michael J.; Thourani, Vinod H. (October 2017). "ACC/AATS/AHA/ASE/EACTS/HVS/SCA/SCAI/SCCT/SCMR/STS 2017 Appropriate Criteria for the Treatment of Patients With Severe Aortic Stenosis". Journal of the American College of Cardiology . doi: 10.1016/j.jacc.2017.09.018.

Source of the article : Wikipedia