Aortic Stenosis

Aortic valve stenosis

Aortic valve stenosis (AS) is a valvular heart disease caused by the incomplete opening of the aortic valve.[1]

The aortic valve controls the direction of blood flow from the left ventricle to the aorta. When in good working order, the aortic valve does not impede the flow of blood between these two spaces. Under some circumstances, the aortic valve becomes narrower than normal, impeding the flow of blood. This is known as aortic valve stenosis, or aortic stenosis, often abbreviated as AS.

Pathophysiology:
When the aortic valve becomes stenotic, it causes a pressure gradient between the left ventricle (LV) and the aorta.[2] The more constricted the valve, the higher the gradient between the LV and the aorta. For instance, with a mild AS, the gradient may be 20 mmHg. This means that, at peak systole, while the LV may generate a pressure of 140 mmHg, the pressure that is transmitted to the aorta will only be 120 mmHg. So, while a blood pressure cuff may measure a normal systolic blood pressure, the actual pressure generated by the LV would be considerably higher.

In individuals with AS, the left ventricle (LV) has to generate an increased pressure in order to overcome the increased afterload caused by the stenotic aortic valve and eject blood out of the LV. The more severe the aortic stenosis, the higher the gradient is between the left ventricular systolic pressures and the aortic systolic pressures. Due to the increased pressures generated by the left ventricle, the myocardium (muscle) of the LV undergoes hypertrophy (increase in muscle mass). This is seen as thickening of the walls of the LV. The type of hypertrophy most commonly seen in AS is concentric hypertrophy, meaning that all the walls of the LV are (approximately) equally thickened.

Etiology:
Major causes and predisposing conditions of aortic stenosis include acute rheumatic fever and bicuspid aortic valve. As individuals age, calcification of the aortic valve may occur and result in stenosis. This is especially likely to occur in people with a bicuspid aortic valve, but also occurs in the setting of perfectly normal valves as a result of age-induced 'wear and tear'. Typically, aortic stenosis due to calcification of a bicuspid valve occurs in the 4th or 5th decade of life, whereas that due to calcification of a normal valve tends to occur later - around the 7th or 8th decade.

Of the various forms of aortic stenosis, the calcific type is predominant. Since calcific aortic stenosis shares many pathological features and risk factors with atherosclerosis, and since atherosclerosis may be prevented and/or reversed by cholesterol lowering, there has been interest in attempting to modify the course of calcific aortic stenosis by cholesterol lowering with statin drugs. Although a number of small, observational studies demonstrated an association between lowered cholesterol and decreased progression, and even regression, of calcific aortic stenosis, a recent, large randomized clinical trial, published in 2005, failed to find any predictable effect of cholesterol lowering on calcific aortic stenosis. A 2007 study did demonstrate a slowing of aortic stenosis with the statin rosuvastatin.[3] However, what is likely to be considered the definitive trial, published in the New England Journal of Medicine in 2008, failed to find any beneficial effect of intensive cholesterol lowering on the course of aortic stenosis [4].

Prevalence:
Aortic stenosis is a common problem. Approximately 2% of people over the age of 65, 3% of people over age 75, and 4% percent of people over age 85 have the disorder. In North America and Europe, at least, the population is aging. Hence, the prevalence of aortic stenosis is increasing. Since the disease carries with it considerable morbidity and mortality, both with large personal and economic impact, aortic stenosis is a major health problem.[5]

Symptoms of aortic stenosis:
The Triad of AS is Dyspnea on exertion, Angina and Syncope ("Aortic Stenosis is a S.A.D. story" may be a helpful mnemonic for remembering this triad). Aortic stenosis can cause dizziness, syncope and congestive heart failure. More symptoms indicate a worse prognosis. Treatment requires replacement of the diseased valve with an artificial heart valve.

Congestive heart failure:
Congestive heart failure (CHF) carries a grave prognosis in patients with AS. Patients with CHF that is attributed to AS have a 2 year mortality rate of 50%, if the aortic valve is not replaced.

CHF in the setting of AS is due to a combination of systolic dysfunction (a decrease in the ejection fraction) and diastolic dysfunction (elevated filling pressure of the LV).

Syncope:
Syncope (fainting spells) in the setting of heart failure increases the risk of death. In patients with syncope, the 3 year mortality rate is 50%, if the aortic valve is not replaced.

It is unclear why aortic stenosis causes syncope. One popular theory is that severe AS produces a nearly fixed cardiac output. When the patient exercises, their peripheral vascular resistance will decrease as the blood vesels of the skeletal muscles dilate to allow the muscles to receive more blood to allow them to do more work. This decrease in peripheral vascular resistance is normally compensated for by an increase in the cardiac output. Since patients with severe AS cannot increase their cardiac output, the blood pressure falls and the patient will syncopize due to decreased blood perfusion to the brain.

A second theory as to why syncope may occur in AS is that during exercise, the high pressures generated in the hypertrophied LV cause a vasodepressor response, which causes a secondary peripheral vasodilation which in turn causes decreased blood flow to the brain. Indeed, in aortic stenosis, because of the fixed obstruction to bloodflow out from the heart, it may be impossible for the heart to increase its output to offset peripheral vasodilation.

A third mechanism may sometimes be operative. Due to the hypertrophy of the left ventricle in aortic stenosis, including the consequent inability of the coronary arteries to adequately supply blood to the myocardium (see "Angina" below), arrhythmias may develop. These can lead to syncope.

Finally, in calcific aortic stenosis at least, the calcification in and around the aortic valve can progress and extend to involve the electrical conduction system of the heart. If that occurs, the result may be heart block - a potentially lethal condition of which syncope may be a symptom.

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

Angina in the setting of AS is secondary to the left ventricular hypertrophy (LVH) that is caused by the constant production of increased pressure required to overcome the pressure gradient caused by the AS. While the myocardium (i.e. heart muscle) of the LV gets thicker, the arteries that supply the muscle do not get significantly longer or bigger, so the muscle may become ischemic (i.e. doesn't receive an adequate blood supply). The ischemia may first be evident during exercise, when the heart muscle requires increased blood supply to compensate for the increased workload. The individual may complain of exertional angina. At this stage, a stress test with imaging may be suggestive of ischemia.

Eventually, however, the muscle will require more blood supply at rest than can be supplied by the coronary artery branches. At this point there may be signs of ventricular strain pattern (ST segment depression and T wave inversion) on the EKG, suggesting subendocardial ischemia. The subendocardium is the region that becomes ischemic because it is the most distant from the epicardial coronary arteries.

Associated symptoms:
In Heyde's syndrome, aortic stenosis is associated with angiodysplasia of the colon. Recent research has shown that the stenosis causes a form of von Willebrand disease by breaking down its associated coagulation factor (factor VIII-associated antigen, also called von Willebrand factor), due to increased turbulence around the stenosed valve.

Aortic valve stenosis Diagnostic tests:

The electrocardiogram (ECG): Although aortic stenosis does not lead to any specific findings on the ECG, it still often leads to a number of electrocardiographic abnormalities. ECG manifestations of left ventricular hypertrophy (LVH) are common in aortic stenosis and arise as a result of the stenosis having placed a chronically high pressure load on the left ventricle (with LVH being the expected response to chronic pressure loads on the left ventricle no matter how caused).

As noted above, the calcification process which occurs in aortic stenosis can progress to extend beyond the aortic valve and into the electrical conduction system of the heart. Evidence of this phenomenon may include heart block that is apparent on the ECG but otherwise undetectable.

Heart catheterization: The heart may be catheterized to directly measure the pressure on both sides of the aortic valve. The pressure gradient may be used as a decision point for treatment. Catheterization is accurate for moderate velocity stenosis, while Doppler echo is more accurate at faster velocities.[citation needed]

Aortic valve stenosis Treatment

Medical:

Stabilize with prostaglandin E1(PGE) infusion to maintain cardiac output through PDA.
Inotropic support as needed.

Surgical: In adults, aortic stenosis usually requires aortic valve replacement if medical management does not successfully control symptoms. According to a prospective, single-center, nonrandomized study of 25 patients, percutaneous implantation of an aortic valve prosthesis in high risk patients with aortic stenosis results in marked hemodynamic and clinical improvement when successfully completed.[8]. Medium- and long-term results are unknown. When selecting the optimal therapy for individual patients, the percutaneous approach must be carefully weighed against the excellent results achieved with conventional surgery.

For infants and children, balloon valvuloplasty, where a balloon is inflated to stretch the valve and allow greater flow, may also be effective[1]

Aortic Stenosis
Campylobacter Infections Pneumonia Carcinoid Tumors Spleen Diseases Bacterial vaginosis Toxoplasmosis Meningococcal Disease Vaginal Diseases Stomach cancer Ingrown Nail Giardiasis Cardiogenic shock Scoliosis Chronic Diarrhea Urinary Tract And Bladder Infections Aortic Stenosis Mitral Valve Prolapse Colorectal cancer Liver cancer Yersinia Enterocolitica Kaposi's Sarcoma Leukemia, Adult Acute Shigellosis Sickle-cell disease Adenoviridae Coming Soon	Aortic valve stenosis Aortic valve stenosis (AS) is a valvular heart disease caused by the incomplete opening of the aortic valve.[1] The aortic valve controls the direction of blood flow from the left ventricle to the aorta. When in good working order, the aortic valve does not impede the flow of blood between these two spaces. Under some circumstances, the aortic valve becomes narrower than normal, impeding the flow of blood. This is known as aortic valve stenosis, or aortic stenosis, often abbreviated as AS. Pathophysiology: When the aortic valve becomes stenotic, it causes a pressure gradient between the left ventricle (LV) and the aorta.[2] The more constricted the valve, the higher the gradient between the LV and the aorta. For instance, with a mild AS, the gradient may be 20 mmHg. This means that, at peak systole, while the LV may generate a pressure of 140 mmHg, the pressure that is transmitted to the aorta will only be 120 mmHg. So, while a blood pressure cuff may measure a normal systolic blood pressure, the actual pressure generated by the LV would be considerably higher. In individuals with AS, the left ventricle (LV) has to generate an increased pressure in order to overcome the increased afterload caused by the stenotic aortic valve and eject blood out of the LV. The more severe the aortic stenosis, the higher the gradient is between the left ventricular systolic pressures and the aortic systolic pressures. Due to the increased pressures generated by the left ventricle, the myocardium (muscle) of the LV undergoes hypertrophy (increase in muscle mass). This is seen as thickening of the walls of the LV. The type of hypertrophy most commonly seen in AS is concentric hypertrophy, meaning that all the walls of the LV are (approximately) equally thickened. Etiology: Major causes and predisposing conditions of aortic stenosis include acute rheumatic fever and bicuspid aortic valve. As individuals age, calcification of the aortic valve may occur and result in stenosis. This is especially likely to occur in people with a bicuspid aortic valve, but also occurs in the setting of perfectly normal valves as a result of age-induced 'wear and tear'. Typically, aortic stenosis due to calcification of a bicuspid valve occurs in the 4th or 5th decade of life, whereas that due to calcification of a normal valve tends to occur later - around the 7th or 8th decade. Of the various forms of aortic stenosis, the calcific type is predominant. Since calcific aortic stenosis shares many pathological features and risk factors with atherosclerosis, and since atherosclerosis may be prevented and/or reversed by cholesterol lowering, there has been interest in attempting to modify the course of calcific aortic stenosis by cholesterol lowering with statin drugs. Although a number of small, observational studies demonstrated an association between lowered cholesterol and decreased progression, and even regression, of calcific aortic stenosis, a recent, large randomized clinical trial, published in 2005, failed to find any predictable effect of cholesterol lowering on calcific aortic stenosis. A 2007 study did demonstrate a slowing of aortic stenosis with the statin rosuvastatin.[3] However, what is likely to be considered the definitive trial, published in the New England Journal of Medicine in 2008, failed to find any beneficial effect of intensive cholesterol lowering on the course of aortic stenosis [4]. Prevalence: Aortic stenosis is a common problem. Approximately 2% of people over the age of 65, 3% of people over age 75, and 4% percent of people over age 85 have the disorder. In North America and Europe, at least, the population is aging. Hence, the prevalence of aortic stenosis is increasing. Since the disease carries with it considerable morbidity and mortality, both with large personal and economic impact, aortic stenosis is a major health problem.[5] Symptoms of aortic stenosis: The Triad of AS is Dyspnea on exertion, Angina and Syncope ("Aortic Stenosis is a S.A.D. story" may be a helpful mnemonic for remembering this triad). Aortic stenosis can cause dizziness, syncope and congestive heart failure. More symptoms indicate a worse prognosis. Treatment requires replacement of the diseased valve with an artificial heart valve. Congestive heart failure: Congestive heart failure (CHF) carries a grave prognosis in patients with AS. Patients with CHF that is attributed to AS have a 2 year mortality rate of 50%, if the aortic valve is not replaced. CHF in the setting of AS is due to a combination of systolic dysfunction (a decrease in the ejection fraction) and diastolic dysfunction (elevated filling pressure of the LV). Syncope: Syncope (fainting spells) in the setting of heart failure increases the risk of death. In patients with syncope, the 3 year mortality rate is 50%, if the aortic valve is not replaced. It is unclear why aortic stenosis causes syncope. One popular theory is that severe AS produces a nearly fixed cardiac output. When the patient exercises, their peripheral vascular resistance will decrease as the blood vesels of the skeletal muscles dilate to allow the muscles to receive more blood to allow them to do more work. This decrease in peripheral vascular resistance is normally compensated for by an increase in the cardiac output. Since patients with severe AS cannot increase their cardiac output, the blood pressure falls and the patient will syncopize due to decreased blood perfusion to the brain. A second theory as to why syncope may occur in AS is that during exercise, the high pressures generated in the hypertrophied LV cause a vasodepressor response, which causes a secondary peripheral vasodilation which in turn causes decreased blood flow to the brain. Indeed, in aortic stenosis, because of the fixed obstruction to bloodflow out from the heart, it may be impossible for the heart to increase its output to offset peripheral vasodilation. A third mechanism may sometimes be operative. Due to the hypertrophy of the left ventricle in aortic stenosis, including the consequent inability of the coronary arteries to adequately supply blood to the myocardium (see "Angina" below), arrhythmias may develop. These can lead to syncope. Finally, in calcific aortic stenosis at least, the calcification in and around the aortic valve can progress and extend to involve the electrical conduction system of the heart. If that occurs, the result may be heart block - a potentially lethal condition of which syncope may be a symptom. Angina: Angina in the setting of heart failure also increases the risk of death. In patients with angina, the 5 year mortality rate is 50%, if the aortic valve is not replaced. Angina in the setting of AS is secondary to the left ventricular hypertrophy (LVH) that is caused by the constant production of increased pressure required to overcome the pressure gradient caused by the AS. While the myocardium (i.e. heart muscle) of the LV gets thicker, the arteries that supply the muscle do not get significantly longer or bigger, so the muscle may become ischemic (i.e. doesn't receive an adequate blood supply). The ischemia may first be evident during exercise, when the heart muscle requires increased blood supply to compensate for the increased workload. The individual may complain of exertional angina. At this stage, a stress test with imaging may be suggestive of ischemia. Eventually, however, the muscle will require more blood supply at rest than can be supplied by the coronary artery branches. At this point there may be signs of ventricular strain pattern (ST segment depression and T wave inversion) on the EKG, suggesting subendocardial ischemia. The subendocardium is the region that becomes ischemic because it is the most distant from the epicardial coronary arteries. Associated symptoms: In Heyde's syndrome, aortic stenosis is associated with angiodysplasia of the colon. Recent research has shown that the stenosis causes a form of von Willebrand disease by breaking down its associated coagulation factor (factor VIII-associated antigen, also called von Willebrand factor), due to increased turbulence around the stenosed valve. Aortic valve stenosis Diagnostic tests: The electrocardiogram (ECG): Although aortic stenosis does not lead to any specific findings on the ECG, it still often leads to a number of electrocardiographic abnormalities. ECG manifestations of left ventricular hypertrophy (LVH) are common in aortic stenosis and arise as a result of the stenosis having placed a chronically high pressure load on the left ventricle (with LVH being the expected response to chronic pressure loads on the left ventricle no matter how caused). As noted above, the calcification process which occurs in aortic stenosis can progress to extend beyond the aortic valve and into the electrical conduction system of the heart. Evidence of this phenomenon may include heart block that is apparent on the ECG but otherwise undetectable. Heart catheterization: The heart may be catheterized to directly measure the pressure on both sides of the aortic valve. The pressure gradient may be used as a decision point for treatment. Catheterization is accurate for moderate velocity stenosis, while Doppler echo is more accurate at faster velocities.[citation needed] Aortic valve stenosis Treatment Medical: Stabilize with prostaglandin E1(PGE) infusion to maintain cardiac output through PDA. Inotropic support as needed. Surgical: In adults, aortic stenosis usually requires aortic valve replacement if medical management does not successfully control symptoms. According to a prospective, single-center, nonrandomized study of 25 patients, percutaneous implantation of an aortic valve prosthesis in high risk patients with aortic stenosis results in marked hemodynamic and clinical improvement when successfully completed.[8]. Medium- and long-term results are unknown. When selecting the optimal therapy for individual patients, the percutaneous approach must be carefully weighed against the excellent results achieved with conventional surgery. For infants and children, balloon valvuloplasty, where a balloon is inflated to stretch the valve and allow greater flow, may also be effective[1]
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