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16-September-2008 16:15:06 - Aortic valve stenosis Redirected from Aortic stenosis Aortic valve stenosis Classification and external resources ICD-10 I35.0, I06.0, Q23.0 ICD-9 395.0, 396.0, 746.3 DiseasesDB 844 MedlinePlus 000178 eMedicine med/157 Aortic valve stenosis AS is a valvular heart disease caused by the incomplete opening of the aortic valve. 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. Contents 1 Pathophysiology 2 Etiology 3 Prevalence 4 Symptoms of aortic stenosis 4.1 Congestive heart failure 4.2 Syncope 4.3 Angina 4.4 Associated symptoms 5 Physical examination 6 Diagnostic tests 6.1 The electrocardiogram ECG 6.2 Heart catheterization 6.3 Echocardiogram 7 Cautions 8 Treatment 8.1 Medical 8.2 Surgical 9 References 10 See also 11 External links Pathophysiology An aortic valve that, due to rheumatic heart disease, has a severe stenosis centre of image. The pulmonary trunk is seen at the lower right of the image. The proximal portion of right coronary artery and its ostium can be seen at the lower left of the image. The proximal left main coronary artery and its ostium are seen on the right of the image. Autopsy specimen. An aortic valve that, due to rheumatic heart disease, has a severe stenosis centre of image. The pulmonary trunk is seen at the lower right of the image. The proximal portion of right coronary artery and its ostium can be seen at the lower left of the image. The proximal left main coronary artery and its ostium are seen on the right of the image. Autopsy specimen. Simultaneous left ventricular and aortic pressure tracings demonstrate a pressure gradient between the left ventricle and aorta, suggesting aortic stenosis. The left ventricle generates higher pressures than what is transmitted to the aorta. The pressure gradient, caused by aortic stenosis, is represented by the green shaded area. AO = ascending aorta; LV = left ventricle; ECG = electrocardiogram. Simultaneous left ventricular and aortic pressure tracings demonstrate a pressure gradient between the left ventricle and aorta, suggesting aortic stenosis. The left ventricle generates higher pressures than what is transmitted to the aorta. The pressure gradient, caused by aortic stenosis, is represented by the green shaded area. AO = ascending aorta; LV = left ventricle; ECG = electrocardiogram. When the aortic valve becomes stenotic, it causes a pressure gradient between the left ventricle LV and the aorta.1 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 of 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. However, a 2007 study did demonstrate a slowing of aortic stenosis with the statin rosuvastatin.2 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. Symptoms of aortic stenosis When symptomatic, aortic stenosis can cause dizziness, syncope, angina 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. Physical examination Aortic stenosis is most often diagnosed when it is asymptomatic and can sometimes be detected during routine examination of the heart and circulatory system. Good evidence exists to demonstrate that certain characteristics of the peripheral pulse can rule in the diagnosis.3 In particular, there may be a slow and/or sustained upstroke of the arterial pulse, and the pulse may be of low volume. This is sometimes referred to as pulsus tardus et parvus. There may also be a noticeable delay between the first heart sound on auscultation and the corresponding pulse in the carotid artery so-called 'apical-carotid delay'. Similarly, there may be a delay between the appearance of each pulse in the brachial artery in the arm and the radial artery in the wrist. An easily heard systolic, crescendo-decrescendo i.e. 'ejection' murmur is heard loudest at the upper right sternal border, and radiates to the carotid arteries bilaterally. The murmur increases with squatting, decreases with standing and isometric muscular contraction, which helps distinguish it from hypertrophic obstructive cardiomyopathy HOCM. The murmur is louder during expiration, but is also easily heard during inspiration. The more severe the degree of the stenosis, the later the peak occurs in the crescendo-decrescendo of the murmur. The 2nd heart sound tends to become softer as the aortic stenosis becomes more severe. This is a result of the increasing calcification of the valve preventing it from snapping shut and producing a sharp, loud sound. Due to increases in left ventricular pressure from the stenotic aortic valve, over time the ventricle may hypertrophy, resulting in a diastolic dysfunction. As a result, one may hear a 4th heart sound due to the stiff ventricle. With continued increases in ventricular pressure, dilatation of the ventricle will occur, and a 3rd heart sound may be manifest. Finally, aortic stenosis often co-exists with some degree of aortic insufficiency. Hence, the physical exam in aortic stenosis may also reveal signs of the latter, for example an early diastolic decrescendo murmur. Indeed, when both valve abnormalities are present, the expected findings of either may be modified or may not even be present. Rather, new signs emerge which reflect the presence of simultaneous aortic stenosis and insufficiency, e.g. pulsus bisferiens. According to a meta analysis, the most useful findings for ruling in aortic stenosis in the clinical setting were slow rate of rise of the carotid pulsepositive likelihood ratio ranged 2.8-130 across studies, mid to late peak intensity of the murmurpositive likelihood ratio, 8.0-101, and decreased intensity of the second heart soundpositive likelihood ratio, 3.1-50.4 Peripheral signs include: a slow-rising, small volume carotid pulse narrowed pulse pressure sustained, thrusting apex beat which is usually not displaced unless the stenosis is severe 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 below, 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 Echocardiogram Echocardiogram heart ultrasound is the best non-invasive test to evaluate the aortic valve anatomy and function. The aortic valve area can be calculated non-invasively using echocardiographic flow velocities. Using the velocity of the blood through the valve, the pressure gradient across can be calculated by the modified Bernoulli's equation: Gradient = 4velocity² mmHg A normal aortic valve has no gradient. If the mean gradient is 25 mm Hg, the stenosis is mild; if the mean gradient is between 25 mm Hg and 50 mm Hg, the stenosis is moderate; if the mean gradient is 50 mm Hg the stenosis is severe; and when the gradient is greater than 70 mm Hg, the stenosis is critical. A normal aortic valve area is 2 cm2. If the valve area is between 1.3 and 2.0 cm2, the stenosis is mild; if the valve area is between 1.0 and 1.3 cm2, the stenosis is moderate; if the valve area is between 0.7 and 1.0 cm2, the stenosis is moderate-severe; areas of less than 0.7 cm2 constitute severe aortic stenosis. Cautions People with aortic stenosis of any aetiology are at risk for the development of infection of their stenosed valve, i.e. infective endocarditis. To lessen the chance of developing that serious complication, people with AS are usually advised to take antibiotic prophylaxis around the time of certain dental/medical/surgical procedures. Such procedures may include dental extraction, deep scaling of the teeth, gum surgery, dental implants, treatment of esophageal varices, dilation of esophageal strictures, gastrointestinal surgery where the intestinal mucosa will be disrupted, prostate surgery, urethral stricture dilation, and cystoscopy. Note that routine upper and lower GI endoscopy i.e. gastroscopy and colonoscopy, with or without biopsy, are not usually considered indications for antibiotic prophylaxis. Notwithstanding the foregoing, the American Heart Association has recently changed its recommendations regarding antibiotic prophylaxis for endocarditis. Specifically, as of 2007, it is recommended that such prophylaxis be limited only to 1. those with prosthetic heart valves, 2. those with previous episodes of endocarditis, and 3. those with certain types of congenital heart disease.5 Since the stenosed aortic valve may limit the heart's output, people with aortic stenosis are at risk of syncope and dangerously low blood pressure should they use any of a number of common medications. Ironically, these same medicines are used to treat a variety of cardiovascular diseases, many of which may co-exist with aortic stenosis. Examples include nitroglycerin, nitrates, ACE inhibitors, terazosin Hytrin, and hydralazine. Note that all of these substances lead to peripheral vasodilation. Normally, however, in the absence of aortic stenosis, the heart is able to increase its output and thereby offset the effect of the dilated blood vessels. In some cases of aortic stenosis, however, due to the obstruction of blood flow out of the heart caused by the stenosed aortic valve, cardiac output cannot be increased. Low blood pressure or syncope may ensue. Treatment Medical Aortic stenosis may be medically treated to control symptoms. 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.6 For infants and children, balloon valvuloplasty, where a balloon is inflated to stretch the valve and allow greater flow, may also be effective1. References ^ Lilly LS or 2003. Pathophysiology of Heart Disease, 3rd ed., Lippincott Williams Wilkins. ISBN 0-7817-4027-4. ^ Moura LM, Ramos SF, Zamorano JL, et al 2007. Rosuvastatin affecting aortic valve endothelium to slow the progression of aortic stenosis. J. Am. Coll. Cardiol. 49 5: 554-61. doi:10.1016/j.jacc.2006.07.072. PMID 17276178. ^ JAMA - Abstract: Does this patient have an abnormal systolic murmur?, February 19, 1997, Etchells et al. 277 7: 564 ^ Etchells E, Bell C, Robb K 1997. Does this patient have an abnormal systolic murmur?. JAMA 277 7: 564-71. doi:10.1001/jama.277.7.564. PMID 9032164. ^ Infective Endocarditis previously referred to as bacterial endocarditis ^ Grube E, Laborde JC, Gerckens U, et al 2006. Percutaneous implantation of the CoreValve self-expanding valve prosthesis in high-risk patients with aortic valve disease: the Siegburg first-in-man study. Circulation 114 15: 1616-24. doi:10.1161/CIRCULATIONAHA.106.639450. PMID 17015786. See also Aortic valve area calculation External links Aortic stenosis information from Seattle Children's Hospital Heart Center Mitral Valve Repair at The Mount Sinai Hospital v d e Cardiovascular disease: heart disease - Circulatory system pathology I00-I52, 390-429 Ischaemic/ Acute coronary CHD: CAD - Coronary thrombosis - Coronary vasospasm - Coronary artery aneurysm Angina pectoris Prinzmetal's angina - Myocardial infarction heart attack Myocardial rupture - Dressler's syndrome Layers Pericardium Pericarditis Acute, Constrictive - Pericardial effusion - Cardiac tamponade - Hemopericardium Myocardium Myocarditis Cardiomyopathy: Dilated Alcoholic - Hypertrophic - Restrictive Loeffler endocarditis, Cardiac amyloidosis Arrhythmogenic right ventricular dysplasia Endocardium/ valves Endocarditis Subacute bacterial endocarditis, Libman-Sacks endocarditis, Nonbacterial thrombotic endocarditis mitral regurgitation, prolapse, stenosis - aortic stenosis, insufficiency - tricuspid stenosis, insufficiency - pulmonary stenosis, insufficiency Conduction/ arrhythmia Heart block AV 1°, 2°, 3° - Bundle branch Left, Right - Bifascicular/Trifascicular - Sinoatrial - Sick sinus syndrome - Adams-Stokes syndrome Pre-excitation syndrome Wolff-Parkinson-White - Lown-Ganong-Levine Tachycardia Paroxysmal - Supraventricular AV nodal reentrant, Accelerated idioventricular rhythm, Sinus - Ventricular Torsades de pointes, Catecholaminergic polymorphic Premature contraction Atrial - Ventricular Flutter/fibrillation Atrial flutter - Ventricular flutter - Atrial fibrillation Familial - Ventricular fibrillation Pacemaker Wandering pacemaker - Ectopic pacemaker - Parasystole Long QT syndrome Romano-Ward syndrome - Andersen-Tawil syndrome - Jervell and Lange-Nielsen syndrome Cardiac arrest Sudden cardiac death - Asystole Other Cardiomegaly - Ventricular hypertrophy Left, Right/Cor pulmonale Heart failure Cardiac asthma - Rheumatic fever See also congenital, neoplasia v d e Congenital malformations and deformations of circulatory system Q20-Q28, 745-747 Heart R→L, L→R Cardiac chambers and connections Persistent truncus arteriosus - Double outlet right ventricle Taussig-Bing syndrome - Transposition of the great vessels dextro, levo - Brugada syndrome Cardiac septa Ventricular septal defect - Atrial septal defect Lutembacher's syndrome - Atrioventricular septal defect Ostium primum - Tetralogy of Fallot - Eisenmenger's syndrome Valvular heart disease/ heart chambers Right pulmonary valves stenosis, insufficiency - tricuspid valves stenosis, atresia, Ebstein's anomaly Left aortic valves stenosis, insufficiency, bicuspid - mitral valves stenosis, regurgitation - Hypoplastic left heart syndrome Other Dextrocardia - Levocardia - Cor triatriatum - Crisscross heart Vascular Great arteries aorta: Patent ductus arteriosus - Aortic coarctation - Interrupted aortic arch - Overriding aorta - Aneurysm of sinus of Valsalva - Vascular ring pulmonary artery: Pulmonary atresia Great veins superior vena cava: Persistent left superior vena cava pulmonary vein: Total anomalous pulmonary venous connection - Scimitar syndrome Other Arteriovenous malformation Cerebral arteriovenous malformation See also non-congenital conditions I, 390-459 Retrieved from http://en..org/wiki/Aortic_valve_stenosis Categories: Valvular heart diseaseHidden categories: All articles with statements | Articles with statements since June 2007 Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Deutsch Español Français Norsk bokmål Norsk nynorsk Polski Português Svenska This page was last modified on 19 June 2008, at 12:1
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