Aortic valve stenosis
From Wikipedia, the free encyclopedia
| 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 heart condition 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.
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[edit] Pathophysiology
[[Image:Aortic Stenosis - Hemodynamic Pressure Tracing.png|thumb|right|300px|Simultaneous left ventricular and aortic pressure tracings demonstrate a pressure gradient between the left ventricle and aorta, suggesting aortic stenosis. The left ventricle generates
[edit] 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.
[edit] 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.
[edit] 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[1]. 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 murmur is heard loudest at the upper right sternal border, and radiates to the carotid arteries. The murmur increases with squatting, decreases with standing and isometric muscular contraction, which helps distinguish it from hypertrophic obstructive cardiomyopathy (HOCM). Respiration has no effect on the loudness of the murmur. 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. 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 relflect the presence of simultaneous aortic stenosis and insufficiency, e.g. pulsus bisferiens.
[edit] The electrocardiogram (ECG) in aortic stenosis
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.
[edit] Major complcations 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 either a porcine aortic valve or a cadaveric aortic valve, or an prosthetic aortic valve.
[edit] Congestive heart failure
Congestive heart failure (CHF) is 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).
[edit] Syncope
Syncope 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.
[edit] 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 of the LV gets thicker, the arteries that supply the muscle do not get significantly longer or bigger, so the muscle may become ischemic. The ischemia may first be evident during exercise, when the 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 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.
[edit] 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.
[edit] 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.
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.
[edit] Calculation of valve area
There are many ways to calculate the valve area of aortic stenosis. The most commonly used methods involve measurements taken during echocardiography. For interpretation of these values, the area is generally divided by the body surface area, to arrive at the patient's optimal aortic valve orifice area.
The calculated aortic valve orifice area is currently one of the measures for evaluating the severity of aortic valve stenosis. A valve area of less than 0.8 cm² is considered to be severe aortic stenosis.[2][3]
[edit] Planimetry
Planimetry is the tracing out of the opening of the aortic valve in a still image obtained during echocardiographic acquisition during ventricular systole, when the valve is supposed to be open. While this method directly measures the valve area, the image may be difficult to obtain due to artifacts during echocardiography, and the measurements are dependant on the technician who has to manually trace the perimeter of the open aortic valve.
[edit] The continuity equation
The continuity equation states that the flow in one area must equal the flow in a second area if there are no shunts in between the two areas. In practical terms, the flow from the left ventricular outflow tract (LVOT) is compared to the flow at the level of the aortic valve. Using echocardiography, the peak velocity at the level of the aortic valve and in the LV outflow tract can be measured, and the area of the LV outflow tract can be measured. From these, it is easy to calculate the area of the aortic valve.
| Example: An individual undergoes trans thoracic echocardiography for the evaluation of a systolic ejection murmur with delayed carotid upstroke noted on physical examination. During echocardiography, the following measurements were made. LVOT diameter of 2 cm, peak velocity in the LVOT of 1 m/s, and a peak velocity at the level of the aortic valve of 2.9 m/s. What is the aortic valve area? | ||
Answer: An LVOT diameter of 2 cm gives a LVOT area of π. This gives  |
The weakest aspect of this calculation is the variability in measurement of LVOT area, because it involves squaring the LVOT dimension. Some doctors prefer to read just the velocity ratio, to eliminate this.
[edit] The Gorlin equation
The Gorlin equation states that the aortic valve area is equal to the flow through the aortic valve during ventricular systole divided by the systolic pressure gradient across the valve times a constant. The flow across the aortic valve is calculated by taking the cardiac output (measured in liters/minute) and dividing it by the heart rate (to give output per cardiac cycle) and then dividing it by the systolic ejection period measured in seconds per beat (to give flow per ventricular contraction).
The Gorlin equation is related to flow across the valve. Because of this, the valve area may be erroneously calculated as stenotic if the flow across the valve is low (ie: if the cardiac output is low). The measurement of the true gradient is accomplished by temporarily increasing the cardiac output by the infusion of positive inotropic agents, such as dobutamine.
| Example: An individual undergoes left and right heart cardiac catheterization as part of the evaluation of aortic stenosis. The following hemodynamic parameters were measured. With a heart rate of 80 beats/minute and a systolic ejection period of 0.33 seconds, the cardiac output was 5 liters/minute. During simultaneous measurement of pressures in the left ventricle and aorta (with the use of one catheter in the left ventricle and a second in the ascending aorta), the mean systolic pressure gradient was measured at 50 mmHg. What is the valve area as measured by the Gorlin equation? | ||
Answer:  |
[edit] The Hakki equation
The Hakki equation[4] is a simplification of the Gorlin equation, relying on the observation that in most cases, the numerical value of 
. The resulting simplified formula is:
| Example: An individual undergoes left and right cardiac catheterization for the evaluation of aortic stenosis. Measurements includes an aortic pressure of 120/60, LV pressure of 170/15, cardiac output of 3.5 liters/minute. What is the aortic valve area? | ||
Answer: The peak gradient between the LV and aorta is 50 mmHg. This gives  |
[edit] References
- ^ http://jama.ama-assn.org/cgi/content/abstract/277/7/564
- ^ Charlson E, Legedza A, Hamel M (2006). "Decision-making and outcomes in severe symptomatic aortic stenosis.". J Heart Valve Dis 15 (3): 312-21. PMID 16784066.
- ^ "Survival in elderly patients with severe aortic stenosis is dramatically improved by aortic valve replacement: results from a cohort of 277 patients aged >/=80 years.". Eur J Cardiothorac Surg. PMID 16950629.
- ^ Hakki A, Iskandrian A, Bemis C, Kimbiris D, Mintz G, Segal B, Brice C (1981). "A simplified valve formula for the calculation of stenotic cardiac valve areas.". Circulation 63 (5): 1050-5. PMID 7471364.
[edit] External links
- Aortic stenosis information from Seattle Children's Hospital Heart Center
- Mitral Valve Repair at The Mount Sinai Hospital
