Aortic stenosis
Aortic stenosis | |
---|---|
Five-year survival ~50% without treatment in symptomatic patients [1] | |
Frequency | 2% of people over 65 (developed world)[1] |
Aortic stenosis (AS or AoS) is the
Causes include being born with a
Aortic stenosis is typically followed using repeated ultrasound scans.
Aortic stenosis is the most common
Signs and symptoms
Angina
Angina in setting 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.[9]
Angina in the setting of AS occurs due to 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 muscular layer of the left ventricle thickens, the arteries that supply the muscle do not get significantly longer or bigger, so the muscle may not receive enough blood supply to meet its oxygen requirement. This 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 anginal chest pain with exertion. Exercise stress testing with or without imaging is strictly contraindicated in symptomatic patients with severe aortic stenosis. Exercise stress test is now recommended by current guidelines in asymptomatic patients and may provide incremental prognostic value.[10]
Eventually, however, the heart muscle will require more blood supply at rest than can be supplied by the
Syncope
Syncope (fainting spells) from aortic valve stenosis is usually exertional.[4][12] In the setting of heart failure it increases the risk of death. In people with syncope, the three-year mortality rate is 50% if the aortic valve is not replaced.[13]
It is unclear why aortic stenosis causes syncope. One theory is that severe AS produces a nearly fixed
A second theory is that during exercise the high pressures generated in the hypertrophied left ventricle cause a vasodepressor response, which causes a secondary peripheral vasodilation that, in turn, causes decreased blood flow to the brain resulting in loss of consciousness. Indeed, in aortic stenosis, because of the fixed obstruction to blood flow out from the heart, it may be impossible for the heart to increase its output to offset peripheral vasodilation.[citation needed]
A third mechanism may sometimes be operative. Due to the hypertrophy of the
Finally, in calcific aortic stenosis
Congestive heart failure
Associated symptoms
In
Complications
Notwithstanding the foregoing[clarification needed], the American Heart Association changed its recommendations regarding antibiotic prophylaxis for endocarditis. Specifically, as of 2007 it is recommended that such prophylaxis should be limited only to those with prosthetic heart valves, those with previous episode(s) of endocarditis, and those with certain types of congenital heart disease.[21]
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 medications for cardiovascular diseases that often coexist with aortic stenosis. Examples include
Causes
Aortic stenosis is most commonly caused by age-related progressive calcific aortic valve disease (CAVD) (>50% of cases), with a mean age of 65 to 70 years. CAVD is the build-up of calcium on the cusps of the valve, and this calcification causes hardening and stenosis of the valve.[22] Another major cause of aortic stenosis is the calcification of a congenital bicuspid aortic valve or, more rarely, a congenital unicuspid aortic valve. Those with unicuspid aortic valves typically need intervention when very young, often as a newborn. While those with congenital bicuspid aortic valve make up 30-40% of those presenting during adulthood[23] and typically presenting earlier (ages 40+ to 50+) than those with tricuspid aortic valves (65+).[7]
Pathophysiology
The human
As a consequence of this stenosis, the left ventricle must generate a higher pressure with each contraction to effectively move blood forward into the aorta.[4][27] Initially, the LV generates this increased pressure by thickening its muscular walls (myocardial hypertrophy). The type of hypertrophy most commonly seen in AS is known as concentric hypertrophy,[4] in which the walls of the LV are (approximately) equally thickened.
In the later stages, the left ventricle dilates, the wall thins, and the systolic function deteriorates (resulting in impaired ability to pump blood forward). Morris and Innasimuthu et al. showed that different coronary anatomy is associated with different valve diseases. Research was in progress in 2010 to see if different coronary anatomy might lead to turbulent flow at the level of valves leading to inflammation and degeneration.[28][29][30]
Diagnosis
Palpation
Aortic stenosis is most often diagnosed when it is
Auscultation
The first heart sound may be followed by a sharp ejection sound ("ejection click") best heard at the
An easily heard
The second heart sound (
Finally, aortic stenosis often co-exists with some degree of
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 pulse (positive likelihood ratio ranged 2.8–130 across studies), mid to late peak intensity of the murmur (positive likelihood ratio, 8.0–101), and decreased intensity of the second heart sound (positive likelihood ratio, 3.1–50).[31]
Other peripheral signs include:[citation needed]
- sustained, heaving left ventriclehas developed
- A precordial thrill[12]
- narrowed pulse pressure
Blood tests
For asymptomatic severe aortic valve stenosis, the European guidelines
Electrocardiogram
Although aortic stenosis does not lead to any specific findings on the
As noted above, the calcification process that occurs in aortic stenosis can progress to extend beyond the aortic valve and into the
Heart catheterization
Echocardiogram
Severity of aortic stenosis[24] | ||
---|---|---|
Degree | Mean gradient (mmHg) |
Aortic valve area (cm2) |
Mild | <25 | >1.5 |
Moderate | 25 - 40 | 1.0 - 1.5 |
Severe | >40 | < 1.0 |
Very severe | >70 | < 0.6 |
The aortic valve area can be
A normal aortic valve has a gradient of only a few mmHg. A decreased valvular area causes increased pressure gradient, and these parameters are used to classify and grade the aortic stenosis as mild, moderate or severe. The pressure gradient can be abnormally low in the presence of mitral stenosis, heart failure, co-existent aortic regurgitation and also ischaemic heart disease (disease related to the decreased blood supply and oxygen causing ischemia).[43]
Echocardiogram may also show left ventricular hypertrophy, thickened and immobile aortic valve, and dilated aortic root.[12] However, it may appear deceptively normal in acute cases.[24]
Chest X-ray
A
Computer tomography
The use of CT calcium scoring is gaining spread as a diagnostic tool to complement echo in the assessment of patients with aortic stenosis.[44][45] Aortic valve calcium scoring by multidetector computed tomography (CT-AVC) is used to quantify the degree of calcification of the aortic valve.[46] According to the 2021 ESC/EACTS Guidelines for the management of valvular heart disease the recommended thresholds indicating severe aortic stenosis are > 1200 AU in women and > 2000 AU in men.[47]
Management
Treatment is generally not necessary in people without symptoms.
Medication
In general, medical therapy has relatively poor efficacy in treating aortic stenosis.[12] However, it may be useful to manage commonly coexisting conditions that correlate with aortic stenosis:[50]
- Any angina is generally treated with Nitrates are contraindicated due to their potential to cause profound hypotension in aortic stenosis.[51]
- Any diastolic blood pressure of 70-90 mmHg.[52]
- Any heart failure is generally treated with digoxin and diuretics, and, if not contraindicated, cautious administration of ACE inhibitors.[24]
Aortic valve repair
Aortic valve repair or aortic valve reconstruction describes the reconstruction of both form and function of the native and dysfunctioning aortic valve. Most frequently it is applied for the treatment of aortic regurgitation. It can also become necessary for the treatment of an aortic aneurysm, less frequently for congenital aortic stenosis.[53]
Aortic valve replacement
In adults, symptomatic severe aortic stenosis usually requires aortic valve replacement (AVR).[4] While Surgical AVR has remained the most effective treatment for this disease process and is currently recommended for patients after the onset of symptoms, as of 2016[update] aortic valve replacement approaches included open-heart surgery, minimally invasive cardiac surgery (MICS), and minimally invasive catheter-based (percutaneous) aortic valve replacement.[54][55] [56] However, surgical aortic valve replacement is well-studied, and generally has a good and well-established longer-term prognosis.[57]
A diseased aortic valve is most commonly replaced using a surgical procedure with either a mechanical or a tissue valve. The procedure is done either in an open-heart surgical procedure or, in a smaller but growing number of cases, a minimally invasive cardiac surgery (MICS) procedure.[citation needed] Minimally invasive approach via right minithoracotomy is most beneficial in the high risk patient such as the elderly, the obese, those with chronic obstructive pulmonary, chronic kidney disease and those requiring re-operative surgery. [58] [59]
Transcatheter aortic valve replacement
Globally more than 250,000 people have received
Balloon valvuloplasty
For infants and children,
Heart failure
Prognosis
If 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%.[63] Prognosis after aortic valve replacement for people younger than 65 is about five years less than that of the general population; for people older than 65 it is about the same.[57]
Epidemiology
Approximately 2% of people over the age of 65, 3% of people over age 75,[4] and 4% percent of people over age 85 have aortic valve stenosis.[64] The prevalence is increasing with the aging population in North America and Europe.[65]
Risk factors known to influence disease progression of AS include factors similar to those of
History
Aortic stenosis was first described by French physician Lazare Rivière in 1663.[6]
Research
People on bisphosphonates were found in a 2010 study to have less progression of aortic stenosis, and some regressed.[66][67] This finding led to multiple trials, ongoing as of 2012[update]. Subsequent research failed to confirm the initial positive result.[68]
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External links
- Aortic stenosis at Curlie
- 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 Use Criteria for the Treatment of Patients With Severe Aortic Stenosis". Journal of the American College of Cardiology. 70 (20): 2566–2598. PMID 29054308.