Aortic regurgitation overview
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Diagnosis |
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Treatment |
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Acute Aortic regurgitation |
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Chronic Aortic regurgitation |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hardik Patel, M.D.; Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S; Usama Talib, BSc, MD [3] Mohammed Salih, MD. [4]
Overview
Aortic insufficiency refers to the retrograde or backward flow of blood from the aorta into the left ventricle during diastole. When the pressure in the left ventricle falls below the pressure in the aorta, the aortic valve is not able to completely close. This causes a leaking of blood from the aorta into the left ventricle. The percentage of blood that regurgitates back through the aortic valve due to AI is known as the regurgitant fraction. The prevalence of aortic regurgitation varies with age, geographic location, and gender. Aortic insufficiency is unusual before the age of 50 and then increases progressively later in life. Aortic regurgitation is more commonly seen in men as compared to women. Worldwide the most common cause of aortic insufficiency is the rheumatic heart disease, particularly in the Asia, the Middle East, and the North Africa. In the United States, degenerative calcific aortic valve disease and bicuspid aortic valve disease are the most common causes. The Framingham Heart Study, a prospective epidemiological study, evaluated the prevalence and severity of aortic regurgitation and other valvular diseases by color Doppler examinations in 1,696 men and 1,893 women. In acute aortic insufficiency symptoms of heart failure often develop acutely. Chronic aortic insufficiency is usually insidious and progressive and the patient may remain asymptomatic for years. Once left ventricular dilation and left ventricular failure occur, dyspnea on exertion and exercise intolerance begin to occur. Later symptoms such as angina, syncope, and other symptoms of heart failure are present. There are two main parameters that reflect the overall outcome in patients with aortic insufficiency: ejection fraction (the lower the ejection fraction, the poorer the outcome) and end systolic diameter. Left ventricular dysfunction develops in patients with aortic insufficiency after decades of the onset of the symptoms. This lag period is longer than that of mitral regurgitation. A detailed history and physical exam and diagnostic techniques like electrocardiogram, chest X-ray, echocardiography and a cardiac MRI can be used to diagnose aortic regurgitation. The symptoms of acute aortic regurgitation (AR) include dyspnea, chest pain (when aortic dissection is the cause of AR), weakness, and symptoms of congestive heart failure. Chronic AR may be without symptoms for several years until there is a decrease in the stroke volume and cardiac output due to heart failure progression. Symptoms of chronic aortic insufficiency include exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and palpitations. The echocardiogram is the single most useful diagnostic imaging study in the diagnosis and ongoing surveillance of the severity of aortic insufficiency. Echocardiography allows for serial assessment of left ventricular volumes which can be critical in determining the timing of aortic valve replacement. Echocardiography is used to assess the following parameters: end-diastolic diameter, end systolic diameter, and ejection fraction. Aortic valve replacement should be performed if the LVEF is ≤ 55% or if left ventricular end-systolic dimension is > 50mm.[1] Pulsed Doppler echocardiography is more sensitive than auscultation specially in patients in whom no murmur is observed. Cardiac MRI may be used for assessing individuals with valvular heart disease in which evaluation of valvular stenosis, regurgitation, para- or perivalvular masses, perivalvular complications of infectious processes, or prosthetic valve disease are needed. CMR may be useful in identifying serial changes in LV volumes or mass in patients with valvular dysfunction. Aortic insufficiency can be treated either medically with vasodilators or surgically with aortic valve replacement, depending upon the acuteness of presentation, the symptoms and signs associated with the disease process, and the degree of left ventricular dysfunction. Nitroprusside and ionotropes can be used to maintain blood pressure. Treatment options that are contraindicated include intra aortic balloon pump, pressors, and beta blockers (except in aortic dissection, where beta blockers can be used cautiously).
ACC/AHA staging system (Stages A-D)
Stage A = at risk;
Stage B = progressive (mild-moderate);
Stage C1 = asymptomatic severe with normal LVEF (>55%) and mild-moderate LV dilation; Stage C2 = asymptomatic severe with LVEF ≤55% or severe LV dilation (LVESD >50 mm);
Stage D = symptomatic severe[1]
Pathophysiology
In aortic insufficiency (AI), when the pressure in the left ventricle falls below the pressure in the aorta, the aortic valve is not able to completely close. This causes a leaking of blood from the aorta into the left ventricle. This means that some of the blood that was already ejected from the heart is regurgitating back into the heart. The percentage of blood that regurgitates back through the aortic valve due to AI is known as the regurgitant fraction. For instance, if an individual with AI has a stroke volume of 100ml and during ventricular diastole 25ml regurgitates back through the aortic valve, the regurgitant fraction is 25%. This regurgitant flow causes a decrease in the diastolic blood pressure in the aorta, and therefore an increase in the pulse pressure (systolic pressure - diastolic pressure). Thus, physical examination will reveal a bounding pulse, especially in the radial artery. The percentage of blood that regurgitates back through the aortic valve due to AI is known as the regurgitant fraction. This regurgitant flow causes a decrease in the diastolic blood pressure in the aorta, and therefore a widening the pulse pressure ).There is decreased effective forward flow in aortic insufficiency.
Difference between pathophysiology of acute and chronic AR
In acute AR, the LV has not had time to dilate and compensate, leading to acute elevation of LV end-diastolic pressure, premature mitral valve closure, pulmonary edema, and cardiogenic shock. In chronic AR, eccentric hypertrophy and LV dilation serve as compensatory mechanisms to maintain forward stroke volume, but eventually lead to irreversible myocardial fibrosis and systolic dysfunction. [2]
Causes
Aortic insufficiency can be an acute illness or a chronic illness and the causes differ depending upon the acuity of the disease. In general, aortic insufficiency is due to abnormalities of the aortic valve itself or the aortic root.While aortic root/ascending aorta dilation is an increasingly recognized cause, the relative frequency depends on the population studied. In Western countries, degenerative disease (including bicuspid aortic valve and calcific degeneration) and aortic root dilation are the leading causes, while rheumatic heart disease remains the most common cause globally[2][3].It can also occur after surgical valve placement.
Drug-induced AR (e.g., from fenfluramine, pergolide, cabergoline) and AR associated with aortitis (e.g., giant cell arteritis, Takayasu arteritis, syphilitic aortitis) are other recognized causes[2]
Epidemiology and Demographics
The prevalence of aortic regurgitation varies with age, geographic location, and gender. Aortic insufficiency is unusual before the age of 50 and then increases progressively later in life. Aortic regurgitation is more commonly seen in men as compared to women. Worldwide the most common cause of aortic insufficiency is the rheumatic heart disease, particularly in the Asia, the Middle East, and the North Africa. In the United States, senile degenerative calcific aortic valve disease and bicuspid aortic valve disease are the most common causes. .The Framingham Heart Study, a prospective epidemiological study, evaluated the prevalence and severity of aortic regurgitation and other valvular diseases by color Doppler examinations in 1,696 men and 1,893 women.The study revealed that the prevalence of aortic regurgitation (ranging in severity from trace to ≥ moderate regurgitation) is 13.0% in men and 8.5% in women. The prevalence of aortic regurgitation increases with age. It is infrequent in young patients, and occurs in < 1% of subjects under the age of 70. However people with congenital aortic valve/root defects such as bicuspid aortic valve disease and Marfan syndrome may develop aortic regurgitation much earlier in life. Clinically significant (moderate or greater) AR is much less common, affecting approximately 0.5% of the general population and increasing with age. [2]
Risk Factors
In the past, the most common risk factor for aortic valvular disease had been the rheumatic fever, with subsequent fibrosis of the scarred valve then leading to retraction of the aortic valve cusps and prevention of their apposition during diastole. In the modern era, a more common risk factor for acquired aortic regurgitation is aortic root dilation degenerative disease of the aorta and aortic valve in which case there is calcification and fibrosis of the cusps. Infective endocarditis remains an important risk factor and cause of aortic insufficiency. Congenital conditions such as congenital bicuspid aortic valve or a ventricular septal defect can also result in aortic insufficiency. Patients with bicuspid aortic valve are at increased risk of developing aortic dissection. Other important risk factors include [2][4]:
- Connective tissue disorders (Marfan syndrome, Loeys-Dietz syndrome, Ehlers-Danlos syndrome),
- Bicuspid aortic valve-associated aortopathy,
- hypertension-related aortic root dilation
Natural History, Complications and Prognosis
In acute aortic insufficiency symptoms of heart failure often develop acutely. Chronic aortic insufficiency is usually insidious and progressive and the patient may remain asymptomatic for years. Once left ventricular dilation and left ventricular failure occur, dyspnea on exertion and exercise intolerance begin to occur. Later symptoms such as angina, syncope, and other symptoms of heart failure are present. There are two main parameters that reflect the overall outcome in patients with aortic insufficiency: ejection fraction (the lower the ejection fraction, the poorer the outcome) and end systolic diameter. Left ventricular dysfunction develops in patients with aortic insufficiency after decades of the onset of the symptoms. This lag period is longer than that of mitral regurgitation. A detailed history and physical exam and diagnostic techniques like electrocardiogram, chest X-ray, echocardiography and a cardiac MRI can be used to diagnose aortic regurgitation.The prognosis and survival of patients with symptomatic aortic regurgitation has improved significantly over the last decade.
Current data indicate that untreated symptomatic severe AR carries a 1-year mortality exceeding 20%, and only 1 in 5 patients with severe AR and LVEF 30-50% are referred for SAVR. The prognosis is excellent after timely surgical intervention but poor without it.[5][6]The prognosis among patients with aortic insufficiency is poor with a high mortality and morbidity due to the acute onset of left ventricular failure, pulmonary edema, or myocardial ischemia due to the abrupt rise in LV wall stress and sudden cardiac death. Early surgical intervention improves the prognosis in these patients.
Asymptomatic patients with severe AR and normal LV function have a rate of progression to symptoms or LV dysfunction of approximately 3-6% per year, and that once LVEF declines below 55% or LVESD exceeds 50 mm, outcomes worsen significantly even after surgery. [1][7]
Diagnosis
History and Symptoms
The symptoms of acute aortic regurgitation (AR) include dyspnea, chest pain (when aortic dissection is the cause of AR), weakness, and symptoms of congestive heart failure. Chronic AR may be without symptoms for several years until there is a decrease in the stroke volume and cardiac output due to heart failure progression. Symptoms of chronic aortic insufficiency include exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and palpitations.
Physical Examination
A patient with suspected aortic insufficiency may have an early diastolic heart murmur which is usually a high-pitched sound best heard at the left sternal border. An ejection systolic 'flow' murmur may also be present. The apex beat is typically displaced down and to the left. A patient with chronic aortic insufficiency may present with signs of congestive heart failure. Other significant findings on physical exam include:
- Bounding pulses may be present.
- Head nodding (de Musset's sign) - rhythmic nodding or bobbing of the head in synchrony with the beating of the heart.
- Capillary pulsations (Quincke's sign) - pulsation of arteriolar and venous plexuses of the nail bed causing alternate blanching and flushing.
- Corrigan's pulse - A rapid upstroke and collapse of the carotid artery pulse.
- Duroziez's sign - 'pistol' shot sounds (audible diastolic murmur heard over the femoral artery)
- The murmur of AR is classically best heard at the left sternal border (Erb's point, 3rd-4th intercostal space) with the patient sitting up and leaning forward. A murmur heard best at the right second intercostal space may suggest AR due to aortic root dilation. . The murmur may be soft in acute AR.
- S3 and S4 may be heard.
Cardiac Stress Test
A cardiac stress test (CST) is an evaluation modality used in cardiology in which the ability of the heart to respond to stress, either actually induced by exercise or stimulated by pharmacologic agents, is measured in a controlled clinical setting. CST for chronic aortic insufficiency is reasonable for assessment of functional capacity and symptomatic response in patients with a history of equivocal symptoms.
Exercise testing should be routinely performed in "asymptomatic" patients with severe AR to unmask symptoms or abnormal hemodynamics (Class IIa, ACC/AHA 2020). Exercise testing is reasonable to confirm symptom status in Stage C patients[1][2]
Electrocardiogram
The echocardiogram is the single most useful diagnostic imaging study in the diagnosis and ongoing surveillance of the severity of aortic insufficiency. ECG findings in AR, which may include LV hypertrophy (voltage criteria), left axis deviation, and left atrial enlargement in chronic AR, or sinus tachycardia in acute AR
Chest X Ray
Chest x ray findings associated with aortic insufficiency may include left ventricular enlargement, cardiomegaly, prominent aortic root with valvular calcification, prosthetic valve dis-lodgement, or aortic dilation. If aortic insufficiency is severe, signs of pulmonary edema may also be present.
Echocardiography
The echocardiogram is the single most useful diagnostic imaging study in the diagnosis and ongoing surveillance of the severity of aortic insufficiency. Echocardiography allows for serial assessment of left ventricular volumes which can be critical in determining the timing of aortic valve replacement. Echocardiography is used to assess the following parameters: end-diastolic diameter, end systolic diameter, and ejection fraction. Aortic valve replacement should be performed if the LVEF is ≤ 55% or if left ventricular end-systolic dimension is > 50mm[1]. Pulsed Doppler echocardiography is more sensitive than auscultation specially in patients in whom no murmur is observed. 3D echocardiography may provide more accurate volumetric assessment than 2D methods, though prognostic data remain limited.[7]
Quantitative criteria for severe AR:
The quantitative criteria for severe AR per current guidelines[1]:
- jet width ≥65% of LVOT,
- vena contracta >0.6 cm,
- holodiastolic flow reversal in the proximal abdominal aorta
- , regurgitant volume ≥60 mL/beat,
- regurgitant fraction ≥50%,
- effective regurgitant orifice ≥0.3 cm²
The Role of GLS ( global longitudinal strain) :
GLS values worse than −18% to −19% predict higher mortality and disease progression in asymptomatic AR with preserved LVEF, and GLS <−15% confers a 2- to 3-fold increased mortality risk. The 2025 AHA scientific statement on speckle-tracking strain echocardiography and the 2025 ASE/EACI consensus statement both support GLS as a prognostic biomarker in AR[2][8]
Cardiac MRI
Cardiac MRI may be used for assessing individuals with valvular heart disease in which evaluation of valvular stenosis, regurgitation, para- or perivalvular masses, perivalvular complications of infectious processes, or prosthetic valve disease are needed. CMR may be useful in identifying serial changes in LV volumes or mass in patients with valvular dysfunction. For patients with suboptimal echocardiograms showing aortic regurgitation, radionuclide angiography or magnetic resonance imaging is indicated to assess left ventricular volume and function at rest.
CMR is recommended as an adjunct when echocardiography is inconclusive or discordant (Class I, ACC/AHA 2020). CMR is the reference standard for direct quantification of regurgitant volume and regurgitant fraction via phase-contrast velocity mapping. CMR-derived regurgitant fraction thresholds of 32-35% (lower than the echocardiographic threshold of 50%) predict adverse outcomes and need for surgery. Holodiastolic retrograde flow in the descending aorta on CMR is independently associated with a 2.8-fold increased risk of death or heart failure hospitalization[2][1][7]
CMR provides volumetric indices (LVESVi ≥45 mL/m², LVEDVi ≥109 mL/m²) that are validated predictors of adverse outcomes and outperform linear dimensions, particularly in patients with preserved LVEF. The 2025 ESC/EACTS guidelines now emphasize these volumetric indices alongside conventional triggers.[2]
CMR offers myocardial tissue characterization via late gadolinium enhancement and T1 mapping/extracellular volume quantification, which can detect focal and diffuse fibrosis — markers of subclinical injury from chronic volume overload that may be irreversible and are associated with impaired postoperative recovery.[2]
Cardiac Catheterization
Although echocardiography is now the primary imaging modality used to evaluate aortic insufficiency, cardiac catheterization is often performed in patients with aortic insufficiency primarily to assess for the presence of epicardial coronary artery disease prior to surgical aortic valve replacement. Aortography can also be performed to assess the severity of aortic insufficiency. The presence or absence of an aortic dissection can be evaluated. Left ventricular function (hemodynamics), size, and systolic function (ejection fraction) can also be evaluated.
Treatment
Aortic insufficiency can be treated either medically with vasodilators or surgically with aortic valve replacement, depending upon the acuteness of presentation, the symptoms and signs associated with the disease process, and the degree of left ventricular dysfunction. Nitroprusside and ionotropes can be used to maintain blood pressure. Treatment options that are contraindicated include intra aortic balloon pump, pressors, and beta blockers (except in aortic dissection, where beta blockers can be used cautiously).
Acute Aortic Insufficiency
Patients with acute severe aortic regurgitation (AR) are managed with emergency aortic valve replacement or repair. Medical therapy is used for the stabilization of patients prior to surgery. Intra-aortic balloon pump is absolutely contraindicated in AR because it augments diastolic pressure and worsens regurgitation. Beta blockers are relatively contraindicated because they prolong diastole and increase regurgitant volume, except in aortic dissection where they are essential. The text should also note that emergency surgery should not be delayed for medical optimization in acute severe AR with hemodynamic instability[2]
Chronic Aortic Insufficiency
In the management of chronic aortic regurgitation, the left ventricular size and function should be monitored closely along with the exercise tolerance of the patient. If the patient develops heart failure symptoms and the disease starts to be symptomatic, then aortic valve replacement or valve repair is indicated. Annual echocardiographic studies are indicated in all patients with significant AR.
Role of Vasodilator Therapy:
There is no evidence that vasodilating drugs reduce severity of AR or alter the disease course in patients with significant AR in the absence of systemic hypertension. Vasodilator therapy is recommended only for:
(1) treatment of hypertension (systolic BP >140 mm Hg) in asymptomatic patients (Class I);
(2) GDMT for reduced LVEF (ACE inhibitors, ARBs, and/or sacubitril/valsartan) in patients with severe AR who have symptoms and/or LV dysfunction but prohibitive surgical risk (Class I).
Medical therapy should not delay timely referral for valve replacement. The greatest benefit of medical therapy is among symptomatic patients and those with heart failure symptoms due to advanced disease, but in general, medical therapy has a limited role in AR because symptomatic cases should be treated with valve replacement if the patient is a good candidate for surgery. Warfarin and long-term anticoagulation is not recommended in AR if there are no other indications for anticoagulation.
Surgery
Severe acute AR requires emergency surgery if there are no absolute contraindications to surgery. The surgery should be performed as early as possible without a delay, particularly if hypotension, decreased perfusion, or pulmonary edema are present.
The 2025 ESC/EACTS guidelines now recommend intervention at lower thresholds than ACC/AHA, including Class IIb consideration for LVESDi >22 mm/m² or LVESVi ≥45 mL/m², and Class IIb (C) for LVESDi >20 mm/m² in low-risk patient[2]
Aortic valve repair should be discussed as an increasingly viable alternative to replacement in selected patients. The 2025 ESC/EACTS guidelines give aortic valve repair a Class IIa recommendation in selected patients at experienced centers. Valve-sparing aortic root surgery (David procedure) is recommended particularly in patients <65 years with aortic root dilation and normal or near-normal cusps. Freedom from reoperation after repair is approximately 88% at 5 years and 73% at 10 years in experienced centers.[1][2]
The Ross procedure (pulmonary autograft) should be mentioned as an expanding option for younger patients with AR, offering survival comparable to the general population in expert centers.[2]
In chronic AR, aortic valve replacement (AVR) is indicated in patients with :
- Severe AR who are either symptomatic regardless of LV systolic function,
- Class I: Symptomatic severe AR (Stage D) regardless of LV function; asymptomatic severe AR with LVEF ≤55% (Stage C2); severe AR (Stage C or D) undergoing cardiac surgery for other indications.[1]
- Class IIa: Asymptomatic severe AR with LVEF >55% but LVESD >50 mm or indexed LVESD >25 mm/m². [1]
- Class IIb: Asymptomatic severe AR with LVEF >55% and progressive decline in LVEF to 55-60% on ≥3 serial studies, or progressive increase in LVEDD >65 mm. [1]
- Class III (Harm): TAVR should not be performed in patients with isolated severe AR who are candidates for SAVR (ACC/AHA 2020). JACC[1]
Treatment — TAVR for AR
Per the 2020 ACC/AHA guidelines, TAVR is Class III (Harm) for isolated severe AR in surgical candidates.[1]
However, the 2025 ESC/EACTS guidelines now give TAVR a Class IIb recommendation for inoperable/high-risk patients with suitable anatomy following heart team consensus.[2]
The ALIGN-AR trial (2024-2025) demonstrated that transfemoral TAVR with a dedicated device (Trilogy valve) was effective in eliminating AR in high-risk patients, with substantial improvements in LV remodeling and functional status at 1 year.[3][6]
Follow Up and Surveillence
Per the 2020 ACC/AHA guidelines and 2025 ESC/EACTS guidelines, recommended surveillance intervals are[1][2]:
- Mild AR (Stage B): echocardiography every 3-5 years
- Moderate AR (Stage B): echocardiography every 1-2 years
- Severe asymptomatic AR (Stage C1): echocardiography every 6-12 months; more frequently if LV is dilating
- Annual history and physical examination for all patients with significant AR
Prevention
Primary prevention
Limiting the factors that lead to the development of Aortic regurgitation will decrease its incidence. Optimal blood pressure control, especially in elderly population is of utmost importance. cessation of smoking and opting for a healthy life style that includes balanced diet and regular exercise. Prevention of the initial development of acute rheumatic fever by prompt diagnosis and antibiotic treatment of group A streptococcal (GAS) infection predominantly due to tonsillopharyngitis. In tropical countries, a link between GAS pyoderma and subsequent ARF/RHD is highly likely.
Secondary prevention
Per the 2020 ACC/AHA guidelines, antibiotic prophylaxis is not recommended for native valve AR (including bicuspid aortic valve). Prophylaxis is recommended only for the highest-risk groups: prosthetic cardiac valves (including TAVR), prosthetic material used for valve repair, previous IE, unrepaired cyanotic congenital heart disease, and cardiac transplant with valve regurgitation[1].
Prophylaxis is recommended only before dental procedures involving manipulation of gingival tissue, the periapical region of teeth, or perforation of the oral mucosa. Prophylaxis is not recommended for nondental procedures (TEE, EGD, colonoscopy, cystoscopy) in the absence of active infection (Class III: No Benefit)[1] [9]
Clindamycin is no longer recommended for IE prophylaxis due to increased risk of Clostridioides difficile infection. Preferred alternatives for penicillin-allergic patients include cephalexin, azithromycin, or doxycycline.[9]
Secondary prevention of recurrent ARF with continuous antibiotic prophylaxis is recommended for patients with definite history of ARF or diagnosis of definite RHD. Continuous antimicrobial prophylaxis is recommended because recurrent ARF can be triggered by GAS infection even if asymptomatic. Patients should be registered in regional ARF prevention programs, where available.
Special Scenarios
Elderly patients
The incidence of aortic regurgitation in the elderly is low in comparison to the incidence of aortic stenosis and mitral regurgitation. The majority of elderly patients have combined aortic stenosis and aortic insufficiency and the incidence of pure aortic insufficiency is rare.
Pregnancy
Isolated aortic insufficiency in pregnant patients can be managed with combination of diuretics and vasodilators. ACE inhibitors are contraindicated in pregnancy.ARBs are also contraindicated in pregnancy. For hypertension management in pregnant patients with AR, labetalol, nifedipine, or methyldopa are preferred agents per current guidelines[1] Patients with signs and symptoms of left ventricular failure should be monitored throughout labor and delivery with strict attention to volume status and blood pressure.
Young Adults
Congenital aortic insufficiency rarely occurs alone and is often associated with aortic stenosis or ventricular septal defect. It may occasionally be observed in adolescents and young adults with a bicuspid aortic valve, discrete subaortic obstruction, or prolapse of one of the aortic cusp into a ventricular septal defect. Turner syndrome, osteogenesis imperfecta, tetralogy of Fallot, and truncus arteriosus are other congenital disorders that are associated with aortic insufficiency in young patients. Rheumatic heart disease is one of the important causes for acquired aortic insufficiency in young patients in developing countries. It can also occur following an episode of infective endocarditis or as a consequence of attempts to relieve aortic stenosis by either balloon valvuloplasty or surgical valvulotomy, or when the pulmonary artery is relocated in the aortic position during repair of transposition of great vessels.
End-stage Renal Disease
Aortic insufficiency in patients with end stage renal disease can be due to either valvular calcification or infective endocarditis. Valvular/annular thickening, and calcification of heart valves occur commonly in patients undergoing dialysis, thereby leading to valvular regurgitation and/or stenosis. Hyperparathyroidism occurring secondary to renal disease is one of the most significant predisposing factor for valular calcification. Aortic insufficiency is seen less commonly than mitral or tricuspid insufficiency. In a study on 75 patients with end stage renal disease (ESRD) undergoing hemodialysis, 38% of patients were found to have developed aortic insufficiency.
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 https://www.jacc.org/doi/10.1016/j.jacc.2020.11.018
- ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 https://pubmed.ncbi.nlm.nih.gov/41194752/ PMID: 41194752 DOI: 10.1016/j.jacc.2025.10.026
- ↑ 3.0 3.1 https://pubmed.ncbi.nlm.nih.gov/38552656/
- ↑ https://pubmed.ncbi.nlm.nih.gov/38554728/ PMID: 38554728 DOI: 10.1016/S0140-6736(23)02755-1
- ↑ https://pubmed.ncbi.nlm.nih.gov/38552656/ PMID: 38552656 DOI: 10.1016/S0140-6736(23)02806-4
- ↑ 6.0 6.1 https://pubmed.ncbi.nlm.nih.gov/41260228/ PMID: 41260228 DOI: 10.1016/S0140-6736(25)02215-9
- ↑ 7.0 7.1 7.2 https://pubmed.ncbi.nlm.nih.gov/37940233/ PMID: 37940233 DOI: 10.1016/j.jacc.2023.08.051
- ↑ https://pubmed.ncbi.nlm.nih.gov/41010738/
- ↑ 9.0 9.1 https://www.aafp.org/pubs/afp/issues/2026/0200/infective-endocarditis.html