Aortic regurgitation
| Aortic regurgitation | |
|---|---|
| Other names | Aortic insufficiency |
 | |
| Illustration of aortic regurgitation | |
| Specialty | Cardiology  |
| Symptoms | Dyspnea on exertion, Orthopnea[1] |
| Causes | Aortic root dilation[1] |
| Diagnostic method | Transthoracic echocardiography[2] |
| Treatment | Vasodilators(depends on the individuals condition, maybe surgery Aortic valve replacement)[1][3] |
Aortic regurgitation (AR), also known as aortic insufficiency (AI), is the leaking of the
Signs and symptoms
- Dyspnea on exertion
- Orthopnea
- Paroxysmal nocturnal dyspnea
- Palpitations
- Angina pectoris
- Cyanosis (in acute cases)
Causes
In terms of the cause of aortic regurgitation, is often due to the aortic root dilation (
Pathophysiology
The mechanism of aortic regurgitation, comprises the pressure in the left ventricle falling 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 AR is known as the
While diastolic blood pressure is diminished and the pulse pressure widens, systolic blood pressure generally remains normal or can even be slightly elevated, this is because sympathetic nervous system and the renin-angiotensin-aldosterone axis of the kidneys compensate for the decreased cardiac output.
The volume overload, due to elevated pulse pressure and the systemic effects of neuroendocrine hormones causes left ventricular hypertrophy (LVH).[9] There is both concentric hypertrophy and eccentric hypertrophy in AI. The concentric hypertrophy is due to the increased left ventricular pressure overload associated with AI, while the eccentric hypertrophy is due to volume overload caused by the regurgitant fraction.[15]
Diagnosis
In terms of the diagnosis of aortic regurgitation a common test for the evaluation of the severity is transthoracic echocardiography, which can provide two-dimensional views of the regurgitant jet, allow measurement of velocity, and estimate jet volume.[2] The findings in severe aortic regurgitation, based on the 2012 American College of Cardiology/American Heart Association guidelines include:[20][21]
- An AI color jet width > 65 % of the left ventricularoutflow tract diameter
- Doppler vena contracta width > 0.6 cm
- The pressure half-time of the regurgitant jet is < 200 ms
- Early termination of the mitralinflow
- Holodiastolic flow reversal in the descending aorta.
- Regurgitant volume > 60 ml
- Regurgitant fraction > 50 %
- Estimated regurgitant orifice area > 0.3 cm2
- Increased left ventricular size
Physical examination
-
Aortic valve regurgitation vs aortic valve stenosis -
Phonocardiogramsfrom normal and abnormal heart sounds
The physical examination of an individual with aortic regurgitation involves auscultation of the heart to listen for the murmur of aortic regurgitation and the S3 heart sound (S3 gallop correlates with development of LV dysfunction).[1] The murmur of chronic aortic regurgitation is typically described as early diastolic and decrescendo, which is best heard in the third left intercostal space and may radiate along the left sternal border.[22]
If there is increased stroke volume of the left ventricle due to volume overload, an ejection systolic 'flow' murmur may also be present when auscultating the same aortic area. Unless there is concomitant
Characteristics- indicative of aortic regurgitation are as follow:
- Corrigan's pulse:[25]Rapid upstroke and collapse of pulses
- De Musset's sign:[26] Head bob with each heartbeat
- Quincke's sign:[26] Capillary pulsations
- Traube's sign:[27] Systolic and diastolic sounds heard over femoral arteries
- Duroziez's sign:[26] Systolic and diastolic bruit heard with compression of femoral artery
- Landolfi's sign [27]
- Becker's sign[27]
- Müller's sign[26]
- Mayne's sign[27]
- Rosenbach's sign [27]
- Gerhardt's sign [27]
- Hill's sign [27]
- Lincoln sign[27]
- Sherman sign [27]
Classification
The hemodynamic sequelae of AI are dependent on the rate of onset of AI.[28] Therefore, can be acute or chronic as follows:
- Acute aortic regurgitation In acute AR, as may be seen with acute perforation of the aortic valve due to left atrium to rise, and the individual will develop pulmonary edema. Severe acute aortic regurgitation is considered a medical emergency. There is a high mortality rate if the individual does not undergo immediate surgery for aortic valve replacement.[9]
- Acute AR usually presents as florid congestive heart failure, and will not have any of the signs associated with chronic AR since the left ventricle had not yet developed the eccentric hypertrophy and dilatation that allow an increased stroke volume, which in turn cause bounding peripheral pulses. On auscultation, there may be a short diastolic murmur and a soft S1. S1 is soft because the elevated filling pressures close the mitral valve in diastole.[medical citation needed]
- Chronic aortic regurgitation If the individual survives the initial hemodynamic derailment that acute AR presents, the left ventricle adapts by its eccentric hypertrophy and dilatation with a subsequent compensated volume overload. The left ventricular filling pressures will revert to normal and the individual will no longer have overt heart failure. In this compensated phase, the individual may be totally asymptomatic and may have normal exercise tolerance. Eventually (typically after a latency period) the left ventricle will become decompensated, and filling pressures will increase. Some individuals enter this decompensated phase asymptomatically, treatment for AR involves aortic valve replacement prior to this decompensation phase.[30]
Treatment
Aortic regurgitation can be treated either medically or surgically, depending on the acuteness of presentation, the symptoms and signs associated with the disease process, and the degree of left ventricular dysfunction.[5][31] Surgical treatment in asymptomatic patients has been recommended if the ejection fraction falls to 50% or below, in the face of progressive and severe left ventricular dilatation, or with symptoms or abnormal response to exercise testing. For both groups of patients, surgery before the development of worsening ejection fraction/LV dilatation is expected to reduce the risk of sudden death, and is associated with lower peri-operative mortality. Also, surgery is optimally performed immediately in acute cases.[1][5]
Medical treatment
Medical therapy of chronic aortic regurgitation that is stable and asymptomatic involves the use of vasodilators.
As of 2007, the American Heart Association no longer recommends antibiotics for endocarditis prophylaxis before certain procedures in patients with aortic regurgitation.
Surgery
A surgical treatment for AR is
| Symptoms | Ejection fraction | Additional Findings |
|---|---|---|
| Present ( NYHA II-IV) |
Any | none |
| Absent | > 50% | Abnormal exercise test, severe LV dilatation (systolic ventricular diameter >55 mm) |
| Absent | <=50 % | none |
| Cardiac surgery for other cause (i.e.: CAD, other valvular disease, ascending aortic aneurysm) | ||
Prognosis
The risk of death in individuals with aortic regurgitation, dilated ventricle, normal ejection fraction who are asymptomatic is about 0.2 percent per year. Risk increases if the ejection fraction decreases or if the individual develops symptoms.[36]
Individuals with chronic (severe) aortic regurgitation follow a course that once symptoms appear, surgical intervention is needed. AI is fatal in 10 to 20% of individuals who do not undergo surgery for this condition.
References
- ^ ISBN 978-0-7817-7153-5.
- ^ PMID 20375260. Retrieved 4 June 2016.
- ^ a b Choices, NHS. "Aortic valve replacement - Why it's done - NHS Choices". www.nhs.uk. Retrieved 4 June 2016.
- ^ "Aortic insufficiency: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2016-05-16.
- ^ a b c d e f "Aortic Regurgitation: Background, Pathophysiology, Etiology". 2018-11-19.
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- ^ "Aortic Valve Anatomy: Overview, Gross Anatomy, Microscopic Anatomy". 2018-09-25.
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- ^ "UOTW#69 - Ultrasound of the Week". Ultrasound of the Week. 3 April 2016. Retrieved 27 May 2017.
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- ^ "Aortic Regurgitation. Health Information and treatment | Patient". Patient. Retrieved 2016-06-04.
- ^ "Heart Failure Medication: Beta-Blockers, Alpha Activity, Beta-Blockers, Beta-1 Selective, ACE Inhibitors, ARBs, Inotropic Agents, Vasodilators, Nitrates, B-type Natriuretic Peptides, I(f) Inhibitors, ARNIs, Diuretics, Loop, Diuretics, Thiazide, Diuretics, Other, Diuretics, Potassium-Sparing, Aldosterone Antagonists, Selective, Alpha/Beta Adrenergic Agonists, Calcium Channel Blockers, Anticoagulants, Cardiovascular, Opioid Analgesics". emedicine.medscape.com. Retrieved 2016-06-04.
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Further reading
- Hamirani, Yasmin S.; Dietl, Charles A.; Voyles, Wyatt; Peralta, Mel; Begay, Darlene; Raizada, Veena (2012-08-28). "Acute Aortic Regurgitation". Circulation. 126 (9): 1121–1126. PMID 22927474.
- Dujardin, Karl S.; Enriquez-Sarano, Maurice; Schaff, Hartzell V.; Bailey, Kent R.; Seward, James B.; Tajik, A. Jamil (1999-04-13). "Mortality and Morbidity of Aortic Regurgitation in Clinical Practice A Long-Term Follow-Up Study". Circulation. 99 (14): 1851–1857. PMID 10199882.
External links
