chapter ii-aortic regurgitation hearth refrat

8/13/2019 Chapter II-Aortic Regurgitation hearth refrat

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CHAPTER II

REVIEW

2.1. Chronic Aortic Regurgitation

2.1.1. Definition

Chronic aortic regurgitation imposes a volume overload on the left ventricle,

resulting in a number of compensatory processes that serve to maintain normal

left ventricular function despite the increased workload.1

2.1.2. Etiology

Chronic aortic regurgitation may be the result of a number of pathologic

process affecting the aortic valve, both common and uncommon. The more

common etiologies are idiopathic dilatation, congenital abnormalities of the aortic

valve (especially bicuspid valves), calcific degenerative valves, systemic

hypertension, rheumatic heart disease, infective endocarditis, myxomatous

degeneration, and diseases of ascending aorta such as disections and Marfans

syndrome. Among the less common etiologies are traumatic injuries to the aorticvalves, ankylosing spondylitis, syphilitic aortitis, rheumatoid arthritis, discrete

subaortic stenosis, and ventricular septal defects with prolapse of an aortic cusp. 1

Although a congenitally bicuspid aortic valve frequently leads to AS in

adulthood, approximately 10% of bicuspid valve patients who require surgery

present with pure aortic regurgitation without stenosis; these patients are usually

younger, averaging approximately 40 years of age. Aortic regurgitation from a

bicuspid aortic valve often results from leaflet prolapse, especially when one cusp

is larger than the other. Although rheumatic heart disease primarily attacks the

mitral valve, leading to mitral stenosis, many patients with rheumatic involvement

also have some degree of aortic regurgitation, and in some patients aortic

regurgitation is the predominant lesion. As mentioned, the presence of rheumatic

mitral valve findings is the hallmark of diagnosing rheumatic aortic valve

involvement. Infective endocarditis is the most common cause of acute aortic

regurgitation.4

3


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Figure 1. Etiologies of chronic aortic regurgitation

Diseases of the aortic root leading to aortic regurgitation include

atherosclerosis, Marfan syndrome, aortic dissection, hypertension with associated

annuloaortic ectasia, syphilitic aortitis, ankylosing spondylitis, osteogenesis

imperfecta, and systemic lupus. In Marfan syndrome and annuloaortic ectasia,

dilation of the proximal root increases the aortic diameter at the level of the

sinotubular ridge, lifting the cusp suspension superiorly, causing cusp separation

and lack of central coaptation. Although annuloaortic ectasia is often associated

with hypertension, its presence usually correlates better with age than elevated

blood pressure. In Marfan syndrome, hypertension, and some patients with

bicuspid aortic valves, cystic medial necrosis of the aorta occurs, and in some

patients, it arises in isolation. Whether an aneurysm is caused by atherosclerosis

or cystic medial necrosis, an intimal tear can occur, producing aortic dissection.

Proximal dissection may undermine aortic valve cusp or commissural support.

Ankylosing spondylitis, aortitis, and syphilis also cause ascending aortic dilation,

but they also produce aortic wall thickening, which itself may distort the

commissures and prevent leaflet coaptation.4


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2.1.3. Pathophysiology

The volume load of chronic aortic regurgitation sets a number of

compensatory processes. The magnitude and progressive nature of these

compensatory changes are a manifestation of the severity of the regurgitant

volume. The LV end-diastolic volume increases to accommodate the regurgitant

volume and does so with an increase in chamber compliance so that the

augmented end-diastolic volume is not associated with an increase in diastolic

filling pressure. The increased end-diastolic volume translates into an increase

total stroke volume. So the stroke volume maintained within the normal range.1

In addition, the ventricle adapts to the volume load by producing new

sarcomeres leads to development of eccentric LV hypertrophy. As a result,

although preload is increased, there is still normal contractile performance results

in enhanced total stroke volume. The augemented LV chamber volume results in

an increase in systolic wall stress and afterload. It is also a stimulus for concentric

hypertrophy. For this reason, aortic regurgitation represents a condition of

combined volume overload and pressure overload, with combined hypertrophic

response of both eccentric and concentric hypertrophy.1,4


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Figure 2. Hemodynamic of the clincal stages of aortic regurgitation


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Figure 3. Pathophysiology of chronic aortic regurgitation

The enlarged compliant left ventricle accommodates filling at a lower

pressure, more normal than in acute aortic regurgitation. In this stage, the patient

may be entirely asymptomatic even during fairly strenuous activity. The large

total SV interacts with the aorta to produce a wide pulse pressure, causing systolic

hypertension. The wide pulse pressure produces most of the physical signs of

aortic regurgitation.4

At some points, the balance between excessive afterload and the

combination of preload reserve and compensatory hypertrophy can not be achieve.

Compensatory mechanism fail, left ventricular contractility deteriorated, the

ventricle dilated further, and interstitial fibrosis contributes to a decline in

compliance. Symptoms of dyspnea or fatigue often develop at this transition point

as a result of declining systolic function. The transition from compensated to

decompensated state can occur in a silent and insidious manner.4,6


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2.1.4. Natural History of Asymptomatic Patients

2.1.4.1. Patients with Normal Left Ventricular Systolic Function

The natural history of asymptomatic patients with chronic sever aortic

regurgitation and normal LV systolic function characterized by a very gradual rate

of deterioration to symptoms, LV systolic dysfunction, or death. According to

American College of Cardiology/ American Heart Association guidelines for

managing of patients with valvular heart disease, 4,3% of 490 patients developing

LV systolic dysfunction per year and average mortality rate less than 0,2% per

year.1

Thus, the overall outcome of asymptomatic patients with normal LV

systolic function is excellent. Most patients develop symptoms before or

coincident with the onset of LV dysfunction.1

2.1.4.1. Patients with Left Ventricular Systolic Dysfunction

Patients with LV systolic dysfunction in the setting of chronic severe aortic

regurgitation appear to have a much more aggressive natural history with steeper

rate of attrition. Based on the data from small series, most patients do not remain

symptom free for long periods of time but become candidates for operation

because of symptomatic indications within only few years. Two thirds or more of

asymptomatic patients who manifest evidence of ventricular dysfunction develop

symptoms requiring operation within only 2 to 3 years.1

2.1.5. Clinical Presentation

2.1.5.1. Anamnesis

In the absence of complications, patients with aortic regurgitation are

asymptomatic for decades. Some patients are aware of increased vigor of

contraction of the left ventricle, particularly on lying down. Slight orhostatic

dizziness may be reported by otherwise asymptomatic patients with low systemic

diastolic blood pressure.1

Symptoms in patients with aortic regurgitation usually consist of angina

pectoris or heart failure or both. Patients with aortic regurgitation in the chronic

compensated phase are often entirely asymptomatic and can remain so for many

years, even after myocardial dysfunction develops. As LV decompensation


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proceeds, some symptoms occur. There are dyspnea on exertion, orthopnea, and in

advanced cases, paroxysmal nocturnal dyspnea and peripheral edema.1,3 Other less

common symptoms of aortic regurgitation include angina associated with

vasoactive flushing, an unpleasant awareness of the heartbeat, and carotid artery

pain.4

Angina pectoris may be associated with coronary atherosclerosis or it may

occur with widely patent coronary arteries. In latter situation, angina pectoris is

the result of low aortic diastolic pressure that leads to decreased myocardial

perfusion in the face of increased myocardial oxygen demands secondary to

increased left ventricular volume an systolic pressure. Angina is not common in

patients with aortic regurgitation.1,4

Congestive heart failure is the most common symptom that develops in

patients with aortic regurgitation. It usually appears after decades during which

the patient reported no symptoms whatsoever. Symptoms may be insidious in

onset with patients initially noting only slightly decreased exercise tolerance.

Dyspnea on exertion may occur for a short of time, before more severe symptoms

of left ventricular failure occur (orthopnea, paroxysmal nocturnal dyspnea).1

2.1.5.2. Physical Findings

The diastolic blood pressure is frequently low in persons with moderate to

severe degrees of aortic insufficiency. In patients with severe aortic regurgitation

occasionally we can even heard Korotkov sounds when pressure in the blood

pressure cuff reaches zero. The systolic blood pressure is normal or elevated so

that the pulse pressure is usually wide in these patients. The low diastolic pressure

is due to the draining of blood into the left ventricle during diastole.1

On inspection and palpation, it is usually revealed that the left ventricle is

enlarge and hyperactive. The murmur of aortic regurgitation is heard on

auscultation. It is best heard at the base of the heart (along the left sternal edge or

in the second right intercostal space). It is relatively soft, high-pitched, and

blowing. It is best heard early in diastole but may fill almost all of diastole. The

murmur is characteristically decresendo. On occasion, the murmur is loud and

musical in quality. This musical murmur of aortic regurgitation has been reffered


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to as the seagull, or cooing-dove, murmur. It is usually the result of eversion or

perforation of an aortic cusp (usually in patients with syphillis, infectious

endocarditis, rheumatic fever, or trauma). The duration of murmur depends on the

severity of aortic regurgitation. In mild case, the murmur is early diastolic.1,4

Ejection clicks are occasionally heard in early systole in patients with aortic

regurgitation and a dilated aortic root. A fourth heart sound is heard in patients

with prominent left ventricular hypertrophy, and a third heart sound is audible in

many patients with left ventricular failure.1

Occasionally, a patient with isolated aortic regurgitation has a soft, low

pitched mid-diastolic to late diastolic rumbling murmur which is termed as Austin

Flint murmur. This murmur is caused by increased left ventricular filling pressure

in late diastole, relative mitral stenosis due to aortic regurgitation jet pushing the

anterior leaflet upward impending the flow of blood from left atrium, and low

pitched vibrations of the aortic regurgitant murmur it self.1

Table 1. Signs of aortic regurgitation6

Less used signs include:

Lighthouse sign (blanching & flushing of forehead) Landolfi's sign (alternating constriction & dilatation of pupil) Becker's sign (pulsations of retinal vessels) Mller's sign (pulsations of uvula) Mayen's sign (diastolic drop of BP>15 mm Hg with arm raised) Rosenbach's sign (pulsatile liver) Gerhardt's sign (enlarged spleen)


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Hill's sign - a 20 mmHg difference in popliteal and brachial systolic cuffpressures, seen in chronic severe aortic regurgitation. Considered to be an

artefact of sphygmomanometric lower limb pressure measurement.

Lincoln sign (pulsatile popliteal) Sherman sign (dorsalis pedis pulse is quickly located and unexpectedly

prominent in age>75 years)

Ashrafian sign (Pulsatile pseudo-proptosis)Peripheral signs of aortic regurgitation are important clues to the presence

and severity of aortic regurgitation. The pulse has a characteristic quality, striking

the finger rapidly and forcefully and then suddenly disappearing (Corrigans or

water-hammer pulse). This quality of the pulse is a result of the large, forcefully

ejected left ventricular stroke volume in early systole. Corrigan and water-hammer

pulse may also be present in patients with patent ductus arteriosus, arteriovenosus

fistula, or marked peripheral vasodilatation secondary to fever, thyrotoxicosis, or

anemia.1,4,6

2.1.5.3. Laboratory Findings

1. Electrocardiograph

The ECG usually demonstrates left ventricular preponderance in patients

with aortic regurgitation. The rhythm is usually sinus. Left axis deviation and

increased ventricular voltage are common. In moderate aortic regurgitation the

lateral precordial leads often demonstrate a small Q wave, a tall R wave, an

isoelectric S-T segment, and an upright T wave (so called diastolic overload of the

left ventricle). In severe cases, S-T segment may be depressed or down sloping or

both, and T wave are inverted in lateral precordial leads. The presence of atrial

fibrillation should make one suspect the presence of associated mitral valve

disease or heart failure.1,5

Patients with aortic regurgitation secondary to inflammatory processes may

have prolonged P-R interval, Mobitz type-1 atrioventricular block, or conduction

defects. Patients with aortic insufficiency caused by severe calcific aortic valve

disease may also demonstrate conduction defects.1


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2. Chest Roentgenogram

With more severe degrees of regurgitation, the left ventricular contour

enlarges downward and to the left producing boot-shape heart silhouette

characteristic of this valvular lesion.The aortic knob and ascending aorta are often

prominent in persons with moderate to severe aortic regurgitation.1

When left ventricular failure develops, chest roentgenogram may reveal

pulmonary vascular redistribution and interstitial or alveolar pulmonary edema.

The left atrium may become modestly dilated secondary to elevated left

ventricular filling pressure with or without concomitant functional mitral

regurgitation. The roentgenographic distinction of aortic stenosis from aortic

regurgitation rests on the finding of a marked left ventricular enlargement in

patient with aortic regurgitation.1

3. Echocardiography

Echocardiography interrogation of LV size and function, as a repeatable,

noninvasive method, has become preeminent in predicting outcome and in timing

surgery. Shortening fraction and systolic diameter, the minor axis one-

dimensional equivalents of EF, and end-systolic volume, respectively, are the

most useful indices for predicting outcome in patients with chronic minimally

symptomatic aortic regurgitation. A shortening fraction less of than 27% or a

resting EF of less than 55% should prompt consideration of AVR, even in the

asymptomatic patient. End-systolic diameter or volume, indices that are more

preload independent than EF, have also proved helpful in timing surgery. When

the end-systolic diameter is 50 mm or greater, surgery should be strongly

considered; postoperative survival is significantly decreased when it is 55 mm or

larger. If surgery is performed within 18 months or so after these thresholds are

crossed, systolic function is likely to return to normal. Regarding frequency of

follow-up echocardiographic studies, when the end-systolic diameter is less than

40 mm, echocardiography should be performed biannually, when it is 40 to 50

mm, yearly follow-up is recommended.4

The sign of aortic regurgitation on echocardiography is diastolic fluttering

of the anterior leaflet of the mitral valve. Echocardiography can easily exclude the


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presence of associated mitral stenosis. LV dimensions are increased, and if LV

function is normal, the percent of dimensional shortening is normal. The increase

in LV dimensions caused by volume overload, results in separation between the

open anterior leaflet of the mitral valve and the endocardial surface of the

interventricular septum (septal-E point separation). In aortic regurgitation, as in

other volume-overload lesions, the response in mild volume overload is an

elongation of the heart.5

Other abnormality of mitral valve echo in aortic regurgitation are rapid

diastolic closure rate and mitral valve closure occuring prior to the onset of the

QRS complex. The aortic root is often dilated in patients with aortic regurgitation.

Coarse diastolic oscillations of the aortic valve leaflet are occasionally noted. Left

ventricular end-diastolic dimensions is often increased in patients with aortic

regurgitation. The left ventricle frequently demonstrates hyperdynamic wall

motion.1

4. Cardiac catheterization and Angiography

In patients with severe aortic regurgitation diagnosed by physical

examination and ultrasound, cardiac catheterization need not be performed before

AVR. Valve surgery without catheterization is more reasonable in men younger

than 40 years or in women younger than 50 years, but atherosclerotic risk factors

and symptoms should also be considered in this decision. In addition to the issue

of defining concomitant coronary disease, when the severity of aortic

regurgitation is in question, aortography can be useful. Unlike echocardiography,

which visualizes the velocity of flow, aortography visualizes the opacification of

the left ventricle with contrast injected into the aorta, which is more dense in more

severe aortic regurgitation.4

Hemodynamic measurements in patients with left ventricular dysfunction

usually reveal elevated left ventricular filling pressures (left ventricular mean

diastolic, left atrial, pulmonary capillary wedge, pulmonary arterial diastolic),

often with associated depression of cardiac output.1

Left ventriculopathy in patients with severe and long standing aortic

regurgitation can demonstrate a number of abnormalities :


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Increased end-diastolic volume

Abnormal roundness (increased eccentricity) Reduced regional and global systolic contractile function with

resultant decreased ejection fraction and abnormal apex-to-base

shortening

Abnormally elevated endsystolic volume and abnormal endsystolicpressure volume relationship

A more accurate method of quantitating aortic regurgitation involves the

calculation of total left ventricular cardiac output from the left ventriculogram and

forward cardiac output by the Fick technique. The volume of aortic regurgitant

blood flow is divided by the total left ventricular output called the regurgitant

fraction. Patients with mild to moderate aortic regurgitation have regurgitant

fraction less than 0,50. While severe aortic regurgitation is associated with a

regurgitant fraction greater than 0,50-0,60.1


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2.1.6. Therapy

The diagram of management of patients with aortic regurgitation can be

seen below.

Figure 4. Management of Aortic Regurgitation

Based on the diagram above, the first thing to do is to determine whether

there is an enlargement of ascending aorta or not. Patients with enlargement of

ascending aorta will undergo surgery to correct the enlargement. Patients who

diagnosed with severe aortic regurgitation and developed symptoms will go

straight to have valve surgery. Patients who diagnosed with severe aortic

regurgitation and have no symptom will be checked for LVEF, EDD, or ESD to

determine whether the patients will undergo surgery or just have periodically

follow up.


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Basically, there are two options in treating patients with aortic

regurgitation. There are medical intervention and surgical intervention. Each of

them has its own indication.

Medical therapy

Nitroprusside and inotropic agents such as dopamine or dobutamine may

be useful to treat patients before surgery. It is used to stabilize patients clinical

condition. In patients with chronic severe aortic regurgitation coincident with

heart failure, ACE inhibitors are the treatment of choice. Although initial studies

had suggested that vasodilators such as calcium channel blockers or ACE

inhibitors may be effective in halting the progression of left ventricular dilatation,

subsequent studies have shown that these medications are not effective in the

patient with normal blood pressure.8,9

The rationale for treating patients with chronic severe aortic regurgitation

with vasodilating agents is that the beneficial hemodynamic effects should

translate into prolongation of the stable compensated phase in asymptomatic

patients who have volume loaded left ventricles but preserved systolic function.

But it is possible that afterload reducing therapy may have deleterious effect.

Thus, patients who develop symptoms of LV dysfunction while receiving

effective vasodilator therapy may do so at a more advanced stage in the natural

history of the disease than patients reaching the same end points without medical

therapy.1,5

Chronic therapy with vasodilators should be given only to asymptomatic

patients with severe aortic regurgitation and normal LV systolic function.

Vasodilator therapy should not be considered an alternative to AVR in

asymptomatic or symptomatic patients with LV systolic dysfunction because such

patients should be considered surgical candidates rather than candidates for long

term medical therapy.1

In patients with Marfans syndrome, beta blockers slow the progression of

the aortic dilatation. The used of beta blockers should be use cautiously because

beta blockers lengthen diastolic phase. Thus, increase the regurgitant volume too.8


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All patients with aortic regurgitation need antibiotic prophylaxis to prevent

infective endocarditis. Patients with aortic regurgitation of a rheumatic origin need

antibiotic prophylaxis to prevent recurrences of rheumatic carditis. Patients with

syphilitic aortic regurgitation need a course of antibiotics to treat syphilis .5

Surgical Therapy8

Table 2. Recommendations for aortic valve replacement in chronic severe

aortic regurgitation

In chronic aortic regurgitation, the goals of operation are to improve

outcome, diminish symptoms, prevent post operative heart failure, and avoid

aortic complications. The development of symptoms is an indication for surgery.


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In asymptomatic patients with severe aortic regurgitation, measurements of

left ventricular size and function determine the need for operation. An ejection

fraction of less than 50-55 percent or an end-systolic dimension of greater than 55

mm, indicates the presence of left ventricular systolic dysfunction.9Even in mild

cases, patients with Marfans syndrome is considered to have aortic valve

surgery.8

In considering operation, it is necessary to also examine the size of the

ascending aorta. In patients with a dilated aorta greater than 5.0 cm, concomitant

aortic replacement as well as aortic valve replacement is indicated. There are

some patients in whom there is rapid dilatation of the ascending aorta and even if

the aortic regurgitation is not severe, operation is indicated for the ascending aorta

of greater than 5.5 cm.9

Transcutaneous Aortic Valve Implantation (TAVI)

Till recently surgical aortic valve replacement (AVR) was the only

effective treatment to severe symptomatic aortic stenosis. Cribier and colleagues

have performed the first in man transcutaneous aortic valve implantation (TAVI)

in 2001. Since then rapid advance in technology has provided a new therapeutic

niche and a high or prohibitive surgical risk. To date more than 10.000 implants

have been performed worldwide.10

There are two TAVI systems which have been applied worldwide. They

are the balloon-expandable Edwards valve (Edwards Lifesciences, Irvine,

California) and the self-expandable CoreValve ReValving system (CoreValve,

Irvine, California). Retrograde transarterial or antegrade transapical approaches

are currently used to access the aortic valve. Balloon aortic valvuloplasty is

performed before valve insertion to facilitate passage of the prosthesis through the

native valve.11

The relatively large diameter of the delivery catheter has been a major

limitation of transarterial TAVI. Early systems used 22- to 25-F sheaths (outer

diameter 9 to 10 mm), and in the absence of adequate screening the incidence of

arterial dissection and perforation was relatively high. Nowadays, newer low-

profile systems (e.g., CoreValve and Edwards NovaFlex) are compatible with


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smaller 18-F sheaths (outer diameter approximately 7 mm). With technological

advances, it is should be associated with further reductions in the risk of vascular

injury and less stringent criteria for a transarterial approach.11

Angiography and multislice computed tomography are the main imaging

modalities used to assess the presence and severity of ilio-femoral disease and

determine the feasibility of an arterial approach. Minimal lumen diameter as well

as the amount and distribution of atheroma, tortuosity, and calcification will

determine the risk for vascular injury related to sheath insertion. Ideally the

minimal lumen diameter should exceed the diameter of the delivery system.

However, in the absence of extensive calcification, bulky atheroma, or severe

tortuosity, short segments of relatively compliant artery 1 to 2 mm smaller in

diameter than the intended sheath can often be safely cannulated.11

Direct access to the left ventricle is typically obtained through an

intercostal mini-thoracotomy. The risk for lung injury, pneumothorax, or pleural

bleeding seems low. Perhaps the most common concern related to the mini-

thoracotomy is chest wall discomfort and associated potential for respiratory

compromise and prolonged ventilation.11

1. Core Valve ReValving System

Figure 5. Core Valve ReValving System.

Consists of 3 leaflets of porcine pericardium mounted on a self-expandable

nitinol frame, which expands from the left ventricular outflow tract (LVOT) to the

ascending aorta. The initial device had a 25F profile, but rapidly evolved to the

current 18F device. This model has facilitated the conversion of this method into a


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strictly percutaneous technique. The currently available third generation device

measures 50 mm in height, and has 3 sections:

a. An inflow portion designed to fix the valve to the annulus has the highestradial strength.

b. An outflow portion (40 mm in diameter in the third generation valve) hasthe lowest radial force and is designed to attach the frame to the ascending

aorta to stabilize it.

c. A central portion constrained to avoid obstructing the coronaries. Despitethis valve being implanted intraannularly, its function (coaptation point) is

supraannular. Available sizes are 26 and 29 mm in diameter, designed for

annuli between 20 and 27 mm.

2. Edwards SAPIEN Prosthesis

Figure 6.Edwards SAPIEN prosthesis.

This prosthesis is the second generation of the Cribier- Edwards valve.

This is a balloon-expandable valve consisting of a stainless steel frame covered by

a Dacron skirt, in which 3 leaflets of pericardium are sutured. It is deployed in a

subcoronary position during rapid ventricular pacing, via a retrograde

transfemoral (TF) or transapical (TA) approach. The leaflets in the first generation

were made of equine pericardium, and in the second generation are made of

bovine pericardium, with improvements in the suture to the frame and an increase

in the skirt length to reduce aortic regurgitation. There are 2 sizes, 23 mm

(diameter) 14 mm (height), and 26 mm 16 mm.


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Patient Selection :

In patients with a prohibitive surgical risk, TAVI may be offered in centers

performing this procedure. Surgical risk is calculated using Logistic Euro SCORE

(LES) or Society of Thoracic Surgeons (STS) score. Patients with LES >15 to

20% and/or STS >10% are considered to have a prohibitive surgical risk.

Selection criteria depend on thorough evaluation of the aortic valve, mitral valve,

ejection fraction, vascular access and coronary angiography. Echocardiographic

interrogation of the aortic valve assesses valve area, peak velocity, transvalvular

gradient and aortic annulus. Degree of calcification of the aortic valve is

determined, Size of ascending aorta and aortic sinuses and degree of

accompanying mitral regurgitation are determined. Aortic valve morphology and

function can assessed by multidetector CT scan. PCI if needed is a prerequisite. In

patients with good femoral vascular access, the retrograde transfemoral technique

is used. In poor femoral vascular access patients, the transapical access is used or

recently through trans-subclavian artery access.10

Outcome :

Generally: transaortic pressure gradient significantly decreases; aorticvalve area increases significantly post TAVI with around 90% 30 days survival in

most studies. Left ventricular ejection fraction improves post TAVI. The

procedure is not without complications. Permanent pacing is required for new AV

block in 3% to 18%. Vascular injury is reported in 15% of TAVI procedures and

significantly increases mortality. Other complications described include valve

malpositioning, cardiac perforation and tamponade, stroke and myocardial

infarction.10

Serial Testing

Patients with mild to moderate aortic regurgitation should undergo

echocardiography every 2 years. All patients with severe aortic regurgitation but

still have normal LV function is recommended to have follow up every 6 month.8

The follow-up should be performed initially at three months to make sure

there is not rapid progression. Following that, the evaluation should be performed

every six months if there is moderate to severe dilatation, (end-systolic dimension


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of 45-50 mm) or every year if there is mild to moderate dilatation (end-systolic

dimension of less than 45 mm). Exercise testing is indicated in the initial

screening, to determine whether or not the patient truly is asymptomatic, as this

provides an objective measurement of exercise tolerance. The ventricular response

to exercise is not a clear-cut indication for operation.9

2.1.7. Prognosis

Patients with mild aortic regurgitation only have major risk for development

of infective endocarditis and further valve destruction. Patients with unprogressed

moderate aortic regurgitation would be expected to have a life close to the normal

range. If the disease progress, mortality at the end of 10 years appears to be

approximately 15 percent.5

In asymptomatic patients with normal LV function at rest, symptoms and

LV dysfunction even sudden death develops at the rate of approximately 3 to 6

percent per year. The predictor of development of symptoms is LV systolic

dysfunction at rest. In patients with normal LV systolic function at rest, the

predictors of development of LV systolic dysfunction and symptoms are an

increased LV size.5

The 5-year mortality of symptomatic patients with severe aortic

regurgitation is approximately 25 percent, and the 10-year mortality averages 50

percent. Once symptoms occur in patients with aortic regurgitation, it is likely that

the rate of deterioration will be rapid. Most patients with angina are dead within 4

years. The 2- to 3-year mortality of those with heart failure is 50 to 70 percent. 5

2.2. Acute Aortic Insufficiency

2.2.1. Definition

Acute severe aortic insufficiency is defined as hemodynamically important

aortic insufficiency of sudden onset, occuring across a previously competent

aortic valve into a left ventricle not previously subjected to volume overload.3

2.2.2. Etiology

The causes of acute aortic insufficiency are infective endocarditis, dissection

of ascending aorta, traumatic disruption of the aortic valve, spontaneus rupture or

prolaps of aortic valve secondary to degenerative disease of the valve, after


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operative or catheter valvuloplasty, sudden dehiscence of part or all of the sewing

ring of a prothetic aortic valve, and connective tissue disease with inflammation

involving the aortic valve.3

Infective Endocarditis

Bacterial or fungal organism infecting and damaging a native or prosthetic

aortic valve are the most common cause of acute severe aortic insufficiency. In

this setting, bacterial endocarditis is often the result of Staphylococcus aureus,

which produces necrosis, perforation, and detachment of one or more aortic valve

leaflets. Other aggressive organisms are Enterococcus, Aspergillus, Candida

albicans, and Histoplasma capsulatum. Often mistaken for influenza, the sudden

development of a high fever, malaise, and the early symptoms of CHF should be

given immediate attention. Cutaneous manifestations of endocarditis, systemic

emboli, a new or changing aortic regurgitation murmur, bacteremia, and

vegetations by echocardiography are elements of the diagnosis.3,4

Acute endocarditis is often associated with organism of sufficient virulence

to infect a previously normal valve. Such infections are often seen in narcotic

addicts as a result of nonsterile intravenous injections or secondary to skin abscess

formation that complicates subcutaneus drug use.3

Dissection of the Ascending Aorta

Dissection of the ascending aorta with development of a medial hematoma

can involve the aortic valve. The hematoma can dissect retrograde and displace

the attachments of the aortic valve cusps downward and medially so that one or

more aortic valve cusps prolapse into the outflow tract of the left ventricle during

diastole, thereby leading to incompetence of the valve.3

Suggestive clinical features of aortic dissection include severe chest pain

and or evidence of vascular compromise to the head, upper, and lower extremities,

gut, and kidney. Acute aortic insufficiency may be overlooked in patients with

dissection who present with other manifestations. Some additional hemodynamic

manifestations are hemopericardium with tamponade, myocardial infarction from

coronary dissection, or aortic rupture, often more problematic than aortic

regurgitation itself.3,4


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Connective Tissue Disease

Cute severe aortic insufficiency can complicate systemic lupus

erythematosus as a result of sterile perforation of one or more aortic valve cusps

secondary to fibrinoid necrosis of the valve parenchyma.3

Trauma

Aortic insufficiency is the most common valve lesion observed on patients

with closed-chest trauma. Many of these patients do not have signs of chest

injury. Initially, there may be no detectable murmur of aortic regurgitation, the

murmur and clinical signs associated with acute aortic insufficiency may be first

observed several days after the occurrence of chest trauma.3

Spontaneous Aortic Insufficiency Secondary to Myxomatous Degeneration of

the Aortic Valve.

Sudden eversion or prolapse of an aortic cusps may result in spontaneous

acute severe aortic insufficiency. This event is almost invariably associated with a

myxomatous valve. Myxomatous valve can also spontaneously perforated.3

Prosthetic Valve Aortic Insufficiency

Sudden partial dehiscence of the sewing ring of a prosthetic valve from the

aortic annulus causes acute severe aortic insufficiency. This occurs after

emergency AVR for bacterial endocarditis when the valve is implanted into an

infected annulus.3

Acute aortic insufficiency is particularly dangerous in patients who have

undergone AVR for aortic stenosis. In this condition, the ventricle is

hypertrophied and noncompliant. To increase stroke volume, it needs to elevate

ventricular filling pressure resulting in pulmonary congestion.3

2.2.3. Pathophysiology

On the contrary to chronic aortic regurgitation, in individuals with acute

aortic insufficiency, eccentric hypertrophy is not present and ventricular

compliance is normal and remains so despite the sudden regurgitant volume

overload. This situation is poorly tolerated because the left ventricle is now

overfilled and operating on the steep portions of its diastolic pressure-volume

relationship.3


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Figure 4. Pathophysiology of acute aortic insufficiency

With its large total stroke volume and wide pulse pressure causing the

bedside physical signs. Indeed, the only clue that this deadly disease is present

may be the new murmur of aortic regurgitation, which may be quite short in early

diastole because of rapid equilibration of left ventrcicle and aortic pressures. In

acute severe aortic regurgitation, the first heart sound (S1) may be soft because

the high left ventricular diastolic pressure closes the mitral valve before the onset

of left ventricular systole, an ominous sign that often indicates the need for urgent

surgery.4,7

If the volume of regurgitant is large, end diastolic left ventricular pressure is

increased. Previously normal ventricle can not acutely increase its total left


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ventricular stroke volume. Because left ventricular stroke volume is not markedly

increased, arterial pulse pressure remains unchanged and so does the bounding

arterial pulse.7 The patient also experiencce reduced cardiac output which has

impaired regional arterial blood flow, manifested as oliguria, pallor, and coolness

of skin, deranged temperature regulation secondary to reduced cutaneus blood

flow, gastrointestinal and hepatic dysfunction.3

2.2.4. Clinical Presentation

2.2.4.1. History3

The patient presents with symptoms of rapid onset due to the precipitous

rise in left arterial pressure (pulmonary congestion) and the abrupt reduction in

forward cardiac output. Progressive symptoms include dyspnea on exertion,

orthopnea, minimally productive cough, paroxysmal nocturnal dyspnea, and

dyspnea at rest even while sitting upright.

The patient also showed symptoms of heart failure in the late stage.

Symptoms of right ventricular failure such as abdominal distention is not common

in acute aortic insufficiency. The clinical picture is dominated by symptoms of

acute left ventricular failure.

A number of other symptoms relate to the etiology of acute aortic

insufficiency. There is severe chest pain characterized aortic dissection. Hence,

fever, chill, and malaise suggest the diagnosis of infective endocarditis. The most

common cause of acute aortic insufficiency is infective endocarditis in a bicuspid

aortic valve. This is more common in men than in women. The absence of

ancillary symptoms or known heart disease suggests sudden disruption or

perforation of an aortic valve intrinsically weakened by myxomatous

degeneration.

2.2.4.2. Physical Examination

Physical findings in patients with acute aortic insufficiency reflect the

severity of pulmonary congestion and impaired cardiac output. A variety of signs

relate to the underlying etiology.

As noted earlier, the most prominent features are the manifestations of

pulmonary congestion and impaired cardiac output. Because of the nature of acute


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aortic insufficiency, the left ventricle has not undergone eccentric hypertrophy. So

there is no widened arterial pulse pressure and another peripheral arterial findings

like in chronic aortic regurgitation.3,7

In acute severe aortic insufficiency, ventricular output is reduced then lead

to tachycardia. The precordium is usually quiet because the left ventricle is neither

dilated nor hyperdynamic. The pulse pressure is not widened, systolic blood

pressure is normal or slightly elevated, and diastolic blood pressure is elevated.

The first heart sound is usually soft as the regurgitant volume rapidly fills the

ventricle and pushes the mitral leaflets toward closed position before left

ventricular activation. Occasionally, the first heart sound is completely absent.3,7

The second heart sound is also soft and may be absent if one or more aortic

valve leaflets have been damaged to the point of little or no diastolic coaptation.

An ejection type murmur of variable intensity is often heard, localized to the base.

This reflects turbulent flow across the aortic valve resulting from augmented

stroke output through the damaged valve. An Austin-Flint murmur is often present

in acute aortic insufficiency. A third heart sound is also frequently present,

reflecting rapid early diastolic ventricular filling.3

Rising pulmonary pressure lead to an increase in right ventricular failure. So

the jugular venous distention with a prominent A wave may be present. In acute

aortic insufficiency, prominent neck pulsation is venous origin rather than arterial.

Other signs can help to differentiate acute and chronic aortic regurgitation.

Distal extremities are cool and pale because of systemic vasoconstiction can be

found in acute state. Fever, ptechiae, purpura, and small or large arterial embolic

events implicate infective endocarditis.3

2.2.4.3. Laboratory Findings

1. Chest x-ray

The chest x-ray in patients with acute aortic insufficiency usually reveals

bilateral patchy interstitial infiltrates that progress to confluent alveolar infiltrates

emanating from the hilar regions as pulmonary congestion progresses to fulminant

pulmonary edema. There is apical redistribution in pulmonary veins. The cardiac

silhoutte is not enlarged unless there is preexisting chronic valvular, myocardial,


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or pericardial dysfunction. The patients with severe aortic insufficiency secondary

to ascending aortic dissection usually demonstrate a widened transverse

mediastinal shadow on the chest x-ray.3

2. Electrocardiogram

Electrocardiogram findings are neither sensitive nor specific for acute aortic

regurgitation. Sinus tachycardia only indicative for the severity of cardiac

decompensation. Left ventricular hypertrophy is absent in pure acute aortic

insufficiency. The electrocardiogram may demonstrate nonspecific ST segment

and T wave abnormalities related to subendocardial ischemia, hypoxemia,

acidosis, and other metabolic or electrolytes abnormalities.

3. Echocardiography

Once acute aortic regurgitation is suspected, echocardiography should be

performed immediately to help detect aortic regurgitation, assess the etiology,

assess the severity, and assess hemodynamic effect.7

Figure 5. Color Doppler echocardiographic of patients with mild (A) and

severe (B) aortic regurgitation

(A) (B)It should be performed at the time of initial presentation and at regular

intervals during the acute course of illness. The echo often provide information

about the cause of aortic insufficiency. For example, shaggy large irregular echo

dense masses is associated with vegetations as seen in infective endocarditis. The


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echo of a redundant echo-dense band located centrally or eccentrically in the

proximal aortic root is indicated for aortic dissection. Transesophageal

echocardiography is particularly helpful in diagnosing endocarditis, perivalvular

abscesses, and aortic dissection.3,4

4. Cardiac Catheterization

Figure 6. Aortic regurgitation at cardiac catheterization

Before the era of using Doppler echocardiography begin, the evaluation of

severity of aortic regurgitation required invasive testing by cardiac catheterization.

Nowadays, routine cardiac catheterization is no longer necessary in the majority

of patients. At catheterization, the detection of aortic regurgitation is achieved

with injection of radioopaque contrast into the aortic root and the appearance of

dye in the left ventricle.7

2.2.5. Treatment

The treatment for patients with acute aortic insufficiency are classified into

three, general supportive cardiovascular measures, pharmacologic management,

and surgical management. It is emphasized that medical and surgical interventions

are mutually complementary in the total management of these patients.3


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aortic ring abscess. Repeat echocardiography is useful to look for changes in

vegetation size and worsening of aortic regurgitation.4

Vasodilator therapy can be one of the choice. Nitropruside in a total dose of

3-6 g/kg/min with titration may produce as much as a 30% to 50% increase in

cardiac output. Nitropruside reduced the regurgitant volume per beat, improve

cardiac output, and lowers left ventricular filling pressure, promoting resolution of

pulmonary edema.3

If the cardiac index is not maintained above 2,0 to 2,2 L/min/m2in response

to nitropruside or nitroglyserin infusion despite doses sufficient to lower systolic

blood pressure to 90 mmHg or reduce mean arterial blood pressure by at least 15

mmHg, a sympathomimetic agent should be added. This is necessary to increase

cardiac output in order to maintain adequate coronary and cerebral perfusion.

Dobutamine, unlike dopamine, lacks intrinsic alpha adrenergic agonist activity. It

elevates neither arterial resistance nor venous tone. Dobutamine instituted at 3-5

g/Kg/min and is increased by 2-4 g/Kg/min every 15 to 30 minutes.3

All patients with severe acute aortic insufficiency require frequent

monitoring of renal function, serum electrolytes, and arterial blood gas. All

processes related to inadequate tissue perfusion and pulmonary congestion may be

cause disturbance to renal, liver, and other organs.3

Definitive management for severe acute aortic insufficiency is aortic valve

replacement.1 Although there is always a concern that early implantation of a

prosthesis in an infected patient may lead to prosthetic endocarditis, persistence of

infection occurs in 10%, irrespective of timing of surgery. Therefore, once the

need for surgery is established further delay is unwarranted and risks spread of the

infection or embolization. In patients with extension of the infection into tissue

around the aortic valve (annular ring abscess), an aortic homograft may be

advantageous because it has reduced postoperative infection.4

In order to prevent infection, it is recommended to administer antibiotic

before aortic valve replacement. In case of cardiogenic shock caused by acute

aortic insufficiency, aortic valve replacement should be undertaken immediately


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even though there is little or no time for antibiotic administration. The patients

then have to receive 4-6 weeks of antibiotic after aortic valve replacement.3

chapter ii-aortic regurgitation hearth refrat

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