Aortic regurgitation

1. AORTIC REGURGITATION
SEMINAR ON 13/08/2018
Dr Sachin Sondhi
IGMC SHIMLA

2. Causes and Pathology

3. • Degenerative aortic dilation,
• cystic medial necrosis of the aorta (either isolated or associated with
classic Marfan syndrome),
• aortic dilation related to bicuspid valves
• aortic dissection,
• osteogenesis imperfecta,
• syphilitic aortitis,
• ankylosing spondylitis,
• Behçet syndrome,
• psoriatic arthritis, arthritis associated with ulcerative colitis, relapsing
polychondritis,
• reactive arthritis, giant cell arteritis, and systemic hypertension, as well
as exposure to some appetite-suppressant drugs.

4. PATHOPHYSIOLOGY
1. Volume overload in LV EDV Increases Increase in chamber compliance (no increase
in EDP)
2. Increase in total SV, Forward stroke volume is maintained
3. New sarcomere (series) produces ecc. Hypertrophy
4. Although LV preload increases, LV preload at sarcomere level remains normal, Hence LV preload reserve
is maintained.
5. Augmented LV chamber volume increases wall stress and afterload, which causes concenteric hypertrophy
(AR is condition of both pressure and volume overload)
6. This produces compensated phase
7. Results in maintenance of EF, Forward stroke volume, normal diastolic pressure
8. Hemodynamic compensation lasts for decade
9. Balance between excessive afterload and combination of preload reserve and compensatory hypertrophy
cannot be maintained indefinitely.
10. Any further increase in afterload at this point decreases systolic ejection performance.
11. Symptoms of dyspnea or fatigue develop at this stage of transition.
12. Depressed LV function initially is potentially reversible process related to afterload mismatch and complete
reversal after AVR.
13. With time severe LV enlargement and remodeling and depressed function may predominate over
excessive loading as principal mechanism for declining function, at this stage AVR will not help in
regaining LV function.

7. • In compensated AR, sufficient wall thickening has occurred that the
ratio of ventricular wall thickness to cavity radius remains normal.
Under these conditions, end-diastolic wall stress is maintained at or
returns to normal levels.
• As AR persists and increases in severity over time, however, wall
thickening fails to keep pace with the hemodynamic load, and end-
systolic wall stress rises. At this point, the afterload mismatch results in
a decline in systolic function, and the ejection fraction falls

8. A, Normal conditions. B, The hemodynamic changes that occur in
severe acute AR. Although total stroke volume is increased, forward
stroke volume is reduced. LV end-diastolic pressure (LVEDP) rises
dramatically.

9. Hemodynamic changes occurring in chronic compensated aortic regurgitation are
shown. Eccentric hypertrophy produces increased end-diastolic volume (EDV), which
permits an increase in total, as well as forward, stroke volume. The volume overload is
accommodated, and LV filling pressure is normalized. Ventricular emptying and end-
systolic volume (ESV) remain normal.

11. • In more severe cases of AR, the regurgitant flow may exceed 20 liters/min,
so the total LV output at rest approaches 25 liters/min, a level that can be
achieved acutely only by a trained endurance runner during maximal
exercise. Thus the adaptive response to gradually increasing, chronic AR
permits the ventricle to function as an effective high-compliance pump,
handling a large stroke volume, often with little increase in filling pressure.
• During exercise, peripheral vascular resistance declines and, with an increase
in heart rate, diastole shortens and the regurgitation per beat decreases,
facilitating an increment in effective (forward) cardiac output without
substantial increases in end-diastolic volume and pressure. The ejection
fraction and related ejection phase indices are often within normal limits,
both at rest and during exercise, even though myocardial function, as
reflected in the slope of the end-systolic pressure-volume relationship, is
depressed.

12. D, In chronic decompensated AR, impaired LV emptying produces an increase
in end-systolic volume and a fall in ejection fraction (EF), total stroke volume,
and forward stroke volume. Further cardiac dilation and re-elevation of LV
filling pressure occur. E, Immediately after valve replacement, preload estimated
by EDV decreases, as does filling pressure. ESV also is decreased, but to a lesser
extent. The result is an initial fall in EF. Despite these changes, elimination of
regurgitation leads to an increase in forward stroke volume, and with time
ejection fraction

27. SYMPTOMS
• In chronic severe AR, the left ventricle gradually enlarges while the patient remains
asymptomatic for decades.
• Palpititions on lying down
• Forcefull pulsations in neck vessels
• Angina – 1. atherosclerosis 2. increased demand due to increase in mass 3. Low
coronary perfusion due to low diastolic pressure 4. osteal atherosclerotic narrowing in
luteal AR
• Nocturnal Angina - nocturnal angina may be troublesome and often is accompanied
by diaphoresis, which occurs when the heart rate slows and arterial diastolic pressure
falls to extremely low levels, attacks are frequently associated nightmares, dyspnea,
forceful heart skin flushing and profuse sweating.
• Symptoms of HF may be insidious dyspnea may occur for short periods of time or
may present before number of years before more severe symptoms of orthopnea or
PND develops.

28. Physical signs
• BP – Presence of completely normal BP excludes severe AR (SEV. AR – DBP around
40-50mm Hg)
• Heart Rate. Tachycardia shortens the time for diastolic reflux and thus may increase the
diastolic blood pressure in aortic regurgitation. Conversely, bradycardia will accentuate
the decrease in diastolic blood pressure because of the increased duration of aortic
regurgitation.
• Leg Blood Pressure. The normal increase in systolic blood pressure found in arteries
distal to the proximal aorta is exaggerated in aortic regurgitation. In severe aortic
incompetence, systolic pressure in the popliteal artery is much higher than in the
brachial artery (Hill's sign). A difference in systolic blood pressure between the arms and
the legs of greater than 40 to 50 mmHg typically is seen in major degrees of aortic
regurgitation.

29. Collapsing pulse in AR
1. Increased upstroke
due to increased
volume of ejection.
2. Downstroke -
Sudden fall in DBP
due regurgitation.
3. Due to rapid
emptying of arterial
system because of
aortic run off).
4. Aortic run off is
because of reflex
vasodilataion due to
over activation
baroreceptors (LOW
SVR).

30. Low cardiac output or heart failure may attenuate these signs. Arterial vasoconstriction occurs as stroke volume
falls. An increased heart rate in congestive heart failure (CHF) may also play a role in blunting the signs of aortic
regurgitation.

31. APEX BEAT

32. • S1 – Normal to soft (increase PR, decreased LV contractility, increased
LVEDP premature closure of MV), sometimes appears loud due to
fusion of ejection click
• S2 – Intensity is variable ( A2 soft in valvular and loud in aortic root
disease), splitt is narrow or single in severe AR (A2 moves to P2 due to
prolonged ejection time)
• S3 – In severe AR,
• An S3 often initiates an Austin Flint rumble when present
• S4 – In severe AR

34. • Prominent murmur on right side – aortic aneurysm, sinus of
valsalva aneurysm, aortic dissection
• Sea gull or cooing dove murmer – loud musical quality due to
eversion or perforation of aortic cusp ( IE, Syphilis, trauma, ARF)
• When mitral stenosis coexists with AR, the obstruction to inflow
to left ventricular filling may attenuate the full expression of the
aortic regurgitation on clinical examination.

35. • Systolic Murmur. A systolic ejection murmur is common in moderate to severe aortic
regurgitation. It results from an abnormally large stroke volume that is ejected with
rapid force often across an anatomically deformed aortic valve into an enlarged
proximal aorta.
• Practical Point: A loud systolic murmur in a patient with severe aortic regurgitation
does not necessarily imply coexisting aortic stenosis. Typically, this systolic murmur is
short and peaks before the second half of systole if there is no aortic valve obstruction
(Figs. 15-5, 15-6B, C, 15-7A). However, with a very large ejected stroke volume the
systolic murmur lengthens in proportion to the increase in left ventricular ejection
time. Thickened aortic valve leaflets with minimal reduction in area of the aortic
orifice in the absence of a systolic left ventricular-aortic gradient may accentuate the
intensity and duration of the systolic murmur

36. • . In such instances, the systolic ejection murmur may be both loud
and long without true aortic stenosis being present. Severe aortic
regurgitation without stenosis rarely may be associated with a
grade 4/6 systolic murmur and an accompanying thrill. In these
difficult cases, the focus should be on any nonauscultatory signs of
aortic regurgitation, the blood pressure, and the quality of the
carotid pulse to assess the possibility of associated aortic stenosis.
Ifthe diastolic blood pressure is low,the pulse volume is full and
bounding, and there is evidence of peripheral vasodilation, aortic
stenosis can usually be readily excluded.

37. Austin Flint Murmur.
AFM is a low-pitched, rumbling apical diastolic murmur
that sounds exactly like the murmur of mitral stenosis
The mechanism for the genesis of the AFM has been
the focus of many investigators. Its presence generally
indicates a large diastolic leak with a regurgitant
fraction of over 50%.

38. • The mechanism appears to be related to an incomplete opening of the anterior leaflet of the mitral
valve during diastole as a result of the impact of the regurgitant stream of blood into the left
ventricular cavity.
• This premature closure of the mitral valve in mid-late diastole prevents left atrial contraction from
reopening the valve, and therefore, the presystolic component of the AFM is absent
• Other postulated mechanisms for the AFM include "relative or functional
mitral stenosis" (small left atrium, large left ventricle), diastolic mitral
regurgitation, fluttering or. vibration of the anterior leaflet of the mitral
valve resulting from the aortic diastolic jet, and selective transmission of low
to medium frequency vibrations of the aortic regurgitation murmur to the
apex. None of these phenomena adequately explain the AFM.

40. Natural history

41. Asymptomatic Severe AR
AUTHOR PATIENTS AND
FOLLOW UP
PROGRESSION
TO
SYMPTOMS/LV
DYSFUNCTION/
DEATH
PROGRESSION
TO
ASYNPTOMATIC
LV dysfunction
BONOW ET AL 104 –
8YEARS
3.8%/YEAR 0.5%/year
TORNOS 101 –
4.6 YEARS
3%/YEAR 1.3%/YEAR
BORER 104 –
7.3 YEARS
6.2%/YEAR 0.9%/YEAR
AVERAGE 6.4 4.3%/YEAR 1.3%/YEAR
SUDDEN DEATH
0.19%/YEAR
BONOW ET AL – ESD IS SINGLE MOST IMPORTANT PREDICTOR ( ESD>50 HAS 19%
LIKLEHOOD OF PER YEAR DEATH/SYMPTOMS AND LV DYSFUNCTION. THOSE WITH
ESD BETWEEN 40-50 HAD 6% LIKEHOOD. THOSE WITH <40 HAD NO LIKLEHOOD

43. ASYMPTOMATIC SEVERE AR WITH
LV DYSFUNCTION
SYMPTOMATIC SEVERE AR
PROGRESSION TO SYMPTOMS
25%/YEAR
>66% BECOME SYMPTOMATIC IN
2-3 YEARS
MORTALITY 10%/YEAR
HF 20%/YEAR

44. VASODILATOR THERAPY IN AR
• No specific therapy to prevent disease progression in chronic AR is currently
available. Uncertainty remains about whether patients with chronic AR and
evidence of significant volume overload (increased end-diastolic dimension or
volume) should be considered for vasodilator therapy to alter the natural
history of chronic LV volume overload.Short-term studies spanning 6 months
to 2 years have demonstrated beneficial hemodynamic effects of oral
hydralazine, nifedipine, felodipine, and ACE inhibitors.
• One concern about the use of any agent that appears to preserve the ejection
fraction is that it may mask progressive myocardial dysfunction; thus, when
the ejection fraction falls or becomes abnormal, myocardial dysfunction may
have progressed to such a degree that successful valve replacement may no
longer improve the ejection fraction.

45. randomly assigned 143 asymptomatic patients with isolated, severe aortic regurgitation and
normal left ventricular systolic function to receive either nifedipine (20 mg twice daily, 69
patients) or digoxin (0.25 mg daily, 74 patients).
Results
By actuarial analysis, we determined that after six years a mean (±SD) of 34 ±6 percent of the
patients in the digoxin group had undergone valve replacement, as compared with only 15 ±3
percent of those in the nifedipine group (P<0.001).

48. Determinants of outcome after valve
replacement
• Preoperative EF is most important
• Degree of Preoperative symptoms with same
degree of LV dysfunction
• Duration of preoperative symptoms
• EF <50%, LV DYSFUNCTION >18 MONTHS, ESD
> 55 MM, POOR EXERCISE TIME AND HIGHER
NYHA CLASS.

49. Indications of operation
• Because of their excellent prognosis in the short and
medium term, operative correction should be deferred in
patients with chronic severe AR who are asymptomatic,
exhibit good exercise tolerance, and have an ejection
fraction greater than 50% without severe LV dilation (i.e.,
end-systolic diameter 50 mm or less) or progressive LV
dilation on serial echocardiograms

50. • In the absence of obvious contraindications or
serious comorbidity, surgical treatment is advisable
for symptomatic patients with severe AR and for
asymptomatic patients with either an ejection
fraction of 50% or less or severe LV dilation (end-
systolic diameter >50 mm).

52. • Asymptomatic patients with severe AR but normal LV
function have an excellent prognosis and do not require
prophylactic operation. On average, less than 6% of
patients/year require operation because of the development
of symptoms or of LV dysfunction

53. • Even after successful correction of AR,
patients with severe LV dysfunction may have
persistent cardiomegaly and depressed LV
function. Such patients often exhibit
persistent histologic changes in the left
ventricle, including massive fiber hypertrophy
and increased interstitial fibrous tissue.
Therefore it is highly desirable to operate on
patients before irreversible LV changes have
occurred.

54. • The indications for surgery for patients with severe AR secondary
to aortic sinus or ascending aortic disease are similar to those for
patients with primary valvular disease.
• However, progressive expansion of the aortic sinuses and/or
ascending aorta to a diameter greater than 55 mm with any degree
of regurgitation in patients with a bicuspid valve (or other
connective tissue disorder) also is an indication for repair of the
aortic sinuses or replacement of the ascending aorta.1

55. • This threshold is decreased to 50 mm in patients with risk factors
for dissection (family history of aortic dissection or rate of increase
in diameter of ≥0.5 cm/year). In addition, in patients with
indications for AVR as noted previously, concomitant surgery on
the aortic sinuses or ascending aorta is indicated if the amount of
aortic dilation is greater than 45 mm.

62. • THANKS