D . B A S E M E L S A I D E N A N Y
L E C T U R E R O F C A R D I O L O G Y
A I N S H A M S U N I V E R S I T Y
Chronic Aortic regurge
--Aortic regurgitation may be due to disease of the
valve leaflets or to enlargement of the aortic root.
--In the developing world, the most common cause of
AR is rheumatic heart disease.
--However, in developed countries, AR is most often
due to aortic root dilation or a congenital bicuspid
--Added volume of regurgitant blood produces an
increase in left ventricular end-diastolic volume and an
elevation in wall stresscompensatory myocardial
hypertrophy increase SV, end-diastolic pressure
remains normal due to an increase in ventricular
--Asymptomatic for decades
--Due to increased mass of the enlarged left ventricle:
A sense of pounding and an uncomfortable awareness of the heartbeat.
Atypical chest pain induced by a mechanical interaction between the heart
and the chest wall. Palpitations due to tachycardia or premature beats.
--Symptoms of left-sided heart failure (dyspnea on exertion, orthopnea,
paroxysmal nocturnal dyspnea, and eventual pulmonary edema)
--Angina pectoris is uncommon coronary arteries are typically large.
underlying coronary artery disease
marked left ventricular hypertrophy, subendocardial ischemia
At night when the heart rate slows and arterial diastolic pressure falls to
very low levels
--Increased SV abrupt distension of the peripheral arteries and an elevation in systolic pressure.
--Regurgitation rapid fall in pressure with quick collapse of the arteries and a low diastolic
--wide pulse pressure= "water hammer" or Corrigan pulse. This finding may be best appreciated
by palpation of the radial or brachial arteries (exaggerated by raising the arm) or the carotid pulses
--deMusset's sign — A head bob occurring with each heart beat.
Traube's sign — A pistol shot pulse (systolic and diastolic sounds) heard over the femoral arteries.
Duroziez's sign — A systolic and diastolic bruit heard when the femoral artery is partially
Quincke's pulses — Capillary pulsations in the fingertips or lips.
Mueller's sign — Systolic pulsations of the uvula.
Becker's sign — Visible pulsations of the retinal arteries and pupils.
Hill's sign — Popliteal cuff systolic pressure exceeding brachial pressure by more than 60 mmHg.
Mayne's sign — More than a 15 mmHg decrease in diastolic blood pressure with arm elevation
from the value obtained with the arm in the standard position.
Rosenbach's sign — Systolic pulsations of the liver.
Gerhard's sign — Systolic pulsations of the spleen.
--DD=sympathetic hyperactivity, anemia, fever, pregnancy, thyrotoxicosis, large arteriovenous
fistula, patent ductus arteriosus, and severe bradycardia
What is the significance of a brisk carotid arterial upstroke?
It depends on whether it is associated with normal or widened pulse pressure.
==If associated with normal pulse pressure, a brisk carotid upstroke usually
indicates two conditions:
Simultaneous emptying of the left ventricle into a high-pressure bed (the
aorta) and a lower pressure bed: The latter can be the right ventricle (in patients
with ventricular septal defect [VSD]) or the left atrium (in patients with mitral
regurgitation [MR]). Both will allow a rapid left ventricular emptying, which, in turn,
generates a brisk arterial upstroke. The pulse pressure, however, remains normal.
Hypertrophic cardiomyopathy (HCM): Despite its association with left
ventricular obstruction, this disease is characterized by a brisk and bifid pulse, due to
the hypertrophic ventricle and its delayed obstruction.
==If associated with widened pulse pressure, a brisk upstroke usually indicates aortic
regurgitation (AR). In contrast to MR, VSD, or HCM, the AR pulse has rapid upstroke
and collapse. Others: anemia, fever, exercise, thyrotoxicosis, pregnancy, cirrhosis,
beriberi, Paget disease, arteriovenous fistulas, patent ductus arteriosus
--Apical impulse being displaced laterally and inferiorly and being diffuse and
hyperdynamic. A prominent pulsation (and occasionally a thrill) may be felt at the
sternal notch due to concurrent dilatation of the ascending aorta
S1 may be soft, often reflecting a long PR interval
S2 is variable; it may be soft, absent, or single
A2 is often soft or absent while P2 may be normal, but obscured by the diastolic
A systolic ejection sound may be due to abrupt aortic distension caused by the large
A third heart sound (S3 gallop) is heard when left ventricular function is severely
--Diastolic murmur begins immediately after A2. It is high pitched, often blowing in
quality, and may be sustained in intensity or decrescendo. It may be soft and barely
audible, often appreciated only when the patient is sitting up, leaning forward, and
holding his or her breath in expiration, the murmur increases with squatting and
decreases with the Valsalva maneuver
-The intensity of the murmur does not correlate well with the severity of AR. However,
the timing and duration of the murmur may be helpful.
--In very severe regurgitation with ventricular decompensation, and acute AR the
murmur may become soft or even absent (increase enddiastolic pressure)
There are two golden and three silver rules:
& The first golden rule is to always judge (systolic) murmurs like people: by
the company they keep. Hence, murmurs that keep bad company (like
symptoms; extra sounds; thrill; and abnormal arterial or venous pulse,
electrocardiogram [ECG], or chest radiograph) should be considered
pathologic until proven otherwise. These murmurs should receive lots of
evaluation, including technology based.
& The second golden rule is that a diminished or absent S2 usually indicates a
poorly moving and abnormal semilunar (aortic or pulmonic) valve. This is the
hallmark of pathology.
As a flip side, functional systolic murmurs are always accompanied by a well-
preserved S2, with normal split.
The three silver rules are:
& All holosystolic (or late systolic) murmurs are pathologic.
& All diastolic murmurs are pathologic.
& All continuous murmurs are pathologic.
--The murmur is heard best along the left sternal border, at
the third and fourth intercostal space, when AR is due to
valvular disease. In contrast, abnormalities of the aortic
root produce murmurs that are best heard at the right
sternal border and apex.
--Systolic murmur can be heard in many patients
--Second diastolic murmur (the Austin Flint murmur) may
also be appreciated mid to late diastolic rumble, heard at
the apex (competing with mitral flow)
absence of both a loud S1 and an opening snap of the mitral
--Left ventricular hypertrophy
--Isolated atrial and ventricular premature beats are
--Conduction abnormalities, sustained
supraventricular or ventricular tachyarrhythmiasare
usually not seen.
--Cardiomegaly due to the dilatation of the left
--The ascending aorta (and often the aortic arch or
knob) are typically markedly dilated
--Left atrial enlargement significant left ventricular
dysfunction. Thus, its presence in patients with mild to
moderate AR suggests associated mitral valve disease
--The valve leaflets may be normal or abnormal (thickening,
vegetations, calcification, and prolapsed or flail leaflets).
--The aortic root is often dilated and there may be evidence of
an aneurysm (dissecting or saccular).
--There is often high frequency, diastolic fluttering of the
anterior leaflet of the mitral valve which is due to the diastolic
regurgitant jet of blood from the aorta.
--Doppler echocardiography detecting the regurgitant jet AR.
--The left ventricular end-systolic and end-diastolic volumes are
increased in chronic AR
---TOE for good assessment of valve leaflet, Ao root,
intraoperative is mandatory in aortic valve repair, to assess the
functional results and identify patients who are at risk of early
recurrence of AR
1. Exercise testing is reasonable in selected patients
with asymptomatic severe VHD to 1) confirm the
absence of symptoms, or 2) assess the hemodynamic
response to exercise, or 3) determine Prognosis .
(Level of Evidence: B)
CMR is indicated in patients with moderate or severe
AR (stages B, C, and D) and suboptimal
echocardiographic images for the assessment of LV
systolic function, systolic and diastolic volumes, and
measurement of AR severity. (Level of Evidence: B)
-In addition to symptom status, prognosis in patients
with AR is assessed by measurements of LV size and
function, usually by echocardiography, as
recommended by the 2006 ACC/AHA valvular
guidelines (with 2008 update)
-Echocardiography every one to two years
-Yearly testing (CT or MRI) is recommended in
patients with an aortic root or ascending aortic
diameter greater than 40 mm
---Marfan patients, bicuspid with aortic root
diseasefirst-degree relatives should be scanned
PHYSICAL ACTIVITY AND EXERCISE
-Asymptomatic patients with mild or moderate AR with a left
ventricular end-diastolic diameter that is normal (≤55 mm) or
mildly increased can participate in all competitive sports.
-Patients with asymptomatic nonsustained ventricular
tachycardia at rest or with exercise should only participate in
low-intensity competitive sports.
-Patients with AR and significant dilatation of the ascending
aorta (>45 mm, normal ≤35 mm) should participate only in low-
intensity competitive sports.
---This recommendation does not apply to patients with Marfan
syndrome in whom any degree of aortic dilatation should
prohibit competitive sports because of the risk of aortic
dissection and rupture.
Vasodilators such as nifedipine and angiotensin converting enzyme
(ACE) inhibitors may influence LV size and function and slow the rate
of progression of AR.
2-Medical therapy, other than vasodilators, has a limited role in AR
because symptomatic patients should be treated with valve
replacement HF, not candidates for surgery digoxin for
symptoms, diuretics for fluid control, ACE inhibitors and/or
angiotensin II receptor blockers to improve survival.
3-BB relative CI as increase diastole, regurge The 2006 ACC/AHA
guidelines on the management of valvular heart disease concluded
that beta blocker therapy was reasonable in patients with bicuspid
aortic valves who have an aortic root diameter greater than 40 mm
and do NOT have moderate or severe aortic regurgitation
4-ENDOCARDITIS PROPHYLAXIS NO LONGER
5---Rheumatic fever prophylaxis: Till 40, or 10 y after last attack
--AR is considered high risk if associated with NYHA
class III to IV symptoms, an LVEF less than 40%, or
Marfan syndrome definitive surgery up to
termination if refuse:
-- symptomatic diuretics, VD as nifedipine (CI of
--Marfan BB esp dialted aortic root (labetalol)
Operate in refarctory NYHA III, IV symptoms
RF in Marfan
-Family history of dissection
-Size increase >2 mm/year in repeated
examinations using the same technique and confirmed
by another technique
-Desire to become pregnant
1. Operative intervention to repair the aortic sinuses or
replace the ascending aorta is reasonable in patients with
bicuspid aortic valves if the diameter of the aortic sinuses
or ascending aorta is greater than 5.0 cm and a risk factor
for dissection is present (family history of aortic dissection
or if the rate of increase in diameter is ≥0.5 cm per year).
(Level of Evidence: C)
2. Replacement of the ascending aorta is reasonable in
patients with a bicuspid aortic valve who are undergoing
aortic valve surgery because of severe AS or AR if the
diameter of the ascending aorta is greater than 4.5 cm.
(Level of Evidence: C)
2006 ACC/AHA guidelines recommended that patient
age, ability to tolerate warfarin, and patient preference
all be taken into account:
--Patients with a projected long life-span generally
receive a mechanical valve because of far greater
durability and improved patient survival at 15 years.
--The main indications for a bioprosthesis are patients
who cannot or will not tolerate warfarin or for whom
compliance is uncertain, and patients ≥65 years of age
who do not have risk factors for thromboembolism
since valve durability is less of an issue.
The patient and family should be sufficiently
educated by the Heart Valve Team about all
alternatives for treatment so that their expectations
can be met as fully as possible using a shared decision-
Heart Valve Centers of Excellence
1) are composed of experienced healthcare providers with
expertise from multiple disciplines;
2) offer all available options for diagnosis and
management, including complex valve repair, aortic
surgery, and transcatheter therapies;
3) participate in regional or national outcome
4) demonstrate adherence to national guidelines;
5) participate in continued evaluation and quality
improvement processes to enhance patient outcomes; and
6) publicly report their available mortality and success
--Echocardiogrambefore hospital discharge or at the first
postdischarge outpatient visitreduction in left ventricular
end-diastolic dimension in the first 10 to 14 days after surgery
--Increasing experience in some centers with aortic valve repair
in selected patients.
--Moderate AR, who undergo CABG or mitral
valve surgery, the decision to treat the aortic valve should be
Aetiology of the AR
Worsening of LV function
Possibility of valve repair
--Fluroscopy: in prosthetic valves
--CT for coronaries in low risk patients
Other valvular lesions
--When either stenosis or regurgitation is predominant,
management follows the recommendations concerning the
--Interaction between the different valve lesions ex. associated
MR may lead to underestimation of the severity of AS
--Indications for intervention are based on global assessment of
the consequences of the different valve lesions, i.e. symptoms
or presence of LV dilatation or dysfunction
--The decision to intervene on multiple valves should take into
account the extra surgical risk
--The choice of surgical technique should take into account the
presence of the other VHD.
--Asymptomatic patients with severe MR or AR and
preserved LV function, non-cardiac surgery can be
--The presence of symptoms or LV dysfunction should lead
to consideration of valvular surgery, but this is seldom
needed before non-cardiac surgery.
--If LV dysfunction is severe (EF <30%), non-cardiac
surgery should only be performed if strictly necessary, after
optimization of medical therapy for HF.
--Control heart rate (particularly in MS), to avoid fluid
overload as well as volume depletion and hypotension
(particularly in AS)