This document provides information on valvular heart disease, focusing on mitral stenosis and mitral regurgitation. It discusses the etiology, pathophysiology, symptoms, physical exam findings, diagnostic testing, and treatment recommendations for each condition. Mitral stenosis is typically caused by rheumatic fever and leads to pulmonary hypertension from elevated left atrial pressures. Mitral regurgitation can result from several causes including rheumatic heart disease, papillary muscle dysfunction, and mitral valve prolapse. Physical exam findings help distinguish the murmurs associated with each condition. Echocardiography is important for diagnosis and determining treatment approach.

1. Valvular Heart Disease for 5th year Medical Students
Samir Morcos Rafla, FACC, FESC, FHRS
Emeritus professor of cardiology
Alexandria University
smrafla@yahoo.com
01001495577
‫صفحة‬ ‫وعلى‬ ‫يوتيوب‬ ‫على‬ ‫موضوعه‬ ‫المحاضرات‬
Dr. Samir Rafla Lectures

2. MITRAL STENOSIS
ETIOLOGY AND PATHOLOGY: Two-thirds of all patients with mitral stenosis (MS) are
females. MS is generally rheumatic in origin. Pure or predominant MS occurs in
approximately 40% of all patients with rheumatic heart disease. The valve leaflets are
diffusely thickened by fibrous tissue and/or calcific deposits. The mitral commissures
fuse, the chordae tendineae fuse and shorten. The valvular cusps become rigid, and
these changes in turn, lead to narrowing at the apex of the funnel-shaped valve.
Other rare causes of mitral stenosis: Atrial myxoma, ball valve thrombus, congenital
and calcific- atherosclerortic disease.
Valvular Heart Disease

3. • PATHOPHYSIOLOGY: In normal adults the mitral valve orifice is 4 to 6 cm2.
When the mitral valve opening is reduced to 1 cm2, a left atrial pressure of
approximately 25 mmHg is required to maintain a normal cardiac output. The
elevated left atrial pressure, in turn, raises pulmonary venous and capillary
pressures, reducing pulmonary compliance and causing exertional dyspnea.
• Pulmonary hypertension results from (1) the passive backward transmission of
the elevated left atrial pressure, (2) pulmonary arteriolar constriction, (reactive
pulmonary hypertension), and (3) organic obliterative changes in the pulmonary
vascular bed. In time, the resultant severe pulmonary hypertension results in
tricuspid and pulmonary incompetence as well as right-sided heart failure.

4. The cardiac cycle:
Simultaneous
electrocardiogram and
pressure obtained from the
left atrium, left ventricle, and
aorta, and the jugular pulse
during one cardiac cycle.

5. When moderately severe MS has existed for several years, atrial arrhythmias as flutter and
fibrillation occur.
Hemoptysis results from rupture of pulmonary-bronchial venous connections (apoplexy)
secondary to pulmonary venous hypertension. Frank hemoptysis must be distinguished from the
bloody sputum that occurs with pulmonary edema, pulmonary infarction, and bronchitis, three
conditions that occur with increased frequency in the presence of MS.
Recurrent pulmonary emboli, sometimes with infarction are an important cause of morbidity
and mortality late in the course of MS, occurring most frequently in patients with right
ventricular failure. Pulmonary infections, i.e., bronchitis, broncho-pneumonia, and lobar
pneumonia, commonly complicate untreated MS. Infective endocarditis is rare in pure MS but
is not uncommon in patients with combined stenosis and regurgitation.

6. • SYMPTOMS AND COMPLICATIONS: - Dyspnea, hemoptysis. - Orthopnea and
paroxysmal nocturnal dyspnea. Pulmonary edema develops when there is a
sudden surge in flow across a markedly narrowed mitral orifice.
• Summary of Causes of Hemoptysis in mitral stenosis:
• - Congestion
• Bronchitis
• Pulmonary edema
• Pulmonary embolism and infarction
• Pulmonary apoplexy

8. Recommendations for Intervention for Rheumatic MS
I 1. In symptomatic patients (NYHA class II, III, or IV) with severe rheumatic MS
(mitral valve area ≤1.5 cm2 , Stage D) and favorable valve morphology with less
than moderate (2+) MR* in the absence of LA thrombus, PMBC is recommended if
it can be performed at a Comprehensive Valve Center.
I In severely symptomatic patients (NYHA class III or IV) with severe rheumatic MS
(mitral valve area ≤1.5 cm2 , Stage D) who 1) are not candidates for PMBC, 2) have
failed a previous PMBC, 3) require other cardiac procedures, or 4) do not have
access to PMBC, mitral valve surgery (repair, commissurotomy, or valve
replacement) is indicated.
IIa 3. In asymptomatic patients with severe rheumatic MS (mitral valve area ≤1.5 cm2 ,
Stage C) and favorable valve morphology with less than 2+ MR in the absence of LA
thrombus who have elevated pulmonary pressures (pulmonary artery systolic
pressure >50 mmHg), PMBC is reasonable if it can be performed at a
Comprehensive Valve Center.

9. Thrombi and emboli: Thrombi may form in the left atrium, particularly in the enlarged atrial
appendage of patients with MS. If they embolize, they do so most commonly to the brain, kidneys,
spleen, and extremities. Embolization occurs much more frequently in patients with atrial fibrillation.
Rarely, a large pedunculated thrombus or a free-floating clot may suddenly obstruct the stenotic mitral
orifice. Such “ball valve” thrombi produce syncope, angina, and changing auscultatory signs with
alterations in position, findings that resemble those produced by a left atrial myxoma.
PHYSICAL FINDINGS: Inspection: In advanced cases there is a malar flush. When fibrillation is
present, the jugular pulse reveals only a single expansion during systole (c-v wave) (systolic venous
pulse). Palpation: Left parasternal lift along the left sternal border signifies an enlarged right
ventricle. In patients with pulmonary hypertension, the impact of pulmonary valve closure can
usually be felt in the second and third left intercostal spaces just left of the sternum (Diastolic shock).
A diastolic thrill is frequently present at the cardiac apex, particularly if the patient is turned into the
left lateral position.

10. Auscultation: The first heart sound (S1) is generally accentuated and snapping. In
patients with pulmonary hypertension, the pulmonary component of the second heart
sound (P2) is often accentuated, and the two components of the second heart sound
are closely split. The opening snap (OS) of the mitral valve is most readily audible in
expiration at, or just medial to, the cardiac apex but also may be easily heard along
the left sternal edge. This sound generally follows the sound of aortic valve closure
(A2) by 0.05 to 0.12; that is, it follows P2; the time interval between A2 closure and
OS varies inversely with the severity of the MS. It tends to be short (0.05 to 0.07 s)
in patients with severe obstruction, and long, (0.10 to 0.12 s) in patients with mild
MS. The intensities of the OS and S1 correlate with mobility of the anterior mitral
leaflet.

11. • The OS usually precedes a low-pitched, rumbling, diastolic murmur, heard best
at the apex with the patient in the left lateral recumbent position. In general, the
duration of the murmur correlates with the severity of the stenosis. In patients
with sinus rhythm, murmur often reappears or becomes accentuated during
atrial systole, as atrial contraction elevates the rate of blood flow across the
narrowed orifice (presystolic accentuation).
• Associated lesion: With severe pulmonary hypertension, a pansystolic murmur
produced by functional tricuspid regurgitation may be audible along the left sternal
border. Characteristically, this murmur is accentuated by inspiration, and should
not be confused with the apical pansystolic murmur of mitral regurgitation.

12. In the presence of severe pulmonary hypertension and right ventricular failure, a
third heart sound may originate from the right ventricle. The enlarged right
ventricle may rotate the heart in a clockwise direction and form the cardiac apex,
giving the examiner the erroneous impression of left ventricular enlargement.
Under these circumstances, the rumbling diastolic murmur and the other
auscultatory features of MS become less prominent or may even disappear and
be replaced by the systolic murmur of functional tricuspid regurgitation which is
mistaken for mitral regurgitation. When cardiac output is markedly reduced in a
patient with MS, the typical auscultatory findings, including the diastolic
rumbling murmur, may not be detectable (silent MS).

14. • ECG findings: The P wave is wide and may be notched which suggests left atrial
enlargement. It becomes tall and peaked in lead II and upright in lead V1 when severe
pulmonary hypertension.
• Echocardiogram: Two-dimensional echo-Doppler echocardiography for estimation
of the transvalvular gradient and of mitral orifice size, the presence and severity of
accompanying mitral regurgitation, the extent of restriction of valve leaflets, their
thickness, and the subvalvular changes. Transthoracic and transesophageal echo are
needed to verify presence of atrial thrombi.
• X-Ray chest: Straightening of the left border of the cardiac silhouette, prominence of
the main pulmonary arteries, dilatation of the upper lobe pulmonary veins, and backward
displacement of the esophagus by an enlarged left atrium.

15. Summary of symptoms and signs of mitral stenosis:
- Middiastolic rumbling murmur with presystolic accentuation
- Snappy first sound
- Opening snap
- Diastolic thrill
DIFFERENTIAL DIAGNOSIS: The apical middiastolic murmur associated with aortic
regurgitation (Austin Flint murmur) may be mistaken for MS. However, in a patient
with aortic regurgitation, the absence of an opening snap or presystolic accentuation if
sinus rhythm is present points to the absence of MS.
Tricuspid stenosis, a valvular lesion that occurs very rarely in the absence of MS, may
mask many of the clinical features of MS.

16. MANAGEMENT: Penicillin prophylaxis of beta-hemolytic streptococcal infections and
prophylaxis for infective endocarditis are important. In symptomatic patients, some
improvement usually occurs with restriction of sodium intake and maintenance doses of oral
diuretics. Digitalis glycosides usually do not benefit patients with pure stenosis and sinus
rhythm, but they are necessary for slowing the ventricular rate of patients with atrial
fibrillation and for reducing the manifestations of right-sided heart failure in the advanced
stages of the disease. Small doses of beta-blockers (e.g., atenolol 25 mg/d) may be added
when cardiac glycosides fail to control ventricular rate in patients with atrial fibrillation.
Particular attention should be directed toward detecting and treating any accompanying
anemia and infections. Hemoptysis is treated by measures designed to diminish pulmonary
venous pressure, including bed rest, the sitting position, salt restriction, and diuresis.
Anticoagulants should be administered continuously in those with atrial fibrillation.

18. If atrial fibrillation is of relatively recent origin in a patient who’s MS is not severe enough to
warrant surgical treatment, reversion to sinus rhythm pharmacologically or by means of
electrical countershock is indicated. Usually this should be undertaken following 3 weeks of
anticoagulant treatment. Conversion to sinus rhythm is rarely helpful in patients with severe
MS, particularly those in whom the left atrium is especially enlarged or in whom atrial
fibrillation is chronic. Mitral valvotomy by balloon or surgical mitral valvotomy, is indicated in
the symptomatic patient with pure MS whose effective orifice is less than approximately 1.3
cm2 (or 0.8 cm2 / m2 of body surface area). Mitral valve replacement by prosthetic valve is
resorted to only if the valve is heavily calcified and associated with incompetence.
Percutaneous balloon valvuloplasty is an alternative to surgical mitral valvuloplasty in patients
with pure or predominant rheumatic stenosis (it is now the first choice). Young patients without
extensive valvular calcification or thickening or subvalvular deformity are candidates for this.

22. MITRAL REGURGITATION
• ETIOLOGY: Chronic rheumatic heart disease is the cause of severe mitral regurgitation
(MR). -MR also may occur as a congenital anomaly. - MR may occur in patients with
infarction involving the base of a papillary muscle. - MR may occur with marked left
ventricular dilatation. Massive calcification of the mitral annulus of unknown cause, presumably
degenerative, which occurs most commonly inelderly women. Systemic lupus erythematosus,
rheumatoid arthritis, are less common cause. -Mitral prolapse.
Acute MR occur 1- secondary to infective endocarditis involving the cusps or chordae
tendineae, 2- in acute myocardial infarction with rupture of a papillary muscle or one of its
heads, 3- as a consequence of trauma, 4- or following apparently spontaneous chordal
rupture.

25. MITRAL REGURGITATION: SYMPTOMS: Fatigue, exertional dyspnea, and
orthopnea are the most prominent complaints in patients with chronic,
severe MR. Hemoptysis and systemic embolism also occur less frequently in
MR than in MS. Right-sided heart failure, with painful hepatic congestion,
ankle edema, distended neck veins, ascites, and tricuspid regurgitation, may
be observed in patients with MR who have associated pulmonary vascular
disease and marked pulmonary hypertension. In patients with acute, severe
MR, left ventricular failure with acute pulmonary edema and /or
cardiovascular collapse is common.

26. PHYSICAL FINDINGS: Palpation: A systolic thrill is often palpable at the cardiac apex, the
left ventricle is hyperdynamic, and the apex beat is often displaced laterally. Auscultation: The
first heart sound is generally absent, soft (muffled), or buried in the systolic murmur. A low-
pitched third heart sound (S3) occurring 0.12 to 0.17 sec after aortic valve closure, i.e. at the
completion of the rapid-filling phase of the left ventricle, is an important auscultatory feature
of severe MR. A fourth heart sound is often audible in patients with acute, severe MR of recent
onset who are in sinus rhythm. A systolic murmur of at least grade III/VI intensity is the
characteristic auscultatory finding in severe MR. It is usually holosystolic (pansystolic). In
MR due to papillary muscle dysfunction or mitral valve prolapse, the systolic murmur
commences in midsystole. In patients with ruptured chordae tendineae the systolic murmur
may have a cooing or “sea gull” quality; in patients with a flail leaflet the murmur may have a
musical quality.

27. Summary: Signs of mitral incompetence:
Harsh pansystolic murmur over apex, propagated to axilla.
Muffled first heart sound.
Systolic thrill over apex.

28. Electrocardiogram: In patients with sinus rhythm there is evidence of left atrial enlargement (P
mitrale), but right atrial enlargement also may be present when pulmonary hypertension is
severe. Chronic, severe MR with left atrial enlargement is generally associated with atrial
fibrillation. Echocardiogram and color Doppler flow imaging are the most accurate
noninvasive techniques for the detection and estimation of MR. The left atrium is usually
enlarged. Findings which help to determine the etiology of MR can often be identified; these
include vegetations associated with infective endocarditis, incomplete coaptation of the
anterior and posterior mitral leaflets, and annular calcification, as well as left ventricular
dilation, aneurysm, or dyskinesia. X ray: The left atrium and left ventricle are the dominant
chambers; in chronic cases, the former may be massively enlarged and forms the right border
of the cardiac silhouette. Pulmonary venous congestion, interstitial edema, and Kerley B lines
are sometimes noted.

29. TREATMENT: Medical: The non-surgical management of MR is directed toward restricting
those physical activities that regularly produce dyspnea and excessive fatigue, reducing
sodium intake, and enhancing sodium excretion with the appropriate use of diuretics.
Vasodilators and digitalis glycosides increase the forward output of the failing left ventricle.
Angiotensin-converting enzyme inhibitors are given in chronic MR. The same considerations
as in patients with MS apply to the reversion of atrial fibrillation to sinus rhythm. Surgical
treatment should be offered to patients with severe MR whose limitations do not allow them to
perform normal household activities despite optimal medical management. Surgery is
indicated when the end systolic diameter of the left ventricle by echo exceeds 50 mm.

30. Recommendations for Diagnosis of Secondary MR
I 1. In patients with chronic secondary MR (Stages B to D), TTE is useful to
establish the etiology and to assess the extent of regional and global LV
remodeling and systolic dysfunction, severity of MR, and magnitude of
pulmonary hypertension.
I . In patients with chronic secondary MR (Stages B to D), noninvasive imaging
(stress nuclear/ PET, CMR, or stress echocardiography), coronary CT angiography,
or coronary arteriography is useful to establish etiology of MR and to assess
myocardial viability.
I . In patients with chronic secondary MR with severe symptoms (Stage D) that
are unresponsive to GDMT who are being considered for transcatheter mitral
valve interventions, TEE is indicated to determine suitability for the procedure.
I In patients with chronic secondary MR undergoing transcatheter mitral valve
intervention, intraprocedural guidance with TEE is recommended.

31. Cla
ss
Recommendations for Intervention for Chronic Primary MR
I 1. In symptomatic patients with severe primary MR (Stage D), mitral valve
intervention is recommended irrespective of LV systolic function.1,2
I 2. In asymptomatic patients with severe primary MR and LV systolic dysfunction
(LVEF ≤60%, LVESD ≥40 mm) (Stage C2), mitral valve surgery is recommended.
I 3. In patients with severe primary MR for whom surgery is indicated, mitral valve
repair is recommended in preference to mitral valve replacement when the
anatomic cause of MR is degenerative disease, if a successful and durable repair
is possible.
IIa 4. In asymptomatic patients with severe primary MR and normal LV systolic
function (LVEF ≥60% and LVESD ≤40 mm) (Stage C1), mitral valve repair is
reasonable when the likelihood of a successful and durable repair without
residual MR is >95% with an expected mortality rate of <1%, when it can
be performed at a Primary or Comprehensive Valve Center.

32. Recommendations for Intervention for Secondary MR
IIa 1. In patients with chronic severe secondary MR related to LV systolic
dysfunction (LVEF <50%) who have persistent symptoms (NYHA class
II, III, or IV) while on optimal GDMT for HF (Stage D), TEER is reasonable in
patients with appropriate anatomy as defined on TEE and with LVEF between
20% and 50%, LVESD ≤70 mm, and pulmonary artery systolic pressure
≤70 mm Hg.
IIa . In patients with severe secondary MR (Stages C and D), mitral valve surgery is
reasonable when CABG is undertaken for the treatment of myocardial ischemia.
IIb . In patients with chronic severe secondary MR from atrial annular dilation with
preserved LV systolic function (LVEF ≥50%) who have severe persistent
symptoms (NYHA class III or IV) despite therapy for HF and therapy for
associated AF or other comorbidities (Stage D), mitral valve surgery may be
considered.16–20
TEER, transcatheter edge-to-edge repair

33. MITRAL VALVE PROLAPSE
• Mitral valve prolapse (MVP), also termed the systolic click-murmur syndrome, is a
common, but highly variable, clinical syndrome. It is a frequent finding in patients
who have the typical features of the Marfan syndrome. The posterior leaflet is usually
more affected than the anterior, and the mitral valve annulus is often greatly dilated.
MVP may be associated with thoracic skeletal deformities.
• MVP is common in females between the ages of 6 and 30 years. Most patients are
asymptomatic and remain so for their entire lives. Arrhythmia, most commonly
ventricular premature contractions and paroxysmal supraventricular and ventricular
tachycardia, have been reported and may cause palpitations, light-headedness, and
syncope. Many patients have chest pain which is difficult to evaluate.

34. PHYSICAL EXAMINATION: Auscultation: the most important finding is the mid-or
late (nonejection) systolic click, which occurs 0.14 s or more after the first heart sound.
Systolic clicks may be followed by a high-pitched late systolic murmur, heard best at
the apex. A useful echocardiographic definition of MVP is systolic displacement (in the
parasternal view) of the mitral valve leaflets into the left atrium > 3 mm. Thickening of
the mitral valve leaflets is present. Doppler studies are helpful in revealing and
evaluating accompanying MR.
Treatment: The management of patients with MVP consists of reassurance of the
asymptomatic patient without severe MR or arrhythmias; prevention of infective
endocarditis with antibiotic prophylaxis in patients with a systolic murmur and the
relief of the atypical chest pain by beta blockers.

35. Jan 2015

36. AORTIC STENOSIS
• Aortic stenosis (AS) occurs in one-fourth of all patients with chronic valvular heart disease; approximately 80
percent of adult patients with symptomatic valvular AS are male.
• Etiology: 1. AS may be congenital in origin, 2. secondary to rheumatic inflammation of the valve, 3. degenerative
calcification of the aortic cusps of unknown cause.
• PATHOPHYSIOLOGY: A peak systolic pressure gradient exceeding 50 mmHg or an effective aortic orifice less
than approximately 0.5 cm2/m2 of body surface area i.e., less than approximately one-third of the normal orifice,
is considered critical obstruction to left ventricular outflow.
• SYMPTOMS: AS is rarely of hemodynamic or clinical importance until the valve orifice has narrowed to
approximately one-third of normal, i.e., to 1 cm2 in adults.
• Exertional dyspnea, angina pectoris, and syncope are the three cardinal symptoms. Angina pectoris reflects an
imbalance between the augmented myocardial oxygen requirement by the hypertrophied myocardium and the un-
accompanying increase in coronary blood flow. Orthopnea, paroxysmal nocturnal dyspnea, and pulmonary
edema, i.e., symptoms of left ventricular failure, also occur only in the advanced stages of the disease.

37. • PHYSICAL FINDINGS: A palpable double systolic arterial pulse the so-called bisferiens pulse,
excludes pure or predominant AS and signifies dominant or pure aortic regurgitation or obstructive
hypertrophic cardiomyopathy. Palpation: The apex beat is usually sustained and displaced laterally,
reflecting the presence of left ventricular hypertrophy. A systolic thrill is generally present at the base of
the heart in the suprasternal notch, and along the carotid arteries.
• Auscultation: Harsh ejection systolic murmur over aortic area propagated to carotids. The sound of
aortic valve closure, the second sound is very weak or even absent with tight aortic stenosis.
Frequently, a fourth heart sound is audible at the apex in many patients with severe AS and reflects the
presence of left ventricular hypertrophy and an elevated left ventricular enddiastolic pressure; a third
heart sound generally occurs when the left ventricle dilates and fails. The murmur of AS is
characteristically an ejection systolic murmur loudest at the base of the heart, most commonly in the
second right intercostal space. It is transmitted along the carotid arteries. Occasionally, it is transmitted
downward and to the apex and may be confused with the systolic murmur of MR.

38. • Summary : Signs of Aortic Stenosis: -Harsh Ejection systolic Murmur over aortic area
propagated to carotids. Weak or absent second heart sound (Aortic component). Systolic
thrill over aortic area, suprasternal notch and carotids. Strong sustained apex.
• Electrocardiogram: This reveals left ventricular hypertrophy in the majority of patients
with severs AS. Echocardiogram: The key findings are left ventricular hypertrophy. The
transaortic valvular gradient can be estimated by Doppler echocardiography.
Causes of death: sudden death, results from an arrhythmia (ventricular tachycardia or
fibrillation) occurred in 10 to 20 percent. Congestive heart failure in one-half to two-
thirds of patients.

39. Electrocardiogram (ECG), left ventricular, and aortic
pressure curves in a patient with aortic stenosis.
There is a pressure gradient across the aortic valve
during systole

40. Fig. Abnormal sounds and murmurs associated with valvular dysfunction displayed
simultaneously with left atrial (LA), left ventricular (LV), and aortic pressure tracings. AVO,
aortic valve opening; E, ejection click; MVO, mitral valve opening; OS, opening snap of the
mitral valve.

41. Recommendations for Diagnostic Testing: Initial Diagnosis of AS
I 1. In patients with signs or symptoms of AS or a BAV, TTE is indicated for accurate
diagnosis of the cause of AS, assessment of hemodynamic severity, measurement
of LV size and systolic function, and determination of prognosis and timing of
valve intervention.
I 2. In patients with suspected low-flow, low- gradient severe AS with normal LVEF
(Stage D3), optimization of blood pressure control is recommended before
measurement of AS severity by TTE, TEE, cardiac catheterization, or CMR.
IIa 3. In patients with suspected low-flow, low- gradient severe AS with reduced
LVEF (Stage D2), low-dose dobutamine stress testing with echocardiographic or
invasive hemodynamic measurements is reasonable to further define severity
and assess contractile reserve.
IIa 4. In patients with suspected low-flow, low- gradient severe AS with normal or
reduced LVEF (Stages D2 and D3), calculation of the ratio of the outflow tract to
aortic velocity is reasonable to further define severity

42. Stage Definition Valve Anatomy Valve Hemodynamics Hemodynamic
Consequences
C: Asymptomatic severe AS
C1 Asymptomatic
severe AS
Severe leaflet
calcification/
fibrosis or
congenital
stenosis with
severely reduced
leaflet opening
Aortic Vmax ≥4 m/s or mean
∆P ≥40 mm Hg AVA typically
is ≤1.0 cm2 (or AVAi 0.6 cm2
/m2 ) but not required to
define severe AS Very severe
AS is an aortic Vmax ≥5 m/s
or mean P ≥60 mm Hg
LV diastolic
dysfunction
Mild LV
hypertrophy
Normal LVEF
C2 Asymptomatic
severe AS with
LV systolic
dysfunction
Severe leaflet
calcification/
fibrosis or
congenital
stenosis with
severely reduced
leaflet opening
Aortic Vmax ≥4 m/s or mean
∆P ≥40 mm Hg AVA typically
≤1.0 cm2 (or AVAi 0.6 cm2
/m2 ) but not required to
define severe AS
LVEF <50%
AVAi=Aortic Valve Area index

43. Recommendations for Timing of Intervention of AS

44. Recommendations for Timing of Intervention of AS

46. AORTIC REGURGITATION
• ETIOLOGY: Approximately three-fourths of patients with pure or predominant aortic
regurgitation (AR) are males; females predominate among patients with AR who have
associated mitral valve disease. Causes:
1. In approximately two-thirds of patients with AR the disease is rheumatic in origin, resulting in thickening,
deformation and shortening of the individual aortic valve cusps, changes which prevent their proper opening
duringsystoleandclosureduring diastole.
2. Acute AR also may result from infective endocarditis, which may attack a valve previously affected by
rheumatic disease, a congenitally deformed valve, or rarely a normal aortic valve, and perforate or erode one
ormoreofthe leaflets.
3. Patients with discrete membranous subaortic stenosis often develop thickening of the aortic valve leaflets,
whichinturnleadstomildormoderatedegreesofAR.

47. AORTIC REGURGITATION
Causescont. AR alsomay occur in patientswithcongenitalbicuspidaortic valves.
Aortic dilatation, i.e., aortic root disease, widening of the aortic annulus and separation of the
aorticleafletsareresponsiblefor theAR.
Syphilis and ankylosing rheumatoid spondylitis may lead to aortic dilatation, aneurysm
formation,and severe regurgitation.
Cystic medial necrosis of the ascending aorta, associated with other manifestations of the
Marfan syndrome, idiopathic dilatation of the aorta, and severe hypertension all may widen
theaorticannulusand leadto progressiveAR.
Occasionally,AR is causedby retrogradedissectionof theaortainvolvingtheaortic annulus.

48. • History: Patients with severe AR may remain asymptomatic for 10 to 15 years.
• Sinus tachycardia during exertion may produce particularly uncomfortable
palpitations. Exertional dyspnea is the first symptom of diminished cardiac reserve.
This is followed by orthopnea, paroxysmal nocturnal dyspnea, and excessive
diaphoresis. Chest pain occurs frequently, even in younger patients, due to
diminished coronary filling during diastole.
• Nocturnal angina may be a troublesome symptom. The anginal episodes can be
prolonged and often do not respond satisfactorily to sublingual nitroglycerin. Late
in the course of the disease, evidence of systemic fluid accumulation, including
congestive hepatomegaly, ankle edema, and ascites, may develop.

49. • PHYSICAL FINDINGS: Peripheral signs: Arterial pulse: A rapidly rising “water-hammer”
pulse, which collapses suddenly as arterial pressure falls rapidly during late systole and
diastole, and capillary pulsations, an alternate flushing and paling of the root of the nail while
pressure is applied to the tip of nail, are characteristic of free AR. A booming, “pistol-shot”
sound can be heard over the femoral or brachial arteries, and a to - fro murmur is audible if the
femoral artery is lightly compressed with a stethoscope.
• The arterial pulse pressure is widened, with an elevation of the systolic pressure and a
depression of the diastolic pressure. The severity of AR does not always correlate directly with
the arterial pulse pressure, and severe regurgitation may exist in patients with arterial pressures
in the range of 140/60.
• Palpation: The apex beat is strong and displaced laterally and inferiorly. The systolic expansion
and diastolic retraction of the apex are prominent and contrast sharply with the sustained

50. • Auscultation: A third heart sound is common, and occasionally, a fourth heart sound
also may be heard. The murmur of AR is typically a high-pitched, blowing, decrescendo
early diastolic murmur which is usually heard best in the third left intercostal space.
Unless it is trivial in magnitude, the AR is usually accompanied by peripheral signs
such as a widened pulse pressure or a collapsing pulse. A midsystolic ejection murmur
is frequently audible in AR. It is generally heard best at the base of the heart and is
transmitted to the carotid vessels. This murmur may be quite loud without signifying
organic obstruction; it is often shorter, than the ejection systolic murmur heard in
patients with predominant AS. Differential diagnosis: from the Graham steel murmur of
pulmonary regurgitation in severe pulmonary hypertension: (a loud and palpable
pulmonary component of the second heart sound).

51. • A third murmur which is frequently heard in patients with AR is the Austin Flint
murmur, a soft, low-pitched, rumbling middiastolic or presystolic bruit. It is probably
produced by the displacement of the anterior leaflet of the mitral valve by the aortic
regurgitant stream. Both the Austin Flint murmur and the rumbling diastolic murmur of
MS are loudest at the apex, but the murmur of MS is usually accompanied by a loud first
heart sound and immediately follows the opening snap of the mitral valve, while the
Austin Flint murmur is often shorter in duration than the murmur of MS, and in patients
with sinus rhythm the latter exhibits presystolic accentuation.
• Summary signs of Aortic incompetence over the heart:
• Soft blowing early diastolic murmur over aortic area propagated to apex
• Austin Flint murmur (diastolic murmur over mitral area)
• Echocardiogram: Essential for detection of severity and cause of AR.

52. • TREATMENT: Although operation constitutes the principal treatment of aortic regurgitation,
and should be carried out before the development of heart failure, the latter usually respond
initially to treatment with digitalis, salt restriction, diuretics, and vasodilators, especially
angiotensin-converting enzyme inhibitors.
• In patients with severe AR, careful clinical follow-up and noninvasive testing with
echocardiography at approximately 6-month intervals are necessary. Operation is to be
undertaken at the optimal time, i.e., after the onset of left ventricular dysfunction but prior to
the development of severe symptoms. Valve replacement is indicated if the LV dilates to 50
mm in systole and 65 to 70 mm in diastole.
• ACUTE AORTIC REGURGITATION: Infective endocarditis, aortic dissection, and trauma
are the most common causes of severe, acute AR.

53. TRICUSPID STENOSIS
• It is generally rheumatic in origin and is more common in women than in men. It does not
usually occur as an isolated lesion or in patients with pure MR but is usually observed in
association with MS. Hemodynamically significant TS occurs in 5 to 10 percent of patients
with severe MS; rheumatic TS is commonly associated with some degree of regurgitation.
• SYMPTOMS: Since the development of MS generally precedes that of TS, many patients
initially have symptoms of pulmonary congestion. Amelioration of the latter should raise the
possibility that TS may be developing. Fatigue secondary to a low cardiac output and
discomfort due to refractory edema, ascites, and marked hepatomegaly are common in patients
with TS and / or regurgitation. Severe TS is associated with marked hepatic congestion, often
resulting in cirrhosis, jaundice, serious malnutrition, anasarca, and ascites. The jugular veins
are distended, and in patients with sinus rhythm there may be giant “a” waves.

54. • On auscultation, the pulmonic closure sound is not accentuated, and occasionally, an OS
of the tricuspid valve may be heard approximately 0.06 s after pulmonic valve closure.
The diastolic murmur of TS has many of the features of the diastolic murmur of MS.
The murmur is augmented during inspiration, and it is reduced during expiration.
Surgical treatment of the tricuspid valve is not indicated at the time of mitral valve
surgery in patients with mild TS. On the other hand, definitive surgical relief of the TS
should be carried out, at the time of mitral valvotomy, in patients with moderate or
severe TS who have mean diastolic pressure gradients exceeding 4 to 5 mmHg and
tricuspid orifices less than 1.5 to 2.0 cm2. TS is almost always accompanied by
significant tricuspid regurgitation.

55. Most commonly, tricuspid regurgitation (TR) is functional and secondary to
marked dilatation of the right ventricle and the tricuspid annulus. Functional TR
may complicate right ventricular enlargement of any cause, including inferior
wall infarcts that involve the right ventricle, and is commonly seen in the late
stages of heart failure due to rheumatic or congenital heart disease with severe
pulmonary hypertension, as well as in ischemic heart disease, cardiomyopathy,
and cor pulmonale. It is in part reversible if pulmonary hypertension is relieved.
Rheumatic fever may produce organic TR, often associated with TS.
Endomyocardial fibrosis, infective endocarditis may produce TR.
Tricuspid Regurgitation

56. • The clinical features of TR result primarily from systemic venous congestion and
reduction of cardiac output. The neck veins are distended with prominent V
waves, and marked hepatomegaly, ascites, pleural effusions, edema, systolic
pulsations of the liver and positive hepato-jugular reflux are common. A
prominent right ventricular pulsation along the let parasternal region and a
blowing holosystolic murmur along the lower left sternal margin which may be
intensified during inspiration and reduced during expiration or the Valsalva
maneuver are characteristic findings; AF is usually present.

57. Echocardiography and Doppler: for detection of severity of TR, estimation of
pulmonary pressure and search for vegetations of infective endocarditis.
Treatment of the underlying cause of heart failure usually reduces the severity of
functional TR. In patients with mitral valve disease and TR due to pulmonary
hypertension and massive RV enlargement, effective surgical correction of the
mitral valve abnormality results in lowering of the pulmonary vascular pressure
and gradual reduction or disappearance of the TR.
Tricuspid valvuloplasty by De Vega procedure and Carpentier ring can be done.

58. Pulmonary Stenosis: See congenital pulmonary stenosis
Pulmonary Regurgitation
Dilatation of the pulmonary artery in cases of pulmonary hypertension may
produce pulmonary regurgitation. This is called Graham Steel murmur. It is
differentiated from the early diastolic murmur of aortic regurgitation by the
associated signs of pulmonary hypertension, and by Doppler study.

59. Valvular Heart Disease for 5th year Medical Students
Samir Morcos Rafla, FACC, FESC, FHRS
Emeritus professor of cardiology
Alexandria University
smrafla@yahoo.com
01001495577
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Dr. Samir Rafla Lectures