AJITH KUMAR P

MPT CARDIOPULMONARY SCIENCES

▪ The heart valves allow forward movement of blood through the
cardiac chambers when they are open and prevent backward flow
when they are closed.
▪ That is, presence of heart valves is to facilitate unidirectional
blood flow.
▪ Diseased valve may become narrowed, obstructing forward flow,
or become leaky, causing backward flow or regurgitation.
▪ Breathlessness is a common symptom of valve disease, and acute
severe breathlessness may be a presenting symptom of valve
failure.
▪ Predisposition to valvular disease may be genetically determined, can arise as the
result of rheumatic fever or infections, or can occur in association with dilatation of
the cardiac chambers in heart failure.
▪ Acute rheumatic fever results from the body’s autoimmune response to a throat
infection caused by Streptococcus pyogenes, also known as the group A
Streptococcus bacteria.
▪ Pathogenesis:
▪ The condition is triggered by an immune-mediated delayed response to infection
with specific strains of group A streptococci, which have antigens that cross-react
with cardiac myosin and sarcolemmal membrane proteins.
▪ Antibodies produced against the streptococcal antigens cause inflammation in the
endocardium, myocardium and pericardium, as well as the joints and skin.
▪ Symptoms:
1. Fever
2. Anorexia
3. lethargy and
4. joint pain, 2–3 weeks after an episode
of streptococcal pharyngitis.
▪ There may be no history of sore throat,
however., Arthritis occurs in
approximately 75% of patients.
▪ Other features include rashes,
subcutaneous nodules, carditis and
neurological changes.
▪ The diagnosis, made using the revised
Jones criteria which is based on two or
more major manifestations, or one major
and two or more minor manifestations,
along with evidence of preceding
streptococcal infection

Reference : harrison’s cardiovascular

medicine 17th edition
▪ Chronic valvular heart disease develops in at least half of those affected by
rheumatic fever with carditis. Two-thirds of cases occur in women.

▪ The mitral valve is affected in more than 90% of cases; the aortic valve is the next
most frequently involved, followed by the tricuspid and then the pulmonary valve.
Isolated mitral stenosis accounts for about 25% of all cases, and an additional 40%
have mixed mitral stenosis and regurgitation

▪ The main pathological process in chronic rheumatic heart disease is progressive

fibrosis . Fusion of the mitral valve commissures and shortening of the chordae
tendineae may lead to mitral stenosis with or without regurgitation. Similar
changes in the aortic and tricuspid valves produce distortion and rigidity of the
cusps, leading to stenosis and regurgitation.
▪ This is caused by microbial infection of a heart valve, the lining of a cardiac chamber or
blood vessel, or by a congenital anomaly. Both native and prosthetic valves can be
affected. The most common causes of infective endocarditis are streptococci and
staphylococci but other organisms may also be involved.

▪ Infective endocarditis typically occurs at sites of pre-existing endocardial damage, but

infection with particularly virulent or aggressive organisms such as Staphylococcus
aureus can cause endocarditis in a previously normal heart.

▪ Infection tends to occur at sites of endothelial damage because they attract deposits of
platelets and fibrin that are vulnerable to colonization by blood-borne organisms. The
avascular valve tissue and presence of fibrin and platelet aggregates help to protect
proliferating organisms from host defense mechanisms.
▪ If the affected valve is damaged by tissue distortion, cusp perforation or disruption of
chordae, Valve regurgitation may develop or increase.

REF: Davidson’s principles and practice of

medicine 23rd edition
▪ Stenosis – As a result of thickening,
the valves become narrowed.
▪ Regurgitations – as a result of the
ineffective closing of valves the
leakage of blood flow occurs, or
backward flow of blood occurs.
CONDITION CAUSE CONDITION CAUSE
Mitral stenosis Rheumatic fever Mitral regurgitation Endocarditis
Congenital Acute Papillary muscle rupture (post-MI)
Severe mitral annular calcification Trauma
SLE, Chordal rupture/Leaflet flail (MVP,
RA IE)

Chronic MR Myxomatous (MVP)

Rheumatic fever
Endocarditis (healed)
Mitral annular calcification
Congenital (cleft, AV canal)
HOCM with SAM
• MVP- mitral valve prolapse Ischemic (LV remodeling)
• HOCM- hypertrophic obstructive
cardiomyopathy Dilated cardiomyopathy
• SAM- systolic anterior motion of the anterior
mitral valve leaflet
• IE- infective endocarditis
CONDITION CAUSE
Aortic stenosis Congenital (bicuspid,
unicuspid)
Degenerative
calcific Rheumatic fever

Aortic regurgitation Valvular

Congenital (bicuspid)
Endocarditis Rheumatic
fever
Myxomatous (prolapse)
Traumatic
Syphilis
Ankylosing spondylitis
Root disease
Aortic dissection
Cystic medial degeneration
Marfan syndrome
Bicuspid aortic valve
Nonsyndromic familial
aneurysm Aortitis
Hypertension
CONDITION CAUSE
Tricuspid stenosis Rheumatic Congenital
Tricuspid regurgitation Rheumatic Endocarditis
Primary Myxomatous (TVP)
Carcinoid
Congenital (Ebstein’s)
Trauma
Papillary muscle injury (post-MI)

Tricuspid regurgitation RV and tricuspid annular dilatation

Secondary Multiple causes of RV enlargement
(e.g., longstanding pulmonary HTN)
Chronic RV apical pacing

TVP - tricuspid valve prolapse.

CONDITION CAUSE

Pulmonic stenosis Congenital Carcinoid

Pulmonic regurgitation Valve disease

Congenital Postvalvotomy Endocarditis
Annular enlargement
Pulmonary hypertension
Idiopathic dilatation
Marfan syndrome

Ref : Harrison’s cardiovascular

medicine
▪ Usually asymptomatic
▪ Fatigue
▪ Exertional dyspnoea
▪ Orthopnoea
▪ Palpitations
▪ Ankle refractory oedema
▪ Distended neck veins
▪ Ascites - hepatomegaly
▪ Angina pectoris
▪ Exertional syncope after exercise
▪ Peripheral cyanosis
▪ Cachexia
▪ Paroxysmal nocturnal dyspnoea
Valvular pathology resulted in
cardiomegaly and pleural effusion
AORTIC STENOSIS The typical finding on electrocardiography
(ECG) in patients with AS is LV hypertrophy,
often with secondary repolarization
abnormalities. This is found in 85% of patients
with severe AS.
AORTIC REGURGITATION Findings on ECG may be normal early in the
disease or show LV hypertrophy with or
without associated repolarization
abnormalities. Left axis deviation may also be
present. With early LV volume overload, there
are prominent Q waves in leads I, aVL, and V3
through V6. As the disease progresses, the
prominent initial forces decrease, but the total
QRS amplitude increases

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2861980/
▪ Surgical treatment of valvulopathies started closed mitral
commissurotomy by passing a finger or instrument through the
narrow orifice of the mitral stenosis to dilate or cut it as did Cutler
in 1923 for the first time.
▪ The Hufnagel cage and ball valve was the first artificial valve
introduced in 1952. It was placed in the descending thoracic
aorta to prohibit blood flow reversal in aortic regurgitation.
▪ In 1967 a similarly structured valve, the Edwards cage and ball
valve, had been implanted 1000 times for mitral valve disease.
▪ Surgical techniques improved from early, single valve procedures
to 4-valve replacement in 1992.
▪ Special techniques were introduced, for example, the Ross
procedure replacing the aortic valve with pulmonic valve
autograft.

ref:https://www.statpearls.com/ArticleLibrary/viewarticle/18904
▪ The results of replacement of any
valve are dependent primarily on
(1) The patient’s myocardial function
and general medical condition at
the time of operation.
(2) The technical abilities of the
operative team and the quality of
the postoperative care.
(3) The durability, hemodynamic
characteristics, and
thrombogenicity of the prosthesis.
▪ Increased perioperative mortality is associated with advanced age and
comorbidity (e.g., pulmonary or renal disease, the need for nonvalvular
cardiovascular surgery, diabetes mellitus) as well as with greater levels of
preoperative functional disability and pulmonary hypertension.
▪ Late complications of valve replacement include paravalvular leakage, thrombo-
emboli, bleeding due to anticoagulants, structural deterioration of the prosthesis,
and infective endocarditis.
 Bio Prosthesis Artificial Prothesis
1. The primary advantage of bio prostheses 1. All patients who have undergone
over mechanical prostheses is the virtual replacement of any valve with a mechanical
absence of thromboembolic complications 3 prosthesis are at risk of thromboembolic
months after implantation, and except for complications and must be maintained
patients with chronic AF, few such instances permanently on anticoagulants, a treatment
have been associated with their use. that imposes a hazard of hemorrhage.
2. The major disadvantage of bioprosthetic 2. They more durable.
valves is their structural deterioration. 3. Traditionally, a mechanical prosthesis was
3. Bioprostheses were recommended for older considered preferable for a patient younger
(>65 years) patients who did not otherwise than 65 years who could take anticoagulation
have an indication for anticoagulation (e.g.,, reliably.
AF).
Reference: https://www.heart-valve-surgery.com/
▪ For patients being considered for
aortic valve surgery, especially due
to aortic stenosis, transcatheter
aortic valve implantation (TAVI) is
an emerging alternative to surgical
aortic valve replacement.
▪ The native valve is not removed but
is compressed by the new
bioprosthetic valve, which is
implanted within it.
▪ The bioprosthetic valve is mounted
on a large stent-like structure and is
implanted through a catheter
inserted in the femoral artery.
TAVI has several major advantages.
▪ It avoids the need for a sternotomy,
▪ It is associated with a short recovery period,
▪ It can be used in high-risk and
▪ In inoperable patients, and
▪ It is much better tolerated by elderly patients.

▪ Complications includes,
1. Stroke (2%) and
2. Heart block necessitating pacemaker implantation (5–15%)
▪ REF: Davidson’s principles and practice of medicine 23rd edition
▪ Ref : Harrison’s cardiovascular medicine17TH EDITION
▪ ref:https://www.statpearls.com/ArticleLibrary/viewarticle/18904
▪ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2861980/
▪ Reference: https://www.heart-valve-surgery.com/