Well informative

1. Valvular Heart Disease
4th year Medical Students

2. Introduction
• Valvular heart disease (VHD) is any disease process involving one or more of
the four valves of the heart (the aortic and mitral valves on the left and the
pulmonary and tricuspid valves on the right).
• There are two types of heart valve disease:
• Valvular stenosis, that occurs when a heart valve doesn’t fully open due to
stiff or fused leaflets.
• Valvular insufficiency (regurgitation,incompetence, "leaky valve“), that
occurs when a valve does not close tightly

3. case
• A 67-year-old male complains of dyspnea on exertion, attacks of retrosternal
pain, dizziness. He has no history of rheumatism.
• Objectively: pale skin, acrocyanosis.There are rales in the lower parts of
lungs.There is systolic thrill in the II intercostal space on the right, coarse
systolic murmur conducted to the vessels of neck.AP- 130/90 mm Hg, heart
rate - 90/min, regular rhythm.The liver extends 5 cm under the edge of costal
arch, lower limb edema are present. Specify the assumed valvular defect?

4. Aortic stenosis
• an obstruction that impedes blood flow from the LV to the aorta and is mostly
secondary to aortic valvular disease.
• Aortic valvular stenosis is the most common valvular ds.
• It can be congenital, rheumatic, or calcific or degenerative.
• A bicuspid aortic valve leads to flow turbulence and valve trauma, which in
return precipitates fibrosis, stiffness, and calcification.
• Atherosclerosis.
• statin therapy?
• streptococcal infection

5. • The aortic valve surface area is normally 3.0 to 4.0 cm2.
• Symptoms typically do not appear unless the valve is narrowed to at least one
fourth of its normal surface area.
• Stenosis is graded as :
• mild (valve area >1.5 cm2)
• moderate (>1.0-1.5 cm2)
• severe (≤1 cm2) .
• The valve area narrows at an average rate of 0.12 cm2 per year .

6. • As the valve narrows, cardiac output remains stable at rest but diminishes with
exercise.
• As disease progresses, LV mass increases, and diastolic dysfunction becomes
evident with an increase in LV filling pressure.
• Patients withAS have a good prognosis if they do not have symptoms of angina,
CHF, or syncope during activity.
• Surgical management of the valve becomes necessary in symptomatic patients
because the incidence of sudden cardiac death increases in these patients.

7. • Patients with severe aortic valve stenosis describe progressive dyspnea; chest
pain and syncope with exertion; and symptoms of HF, including orthopnea,
paroxysmal nocturnal dyspnea, and edema.
• Syncope at rest is typically arrhythmia induced.
• Patients with severe aortic valve stenosis have an approximate 5% history of
sudden cardiac death.

8. physical signs of severe aortic valve stenosis
A. diminished carotid pulses (delayed and weak)
B. a sustained apical impulse
C. a single second heart sound
D. S4 gallop
E. a midsystolic crescendo–decrescendo murmur .
• Aortic valve stenosis can be distinguished clinically from dynamic left
ventricular outflow tract (LVOT) obstruction such as in hypertrophic
obstructive cardiomyopathy (HOCM) by certain clinical maneuvers at the
bedside.

9. Diagnostic tests
chest radiography:
• which could show a calcified valve, pulmonary venous congestion, or an increase
in ascending aortic root size secondary to poststenotic dilation.
• 12-lead ECG may show LVH and conduction abnormalities.
• An echocardiogram typically confirms the diagnosis (presence of calcification,
reduction in cusp motion, and congenital abnormalities )
• A gradient can be measured across the valve and the valve area can be determined
using Doppler flow with reasonable accuracy .
• The presence of concomitant aortic valve insufficiency can also be visualized using
color Doppler flow characteristics.

10. • echocardiography : - the presence or absence of LVH and assessment of LV
compliance, atrial size, and associated other valvular abnormalities.
• If noninvasive findings support the diagnosis of severeAS and the patient is
symptomatic, then diagnostic angiography is indicated to confirm the presence
of severe aortic valve stenosis and assess the coronary arteries.
• Stress testing is contraindicated in the setting of symptomatic, severe aortic
valve stenosis.

11. Treatment
• aortic valve stenosis depends on the presence or absence of symptoms.
• Symptomatic severe aortic valve stenosis carries a poor prognosis, with an average
life expectancy of 2 to 3 years .
• The 5- and 10-year mortality rates are approximately 52% to 80% and 80% to
90%, respectively
• Aortic valve surgery with or without coronary artery bypass grafting is the
treatment of choice

12. • Aortic valvuloplasty carries a poor outcome and is reserved as a palliative
therapy for inoperable patients.
• Typically, the improvement in the aortic valve gradient is mild with
valvuloplasty, and a recurrence of severe stenosis can be expected within 6
months
• Surgery is typically not advised for patients with asymptomatic severe valvular
stenosis

13. • Patients with dyspnea and progressive LV dysfunction need to be considered for
valve replacement.
• Most patients with asymptomatic, severe aortic valve stenosis will, however,
develop symptoms within 5 years of follow-up.
• A low threshold to intervene in patients with asymptomatic severeAS may be
considered, particularly when peak systolic velocity (PSV) is 4.5 m/sec or
greater on Doppler echocardiography if associated with moderate or severe
valvular calcification
• It is currently recommended that patients with severeAS undergo aortic valve
replacement if they have symptoms (chest pain, syncope, or HF), if EF is less
than 50%, or in conjunction with another valve surgery or bypass surgery (even
if the aortic valve is moderate in severity).

14. • European guidelines currently favor aortic valve replacement in patients with
severeAS with a valve area less than 0.6 cm2 (irrespective of symptoms),
rapidly progressing valve area severity, or an abnormal response to exercise
testing
• Patients need to be advised about antibiotic prophylaxis to prevent
endocarditis, especially with rheumatic valve disease.
• Patients with moderate to severe aortic valve stenosis need to avoid moderate
to severe physical exertion
• Arrhythmias need to be corrected promptly in patients with severeAS.
• Follow up

15. Prophylaxis of bacterial endocarditis

16. • Aortic valve replacement can be performed with a mechanical valve or a tissue
valve.
• Mechanical valves are more durable than bioprosthetic valves but require
lifetime anticoagulation.
• The choice of the valve depends on the patient clinical situation but takes into
consideration the patient’s age, need for future pregnancies, ability to take
anticoagulants, compliance, and preference.
• Antibiotic prophylaxis to prevent endocarditis is strongly recommended in
patients with prosthetic valves.

17. • Transcatheter aortic valve replacement (TAVR) using a stent valve has recently
emerged as a less invasive procedure to replace severe aortic valve stenosis in
patients who are deemed inoperable or are at high risk for conventional aortic
valve surgery.
• No difference in mortality was seen with both modalities, but there was more
bleeding and atrial fibrillation (AF) with surgery and more vascular
complications withTAVR.
• TAVR is approved at this time for both inoperable and high-risk patients for
open aortic valve replacement.

18. Aortic valve regurgitation
• (AR) is defined as blood flow from the aorta to the LV in diastole because of an
incompetent aortic valve .
• Aortic valve insufficiency is generally acquired because of valve infection,
dilation and dissection of the aortic root, trauma, or long-term degenerative
change of the valve, particularly in the setting of HTN.
• Patients with a history of prosthetic valves) can also have aortic valve
insufficiency.
• Aortic insufficiency can also be caused by a congenital bicuspid aortic valve.

19. • Aortic valve regurgitation leads to volume overload of the LV and an increase in
LV end-diastolic pressure.
• In chronicAR, symptoms might not appear before LV cavity dilation, and a
reduction in LV function develops.
• Patients will have a long diastolic murmur, a wide pulse pressure, and bounding
pulses.
• AcuteAR

20. • Patients are generally acutely symptomatic with HF.
• Patients have a short diastolic murmur and a soft S1 with tachycardia.
• Patients with severeAR will eventually become symptomatic, displaying
symptoms of dyspnea and CHF.
• Angina is less common, but it can occur as a result of reduction in coronary
perfusion pressure.

21. • Physical signs of severeAR include a rapid and quick arterial pulse (Corrigan
pulse); a wide pulse pressure; an early high-pitched, blowing diastolic murmur
heard best over the left sternal border; an S3 gallop.
• The ECG shows LVH and possibly conduction abnormalities.
• Echocardiographic:
• Stress testing can provide information about functional capacity and
hemodynamic response to exercise.
• Diagnostic angiography allows the verification of the severity of theAR and helps
in the assessment of the aortic root size, cavity size, and the presence or absence
of CAD.

22. • The surgical treatment ofAR is indicated in symptomatic patients with dyspnea,
angina, or CHF .
• Asymptomatic patients should undergo surgery if the LVEF is 50% or less, LV
end-systolic dimension approaches 5.5 cm, or there is an LV end-diastolic
dimension of more than 75 mm.
• Patients also should be advised on prophylaxis against infective endocarditis
• Patients with moderate to severeAR should avoid competitive sports, heavy
workloads, and weight lifting.
• After valve replacement forAR, the use of β-blockers may improve cardiac
performance

23. Mitral stenosis
• is defined as the reduced ability of blood to move from the left atrium to the LV
in diastole.
• It is mostly caused by dysfunction in the mitral valve, which lacks the ability to
open its leaflets in diastole.
• MS is predominantly caused by rheumatic carditis and is more prevalent in
females.
• Acute rheumatic carditis leads to valvular disease in approximately 50% of
affected patients.
• The mitral valve is the most commonly affected by rheumatic heart disease,
followed by the aortic valve, and then combined aortic and mitral valves.

24. • MS is considered severe if the valve area is less than 1 cm2 (normal mitral valve
area is 4 to 6 cm2).
• A valve area of 1.5 cm2 or smaller associated with severe dyspnea class or
severe pulmonary HTN is also considered clinically significant and warrants
therapy.
• The main symptom of MS is slowly progressive dyspnea and fatigue.
• Patients might complain of orthopnea and paroxysmal nocturnal dyspnea.
Pulmonary HTN can become severe, and right-sided ventricular failure can
then lead to dependent edema, hepatomegaly, and right upper quadrant pain.

25. • An increase in left atrial size can lead to palpitations secondary toAF as well as
subsequent cardioembolic strokes if not recognized in a timely fashion.
• auscultatory of MS(left lateral decubitus position).
• A low-pitched diastolic rumble, heard with the bell of the stethoscope over the
apex, is also present.
• The high-pitched opening snap (OS), caused by the abrupt stopping of the
domed mitral valve into the LV, is also appreciated in most patients midway
between the left sternal border and apex.
• A shorterA2–OS distance indicates a more severe MS.
• Signs of pulmonary HTN such as a loud P2 and right ventricular hypertrophy
(RVH) can also be present as MS becomes more severe.

26. • The ECG findings in MS might show a biphasic P wave inV1, a large P wave in
lead II, and possiblyAF.
• Chest radiography could show evidence of an enlarged left atrium and an
increase in pulmonary congestion with interstitial edema.
• An echocardiogram can accurately diagnose MS and assess valvular and
subvalvular structure and valve area .
• different causes such as tumors, vegetations, extreme calcification of the
annulus, left atrial myxoma, cor triatriatum, or presence of a large thrombus.

27. • estimate pulmonary pressures and assess for right-sided enlargement.
• Typically, LV function is preserved in MS.
• In addition, echocardiography can help in calculating a mitral valve score that
takes into account leaflet mobility, thickening, valve calcification, and distortion
of the subvalvular apparatus.
• The interventional cardiologist typically uses the valve score to determine the
feasibility of balloon valvuloplasty.
• a transesophageal echocardiogram
• a left and right heart Catheterization

28. Treatment of Mitral Stenosis
• All patients with rheumatic mitral valve disease require bacterial endocarditis
prophylaxis before dental, genitourinary, or GI procedures.
• β-blockers or verapamil .
• Patients withAF need to be aggressively treated with rate control and
anticoagulation with warfarin to reduce embolic strokes.
• Chemoversion (with amiodarone or other antiarrhythmics)
• Transesophageal echocardiography can be performed before cardioversion to rule
out the presence of a left atrial thrombus
• Even when a thrombus is excluded, patients need to be heparinized for at least 48
to 72 hours before cardioversion then maintained on warfarin afterwards.
• The target international normalized ratio (INR) in patients withAF needs to be 2.0
to 3

29. • Patients with moderate to severe symptoms (NYHA class II to IV) or asymptomatic
patients with severe MS (valve area <1.5 cm2) and pulmonary HTN (pulmonary
pressure >50 mm Hg at rest and ≥60 mm Hg with exercise) require percutaneous
valvuloplasty, mitral valve repair, or mitral valve replacement.
• Balloon valvuloplasty leads to commissural separation as the main mechanism that
leads to an improvement in valvular function.
• Mitral valvuloplasty is currently the preferred method of treating severe MS when
no contraindications
• Mitral valve surgery is reserved for those patients with a calcified valve and a high
valve score on echocardiography who are essentially excluded from balloon
valvuloplasty.

31. Mitral regurgitation
• abnormal blood flow into the left atrium in systole as a result of an abnormal closing
of the mitral valve.
• In chronic mitral insufficiency vers acute MR
• Chronic MR is generally asymptomatic or associated with minimal symptoms of
dyspnea or generalized fatigue Later become symptomatic, with symptoms and signs
of HF.
• Patients might provide a history of rheumatic fever, endocarditis, CAD, or CHF.
Acute MR needs to be in the differential diagnosis of a patient with a sudden onset of
pulmonary edema.
• On examination, patients display a systolic murmur, most often holosystolic, high
pitched, and present at the apex with radiation to the axilla, left scapula.

32. • The ECG often displays an enlarged left atrium (biphasic P wave inV1), large
QRS complex secondary to LV enlargement, and possibleAF, and, in ischemic
MR, evidence of old or acute inferior infarcts can be seen.
• The chest radiograph may show an enlarged cardiac silhouette, a calcified mitral
valve, or increased pulmonary vascular congestion.
• Echocardiography provides the diagnosis by assessing the presence of the MR; its
severity; and its cause, such as severe prolapse, endocarditis, calcification,
papillary muscle or chordae rupture, or a degenerative valve.

33. • Regurgitant volume (30-59 mL is moderate; ≥60 mL is severe) and effective
regurgitant orifice (20-39 mm2 is moderate; ≥40 mm2 is severe) can be
calculated.
• Left and right heart catheterization is indicated before corrective surgery to
determine the presence of CAD and confirm the diagnosis of MR with the use
of left ventriculography.

34. Treatment of Mitral Regurgitation
• Patients with a history of mitral insufficiency need to have bacterial endocarditis
prophylaxis.
• Those with chronic MR benefit from long-term afterload reduction?
• Aggressive treatment ofAF with rate control and warfarin anticoagulation is
needed.
• Patients with moderate to severe MR need to be closely monitored for EF and
LV cavity size.

35. • Symptomatic patients (NYHA class II-IV) or asymptomatic patients with a LV end-
systolic dimension approaching 4.0 cm or LVEF of 60% or less should undergo
intervention.
• Patients with lower EF and a bigger cavity size carry a poorer outcome after surgery.
• Asymptomatic patients with preserved LV function and cavity size but with AF might
benefit from surgery.
• Patients with acute MR should be treated aggressively with afterload reduction such
as sodium nitroprusside.
• ?surgery after compensation
• Most regurgitant mitral valves can now be repaired instead of replaced.
Percutaneus repair of mitral valve.

36. Mitral Valve Prolapse
• bulging of one or more of the mitral leaflets into the left atrium in systole .
• MVP carries a benign course . In rare occasions, it can be associated with
significant arrhythmias and sudden cardiac death.
• When associated with MR, patients need to be carefully monitored for
progressive left atrial and LV cavity dilation andAF.
• familial and is inherited as an autosomal dominant trait versa Secondary MVP

37. • Patients with MVP are often asymptomatic. However, some patients describe
palpitations, chest pain, dyspnea, and fatigue with or without MR.
• A high-pitched midsystolic click is often heard that occurs shortly after the
first heart sound and can be associated with a systolic murmur.
• Baseline ECG is quite often unrevealing, and routine stress testing carries a
high false-positive rate.
• Stress imaging is more accurate in evaluating these patients for myocardial
ischemia.

38. • An echocardiogram is the most helpful methodology for making the diagnosis
of MVP.
• Cardiac catheterization is generally not needed for diagnostic purposes.
• Asymptomatic patients with MVP generally do not require treatment unless
they have severe associated MR .
• Symptomatic patients with MVP can be treated with β-blockers.
• Flail mitral leaflets caused by chordae rupture or severe MR associated with
MVP needs to be followed, and mitral valve repair becomes indicated if
patients develop symptoms of dyspnea (NYHA class III or IV), the EF and
cavity size become adversely affected, orAF appears.

39. Tricuspid Valve Disease
• Tricuspid regurgitation (TR) is commonly present on echocardiography in the
majority of patients and therefore, when mild, is considered a normal variant.
• SevereTR can occur, however, and can create significant symptoms of right-
sided CHF (cor pulmonale) and dyspnea.
• IsolatedTR is commonly seen in drug addicts secondary to tricuspid valve
endocarditis but can also be caused by carcinoid syndrome, trauma, RV
infarction, and certain congenital anomalies.
• The most common etiology ofTR is, however, annular dilation caused by RV
cavity dilation.

40. • Typically, dyspnea, right- and left-sided failure, and in the case of endocarditis,
fever and night sweats can be present.
• The RV is generally dilated, and a precordial lift is present.
• The jugular veins are pulsatile and increased.
• A systolic murmur is generally heard along the left sternal border that
increases with respiration.

41. • Patients with severeTR are treated with diuretics and digitalis to treat the
associated right-sided failure.
• ACE inhibitors are indicated if LV dysfunction is present.
• It is recommended that tricuspid valve replacement or repair be performed if
severeTR is present and the patient is undergoing simultaneous mitral valve
surgery or if severeTR is present as a primary disorder in a symptomatic
patient.

42. • mostly caused by rheumatic heart disease and is typically associated with other
valvular involvement.
• TS can also be caused by the carcinoid syndrome (most commonly causesTR)
and certain connective tissue diseases.
• Secondary causes ofTS such as tumors or thrombi can also precipitate
secondaryTS.
Tricuspid valve stenosis

43. • InTS, patients can be dyspneic with activity.
• Typically, there is an increase in the jugular vein, with a large a wave indicating
atrial contraction against a stiff tricuspid valve.
• TS is typically treated with percutaneous valvular commissurotomy unless it is
unfeasible.
• Open commissurotomy is then performed, or valve replacement is then
performed if the leaflets and subvalvular structures are not repairable.
• Bioprosthetic valves are typically used, and patients are generally prescribed
warfarin after tricuspid valve replacement.

44. Pulmonic Valve Disease
• Pulmonary valve regurgitation (PR) is typically acquired because of increased
pulmonic pressures (pulmonary HTN).
• Primary valve abnormalities caused by endocarditis can also cause PR.
• PR due to pulmonary HTN causes a diastolic murmur along the left sternal
border (Graham Steel murmur).
• Surgery on acquired PR is rarely performed.
• Pulmonic valve stenosis (PS) is mostly congenital, but secondary causes such as
tumors, endocarditis, or carcinoid can also cause PS.
• PS is best treated with percutaneous valvuloplasty with good long-term results.

45. Endocarditis
• Endocarditis is defined as an oscillating intracardiac mass without alternate
anatomic classification, the presence of an abscess, or dehiscence of a new
prosthetic valve .
• Endocarditis is treated with a prolonged course of IV antibiotics.
• Surgical management can be considered in patients who develop HF or LV
dysfunction, damage to the valve annulus with an abscess or perforation of the
leaflet, or isolating a resistant organism to antibiotics after 1 week of treatment.

46. • Large vegetations, particularly those that are increasing in size and recurrent
emboli, are to be considered as indications for valve surgery.
• Prophylaxis for endocarditis is now limited to patients with prosthetic valves
or rings, a history of prior endocarditis, congenital heart disease, or transplant
with valvular heart disease.

47. Prosthetic Valves
• Echocardiography (transthoracic, transesophageal, or both) is indicated to evaluate stenotic or
regurgitant prosthetic valves.
• Prosthetic valves are associated with several complications, including infective endocarditis, a
paravalvular leak, thrombosis and embolization, pannus formation, and hemolytic anemia.
• Prosthetic valve thrombosis requires surgery if it is a left-sided valve and is associated with
advanced HF (class III and IV NYHA) and there is large clot burden.
.

48. Rheumatic fever
• systemic inflammatory process initiated by groupA β-hemolytic streptococcal
pharyngitis.
• Often, younger children in particular do not recall antecedent pharyngitis,
which usually occurs 2 to 4 weeks before symptom onset.
• Rheumatic fever most often affects children 4 to 9 years of age, and the onset
is usually characterized by an acute febrile illness that can cause large-joint
migratory arthritis, CNS involvement (Sydenham chorea), characteristic rash,
and carditis with inflammation of heart valves and subsequent damage.
• Antibiotic treatment of GAS pharyngitis greatly reduces the development
of rheumatic fever.

49. revised Jones criteria

50. • Rheumatic fever–related arthritis is often preceded by arthralgias out of
proportion to frank swelling, lasting approximately 1 week.
• Arthralgias
• Carditis .
• Rheumatic heart disease is the most common serious sequela and usually occurs
10 to 20 years after the original attack.
• Patients might also have erythema marginatum
• The antistreptolysin O (ASO) titer is the most useful laboratory .
• TheASO titer rises 4 to 5 weeks after the onset of GAS pharyngitis or 2 to 3
weeks after development of rheumatic fever.
• antistreptococcal antibody, such as anti-DNase, anti-DNase B, and
antihyaluronidase antibody tests.

51. • Aspirin is the drug of choice for acute rheumatic fever and usually results in a
dramatic response.
• Penicillin should also be given for a 10-day course whether or not pharyngitis
is present, and family members and other close contacts should be cultured
and treated if necessary.
• IM penicillin is more effective than oral penicillin in clinical trials.
• No benefit has been shown from IV immune globulin (IVIG) or
corticosteroids for rheumatic fever, but studies continue.

52. • Patients who have had documented rheumatic fever and who develop
subsequent GAS pharyngitis are at high risk for a recurrent rheumatic episode
and thus at increased risk for worsening rheumatic heart disease.
• For this reason, prevention of recurrent episodes requires continuous
antimicrobial prophylaxis .
• Before prophylaxis initiation, a full treatment course for GAS pharyngitis
should be completed.
• typical prophylactic therapy is with long-acting IM benzathine penicillin G
every 4 weeks until early adulthood (≈18 years of age).

53. • END