This document discusses the assessment of severity in valvular heart disease. It addresses three main issues in managing patients with valvular heart disease: assessing disease severity, determining the effect on the cardiovascular system, and deciding the timing and type of intervention. Disease severity is classified as mild, moderate, or severe based on physical exam findings, echocardiography, and other tests. Only severe disease generally causes symptoms and requires intervention. Assessment of severity integrates data from multiple tests and should guide decisions about treatment.
Echocardiographic screening for rheumatic heart diseaseRamachandra Barik
RHD affects ≈20 million people worldwide
highest in developing countries
significant morbidity and mortality
Subclinical detection adds to of secondary prophylaxis
echocardiographic definitions evolving
In 2012, the WHF published evidence-based
guidelines for the echocardiographic diagnosis of RHD
but these criteria have not yet been applied
Echocardiographic screening for rheumatic heart diseaseRamachandra Barik
RHD affects ≈20 million people worldwide
highest in developing countries
significant morbidity and mortality
Subclinical detection adds to of secondary prophylaxis
echocardiographic definitions evolving
In 2012, the WHF published evidence-based
guidelines for the echocardiographic diagnosis of RHD
but these criteria have not yet been applied
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Some of the slides, i hide it from my real presentations for my own reference. Download to see all of them.
comprehensive presentation on 2D echo use in ICu set up. helpful in finding causes of shock and also in monitoring of fluid status in critically ill patients.
A case of missed diagnosis. Presentation can be in form of heart failure. Differentials can be of Constrictive pericarditis. Restrictive cardiomyopathy/Endomyocardial fibrosis, DCM. This presentation contains clinical presentation, differentials, hemodynamics of cath study, echocardiogrpahy in a case of CP
Vitamin D is an important prohormone for optimal intestinal calcium absorption for mineralization of bone. Because the vitamin D receptor is present in multiple tissues, there has been interest in evaluating other potential functions of vitamin D, particularly, in cardiovascular diseases (CVD). Cross-sectional studies have reported that vitamin D deficiency is associated with increased risk of CVD, including hypertension, heart failure, and ischemic heart disease. Initial prospective studies have also demonstrated that vitamin D deficiency increases the risk of developing incident hypertension or sudden cardiac death in individuals with preexisting CVD. Very few prospective clinical studies have been conducted to examine the effect of vitamin D supplementation on cardiovascular outcomes. The mechanism for how vitamin D may improve CVD outcomes remains obscure; however, potential hypotheses include the downregulation of the renin-angiotensin-aldosterone system, direct effects on the heart, and vasculature or improvement of glycemic control. This review will examine the epidemiologic and clinical evidence for vitamin D deficiency as a cardiovascular risk factor and explore potential mechanisms for the cardioprotective effect of vitamin D.
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Hypertension is a common medical and social problem leading to cardiovascular diseases worldwide. Antihypertensive drugs are clinically applied to decrease the morbidity and mortality induced by hypertension itself and its complications. The 2014 hypertension guideline of the Eighth Joint National Committee (JNC8) for hypertension therapy in the United States has made several significant changes with respect to the clinical management of hypertension and the initiative medications, as compared with the previous guidelines. In addition to the instructions that pharmacologic treatment should be initiated when blood pressure (BP) is 150/90 mmHg or higher in adults over 60 years, 140/90 mmHg in adults younger than 60 years, or 140/90 mmHg or higher (regardless of age) in patients with hypertension and diabetes, a thiazide-type diuretic, calcium (Ca2+) channel blocker (CCB), angiotensin-converting enzyme inhibitor (ACEI), or angiotensin receptor blocker (ARB) should be considered to start an initial antihypertensive medication in non-black population. In black population with or without diabetes, initial antihypertensive treatment should include a thiazide-type diuretic or CCB. Thus, CCB has become one of the most important initial agents for antihypertensive monotherapy. Furthermore, since CCBs have been proved not to increase the risk of coronary events and stroke,CCBs appear to be a favorable choice for monotherapy as well as for combination with other agent classes in the treatment of hypertension and may provide specific benefits beyond BP lowering.Nowadays, dihydropyridine (DHP) CCBs are one group of most frequently prescribed antihypertensive medications in China and other Eastern Asian countries.
Among patients with or at high risk of CVD, use of an FDC strategy for blood pressure, cholesterol, and platelet control vs usual care resulted in significantly improved medication adherence.Polypill therapy significantly improved adherence, SBP and LDL-cholesterol in high risk patients compared with usual care, especially among those who were under-treated at baseline.
A transesophageal echocardiogram (TEE) uses echocardiography to assess the structure and function of the heart. During the procedure, a transducer (like a microphone) sends out ultrasonic sound waves. When the transducer is placed at certain locations and angles, the ultrasonic sound waves move through the skin and other body tissues to the heart tissues, where the waves bounce or "echo" off of the heart structures. The transducer picks up the reflected waves and sends them to a computer. The computer displays the echoes as images of the heart walls and valves.
A traditional echocardiogram is done by putting the transducer on the surface of the chest. This is called a transthoracic echocardiogram. A transesophageal echocardiogram is done by inserting a probe with a transducer down the esophagus. This provides a clearer image of the heart because the sound waves do not have to pass through skin, muscle, or bone tissue. The TEE probe is much closer to the heart since the esophagus and heart are right next to each other.
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June 3, 2024 Anti-Semitism Letter Sent to MIT President Kornbluth and MIT Cor...Levi Shapiro
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The US House of Representatives is deeply concerned by ongoing and pervasive acts of antisemitic
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Valvular heart disease assessment of lesion severity
1. Valvular Heart DiseaseValvular Heart Disease
Assessment of Lesion severityAssessment of Lesion severity
Dr Awadhesh kumar sharma
DM Cardiology
PGIMER &Dr RML Hospital,New Delhi
2. In managing the patient with valvular heart disease (VHD)
three major issues must be addressed:-
Assessment of the severity of disease,
The effect the disease is having or is likely to have on the
patient and his/her cardiovascular system
The timing and type of intervention to be used to correct
the lesion.
Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 8th
ed. Philadelphia, PA: WB Saunders; 2007:1625-1712.
3. The distinction between mild, moderate and severe disease
is thought crucial since it is believed that, in most cases,
mild and moderate disease are tolerated indefinitely
(unless severity worsens) and only severe disease (as
defined) causes symptoms and cardiac dysfunction.
Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 8th
ed. Philadelphia, PA: WB Saunders; 2007:1625-1712.
4. Classification of the severity of valve lesions should be
based on multiple criteria, including the initial findings on
the physical examination, which should then be correlated
with data from a comprehensive TTE.
Intervention should primarily be performed on patients
with severe VHD
Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 8th
ed. Philadelphia, PA: WB Saunders; 2007:1625-1712.
6. OBJECTIVE ASSESSMENT OF DISEASE
SEVERITY
The physical examination
In this age of high-tech diagnostic modalities, the physical
examination, and the skill applied when performing it,
seem to be diminishing.
However, the importance of the physical exam cannot be
overemphasized because it lays the Bayesian foundation
for all tests that follow.
7. Mitral stenosis (MS)
Etiology
Most commonly rheumatic fever
——rheumatic heart disease ( RHD )
Symptoms commence mostly in 2nd~4th decade
2/3 of all patients are female
25% of all patients with RHD have pure MS
40% have combined MS and mitral regurgitation (MR)
J Am Coll Cardiol. 1994;24:152-8.
8. Clinical features s/o severe MS
PND
Pulmonary edema
Orthopnea
Atrial fibrillation
Ortner syndrome
Short A2-OS interval
Long duration of diastolic murmur
J Am Coll Cardiol. 1994;24:152-8.
9. Laboratory examination
Electrocardiography (ECG)
Left atrial enlargement
Mitral valve P wave
P-wave duration in lead II > 0.12 s
Large terminal negative P force in lead V1
Right ventricular hypertrophy
Arrhythmia
Premature atrial contraction → atrial fibrillation
10. Radiological findings
“Mitral valve heart”
Marked enlargement of LA
Enlargement of RV
Dilatation of PA
Pulmonary congestion
Interstitial edema (manifested as Kerley B lines)
11. Echocardiography
The most valuable technique for diagnosing MS,
and determining its severity
M-mode echoM-mode echo ::
Thickened, calcified leaflets
open poorly, close slowly (EF slope↓)
The double peaks disappear
Both leaflets move anteriorly during early diastole
Two-dimensional echo:Two-dimensional echo:
Fusion, thickening, doming of the valve leaflets, and poor
leaflet separation in diastole; mitral orifice area↓
Eur J Echocardiogr. 2009;10:1-25.
14. Hemodynamic changes
MS involves mainly LA and RV
1. Effect of MS on left atrioventricular pressure
gradient and left atrial pressure (LAP)
MVA transvalvular gradient LAP
Normal 4 ~ 6cm2
Mild MS > 1.5cm2
<5 mmHg ↑
Moderate 1.0 ~ 1.5cm2
5-10mmHg ↑↑
Severe < 1.0cm2
≥10mmHg 25mmHg
Eur J Echocardiogr. 2009;10:1-25.
16. Doppler echoDoppler echo ::
Most accurate noninvasive technique for quantifying the
severity of MS
Spectrum Doppler: measure transvalvular gradient, MVA
Color Doppler: display high velocity color jet
Provide other important information
Cardiac chamber size (LA, RV)
Left ventricular contractility
Pulmonary arterial pressure
Other coexisted valvular or congenital abnormalities
Mural thrombi
Eur J Echocardiogr. 2009;10:1-25.
17. Cardiac catheterization
Its value in assessment of patients with MS or
suspected MS has been largely superseded by
echocardiography
If surgery is planned, coronary angiography is
performed to ascertain whether or not bypass grafting
is indicated in patients at risk of having coexisting
coronary artery disease
J Am Coll Cardiol. 1994;24:152-8.
18. 2014 AHA/ACC Valvular Heart Disease
Guidelines
J Am Coll Cardiol. March 2014.Online first.
20. Severe dilatation of LV
result in dilatation of the mitral annulus and
lateral movement of papillary muscle
Infective endocarditis
valve leaflets destruction, perforation, retraction;
valve closure interfered by vegetation
Other causes:
Rupture of the chordae
congenital abnormalities
obstructive hypertrophic cardiomyopathy
21. Hemodynamic changes
MR involves mainly LA and LV
Chronic MR
Compensation: MR→ LV volume↑→LV, LA↑→
LVEDV↑→ SV↑→ CO↑, EF↑
Decompensation:
Left HF, LAP and LVEDP↑ → pulmonary congestion,
pulmonary hypertension, right HF
(hepatomegaly, edema, and ascites)
CO↓
Acute MR
MR →LA, LV volume↑→LVEDP↑→LAP↑→
↓ pulmonary congestion, pulmonary edema
SV and CO↓
22. Clinical manifestations
Symptoms
Chronic MR
Mild— no symptom
Severe— left-sided heart failure
Weakness, fatigue (CO↓)
Dyspnea (pulmonary congestion)
RHD: symptoms occur late, once present, LV
dysfunction is usually irreversible
MVP: asymptomatic, or atypical chest pain,
palpitation, fatigue; in severe MR, left
HF occur at late stage
Acute Mild— mild exertional dyspnea
Severe— acute left HF, pulmonary edema,
or cardiac shock
Circulation. 2003;108:2432-2438.
23. Physical examination
Cardiac impulse at apex
Hyperdynamic
Displaced laterally, inferiorly (Chronic)
Changes of heart sounds
S1↓(RHD) or normal (MVP, CAD)
S3 (severe MR): prominent
Mid or late systolic click ( MVP )
( Acute: P2↑ , S4 )
Circulation. 2003;108:2432-2438.
24. Systolic murmur
RHD : Pansystolic, blowing, high-pitched murmurPansystolic, blowing, high-pitched murmur
maximal at the apex
Anterior valve lesion, radiate to the axilla and back
Posterior leaflet abnormality, radiate to the base
MVP : mid- to late-systolic murmur
Dysfunction of papillary muscles:
Variable (early, mid, late or holosystolic)
Rupture of the chordae: musical
(Acute MR: not pansystolic murmur, but lower-pitched,
decrescendo, and softer than the murmur of chronic MR)
Circulation. 2003;108:2432-2438.
25. Severe MR
Hyperdynamic LV type apex
Systolic thrill over apex
S3
Functional flow mid diastolic murmur
Circulation. 2003;108:2432-2438.
26. Laboratory examination
ECG
Chronic (severe) MR:
LA dilation, Atrial fibrillation
LV enlargement and non-specific ST-T changes
Acute MR: sinus tachycardia
Radiological findings
Chronic (severe) MR:
Cardiomegaly with LA, LV↑; pulmonary congestion,
interstitial edema with Kerley B lines (left HF)
C-shaped calcification of mitral annulus
Acute MR:
Normal cardiac silhouette or mild LA dilation
overt pulmonary congestion, edema
J Am Coll Cardiol. 1999;34:1137-44.
27. Echocardiography
1 、 Display anatomy of the mitral valve apparatus
Useful in determining the etiology of MR (2D)
2 、 Confirm the existence of MR
Doppler (color, spectrum): reveal high-velocity jet into LA
during systole
Sensitivity~100%
Estimate the severity of MR
< 4 cm2 Mild
( Color flow jet area ) 4~8 cm2 Moderate
> 8 cm2 Severe
3 、 Measure cardiac chamber sizes, evaluate LV
function, pulmonary artery pressure, provide data
concerning other valvular lesions
J Am Coll Cardiol. 1999;34:1137-44.
29. PISA
Measure the radius of the
hemisphere. (red/blue
interface)
– PISA radius =2πr2
(cm2
)
• Mild MR: <0.4
• Severe MR:>1.0
30. Colour Doppler Indicators of Mitral
Regurgitation Severity
Mild Moderate Severe
Colour Doppler
Jet area (cm2
) Nyquist
50-60cm/s
<4 >10
Ratio of jet area to left
atrial area (%)
<20 >40
Vena contracta width
(cm)
<0.3 >0.7
PISA radius (cm) at
Nyquist 40cm/s
<0.4 >1.0
31. Continuous wave and Pulse wave Doppler
Continuous wave spectral
Strength
– Apical 4Ch view CW of
regurgitant jet
• Faint in mild mitral
regurgitation
• Denser in moderate
and severe
regurgitation.
32. Peak Mitral Valve E velocity
Increased mitral valve E
velocity (>1.2m/s) may
indicate significant
regurgitation.
– Assumes ejection
fraction is>40%)
Decreased mitral valve DT
(<150msec) may indicate
significant regurgitation.
– Assumes normal
diastolic LV function.
33. Pulmonary Vein Systolic Flow Reversal
PW doppler 1cm into the
pulmonary veins
– Systolic S (systolic)
wave is normally larger
than the D (diastolic)
wave.
– If D wave is larger there
is blunting of forward
flow.
– S wave inversion
demonstrates systolic
flow reversal (indicative
of severe MR).
37. Regurgitant Volume, Regurgitant Fraction
and ERO
Regurgitant volume
Step 1
– A4ch view measure
diameter of the mitral
annulus.
• CSAMV=0.785 X
(mitral annulus
diameter)2
38. Regurgitant volume
Step 2
– Apical 4Ch view measure
the VTI of the mitral inflow
(using PWD)
– Commonly at valve tip
level.
• VTIMV in cm
Step 3. Stroke Volume
– SVMV(mL/beat) =CSAMV X
VTIMV
39. Regurgitant volume
Step 4
– In PLAx measure the
diameter of the LVOT
(cm).
– Calculate CSA of the
LVOT (cm2
)
• CSALVOT = 0.785 x (LVOT
diameter)2
40. Regurgitant volume
Step 5
– In the Ap5 Ch view
measure the VTI of the
LVOT outflow (using
PWD)
• VTILVOT (cm)
Step 6. Stroke volume
– SVLVOT = CSALVOT x VTILVOT
42. Regurgitant orifice area
Step 8
– Measure the VTI of the
mitral regurgitation
VTIMR (cm) (using CWD)
– Calculate Regurgitant
Orifice Area (ROA) in
cm2
• ROA = RV / VTIMR
– Mild MR:<0.20
– Mod MR:0.21-0.39
– Severe MR:>0.40
43. Regurgitant Orifice Area
PISA method
Step 1. Measure the radius
of the hemisphere.
(red/blue interface)
– PISA =2πr2
(cm2
)
– Calculate regurgitant
flow rate
– RFR mL/s =PISA X
aliasing velocity
44. Regurgitant orifice area
Step 2. CWD of the mitral
regurgitation. Measure peak
velocity (VMR) in cm/s.
Calculate Regurgitant
Orifice Area in cm2
.
– ROA =Regurgitant flow
rate / VMR
45. Common pitfalls
Measuring regurgitant jet area or VC width on colour
doppler with inappropriate colour gain settings
Underestimating severity of eccentric jets on CFD.
Failure to align the doppler beam with regurgitant flow
during CW doppler interrogation.
Inaccurate measurement of mitral valve orifice area or
LVOT diameter when calculating RV.
Trying to calculate RV when there is coexistant aortic
regurgitation.
Failure to average several readings when the patient is in
AF.
46. Radionuclide angiography and MRI
Evaluate LV function
Estimate the severity of regurgitation
The regurgitant fraction can be estimated from
the ratio of LV to RV (LV/RV) stroke volume
Cardiac catheterization
Confirm the diagnosis of MR and estimate
its severity, evaluate cardiac function and
pulmonary artery pressure
Coronary angiography is performed to
determine presence of CAD prior to surgery
J Am Coll Cardiol. 1999;34:1137-44.
47. 2014 AHA/ACC Valvular Heart Disease
Guidelines
J Am Coll Cardiol. March 2014.Online first.
48. 2014 AHA/ACC Valvular Heart Disease
Guidelines
J Am Coll Cardiol. March 2014.Online first.
49. Aortic stenosis (AS)
Etiology
RHD
Common, + AR and mitral valve disease
Degenerative calcific AS
Common in the elderly, accompanied by calcification of
the mitral annulus
Congenital abnormalities
Calcific stenosis of congenitally bicuspid aortic valve
Congenital aortic stenosis
50. Hemodynamic changes
Normal aortic orifice area (AOA): 3.0~4.0 cm2
AOA ≤1.0cm2, LVSP↑, with significant transvalvular gradient
Compensation
AS→LV pressure load↑
Concentric LVH→compliance↓→LVEDP↑→LAH
Maintain systolic wall stress and CO ↑LVEDV
Decompensation
LVEDV↑→wall stress↑, myocardial ischemia, fibrosis →
left HF
52. Classic symptom triad
Once any of these classic symptoms develop,
prognosis dramatically worsens.
Thus, within 5 years of the development of angina,
approximately 50% of patients will die unless aortic
valve replacement is performed.
For syncope, 50% survival is 3 years
For congestive heart failure, 50% survival is only 2
years unless the valve is replaced.
Angina 5yrs, Syncope 3yrs, and CHF 2yrs.
53. Severe AS
Triad of angina,dyspnoea and syncope
Heaving apex
Slow rising small volume pulse
Reverse splitting of S2
Long duration of systolic murmur
Late peaking of murmur
Presence of S4
54. Laboratory examination
ECG
Severe: LVH and secondary ST-T changes,
LA↑ , arrhythmias
Radiological findings
Normal size or slightly enlarged heart
Calcification of the aortic valve
Poststenotic dilatation of the ascending aorta
Pulmonary congestion
55. Echocardiography
Establish a diagnosis, and determine the severity
of AS
M-mode and 2D echo
Observe aortic valve opening, thickening and
calcification
Helpful in determining the etiology of AS
Also invaluable in detecting associated mitral
valve disease and in assessing LV performance,
hypertrophy, and dilatation
Eur J Echocardiogr. 2009;10:1-25.
56. Doppler echo
Allows calculation of the aortic valve gradient
Estimate the severity of the stenosis
< 20 mmHg Mild AS
MPG 20~40 mmHg Moderate AS
> 40 mmHg Severe AS
Color Doppler flow imaging is helpful in the
detection and determination of the severity of any
accompanying aortic regurgitation
Eur J Echocardiogr. 2009;10:1-25.
57. Enriquez-Sarano, M. et al. N Engl J Med 2004;351:1539-1546
Jet of Aortic Regurgitation, as Shown by Color-Flow Imaging
58. Enriquez-Sarano, M. et al. N Engl J Med 2004;351:1539-1546
Classification of the Severity of Aortic Regurgitation
59. Enriquez-Sarano, M. et al. N Engl J Med 2004;351:1539-1546
Quantitation of Aortic Regurgitation by the Convergence of the Proximal Flow
60.
61.
62.
63. Cardiac catheterization
Determine the severity of AS by measuring systolic
LV and aortic pressure simultaneously, and
calculating the valve area
An average pressure gradient of > 40mmHg or
peak pressure gradient of ≥ 70mmHg represent
severe AS
Coronary angiography is performed in most adults
to assess for concomitant coronary disease
64. Cath data
“Pull back” tracing can be used in pt with NSR but not
accurate in irregular rhythms or low-out put states.
In low cardiac output, the stenosis may be severe, with a
mean gradient <50mm Hg per echo.
Gorlin equation can be used to calculate AVA from
pressure gradients, independent of CO.
AVA= (1000)(CO)
(44)(SEP)(HR)(√∆P)
65.
66. 2014 AHA/ACC Valvular Heart Disease
Guidelines
J Am Coll Cardiol. March 2014.Online first.
67. 2014 AHA/ACC Valvular Heart Disease
Guidelines
J Am Coll Cardiol. March 2014.Online first.
69. Aortic valve disease
① RHD : most common, about 2/3
+ AS and/or mitral valve disease
② Infective endocarditis
③ Congenital deformity: bicuspid valves
④ Myxomatous degeneration of the aortic valve
Aortic root dilatation
① Marfan syndrome
② Aortic dissection (involve annulus or leaflets)
③ Syphilitic aortitis
Clinical practice: aortic regurgitation. N
Engl J Med. 2004;351:1539-1546.
72. Clinical manifestations
Symptoms
Chronic AR
Asymptomatic for many years
Palpitation, precordial discomfort, head pounding
(related to SV↑)
LV failure (dyspnea, fatigue): occur at late stage
Angina pectoris or chest pain: less common
Acute AR
mild—no symptom
severe—Acute LV failure and hypotension
(pulmonary edema)
Clinical practice: aortic regurgitation. N
Engl J Med. 2004;351:1539-1546.
73. Physical examination
Chronic, severe AR
① Peripheral arterial signs: Owing to wide pulse pressure:
SBP↑, DBP↓
Water-hammer pulseWater-hammer pulse (rapid rise and fall)
“Pistol shot soundsPistol shot sounds” (booming systolic & diastolic sounds
heard over femoral artery)
Duroziez’s signDuroziez’s sign (systolic, diastolic murmur over partially
compressed femoral artery)
Quincke’s signQuincke’s sign (subungual capillary pulsations)
de Musset’s signde Musset’s sign (head bobs with each heartbeat )
② Apical impulse: diffuse and forceful, displaced laterally and
inferiorly (hyperactive, enlarged LV)
③ Heart sound: An S3 gallop is common with LV failure
Clinical practice: aortic regurgitation. N
Engl J Med. 2004;351:1539-1546.
74. ④ Heart murmurs
Aortic diastolic murmur:Aortic diastolic murmur:
High-pitched, blowing, decrescendo pattern
When AR is due to primary valvular disease, the diastolic
murmur is best heard along the left sternal border in the
3rd and 4th intercostal spaces
However, when it is due mainly to dilatation of the ascending
aorta, the murmur is often more readily audible along the
right upper sternal border
Austin-Flint murmur:
apical mid or late diastolic low-pitched murmur:
common in severe AR, owing to partial closure of MV by
the regurgitant jet
Circulation. 2005;112(1):125-134.
75. Ejection systolic murmur:
common
harsh
at the base of the heart
accompanied by a systolic thrill
Acute AR
S1 soft or absent , P2↑ , S3 and S4
AR murmur: lower pitched and shorter than
that of chronic AR
Austin-Flint murmur: brief
Circulation. 2005;112(1):125-134.
77. Radiological findings
Acute AR: cardiac size normal or slightly enlarge,signs of pulmonary congestion,
pulmonary edema
Chronic: LV enlargement, associated with dilatation of the ascending aorta
Severe, aneurysmal dilatation of the aorta suggests aortic root disease
Marfan syndrome)
Pulmonary congestion ( LV heart failure )
Chronic Acute
LVE with normal pulmonary
vasculature
Normal size LV with pulmonary
vascular congestion
78. Echocardiography
Confirm diagnosis, estimate severity, identify the cause
2-D echo:
Structural changes of the valve leaflets and/or aortic root
M mode echo:
Diastolic fluttering of the anterior leaflet of the mitral
valve is an important echocardiographic finding in AR
Serial assessments of LV size and function
Doppler echo:
Sensitive, accurate noninvasive technique for detecting AR
LVOT diastolic regurgitant jet, estimate the severity of AR
Cardiac catheterization
Quantify the severity of AR
Evaluate the coronary and aortic root anatomy
J Am Soc Echocardiogr.2003;16:777-802.
86. vitrag24-www.medicalgeek.com
Assessing Severity of AR
Assess severity by impact on peripheral signs and LV-
Duration of murmur >2/3 of diastole
Bisferiens pulse
Hills sign>60 mmHg
Apical impulse down & out
Austin flint murmur
Marked peripheral sign
Circulation. 2005;112(1):125-134.
87. Features AS > AR AR > AS
Symptoms:
Anginal pain, blackout
Palpitation
+++
+
+
+++
Pulse Low volume
Bisferians pulse
High volume
Corrigan’s pulse
Pulse pressure Normal to low Wide
Peripheral signs +/- +
Apex Heaving Hyperdynamic
Thril Always systolic Rarely
S3 Absent May be present
S4 May be present Absent
Ejection click Present Rare
Diastolic murmur Very short Classic murmur of AR
Systolic murmur Classic murmur of AS Function systolic murmur
+/-
Chest X-Ray Calcification + Cardiomegaly
ECG Pressure overload Volume overload
92. Severe TS
Giant a wave in JVP
Duration of diastolic murmur over tricuspid
valve
Signs of right heart failure
N Engl J Med. 1997;337:32-41.
93. ECG-
Absence of evidence of RVH
Right atrial abnormality
Chest X ray
Prominence of right atrium and SVC
N Engl J Med. 1997;337:32-41.
94. 2014 AHA/ACC Valvular Heart Disease
Guidelines
J Am Coll Cardiol. March 2014.Online first.
95. Tricuspid regurgitation
Primary disorders of the tricuspid apparatus
Rheumatic disease
Prolapse
Congenital disease (Ebstein’s)
IE
Radiation
Carcinoid
Blunt chest wall trauma
RV endomyocardial biopsy related trauma
Intra-annular RV pacemaker or implantable cardioverter-
defibrillator leads.
N Engl J Med. 1997;337:32-41.
96. Approximately 80% of cases of significant TR are
functional in nature and related to tricuspid
annular dilation and leaflet tethering in the setting
of RV remodeling due to pressure and/or volume
overload.
J Am Soc Echocardiogr.2003;16:777-802.
98. 2014 AHA/ACC Valvular Heart Disease
Guidelines
J Am Coll Cardiol. March 2014.Online first.
99. 2014 AHA/ACC Valvular Heart Disease
Guidelines
J Am Coll Cardiol. March 2014.Online first.
100. Pulmonary stenosis
Pulmonic stenosis is essentially a congenital
disorder.
Less common etiologies include carcinoid
and obstructing vegetations or tumors.
Assessment with TTE alone is usually
sufficient for diagnosis and clinical decision
making.
N Engl J Med. 1997;337:32-41.
102. 2014 AHA/ACC Valvular Heart Disease
Guidelines
J Am Coll Cardiol. March 2014.Online first.
103. Pulmonary regurgitation
Mild-to-moderate PR seen on echocardiography is
common and does not require further follow-up or
intervention if asymptomatic with normal RV size and
function.
Significant PR in patients is uncommon.
Primary PR that follows in the wake of childhood surgery
for tetralogy of Fallot or other congenital lesions may
progress insidiously
J Am Soc Echocardiogr.2003;16:777-802.
104. 2014 AHA/ACC Valvular Heart Disease
Guidelines
J Am Coll Cardiol. March 2014.Online first.
105. We urgently need research on almost every aspect of VHD
to ensure that patients who already have VHD receive
optimal therapy and to prevent VHD in those at risk.
Approaches to improving outcomes in patients with VHD
include –
1) National and international registries and RCTs
2) Continuous evaluation of outcomes data at each Heart
Valve Center of Excellence
3) Focus on patient-centric care with involvement of the
patient in the decision-making process.
Figure 1. Example of a Jet of Aortic Regurgitation, as Shown by Color-Flow Imaging.
The three components of the regurgitant flow (flow convergence above the orifice, vena contracta through the orifice, and the jet below the orifice) are shown. The width of the vena contracta (as indicated by crosses) can be measured as a surrogate for the regurgitant orifice.
Table 1. Classification of the Severity of Aortic Regurgitation.
Figure 2. Example of Quantitation of Aortic Regurgitation by the Convergence of the Proximal Flow.
Panel A is a color-flow image of the aortic valve; the measured radius of the proximal flow convergence (R) is 0.74 cm, and the regurgitant flow is calculated as 138 ml per second. The &quot;aliasing&quot; velocity of 0.40 m per second (modified by baseline displacement) is the blood velocity at the junction of the orange and blue flows. Panel B shows a continuous-wave Doppler measurement of regurgitant blood velocity, at 455 cm per second (arrow). The effective regurgitant orifice area is determined by dividing the flow by the velocity, which in this case is 0.30 cm2.