Valves Flashcards
(369 cards)
1
Q
What ensures mitral valve competence under normal physiological conditions?
A
Appropriate ventricular contractility (mitral closing force)
Appropriate chordal length/tension (prevents prolapse)
Thin, non-redundant leaflet tissue for tight coaptation
2
Q
What are the 4 types of MR in Carpentier’s classification?
A
Type I: Normal leaflet motion, MR due to leaflet perforation or annular dilatation (e.g., endocarditis, trauma)
Type II: Leaflet prolapse or flail (e.g., MVP, chordae or papillary muscle rupture)
Type IIIa: Restricted leaflet motion in both systole/diastole (rheumatic disease)
Type IIIb: Restricted motion in systole only, due to ventricular remodeling (functional MR)
3
Q
What defines Type II MR?
A
Prolapse >2 mm above annular plane; flail leaflet if free edge turns into LA. Commonly due to chordal or papillary muscle rupture.
4
Q
What is the hallmark of Type IIIb MR?
A
Leaflet tethering from ventricular dysfunction pulling papillary muscles posterolaterally, mostly affecting posterior leaflet.
5
Q
What are the causes of acute MR?
A
Endocarditis (vegetation, perforation)
Papillary muscle rupture (post-MI)
Chordae rupture (trauma, MVP, endocarditis)
Acute functional MR (MI, myocarditis)
Blunt chest trauma during isovolumetric contraction
6
Q
How is EF affected in acute MR?
EF is increased to maintain total stroke volume, though forward stroke volume is reduced; LA pressure is elevated, but LV diastolic pressure may be normal.
A
7
Q
What defines MVP on imaging?
A
Leaflet prolapse >2 mm above annular plane
Leaflet thickness ≥2 mm (myxomatous)
Elongated leaflets/chordae
8
Q
What are the two forms of MVP and how do they differs?
A
Fibroelastic Deficiency: Thin leaflet, localized, common in elderly, rapid progression
Barlow’s Disease: Thickened valves/chordae, diffuse, younger patients, associated with connective tissue disorders
9
Q
What is the most common cause of severe intrinsic MR needing surgery?
A
Fibroelastic deficiency
10
Q
What is the prevalence and demographics of MVP?
A
1–2% of population; more common in women (2:1)
11
Q
What leaflet segment is most often affected in MVP?
A
Posterior cusp, especially P2
12
Q
What are risk factors for severe MVP?
A
Male >50 years
Valve thickness ≥5 mm
Significant baseline MR and murmur
13
Q
What arrhythmias are associated with MVP?
A
PVCs, rarely VT and sudden death, due to papillary muscle scarring
14
Q
What causes ischemic MR?
A
Ventricular remodeling (not valve pathology), particularly posterior/inferior MI that displaces papillary muscles, tethering posterior leaflet
15
Q
What is the role of papillary muscle ischemia in ischemic MR?
A
Minimal; MR is due to wall remodeling, not ischemia of papillary muscles per se
16
Q
What MI location is more commonly associated with ischemic MR?
A
Inferior/inferolateral MI (RCA or LCx) – ~80% of ischemic MR cases
17
Q
Can anterior MI cause ischemic MR?
A
Yes, but only with global remodeling that affects papillary muscle position; requires low EF and large LV volumes
18
Q
What is dynamic MR?
A
MR that worsens with exercise/increased preload due to increased LV volume and tethering
19
Q
What are clinical clues to dynamic MR?
A
Exertional/nocturnal dyspnea or pulmonary edema despite mild MR at rest
MR murmur elicited with leg raise or post-exercise
Stress echo shows worsening MR and PA pressure without ischemia
20
Q
What is an important caution when evaluating ischemic MR intraoperatively?
A
Avoid assessment due to unloading effects of anesthesia which reduce MR severity
21
Q
What is the typical MR jet direction in MVP?
A
Opposite to prolapsed leaflet, often eccentric, hugging LA wall
22
Q
Can ischemic MR have an anteriorly directed jet?
A
No, anterior jet is not typical for ischemic MR
23
Q
What does symmetric leaflet tethering produce?
A
Central MR jet
24
Q
What imaging view should not be used alone to diagnose MVP?
A
Apical 4-chamber view (may give false positives)
25
What is the ratio of leaflet area to annular surface area?
Normally >2:1 — thus, annular dilation alone rarely causes MR
26
What are the structural heart changes leading to atrial functional MR?
LA dilation (with preserved LV function/size), seen in HFpEF or persistent AF.
27
What % of patients with isolated AF or decompensated HFpEF have significant functional MR?
6–7% with isolated AF, up to 18% with decompensated HFpEF.
28
What happens to atrial functional MR after rhythm control in AF?
It improves in >75% of patients.
29
How does atrial functional MR differ from ventricular functional MR in jet direction?
Atrial MR is centrally directed; ventricular MR is typically eccentric.
30
What echocardiographic feature drives atrial functional MR?
Severe annular dilatation, requiring marked LA enlargement.
31
How does hypertension (HTN) influence functional MR?
HTN worsens functional MR by increasing afterload; control improves MR.
32
Name two causes of transient severe MR.
Dynamic MR from transient LV dysfunction (e.g., ischemia)
Dynamic MR from chronic LV dysfunction worsened by preload/afterload increases
33
What echocardiographic finding suggests acute primary MR?
Hypercontractile LV (increased EF)
34
Do loading conditions affect organic MR?
No. Severity is unchanged, though regurgitant volume, LA pressure, and pulmonary edema may vary.
35
How do loading conditions affect functional MR?
Functional MR worsens with increased preload/afterload and improves with reduction.
36
What are TTE criteria for severe MR?
LA jet fills >40%
E wave >1.2 m/s
PISA ≥0.9 cm (at 40 cm/s Nyquist), ERO ≥40 mm²
Flail leaflet (specific)
Pulmonary vein systolic flow reversal
37
Why may acute MR appear mild on TTE?
High LA pressure reduces MR velocity and color jet; MR may be eccentric.
38
What V wave value on RHC suggests severe MR?
V wave >45 mmHg or >2× mean PCWP.
39
What are stress testing/BNP used for in MR?
Determine symptom-limited functional capacity and candidacy for surgery in mild or non-specific symptoms.
40
What is the natural history of severe organic MR (asymptomatic, preserved EF)?
Symptoms or LV dysfunction in 100% by ~5 years.
41
Why is EF often high early in chronic MR?
LV pumps into low-resistance LA; low afterload initially.
42
Why is an EF of 50–60% abnormal in chronic MR?
Indicates intrinsic LV dysfunction; may not recover post-surgery.
43
What are Class I indications for surgery in primary MR?
Symptoms (NYHA II–IV)
EF ≤60% or LVESD ≥40 mm
Severe MR undergoing other cardiac surgery
44
What are Class IIa indications?
New-onset AF
Pulmonary HTN (sPAP >50 at rest or >60 with exercise)
Asymptomatic with EF >60%, LVESD <40 mm if repair likely
45
What is the treatment approach for:
Steady inferior akinesis with MR?
Revascularization + MV repair.
46
What is the treatment approach for:
Off/on inferior akinesis with off/on MR?
Revascularization alone.
47
How is SAM managed postoperatively?
Fluid resuscitation and cessation of inotropes.
48
What is the mechanism behind SAM post MV repair?
Anterior leaflet gets pushed into LVOT by small ring and long leaflet in a small LV, worsened by inotropes.
49
What % of patients with EF <50% have worsening EF post-MV surgery?
Up to 50%.
50
Why does EF drop after MR surgery?
Loss of low-resistance MR leak (↑ afterload),
Pre-existing LV dysfunction,
Disruption of annular–papillary continuity.
51
How is acute leaflet tethering post-MI managed?
Medical therapy + IABP; surgery if no improvement.
52
What is the treatment for papillary muscle rupture post-MI?
Emergent MV surgery + CABG; use IABP and vasodilators pre-op if tolerated.
53
In atrial functional MR with preserved EF, when is surgery considered?
When MR persists despite AF/HFpEF therapy (Class IIb).
54
What class is given to mitral surgery in patients undergoing CABG with severe functional MR?).
Class IIa (repair or replacement
55
What is the EROA cutoff used in ACC surgical recommendations?
40 mm² (based on CTSN trials).
56
What is the EROA cutoff for severe secondary MR per ESC?
30 mm²
57
What anatomical features must be met for MitraClip use in functional MR?
Coaptation depth <11 mm and coaptation length >2 mm.
58
What criteria favor MitraClip candidacy?
LVEDD <7 cm, LVESD <6 cm, ERO >30 mm², and class II–IV symptoms despite therapy.
59
When is MitraClip preferred over surgery?
In isolated functional MR with persistent symptoms despite GDMT and CRT, especially if LV is not severely dilated.
60
When is MV replacement superior to repair in ischemic MR?
In patients with severe ischemic MR and moderate EF (40±10%); replacement gives more durable MR correction.
61
Why might posterior bands fail in annuloplasty?
Both anterior and posterior annuli dilate; posterior-only bands are insufficient.
62
What is the optimal ring for annuloplasty?
Rigid/semi-rigid full ring downsized 2 sizes (24–28 mm).
63
When is annuloplasty most effective in ischemic MR?
When LVEDD <65 mm; provides better remodeling and survival.
64
What complication can occur in 10% of MV repairs post-op?
SAM (Systolic Anterior Motion) with LVOT obstruction and MR.
65
How is anterior MV prolapse repaired?
Chordal transfer or replacement with PTFE chords + annuloplasty ring.
66
When is MV repair preferred over MV replacement?
In isolated posterior leaflet prolapse involving <50% of the leaflet (Class I); MV replacement is contraindicated unless repair fails (Class III).
67
Why is chordal preservation during mitral valve (MV) replacement important?
It maintains the annular–chordal–papillary continuity, preserving LV geometry and preventing ballooning/sagging of the LV.
68
What finding on serial echo suggests early LV dysfunction despite EF >60%?
Rising LVESD ≥37 mm
Declining EF <64% (Class IIb indication for surgery)
69
What BNP value predicts increased long-term mortality under conservative management?
70
What is the benefit of early surgery in asymptomatic severe MR?
Prevents LV remodeling, improves long-term survival, avoids EF decline
71
When is mitral surgery reasonable if EF <30%?
If MR is primary and repair or chordal-preserving replacement is feasible.
72
How does rheumatic fever lead to mitral stenosis?
It causes progressive fibrosis and commissural fusion due to turbulent flow trauma over years.
73
In which population is rheumatic MS more prevalent and at what age?
Women (2:1); 20s–30s in developing countries, later in developed countries.
74
How fast does MS progress symptomatically?
Slowly; 5–10 years from NYHA class II to III–IV.
75
What is the 10-year survival in untreated symptomatic MS (class II–III)?
Around 50%.
76
What is the mean survival in untreated class IV MS?
Less than 1 year.
77
What is Mitral Annular Calcification (MAC) and how does it relate to MS?
MAC is age- and stress-related calcification starting at the posterior annulus; it may mimic MS but usually causes MR or diastolic dysfunction.
78
What congenital abnormality can cause MS?
Parachute mitral valve (single papillary muscle → chordal fusion).
79
Which inflammatory diseases can mimic rheumatic MS?
Lupus, rheumatoid arthritis, carcinoid syndrome.
80
How does the E wave differ in MS vs MR or HF?
MS: Tall E wave with slow downslope; MR/HF: Tall E wave with steep downslope.
81
Why is heart rate essential when evaluating MS by echo?
High HR shortens diastole and exaggerates gradient; low HR may mask severity.
82
What pressures are used to assess MS invasively?
Simultaneous LA (or PCWP) and LV pressures.
83
What happens to LA–LV pressures in true MS throughout diastole?
Gradient persists — pressures do not equalize (no diastasis).
84
How long should anticoagulation be continued after AF ablation or LAA closure?
At least 3 months.
85
What procedure helps reduce stroke risk during surgery?
LA appendage excision.
86
When is a maze procedure for AF indicated?
During cardiac surgery in patients with AF (Class IIa).
87
What is the role of pulmonary vasodilators in MS?
Temporary use postoperatively for severe PA hypertension
88
Is β-blocker therapy acutely helpful in other types of heart failure?
No—only in MS and HOCM.
89
What therapy is useful for decompensated MS with pulmonary edema?
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Acute β-blocker therapy.
90
What happens to PVR and PA pressures after correcting severe MS?
They usually decline significantly, often normalizing over time.
91
What findings suggest a pliable valve suitable for PMBV?
Loud S1 and opening snap; age <60–70 years.
92
When is surgical commissurotomy preferred over PMBV?
When there’s LA thrombus, need for CABG, or unavailable percutaneous therapy.
93
What percent of patients need valve replacement within 5 years post-PMBV?
~25%.
94
Can patients with Wilkins 9–11 still benefit from PMBV?
Yes, especially if MR is mild and surgical risk is high.
95
What Wilkins score is ideal for PMBV?
≤ 8 with no commissural calcium.
96
What defines a successful PMBV?
MVA ≥ 1.5 cm² and ≤ moderate MR (≤2+).
97
What is a contraindication for PMBV?
LA thrombus not resolved after anticoagulation.
98
When is PMBV reasonable in asymptomatic patients?
If PA pressure >50 mmHg at rest, >60 mmHg with exercise, planned pregnancy, or AF (Class IIa–IIb).
99
When is PMBV indicated (Class I)?
Severe MS (MVA ≤1.5 cm²) with NYHA Class II–IV symptoms.
100
101
What rhythm control method is discouraged in chronic MS with AF?
Repeated DC cardioversion due to high recurrence and stroke risk.
102
What is the stroke risk in MS with AF?
10–15% per year.
103
Is medical therapy a standalone option for MS?
Only in select cases, e.g., mild symptoms, poor surgical candidates, or elderly sedentary patients.
104
What heart rate is targeted with β-blockers in MS?
~60 bpm.
105
Why are β-blockers helpful in MS?
They slow heart rate, prolonging diastole for better LA emptying.
106
What medications improve symptoms in MS?
Diuretics and β-blockers.
107
What happens to LV diastolic pressure during stress in MS?
It usually remains unchanged.
108
What findings on stress test suggest significant MS?
Mean transmitral gradient >15 mmHg, systolic PA pressure >60 mmHg, or PCWP >25 mmHg.
109
Why might resting transmitral gradient underestimate MS severity?
Because gradient increases with higher cardiac output or tachycardia.
110
Does TEE help assess the Wilkins score?
No, TTE is better for evaluating subvalvular apparatus.
111
What is TEE primarily used for before PMBV?
To rule out left atrial appendage thrombus and assess MR severity.
112
What Wilkins score indicates suitability for PMBV?
A total score ≤ 8.
113
What are the four components of the Wilkins score?
Valve thickness, valve mobility, valve calcification, chordal thickening/calcification
114
When is intervention indicated in Severe MS with:
Symptoms
Resting PA systolic pressure >50 mmHg
Exercise PA systolic pressure >60 mmHg
115
What does preserved diastasis at low HR (≤60 bpm) imply in MS?
Milder MS — likely not severe.
116
What does a stress-induced PCWP–LV gradient >15 mmHg suggest?
Hemodynamically significant MS.
117
Why can transmitral gradient be misleading?
It is flow-dependent; high-output states or tachycardia can falsely elevate it.
118
What is a better indicator of MS severity — MVA or gradient?
MVA.
119
What are MVA and gradient thresholds for MS severity?
Moderate: MVA >1.5 cm², gradient <5 mmHg
Severe: MVA 1–1.5 cm², gradient 5–10 mmHg
Very Severe: MVA ≤1 cm², gradient >10 mmHg
120
What is the normal mitral valve area (MVA)?
4–6 cm².
121
When is trans-septal LA pressure measurement especially required?
Pulmonary hypertension
Large V wave
Discordant echo/clinical findings
122
What happens to LA–LV pressures in MR or diastolic HF?
Pressures equalize at mid-diastole (diastasis is present).
123
What is the most common cause of aortic stenosis (AS)?
Age-related calcific degeneration.
124
What precedes AS in many elderly patients and is associated with cardiovascular death and CAD?
Aortic valve sclerosis (non-stenotic thickening), found in ~20% of those >65 years.
125
What percentage of aortic sclerosis patients progress to AS in 5 years?
About 10%.
126
What is the most common congenital heart disease?
Bicuspid aortic valve (~1.3% prevalence).
127
Which congenital syndrome is commonly associated with BAV?
Turner syndrome (~10% of women with Turner).
128
Which BAV fusion pattern is most common?
Right and left cusps (80%).
129
What is the risk of developing severe AS in bicuspid valve patients over a lifetime?
~75%.
130
What percentage of BAV patients have aortic dilatation >3.7 cm by age 30?
50–60%.
131
What imaging is recommended at least once for BAV patients?
CT to assess the entire aorta.
132
What is the recommended echo surveillance for BAV with sinus aortic diameter >4 cm?
Annual TTE.
133
How common is rheumatic aortic stenosis today?
Rare.
134
What is the most important diagnostic feature of severe AS on echo?
Aortic valve velocity (used to derive pressure gradient).
135
What is the formula for transaortic pressure gradient?
4 × (aortic velocity)^2.
136
What are the recommended views to assess aortic velocity?
Apical 3- and 5-chamber, suprasternal, and right parasternal.
137
What is the continuity equation for AVA?
AVA = LVOT area × (LVOT velocity / aortic valve velocity).
138
Mild AS
<20 mmHg
2–2.9 m/s
>1.5 cm²
139
Moderate AS
20–40 mmHg
3–3.9 m/s
1–1.5 cm²
140
Severe AS
≥40 mmHg (≥60 very severe)
≥4 m/s (≥5 very severe)
≤1.0 cm² (or indexed ≤0.6 cm²/m²; more specific ≤0.8 cm²)
141
What gradient corresponds to AVA of 1.0 cm² with normal CO (Hakki’s formula)?
~30 mmHg.
142
Why might a patient with AVA ≤1 cm² have <40 mmHg gradient?
Low-flow state or small body habitus leading to low CO.
143
What is more specific for severe AS: AVA ≤1.0 cm² or mean gradient ≥40 mmHg?
Mean gradient ≥40 mmHg.
144
What does AVA-gradient discordance mean in AS assessment?
When AVA is ≤1.0 cm² but gradient is <40 mmHg; can be true severe AS (~50%) or due to AVA underestimation.
145
What is the definition of low-gradient AS with reduced EF?
AVA ≤ 1 cm², EF < 50%, and mean gradient < 40 mmHg.
146
What equation explains the flow dependence of the AVA and gradient in AS?
Gorlin equation: AVA ~ CO / √mean gradient.
147
What AVA and cardiac output may yield a mean gradient of only 15 mmHg in severe AS?
AVA of 1 cm² with CO of 3.5 L/min.
148
What is the starting dose of dobutamine for AS assessment?
5 mcg/kg/min.
149
What is considered a significant increase in stroke volume during dobutamine testing?
≥ 20% increase.
150
What indicates truly severe AS during dobutamine stress testing?
Gradient increases to ≥ 40 mmHg, AVA remains ≤ 1 cm².
151
What do you suspect if stroke volume increases ≥ 20%, gradient stays < 40 mmHg, and AVA increases > 1 cm²?
Pseudo-severe AS.
152
What does no significant increase in stroke volume during dobutamine indicate?
Poor contractile or flow reserve.
153
List causes of low-gradient AS in low EF.
Truly severe AS with low flow
Pseudo-severe AS due to poor valve excursion
154
List causes of low-gradient AS in normal EF.
Hypertension/Concentric LV hypertrophy/Hypovolemia/Mitral valve disease/Bradycardia/
Transthyretin amyloidosis
Echo underestimation
Pressure recovery
155
What is valvuloarterial impedance and its formula?
(SBP + mean gradient) / stroke volume index; reflects total LV afterload.
156
What is the diagnostic role of CT calcium scoring in AS?
Confirms truly severe AS: >2000 AU in men, >1200 AU in women.
157
What is pressure recovery and when is it most significant?
Re-increase in pressure distal to valve due to flow dynamics; significant in small aorta (<3 cm diameter).
158
What is the Energy Loss Index (ELI) used for?
Adjusts AVA in presence of pressure recovery.
159
What are three possible causes of AVA ≤ 1 cm² with normal EF and gradient < 40 mmHg?
Echo underestimation
Truly severe AS with low flow
True severe AS with normal flow but low gradient due to guideline cut-off mismatch
160
What is considered low stroke volume index in AS?
< 35 mL/m².
161
Why might dobutamine not be helpful in low-gradient AS with normal EF?
Flow limitation is due to low preload or high afterload, not contractility.
162
What is the first step in evaluating low-gradient AS with AVA ≤1 cm² and normal EF?
If AVA ≤ 0.8 cm² and gradient 30–40 mmHg → likely truly severe AS.
163
What causes dyspnea in AS?
Elevated LVEDP and impaired CO increase with exercise.
164
What causes syncope in AS?
Fixed CO and exercise-induced vasodilation → systemic pressure drop.
165
What are two mechanisms of angina in AS?
CAD (50%) and increased demand/reduced supply (LVH, ↑LVEDP
166
What is Heyde's syndrome and its relevance to AS?
GI bleeding due to von Willebrand factor degradation; improves after AVR.
167
What are causes of AVA >1 cm² with mean gradient >40 mmHg?
• Severe AS with large body size (indexed AVA <0.6 cm²/m²)
•High-output states (anemia, AI, sepsis)
•AVA overestimation due to LVOT measurement errors
168
What is the expected progression of severe asymptomatic AS?
~50% become symptomatic within 2 years, especially if aortic velocity ≥5 m/s or increases >0.3 m/s/year.
169
What is the annual sudden cardiac death rate in truly asymptomatic severe AS?
Less than 1% per year.
170
How long is the survival once AS becomes symptomatic?
2–3 years, shorter with HF (1–2 years).
171
What is the typical yearly progression rate of moderate/severe AS in terms of AVA, velocity, and gradient?
AVA ↓ by ~0.12 cm²/year, velocity ↑ by 0.3 m/s/year, gradient ↑ by 7 mmHg/year.
172
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What causes fixed subvalvular AS?
A fibrous membrane below the aortic valve; often associated with VSD and causes progressive AI.
174
What is the treatment indication for subvalvular AS?
Surgery if mean gradient >30 mmHg, even if asymptomatic.
175
What diagnostic clues help differentiate sub-/supravalvular AS from valvular AS?
Normal valve anatomy, high-velocity jet on Doppler, turbulence above/below valve, loud A2, no systolic click, and specific murmur radiation.
176
Why must antihypertensives be used cautiously in AS?
Vasodilators can cause hypotension if cardiac output cannot increase due to severe AS.
177
Why is HTN treatment still beneficial in AS?
Reduces total afterload, improving output and symptoms in low-flow/low-gradient states.
178
What are the class I indications for AVR?
a. Severe symptomatic AS (angina, syncope, dyspnea)
b. Severe asymptomatic AS with EF <50%
c. Low-gradient severe AS with low EF (confirmed by dobutamine)
d. Symptomatic low-gradient severe AS with normal EF (after confirming severity)
179
When is AVR indicated in low-gradient AS with no flow reserve?
If CT calcium score confirms severity; TAVR is preferred due to high surgical risk.
180
What are class IIa AVR indications in asymptomatic patients?
Velocity ≥5 m/s
Velocity progression ≥0.3 m/s/year
BNP >300 pg/ml or 3× normal
Abnormal exercise test (drop in SBP or <7 METs)
181
When is AVR performed in patients undergoing other cardiac surgeries?
Always for severe AS (Class I)
For moderate AS to avoid redo surgery (Class IIb)
182
What is the Ross procedure?
Autograft of pulmonary valve to aortic position; pulmonary homograft replaces native PA valve.
183
What are contraindications to the Ross procedure?
Aortic insufficiency with dilated ascending aorta (risk of neoaortic root dilatation).
184
What vena contracta width suggests severe AR?
>6 mm
185
What pressure half-time (PHT) suggests severe AR?
<200 ms
186
What values of EROA and regurgitant volume indicate severe AR?
EROA ≥ 0.3 cm²
RV ≥ 60 mL
RF ≥ 50%
187
What is the significance of holodiastolic flow reversal in the descending aorta on Doppler?
It is a hallmark of severe AR.
188
Which imaging modality is used to confirm severity if echo is unclear?
Cardiac MRI (quantifies regurgitant fraction and LV volumes)
189
What are the main surgical options for AR?
Aortic valve replacement (AVR)
Valve-sparing aortic root replacement (David procedure)
Bentall procedure (valve + root replacement)
190
When is the Bentall procedure preferred?
In cases of connective tissue disease
Bicuspid aortic valve with root dilation
Poor leaflet quality
191
What is the expected LV recovery after AVR in AR?
LV size improves quickly
EF may take weeks–months to normalize
Longstanding AR → incomplete recovery possible
192
What pre-op factor predicts poor post-op recovery in AR?
LV end-systolic diameter > 50 mm
EF < 50% at baseline
Symptomatic status
193
What is the typical follow-up schedule post-AVR?
-Echo at 6–12 weeks post-op
-Yearly echo if valve function stable
-Closer follow-up if prosthetic dysfunction or LV dysfunction
194
What is the target blood pressure in patients with chronic AR?
SBP < 140 mmHg
MAP ~90–100 mmHg
Avoid bradycardia
195
Which antihypertensive medications are preferred in chronic AR?
ACE inhibitors/ARBs
Nifedipine or other vasodilators
Avoid beta-blockers unless otherwise indicated
196
Why should bradycardia be avoided in chronic AR?
Prolonged diastole worsens regurgitation volume.
197
How is acute severe AR managed acutely before surgery?
•Afterload reduction with IV vasodilators (nitroprusside)
•Inotropes if needed
•Avoid beta-blockers
•Urgent surgery
198
Why does chronic AR cause widened pulse pressure?
Large stroke volume → high SBP; regurgitation → low DBP.
199
What murmur is pathognomonic for severe chronic AR?
Diastolic decrescendo murmur along LSB, best heard with patient leaning forward.
200
What is an Austin Flint murmur?
A low-pitched mid-diastolic rumble at the apex, due to regurgitant jet striking the anterior mitral leaflet.
201
What are three causes of acute aortic insufficiency (AI)?
Endocarditis, aortic dissection, and chest trauma.
202
What is the most common cause of chronic severe AI?
Dilatation of the ascending aorta.
203
What BP pattern is typical in acute AI?
Low SBP and DBP (e.g., 90/40 mmHg) with only mildly widened pulse pressure.
204
What is the characteristic blood pressure in chronic compensated AI?
Wide pulse pressure (e.g., 160/60 mmHg
205
What peripheral pulse finding may be seen in chronic AI?
Pulsus bisferiens
206
What happens in chronic decompensated AI?
EF declines, LV compliance worsens, LVEDP rises.
207
Why is AI better tolerated during exercise than MR?
Exercise reduces diastolic time and regurgitant volume in AI.
208
What angiographic grade suggests severe AI?
Grade 3+ (LV opacification equal to aorta) or 4+ (greater than aorta).
209
What is the annual mortality in asymptomatic severe AI with normal LV function?
A: <0.2%.
210
What is the mean survival in symptomatic AI without surgery?
~3 years.
211
What symptom often appears early in AI and may go unnoticed?
Class II dyspnea.
212
What is the mechanism of angina in AI?
Low aortic diastolic pressure and high LVEDP reduce coronary perfusion.
213
When is angina more likely to occur in AI?
At night and during bradycardia.
214
Which medications may be useful in systolic hypertension with AI?
ACE inhibitors and dihydropyridine calcium channel blockers.
215
What is the EF threshold for surgery in asymptomatic severe AI?
A: ≤55%.
216
What LVESD threshold supports surgery for asymptomatic AI?
>50 mm or >25 mm/m².
217
What is the LVEDD threshold suggesting possible need for surgery?
>65 mm.
218
Is an EF <25% a contraindication to surgery in AI?
No, but it suggests possible irreversible damage.
219
What is the earliest sign of LV recovery after AVR in AI?
Decrease in LV diastolic size.
220
At what aortic diameter is replacement indicated in most patients?
≥5.5 cm.
221
What is the surgical cutoff for patients with Marfan or bicuspid valve + family history?
≥5.0 cm.
222
When is ascending aorta replaced even at 4.5 cm?
In patients with severe AI or AS undergoing AVR.
223
Is medical therapy effective in symptomatic severe valvular disease or valvular disease with secondary LV dysfunction?
No, surgery is the only effective therapy, except in severe MR with severe LV dysfunction and MS with very mild symptoms in debilitated patients.
224
What are the indications for TEE in mitral regurgitation (MR)?
To assess MR severity, identify anatomic cause, determine repair feasibility, and guide repair intraoperatively.
225
Is TEE superior to TTE in assessing severity of AS or AI?
No; TEE is inferior for valve gradient measurement but better for anatomical assessment and endocarditis diagnosis.
226
What can TEE detect in mitral stenosis (MS) or atrial fibrillation (AF)?
Left atrial appendage thrombus, which would delay percutaneous valvuloplasty.
227
When is intraoperative TEE indicated?
In all valvular surgeries, especially mitral valve repair and endocarditis with abscess.
228
Why is preoperative TEE not reliable for assessing valvular severity?
General anesthesia alters loading conditions, often underestimating severity of functional MR.
229
When is exercise testing indicated in valvular disease?
For patients with severe valve disease and equivocal symptoms, to assess dyspnea and functional capacity
230
What is concerning in exercise testing for valvular disease?
Functional capacity 1–2 METs below predicted.
231
What are other uses of exercise testing in valvular disorders?
To evaluate exertional PA pressures (in MS), dynamic ischemic MR, and BP response in asymptomatic severe AS.
232
When is coronary angiography indicated before valve surgery?
In men >40, postmenopausal women, those with angina, or >1 CAD risk factor.
233
What dictates combined CABG and valve surgery?
Presence of proximal CAD.
234
When can coronary angiography be omitted before surgery?
In emergent cases: acute regurgitation, endocarditis, or aortic dissection.
235
Is endocarditis prophylaxis routinely recommended for native valve disease?
No, only in high-risk patients.
236
Which patients require endocarditis -prophylaxis before dental or respiratory procedures?
-Prosthetic valve or valve repair with prosthetic material
-History of infective endocarditis
-Unrepaired cyanotic congenital heart disease or partially repaired with defects
-Within 6 months of complete congenital repair
-Transplant valvulopathy
237
Is endocarditis prophylaxis needed for GI or GU procedures?
No
238
What is the echo follow-up for severe valvular disease without symptoms?
Every 6 months; every 3–6 months if LV starts dilating.
239
What is the echo follow-up for moderate valvular disease without symptoms?
Every 1–2 years; every 3–5 years for moderate MS.
240
What is the echo follow-up for mild valvular disease?
Every 3–5 years.
241
How are predicted METs calculated for exercise capacity?
Men: 18 − (0.15 × age)
Women: 14.7 − (0.13 × age)
242
What is the mortality for CABG?
A: ~1–5%
243
What is the mortality for MVR + CABG?.
~11%, mostly due to underlying CAD
244
Do AI, MR, and AS cause heart failure before reduced LVEF?
Yes; LV dysfunction is present before gross drop in EF.
245
How does MS lead to heart failure?
From mitral obstruction; LV function is normal unless there’s coexisting LV disease.
246
What is the most common cause of tricuspid regurgitation (TR)?
Secondary (functional) TR due to RV pressure or volume overload (≈80% of all TR).
247
What PA pressure and PVR suggest TR is secondary to pulmonary hypertension?
PA pressure >50 mmHg or PVR >3 Wood units.
248
Name primary cardiac conditions that cause secondary TR through pulmonary hypertension.
LV dysfunction and left-sided valvular disease (e.g., MS, MR).
249
What structural changes in the RV and tricuspid valve annulus contribute to functional TR?
RV and annular dilatation, leaflet tethering; annular dilatation is most significant.
250
What happens to the tricuspid annulus shape in functional TR?
Becomes circular and planar from its normal oval, saddle shape.
251
What does PA pressure <40–50 mmHg with normal PVR suggest in a patient with TR?
Either primary TR or TR secondary to pure RV volume overload (e.g., ASD, ARVD).
252
What RA pressure findings are typical in severe functional TR?
Elevated RA pressure with large V waves and a dilated IVC.
253
Can RA pressure be normal in severe primary TR? Why?
Yes, due to high RA compliance.
254
Why is TR velocity unreliable in torrential TR?
Because RV and RA become a common chamber, with minimal pressure gradient.
255
Name common causes of primary TR.
Endocarditis, rheumatic fever, blunt trauma (flail leaflet), carcinoid syndrome, Ebstein anomaly, tricuspid prolapse.
256
In rheumatic disease, what % of MS cases involve the tricuspid valve?
About one-third.
257
What are two main causes of isolated TR?
Atrial fibrillation in the elderly and pacemaker/ICD leads
258
How does AF cause isolated TR?
AF causes atrial and annular dilatation, leading to TR.
259
What % of patients develop moderate TR after pacemaker/ICD placement?
Up to 38%.
260
What % develop severe TR by 4 years post-device implantation?
8%.
261
Is device lead the most likely cause of TR in a patient with other causes of functional TR?
No, the lead is unlikely the primary driver if other causes exist.
262
Can severe primary/isolated TR be tolerated long-term?
Yes, if RV is not dilated and PA pressure is normal.
263
What leads to worsening TR over time?
RV dilatation → annular dilatation → more TR (vicious cycle).
264
What TTE annular diameter predicts progressive TR?
>35–40 mm or >21 mm/m².
265
What is the mainstay of medical therapy for TR?
Diuretics, especially for functional or AF-related isolated TR.
266
Are diuretics effective in primary TR?
Less so—they do not prevent RV dysfunction.
267
What are class IIa indications for tricuspid surgery?
Severe, symptomatic primary or isolated TR; annular dilatation.
268
What is a class IIb indication for surgery?
Severe TR with progressive RV dilatation/dysfunction, even if asymptomatic.
269
What is a class I indication for concomitant tricuspid surgery?
Severe secondary TR during mitral valve surgery.
270
When is tricuspid annuloplasty preferred over replacement?
In most surgical cases, unless repair is not feasible.
271
What size of annular dilatation warrants repair during mitral surgery (intraop on arrested heart)?
>70 mm.
272
What are the two types of tricuspid annuloplasty?
Ring annuloplasty (preferred) and suture (De Vega) annuloplasty.
273
Why are bioprosthetic valves preferred over mechanical valves in the tricuspid position?
Lower thrombotic risk and longer durability in low-pressure systems.
274
Why is early surgery important in severe TR?
To prevent irreversible RV dilatation, hepatic and renal failure.
275
What complications of right HF due to TR significantly increase mortality?
Liver failure, cirrhosis, and renal failure.
276
What paradox may occur after surgical correction of severe TR?
Acute RV failure if RV was dependent on TR as a pop-off mechanism.
277
What are causes of tricuspid stenosis?
Rheumatic disease, carcinoid syndrome, cardiac tumors.
278
Why does carcinoid syndrome typically affect right-sided valves?
Serotonin is inactivated in the lungs, sparing left-sided valves unless there's a shunt or lung metastases.
279
What is the valve morphology in carcinoid heart disease?
Thickened, immobile tricuspid leaflets with combined stenosis and regurgitation.
280
What is the most common cause of pulmonic stenosis (PS)?.
Congenital
281
What valve morphology is typical in congenital PS?
Domed valve with commissural fusion and small central orifice (acommissural morphology).
282
How is the domed morphology of the pulmonic valve best recognized?
On angiography.
283
What syndromic condition is associated with dysplastic PS?
Noonan’s syndrome.
284
What are some non-congenital causes of PS?
Rheumatic disease and carcinoid syndrome
285
What is the characteristic RA pressure finding in PS?
Large A wave and normal V wave.
286
Does PS typically lead to RV hypertrophy or dilatation?
RV hypertrophy without dilatation.
287
What should be suspected if RV failure occurs in PS?
A coexisting volume lesion (e.g., ASD, TR, PR).
288
What does chest X-ray show in PS?
Dilated main and left pulmonary arteries (post-stenotic dilatation); normal lung perfusion.
289
How is severe PS defined by Doppler criteria?
Peak velocity >4 m/s or mean gradient >35 mmHg.
290
What is the usual outcome of percutaneous balloon valvotomy for severe PS?
Excellent long-term results with rare recurrence (>20 years).
291
What percentage of patients may develop moderate-to-severe PR after valvotomy?
Up to 20%.
292
Why does dysplastic PS not respond to balloon valvotomy?
Because the pathology is not commissural fusion.
293
What kind of sports can asymptomatic athletes with severe PS participate in?
Low-intensity competitive sports.
294
When can athletes resume full sports after successful valvuloplasty?
2–4 weeks if only mild residual PS and normal ventricular function.
295
What is “suicide RV”?
Dynamic RVOT obstruction after valvuloplasty due to hypertrophy; treated with fluids, β-blockers, and calcium channel blockers.
296
How to differentiate residual RVOT gradient from persistent PS?
Slow PA-to-RV pressure pullback confirms RVOT gradient.
297
What is the most common cause of PR?
Pulmonary hypertension
298
What cardiac condition is classically associated with PR secondary to pulmonary hypertension?
Mitral stenosis (MS).
299
What murmur is associated with PR from pulmonary hypertension?
Graham Steell’s murmur — diastolic, heard at L 2nd ICS, increases with inspiration.
300
When is valve replacement indicated in primary PR?
Class I: Symptomatic RV failure; Class IIa: Asymptomatic but with progressive RV dilation or dysfunction.
301
How long can the RV tolerate severe PR?
Often for decades, unless marked RV enlargement/dysfunction develops.
302
What usually determines the clinical picture in mixed stenosis/regurgitation of the same valve?
The dominant lesion.
303
Why is pulmonary edema more likely in mixed lesions?
The nondominant lesion exacerbates the dominant lesion’s hemodynamic effects.
304
How does regurgitation affect the transvalvular gradient?
Increases it, potentially overestimating stenosis severity by gradient.
305
What finding suggests mixed mitral disease is symptomatic?
PCWP and PA pressures rise disproportionately to LVEDP with exercise.
306
What are common causes of multiple valve disease?
Rheumatic disease, radiation, endocarditis, myxomatous degeneration, connective tissue disorders.
307
What is the effect of AS on MR in combined disease?
Increases MR severity (from moderate to severe).
308
In MS + AI, how are hemodynamics affected?
LA pressure must rise to overcome elevated LVEDP; AI effects are reduced.
309
What is the worst-tolerated valvular combination?
Combined MR–AI (double volume load).
310
How does AVR affect functional MR in AS + MR?
Often improves functional MR; mitral repair needed if organic or severe.
311
What is the most common valvular lesion in radiation heart disease?
AI or combined AS + AI.
312
What unique lesion may result from mitroaortic curtain calcification?
Subvalvular AS (due to calcium protruding into LVOT).
313
What coronary arteries are most affected by radiation?
Left main, ostial RCA, and mid-LAD.
314
What are common conduction issues post-radiation?
RBBB, infranodal block, sick sinus syndrome (up to 75%).
315
Is TEE superior to TTE in assessing AS/AI severity?
No—TTE is preferred for valve gradients.
316
Are S3 and S4 heard in severe MS?
No—LV filling is restricted.
317
Can S4 be heard in atrial fibrillation?
A: No.
318
When is S4 heard?
Diastolic dysfunction with elevated LVEDP.
319
What does S3 indicate?
Elevated LA pressure and decompensated HF.
320
What is a fixed split S2 associated with?
Atrial septal defect (ASD).
321
What is paradoxical splitting of S2?
Split worsens with expiration—seen in LBBB, AS, HOCM.
322
What does a murmur that increases after a pause suggest?
HOCM or AS.
323
What increases regurgitant and VSD murmurs?
Handgrip and squatting (↑ afterload).
324
What increases the murmur of HOCM and MVP?
Standing, Valsalva (decrease in preload/afterload)
325
Which murmurs increase with inspiration?
Right-sided murmurs (except PS click).
326
What are features of benign murmurs?
Mid-systolic, grade ≤2/6, no radiation or change with Valsalva, improves with sitting/standing.
327
What murmur is heard in pulmonary regurgitation (PR)?
Diastolic murmur at LUSB, increases with inspiration.
328
What murmur is heard in coarctation of the aorta?
Mid-systolic murmur at LUSB radiating to the back.
329
What murmur is heard in VSD?
Harsh holosystolic murmur at LLSB.
330
What materials are bioprosthetic valves made from?
Porcine leaflets or bovine pericardial tissue.
331
What is the approximate degeneration rate of bioprosthetic valves at 10–15 years?
1/3 of bioprostheses degenerate.
332
What factors accelerate bioprosthesis degeneration?
Younger age (<65), mitral position, high cardiac output, atherosclerosis.
333
Which position is most prone to bioprosthesis degeneration?
Mitral valve.
334
How does statin therapy affect bioprosthesis durability?
May slow degeneration (data are conflicting).
335
Which valve type is preferred in aortic valve endocarditis?
Homograft.
336
What valve type is preferred for mitral valve replacement in patients ≥65?
Bioprosthesis.
337
What valve type is preferred for aortic valve replacement in patients <50?
Mechanical prosthesis.
338
What are the options for aortic valve replacement in patients aged 50–65?
Either mechanical or bioprosthesis (Class IIa).
339
What is the INR target for an aortic mechanical valve without high-risk factors?
INR 2–3.
340
What are thromboembolic high-risk factors in valve patients?
Prior embolic event, AF, LV dysfunction, thrombophilia.
341
INR target for a mitral mechanical valve or high-risk aortic mechanical valve?
INR 2.5–3.5.
342
Is aspirin recommended routinely with mechanical valves?
No, not by ACC/ESC; Class IIb with atherosclerosis and low bleeding risk.
343
Antithrombotic regimen for bioprosthesis without risk factors?
Aspirin 81 mg indefinitely; warfarin for 3–6 months post-op (Class IIa).
344
Antithrombotic regimen for bioprosthesis with AF?
Warfarin (INR 2–3); NOAC acceptable beyond 3 months (Class I).
345
What do you do if stroke occurs in a patient with a mechanical valve despite anticoagulation?
Increase INR target and consider adding aspirin.
346
What is the INR adjustment after stroke on warfarin with INR 2–3?
Increase to 2.5–3.5 or 3.5–4.5.
347
How do you manage bioprosthetic valve thrombosis?
Warfarin or NOAC; evaluate with TEE or CT.
348
What is the treatment for right-sided mechanical valve thrombosis?
Thrombolysis, even if large clot or severe symptoms.
349
When should warfarin be stopped before a planned procedure?
5 days before.
350
When to resume warfarin after a procedure?
On the day of the procedure.
351
Is bridging needed in bileaflet AVR without high-risk features?
No.
352
What’s the best valve choice in dialysis patients?
Bioprosthesis, unless very young (<35 years).
353
When is baseline post-op echo performed?
At 6 weeks.
354
What carotid pulse abnormality is seen in HOCM?
Brisk, double-peaked pulse (spike-and-dome).
355
What maneuver increases TR murmur intensity?
Inspiration (Carvallo’s sign).
356
What sign is specific for TR?
A: Ventricularized JVP mimicking carotid pulse.
357
What does murmur duration in AI indicate?
Longer murmur = more severe AI.
358
What is a bisferiens pulse and when is it seen?
Double-peaked pulse; seen in severe AI, HOCM, high-output states.
359
What pulse finding is sensitive for chronic severe AI?
Wide pulse pressure.
360
What carotid pulse abnormality is seen in severe AS?
Pulsus parvus et tardus (weak and delayed).
361
What finding excludes severe AS?
Normal A2 at RUSB or apex
362
What murmur mimics MS murmur due to functional mitral obstruction?
Austin-Flint murmur (from severe AI).
363
What is a “seagull cry” murmur associated with?
Ruptured chordae in MR.
364
What does an end-systolic MR murmur suggest?
Mild MR; not consistent with severe MR.
365
Where does the MR murmur radiate in anterior vs. posterior leaflet issues?
Anterior leaflet: to the back/axilla; Posterior leaflet: to the base/aorta.
366
Common pathogen in late prosthetic valve endocarditis?
Streptococcus (viridans, bovis).
367
Most common pathogens in early prosthetic valve endocarditis?
Staph (coag+ and coag-), then enterococci and gram-negatives.
368
Treatment for severe paraprosthetic leak with hemolysis?
Percutaneous plug or surgical repair
369
What is a severe paraprosthetic leak associated with?
HF or hemolysis requiring transfusions
