3. TEE
The physician evaluating a prosthetic device with TEE
should be aware of the range of abnormalities that are
possible in these devices and should match those
possibilities to the patient's presentation. Complications
of prosthetic valves detected by TEE include:
Paravalvular leak
Endocarditis
Extrinsic interference of function (pannus, thrombus,
vegetation) resulting in obstruction or regurgitation
Ball variance
Strut fracture and component escape
Leaflet tears of bioprosthesis
Leaflet calcification/stenosis of bioprosthesis
Echocardiographic evaluation of prosthetic heart valves - Elyse Foster – Uptodate 2012
5. THEO DÕI
- An initial TTE study is recommended in patients after
prosthetic valve implantation for evaluation of valve
hemodynamics (IB)
- Annual TTE is reasonable in patients with a bioprosthetic
valve after the first 10 years, even in the absence of a change
in clinical status. (Class IIa, Level of Evidence: C)
The incidence of bioprosthetic valve dysfunction is low within 10
years of valve implantation but increases markedly after that
point. Earlier evaluation may also be prudent in selected patients
at increased risk of early bioprosthetic valve degeneration.
In patients with mechanical valve prostheses, routine annual
echocardiographic evaluation is not needed if the postoperative
baseline study is normal in the absence of signs or symptoms of
valve dysfunction.
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p111
6. An initial TTE study is recommended in patients after
prosthetic valve implantation for evaluation of valve
hemodynamics (522-525). (Class I, Level of Evidence: B)
An echocardiographic examination performed 6 weeks to 3
months after valve implantation is an essential component of
the first postoperative visit.
Doppler TTE provides accurate measurements of
transvalvular velocities and pressure gradients as well as
detection and quantitation of valvular and paravalvular
regurgitation. Normal Doppler transvalvular velocities and
gradients vary among different types and sizes of prosthetic
valves but are also affected by patient-specific factors,
including body size and cardiac output. In addition to
imaging and Doppler flow data for the prosthetic valve, TTE
provides assessment of other disease(s).
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p111
7. Repeat TTE is recommended in patients with
prosthetic heart valves if there is a change in
clinical symptoms or signs suggesting valve
dysfunction. (Class I, Level of Evidence: C)
Bioprosthetic valves are prone to tissue degeneration
or pannus formation with development of valve
regurgitation and/or stenosis. Bioprosthetic valve
dysfunction typically presents with the insidious
onset of exertional dyspnea or with a louder systolic
murmur (MR or AS) or a new diastolic murmur (AR
or MS) on physical examination. More abrupt and
severe symptoms may occur with bioprosthetic valve
endocarditis or with degenerative rupture of a valve
cusp. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p111
8. Mechanical valve dysfunction present with
symptoms of HF, systemic thromboembolism,
hemolysis, or a new murmur on auscultation.
Signs or symptoms of mechanical valve
dysfunction are often acute or subacute because
of more abrupt impairment of leaflet occluder
opening or closing by thrombus or pannus.
Acute or chronic paravalvular regurgitation may
also be seen due to IE or suture dehiscence.
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p111
9. TEE is recommended when clinical symptoms or
signs suggest prosthetic valve dysfunction. (Class
I, Level of Evidence: C)
TEE provides superior images of the left atrial side of
the mitral prosthesis and is accurate for diagnosis of
prosthetic mitral valve dysfunction.
However, both TTE and TEE are needed for complete
evaluation in a patient with suspected prosthetic valve
dysfunction, particularly for those with prosthetic
aortic valves in whom the posterior aspect of the valve
is shadowed on the TTE approach and the anterior
aspect of the valve is shadowed on the TEE approach.
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p111
10. `
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p124
11.
12.
13. 1. Continuation of VKA anticoagulation with a therapeutic
INR is recommended in patients with mechanical heart
valves undergoing minor procedures (such as dental
extractions or cataract removal) where bleeding is easily
controlled. (Class I, Level of Evidence: C)
2. Temporary interruption of VKA anticoagulation,
without bridging agents while the INR is subtherapeutic,
is recommended in patients with a bileaflet mechanical
AVR and no other risk factors for thrombosis who are
undergoing invasive or surgical procedures. (Level of
Evidence: C)
VKA is stopped 2 to 4 days before the procedure (so the
INR falls to <1.5 for major surgical procedures) and
restarted as soon as bleeding risk allows, typically 12 to
24 hours after surgery. 2014 AHA/ACC Guideline for the Management of Patients With
Valvular Heart Disease, Prosthetic valves, p122 - 123
14. Bridging anticoagulation with either intravenous UFH or
subcutaneous LMWH is recommended during the time
interval when the INR is subtherapeutic preoperatively in
patients who are undergoing invasive or surgical procedures
with a :
1) mechanical AVR and any thromboembolic risk factor
2) older-generation mechanical AVR, or
3) mechanical MVR.
(class I, Level of Evidence: C)
Administration of fresh frozen plasma or prothrombin
complex concentrate is reasonable in patients with
mechanical valves receiving VKA therapy who require
emergency noncardiac surgery or invasive procedures.
(IIa, Level of evidence C)
15. - Excessive anticoagulation (INR ≥5)
greatly increases the risk of hemorrhage.
- High-dose vitamin K should not be
given routinely, because this may create a
hypercoagulable condition
- INR of 5 to 10, excessive anticoagulation
can be managed by withholding VKA and
monitoring the level of anticoagulation
with serial INR determinations
- In patients with an INR >10 who are not
bleeding, it is prudent to administer 1 mg
to 2.5 mg of oral vitamin K1
(phytonadione) in addition to holding
VKA therapy.
- In emergency situations, such as
uncontrollable bleeding, administration
of fresh frozen plasma or prothrombin
complex concentrate is reasonable .
Điều trị kháng đông ‘quá mức’
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p124
Guidelines on the management of valvular heart disease (version 2012), ESC, p34
-If the INR is .10, higher doses of oral
vitamin K (5 mg) should be
considered.
-The oral route should be favoured
over the intravenous route
- In the absence of bleeding, the
management depends on the target
INR, the actual INR, and the half-life
of the vitamin K antagonist used. It is
possible to stop oral anticoagulation
and to allow the INR to fall gradually
or to give oral vitamin K in increments
of 1 or 2 mg.
-Immediate reversal of anticoagulation
is required for severe bleeding causing
haemodynamic instability, or requiring
an emergency surgical procedure or
transfusion.
16. COMPLICATIONS
Structural deterioration, particularly with bioprosthetic
valves
Valve obstruction due to thrombosis or pannus formation
Systemic embolization
Bleeding
Endocarditis and other infections
Left ventricular systolic dysfunction, which may be pre-
existing
Hemolytic anemia
Complications of prosthetic heart valves - William H Gaasch – Uptodate 2012
17. Structural deterioration
- Paravalvular leaks early after surgery, as detected
with (TEE) or (TTE), are common .
- The reported incidence ranges from 18 to 48 percent
of patients with a mitral or aortic prosthesis; the
majority of leaks are trivial or mild and do not
progress over a two to five year follow-up.
- the later development of new, often severe
regurgitation results from prosthetic valve
endocarditis or structural failure.
Complications of prosthetic heart valves - William H Gaasch – Uptodate 2012
18. A variety of factors can contribute to structural failure with
bioprosthetic valves, including:
- mechanical stress
- immunologic rejection
- endocarditis
- cusp tear leading to severe valvular regurgitation.
- The structural failure rate with bioprosthetic valves falls dramatically
with age
Complications of prosthetic heart valves - William H Gaasch – Uptodate 2012
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p132
19. Valve obstruction
- Nguyên nhân:
Đ/v van cơ học: huyết khối, pannus, mảng sùi.
Đ/v van sinh học: xơ hóa và calci hóa lá van.
The clinical manifestations of prosthetic valve
obstruction include :
+ dyspnea,
+ heart failure, and with
+ thrombus formation
+ systemic embolization
Complications of prosthetic heart valves - William H Gaasch – Uptodate 2012
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p130 - 131
20. Pannus is the ingrowth of fibrous tissue into the valve apparatus in case of prosthetic
valves, Pannus formation is more common in the aortic position
http://cardiophile.org/2012/04/pannus-formation-in-prosthetic-valves-2/
21. Prosthetic Valve thrombosis
- PVT can lead to valvular obstruction, occurs with equal
frequency in patients with bioprosthetic valves and in
those with mechanical valves who are treated with
anticoagulants.
- The reported annual incidence of PVT ranges from 0.03 to
5.7 percent; higher rates are observed in patients with
mitral prostheses (in some reports) and/or subtherapeutic
anticoagulation.
- In one report of PVT in mechanical valves, 70 percent of
patients with coagulation tests measured at the time of
PVT were receiving inadequate anticoagulant therapy
- The gold standard for the diagnosis of PVT is transesophageal
echocardiography (TEE) and/or cine-fluoroscopy to assess both
valve motion and clot burden
Complications of prosthetic heart valves - William H Gaasch – Uptodate 2012
22. Thrombolytic regimens include alteplase
(100 mg given as a 10 mg bolus followed by
90 mg as an infusion over 90 minutes) or
streptokinase (500,000 IU over 20 minutes
followed by 1.5 million IU over 10 hours).
Intravenous heparin is typically given
concurrently to achieve an activated partial
thromboplastin time 1.5 to 2.0 times control.
Complications of prosthetic heart valves - William H Gaasch – Uptodate 2012 + 2006 ACC/AHA
23. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves
24. Although fibrinolytic therapy of a left-sided obstructed prosthetic
heart valve is associated with an overall rate of thromboembolism
and bleeding of 17.8%, the degree of risk is directly related to
thrombus size.
When thrombus area is measured in the 2D TEE view showing the
largest thrombus size, an area of 0.8 cm2 provides a useful
breakpoint.
A mobile thrombus or a length >5 mm to 10 mm is also associated
with increased embolic risk. Patients with a small thrombus (<1.0
cm in diameter or 0.8 cm2 in area) have fewer thrombolysis-
related complications, whereas those with a large thrombus (>1.0
cm diameter or 0.8 cm2 in area) have a 2.4-fold rate of
complications per 1.0 cm2 increase in size.
risk for adverse outcomes of fibrinolytic therapy : active internal
bleeding, history of hemorrhagic stroke, recent cranial trauma or
neoplasm, diabetic hemorrhagic retinopathy, large thrombi,
mobile thrombi, systemic hypertension (>200 mm Hg/120 mm
Hg), hypotension or shock, and NYHA class III to IV symptoms.
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves
25. With mild symptoms due to aortic or mitral valve
thrombosis with a small thrombus burden, it is prudent to
reassess after several days of intravenous UFH.
If valve thrombosis persists, fibrinolysis with a
recombinant tissue plasminogen activator dose of a 10 mg
IV bolus followed by 90 mg infused IV over 2 hours is
reasonable.
Heparin and glycoprotein IIb/IIIa inhibitors are held, but
aspirin can be continued.
Alternatively, streptokinase may be used with a loading
dose of 500,000 IU in 20 minutes followed by 1,500,000 IU
over 10 hours.
If fibrinolytic therapy is successful, it is followed by
intravenous UFH until VKA achieves an INR of 3.0 to 4.0
for aortic prosthetic valves and 3.5 to 4.5 for mitral
prosthetic valves
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves
26. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves
Guidelines on the management of valvular heart disease (version 2012), ESC, p 35
27. - DRUG THERAPY:
If embolic events have occurred despite a therapeutic
INR when other contraindications are not present :
-Increase the INR goal from 2.5 (range 2.0 to 3.0) to an INR goal
of 3.0 (range 2.5 to 3.5) for patients with an AVR
- Increase the INR goal from 3.0 (range 2.5 to 3.5) to an INR goal
of 4.0 (range 3.5 to 4.5) for patients with an MVR.
In patients with a bioprosthetic valve with embolic
events who are only on aspirin 75 mg to 100 mg daily, a
possible approach includes consideration of
anticoagulation with a VKA.
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p125
28. TTE is indicated in patients with suspected PVT to
assess hemodynamic severity and follow resolution
of valve dysfunction (604, 605). (Level of Evidence:
B)
TEE is indicated in patients with suspected PVT to
assess thrombus size and valve motion (605-607).
(Level of Evidence: B)
Fluoroscopy or CT is reasonable in patients with
suspected valve thrombosis to assess valve motion.
(Level of Evidence: C)
Huyết khối tại van nhân tạo
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p126-127
29. Hẹp van nhân tạo
- Medical therapies :
There are no medical therapies known to prevent
bioprosthetic valve degeneration other than those
integrated into the valve design.
Medical therapy is not effective for treatment of
symptoms due to significant prosthetic valve
stenosis, except with valve thrombosis, but standard
medical therapy may help stabilize patients before
surgical intervention and may be used for palliative
care in patients who are not surgical candidates.
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p130 - 131
The indications for surgical intervention for prosthetic valve stenosis are the
same as those for native stenosis of the aortic or mitral valve
30. pathogenesis :
Early infection - Microorganisms can reach the valve prosthesis by
direct contamination intraoperatively or via hematogenous spread
during the initial days and weeks after surgery. These pathogens have
direct access to the prosthesis-annulus interface and to perivalvular
tissue along suture pathways because the valve sewing ring, cardiac
annulus, and anchoring sutures are not endothelialized early after
valve implantation. These structures are coated with host proteins,
such as fibronectin and fibrinogen, to which some organisms can
adhere and initiate infection.
Late infection - As the sewing ring, sutures, and adjacent tissues
become endothelialized over the months after valve replacement,
sites for adherence of microorganisms and access to host tissues
adjacent to the prosthesis are altered. The pathogenesis of late PVE
has been postulated to resemble native valve endocarditis (NVE).
Epidemiology, clinical manifestations, and diagnosis of prosthetic valve endocarditis, Adolf W Karchmer
Prosthetic Valve Endocarditis
31. Viêm nội tâm mạc nhiễm trùng (IE)
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p134
32. Viêm nội tâm mạc nhiễm trùng
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p134
33. Viêm nội tâm mạc nhiễm trùng
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p135-136
34. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p141
35. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p139-140
36. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p139-140
37. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p150
38. Viêm nội tâm mạc nhiễm trùng
Điều trị nội khoa
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p141-142
39. Viêm nội tâm mạc nhiễm trùng
Điều trị can thiệp
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p144
40. Viêm nội tâm mạc nhiễm trùng
Điều trị can thiệp
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p147-148
41. Viêm nội tâm mạc nhiễm trùng
Điều trị can thiệp
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease, Prosthetic valves, p149
42. LEFT VENTRICULAR SYSTOLIC
DYSFUNCTION
— Patients with prosthetic heart valves may develop LVSD with or
without HF. The factors may contribute :
Preoperative left ventricular dysfunction that persists or partially
improves
Perioperative myocardial infarction
Progression of other valve disease
Complications of the prosthetic valve
An unrelated disorder such as coronary heart disease or
hypertension
Appropriate testing in such patients includes transthoracic
Doppler echocardiography, TEE if necessary, or, if the cause
remains uncertain, cardiac catheterization with arteriography.
Should be treated with standard medical therapy for systolic
heart failure . Such therapy should be continued even if left
ventricular function improves.
Complications of prosthetic heart valves - William H Gaasch – Uptodate
43. Hemolytic anemia
- Due to mechanical damage, is seen more commonly with prosthetic
mechanical heart valves than with bioprosthetic valves.
Among patients with prosthetic mitral regurgitation, hemolysis is
associated with rapid acceleration and deceleration of the
regurgitant jet and/or high peak shear rates .
Hemolysis is usually mild and subclinical, but is severe in up to 15
percent of patients with certain prostheses, such as ball-cage and
bileaflet valves, or those with paravalvular regurgitation .
It is uncommon with tissue valves, although hemolytic anemia may
be the initial presentation of porcine valve failure .
Presenting features may be subtle and include anemia, heart failure,
jaundice, dark urine, increasing serum LDH, and a new or changed
regurgitant murmur.
The peripheral smear shows variable numbers of schistocytes and
smaller red cell fragments
Complications of prosthetic heart valves - William H Gaasch – Uptodate
44. Oral iron replacement is effective in the majority of
patients, although transfusion may be required;
The administration of erythropoietin may eliminate
the need for transfusion .
Reoperation may be required, especially if hemolysis is
due to regurgitation from a paravalvular leak or valve
failure.
HEMOLYTIC ANEMIA
Complications of prosthetic heart valves - William H Gaasch – Uptodate
Editor's Notes
PANUS : MO XO PHAT TRIEN QUA MUC
increased risk of early bioprosthetic valve degeneration, including those with renal impairment, diabetes mellitus, abnormal calcium metabolism, systemic inflammatory disease, and in patients <60 years of age.
- MECHANICAL VALVE PROSTHESES : However, many of these patients require TTE for other indications, such as residual LV systolic dysfunction, pulmonary hypertension, aortic disease, or concurrent valve disease.
- because it allows for an assessment of the effects and results of surgery and serves as a baseline for comparison should complications or deterioration occur later.
-other disease : valve disease(s), pulmonary hypertension, atrial size, LV and RV hypertrophy, LV and RV size and function, and pericardial disease
Insidious am tham
Mechanical valve dysfunction may be due to thrombosis, pannus formation, or IE.
-TTE is the preferred approach for initial assessment of suspected prosthetic valve dysfunction because it allows correct alignment of the Doppler beam with transvalvular flow for measurement of velocity, gradient, and valve area. TTE also allows quantitation of LV volumes and LVEF, an estimate of pulmonary pressures, and evaluation of right heart function.
-However, the left atrial side of a prosthetic mitral valve is obscured by acoustic shadowing from the TTE approach, resulting in a low sensitivity for detection of prosthetic MR and prosthetic mitral valve thrombus, pannus, or vegetation.
3. Anticoagulation with a VKA is indicated to achieve an INR of 3.0 in patients with a mechanical AVR and additional risk factors for thromboembolic events (AF, previous thromboembolism, LV dysfunction, or hypercoagulable conditions) or an older-generation mechanical AVR (such as ball-in-cage) (564). (Level of Evidence: B)
Anticoagulant therapy with oral direct thrombin inhibitors or anti-Xa agents should not be used in patients with mechanical valve prostheses (589-591). (Level of Evidence: B)
Patients at high risk of thrombosis include all patients with mechanical MVR or tricuspid valve replacements and patients with an AVR and any risk factors for thromboembolism. Such risk factors include AF, previous thromboembolism, hypercoagulable condition, older-generation mechanical valves, LV systolic dysfunction (LVEF <30%), or >1 mechanical valve.
Administration of fresh frozen plasma or prothrombin complex concentrate is reasonable in patients with mechanical valves and uncontrollable bleeding who require reversal of anticoagulation (601, 602). (Level of Evidence: B)
---Excessive anticoagulation (INR ≥5) greatly increases the risk of hemorrhage. However, a rapid decrease in the INR that leads to INR falling below the therapeutic level increases the risk of thromboembolism. High-dose vitamin K should not be given routinely, because this may create a hypercoagulable condition. In most patients with an INR of 5 to 10, excessive anticoagulation can be managed by withholding VKA and monitoring the level of anticoagulation with serial INR determinations. In patients with an INR >10 who are not bleeding, it is prudent to administer 1 mg to 2.5 mg of oral vitamin K1 (phytonadione) in addition to holding VKA therapy. When the INR falls to a safe level, VKA therapy is restarted with the dose adjusted as needed to maintain therapeutic anticoagulation. In emergency situations, such as uncontrollable bleeding, administration of fresh frozen plasma or prothrombin complex concentrate is reasonable because the onset of action of vitamin K is very slow.
---If the INR is .10, higher doses of oral vitamin K (5 mg) should be considered. The oral route should be favoured over the intravenous route, which may carry a higher risk of anaphylaxis
In the absence of bleeding, the management depends on the target INR, the actual INR, and the half-life of the vitamin K antagonist used. It is possible to stop oral anticoagulation and to allow the INR to fall gradually or to give oral vitamin K in increments of 1 or 2 mg.
Immediate reversal of anticoagulation is required only for severe bleeding—defined as not amenable to local control, threatening life or important organ function (e.g. intracranial bleeding), causing haemodynamic instability, or requiring an emergency surgical procedure or transfusion.
Spectrum of paravalvular regurgitation — Paravalvular leaks early after surgery, as detected with intraoperative transesophageal echocardiography (TEE) or postoperative transthoracic echocardiography (TTE), are common. The reported incidence ranges from 18 to 48 percent of patients with a mitral or aortic prosthesis; the majority of leaks are trivial or mild and do not progress over a two to five year follow-up [ 10,11 ]. In contrast, the later development of new, often severe regurgitation results from prosthetic valve endocarditis or structural failure.
---Most mechanical valves can be expected to last at least 20 to 30 years with the exception of the Bjork-Shiley convexoconcave (BSCC) valve described in the next section. In contrast, 10 to 20 percent of human aortic homograft prostheses, and 30 to 35 percent of porcine heterograft prostheses have failed within 10 to 15 years of implantation [ 1,3-6,12 ]. Pericardial prostheses may be more durable than porcine valves [ 13,14 ]. The failure rate with porcine valves is higher with valves in the mitral position (eg, 44 versus 26 percent in the aortic position at 15 years in the Veterans Administration trial)
A variety of factors can contribute to structural failure with bioprosthetic valves, including mechanical stress, immunologic rejection, endocarditis, and cusp tear, leading to severe valvular regurgitation.
The structural failure rate with bioprosthetic valves falls dramatically with age [ 12,15,16 ]. In the Veterans Affairs trial cited above, the rate of valve failure at 15 years varied from 26 percent under age 65 to 9 percent in patients ≥65 years of age [ 12 ]. Similar findings were noted in another study in which the actuarial estimate of the rate of structural deterioration of bioprosthetic aortic valves at 15 years varied from 63 percent between the ages of 40 and 49 (and perhaps higher under age 40) to 10 percent over age 70
The lower rate of bioprosthetic valve failure in elderly adults is due at least in part to decreased activity in older patients. Because of this observation and the apparently lower failure rates with current bioprostheses, the 2006 ACC/AHA guidelines on the choice of valve considered it reasonable to use a bioprosthesis in patients ≥65 years of age who do not have risk factors for thromboembolism and who understand the likelihood that a second valve replacement will be required in the future
Pannus is usually firmly fixed to the valve apparatus and may cause a pre valve jet on colour Doppler. Pannus is highly echogenic and immobile, compared to a thrombus which is less echogenic and mobile.
CENTRIPENTAL : HUONG TAM
. In one report of PVT in mechanical valves, for example, 70 percent of patients with coagulation tests measured at the time of PVT were receiving inadequate anticoagulant therapy [ 18 ].
Diagnosis — The gold standard for the diagnosis of PVT is transesophageal echocardiography (TEE) and/or cine-fluoroscopy to assess both valve motion and clot burden [ 9,21 ]. However, transthoracic Doppler echocardiography can establish the diagnosis in many patients [ 22,23 ] and is also indicated to assess hemodynamic severity
both surgery (appreciable perioperative mortality) and thrombolytic therapy (major bleeding and systemic embolization) have important limitations
Thrombolytic regimens include alteplase (100 mg given as a 10 mg bolus followed by 90 mg as an infusion over 90 minutes) or streptokinase (500,000 IU over 20 minutes followed by 1.5 million IU over 10 hours). Intravenous heparin is typically given concurrently to achieve an activated partial thromboplastin time 1.5 to 2.0 times control.
I
-A lower tissue plasminogen activator dose of a 20 mg IV bolus followed by 10 mg per hour for 3 hours may be appropriate in some situations.
- Urokinase is less effective than tissue plasminogen activator or streptokinase.
In patients on VKA anticoagulation and aspirin 75 mg to 100 mg daily for a mechanical valve who have a definite embolic episode, it is important to document the adequacy of the anticoagulation, including the time within therapeutic range. If there have been periods in which the INR has been documented to be subtherapeutic, appropriate steps to ensure adequate anticoagulation should be taken. If embolic events have occurred despite a therapeutic INR when other contraindications are not present, a prudent approach to antithrombotic therapy is: Increase the INR goal from 2.5 (range 2.0 to 3.0) to an INR goal of 3.0 (range 2.5 to 3.5) for patients with an AVR; or, increase the INR goal from 3.0 (range 2.5 to 3.5) to an INR goal of 4.0 (range 3.5 to 4.5) for patients with an MVR.
In patients with a bioprosthetic valve with embolic events who are only on aspirin 75 mg to 100 mg daily, a possible approach includes consideration of anticoagulation with a VKA.
There are no medical therapies known to prevent bioprosthetic valve degeneration other than those integrated into the valve design. Medical therapy is not effective for treatment of symptoms due to significant prosthetic valve stenosis, except with valve thrombosis, but standard medical therapy may help stabilize patients before surgical intervention and may be used for palliative care in patients who are not surgical candidates.
DEHISCENCE : RACH VAN
LEFT VENTRICULAR SYSTOLIC DYSFUNCTION — Patients with prosthetic heart valves may develop left ventricular systolic dysfunction with or without heart failure. One or more of the following factors may contribute [ 9 ]:
Preoperative left ventricular dysfunction that persists or partially improves
Perioperative myocardial infarction
Progression of other valve disease
Complications of the prosthetic valve
An unrelated disorder such as coronary heart disease or hypertension
Appropriate testing in such patients includes transthoracic Doppler echocardiography, TEE if necessary, or, if the cause remains uncertain, cardiac catheterization with arteriography.
The 2006 ACC/AHA guidelines recommended that patients with left ventricular systolic dysfunction after valve replacement should be treated with standard medical therapy for systolic heart failure [ 9 ]. Such therapy should be continued even if left ventricular function improves. (See "Overview of the therapy of heart failure due to systolic dysfunction" .)