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INTRODUCTION
Prevalence of maternal heart disease -< 1%, itspresence increases the risk of adverse maternal,fetal, and neonatal outcomes
0.24% of all pregnancies in western industrializedcountries. {Am J Obstet Gynecol 1998;179:16431653.}.
In western countries maternal heart disease is nowthe major cause of maternal death duringpregnancy
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RHD dominates in non-westerncountries [5689% ]
Congenital heart disease [just 919%].
Eur J Heart Fail 2008;10:855-860, Circulation 2001;104:515-521.
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STUDY
A Canadian study analyzed the outcomes ofpregnancy in a group of women with congenital oracquired heart disease (562 women and 599pregnancies)
CARPREG study (Circulation.2001;104:515-21.)
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Maternal outcomes Incidence of adverse maternal cardiac events
13% of completed pregnancies
More likely if: EF below 40%
Left heart obstruction (AS with a valve area of less than 1.5 cm2 or
MS with a valve area of less than 2.0 cm2) Previous cardiovascular events or arrhythmia
NYHA class > II or cyanosis.
These events occurred in: 4% of the women with none of these risk factors
27 % of those with one risk factor 62 % of those with two or more risk factors
The 3 women that died had two or more risk factors
Sui et al
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Fetal outcomes NYHA class III or IV and left heart obstruction were
predictors of fetal outcomes also.
Other predictors of adverse fetal outcomes include: The use of anticoagulant drugs Smoking during pregnancy. Multiple gestation. Mothers age (> 35 yrs or < 20 yrs).
ZAHARA study Fetal mortality :
4 % among pregnancies in women with one or more of these riskfactors.
2% among those with none of these risk factors.
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WHO CLASS II
Most arrythmias
WHO CLASS II/III
Mild LV impairmentVHD not included in class IV
WHO CLASS IIIMechanical valve
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CLASS IV
Pulmonary hypertension of anycause
Previous PCM with LV impairmentSevere MS and severe symptomatic
AS
Severe LV dysfunction
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Evaluation
The evaluation- Pre conceptional and entail a full cardiacassessment.
H/o exercise capacity, current or past evidence of heartfailure and associated arrhythmias.
Cardiac hemodynamics -PAP and the severity of valvedysfunction - assessed by echo.
Exercise testing - Assessment of functional capacity.
During pregnancy evaluation of each trimester - Assess anydeterioration in maternal cardiac status.
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INVESTIGATIONS -ECHO Gradients in RVOT and LVOT increase
Increased stroke volume cause increase in severity of
regurgitation. LVEDD increased
TEE can be performed safely
Fetal echo best in 20 weeks gestation.
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TMT 80% of predicted heart rate
No evidence of spontaneous abortion
Dobutamine stress should be avoidedAssessment of myocardial reserve pre pregnancy in
PPCM & VHD
Nuclear stress tests are avoided.
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Fluoroscopy risks
Majority of procedures are < 1mGy to fetus
RCR -2009 guidelines
During the first 14 days of fertilization -no riskAfter 14 days major risk occurs if doses > 100mGy
Doses
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Valvular Heart DiseaseSeverity
Risk Stenotic lesions > Regurgitant lesion
Left sided diseases> Right sided disease
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MS Poorly tolerated [ moderate & severe MS]- Tachycardia, increased plasma
volume
PHT, Trans valvular gradients, PAP measurements are less reliable marker
of severity
Maternal Risks- HF symptoms, Pulmonary edema in II & III trimester. AF[increases risk of T.Emb, pulmonary edema] ( El Kayam etal, 2005 JACC)
Moderate & severe MS counseled against pregnancy without priorintervention
Fetal risks- prematurity 20-30%; IUGR 5-20% ( El Kayam & Hameed 2001)& Silversides
JACC 2001: 37:893-899
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MS INTERVENTIONS NYHA III or IV patients or valve area less than 1 cm2,
BMV or MVR before pregnancy.
BMV - second trimester in NYHA III/ IV or with PAPabove 50 mm Hg despite optimal medical therapy.
MVR during pregnancy- high fetal loss (30%) hencereserved till all measures fail and mother`s life is in
danger.Anticoagulation in AF OR in bed rest.
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BMV OUTCOMES BMV in pregnancy KEM study (Gupta et al) successful
outcomes of 40 pregnancies.
Ribeiro et al (1992)study on maternal outcomes in 78
patients-8 patients developed mod MR, No evidence of PE
De Souza et al(2001) compared the outcomes of PBMV v/sOMC in 21 pts with severe MS -38% fetal death in OMC
Current consensus PBMV to symptomatic patients with
severe MS with OMT/ MVA 0.75-1.2cm2
Complications- CT , AF ,MR ,emboli, uterine contractions& labor
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PERIPARTUM MANAGEMENTVaginal delivery is the usual approach.
Avoidance of volume overload and tachycardia is themain hemodynamic goal.
In unstable patients, monitoring with arterial line and
PCWP aids in optimum hemodynamic management.
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PERIPARTUM MANAGEMENT Epidural analgesia.
Assisted-delivery devices during the second stageof delivery eliminate hemodynamic effects ofvalsalva maneuver during pushing.
Caesarean section for obstetrical indications.
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Pharmacological management of symptoms
MS with symptoms or PAH, restricted activities and 1-selective blockers are recommended. Diuretics are
recommended when congestive symptoms persist despite -
blockers.
BMVNYHA class III/IV or sys PAP > 50mm Hg, preferably after 20
weeks POG. [CI in asymptomatic women]
AnticoagulationParoxysmal or Permanent AF, LA thrombus, prior embolism
Considered in mod/sev MS with spontaneous echo contrast, LA >
40ml/m2, low CO, CCF
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MITRAL REGURGITATIONWell tolerated due to reduction in SVR.
Women with symptomatic MR may benefit frommitral-valve surgery (preferably repair))beforebecoming pregnant.
Diuretics may be indicated.
Outcome data that would help to guide clinical
decision making in this area are lacking.
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AORTIC STENOSIS Congenital valvular abnormalities are usually the cause
of AS in young women in the US.
Severe AS is poorly tolerated during pregnancy.
Maternal and perinatal mortality of 17%and 32% respectively have been reported.
(Pieper et al 2008)
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AORTIC STENOSIS Symptomatic patients - peak outflow gradient > 50 mm
Hg are advised to delay conception until after surgicalcorrection.
Termination of pregnancy- if patient is symptomaticbefore the end of the 1st trimester.
Even severe AS may be asymptomatic
Aortic-valve replacement and palliative aortic balloon
valvuloplasty have been performed during pregnancywith associated maternal and fetal risk.
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CONTD..
Maternal riskHF 10%, Arrhythmias 3-25%(Pieper etal 2008)
Fetal risk- Preterm Labour, IUGR, LBW
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PERIPARTUM MANAGEMENTVaginal delivery is the usual approach.
Oxytocin may decrease the SVR and increase PAP.
Epidural analgesia may be given.Avoid sudden decrease in SVR.
Cesarean section
GA has traditionally being advocated to avoid sudden
decreases of SVR.Case reports of regional anesthesia with positiveoutcomes.
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Pharmacological management of symptoms
HF- treat with diuretics
AF- b-blockers, CCB to control HR, Digoxin also may be
used
Pre- pregnancy intervention
Symptomatic severe AS
LVEF 15mm)
TMT- symptoms or falling BP
Recent progression of ASAsc. Aorta> 50 MM (27.5mm/m2)
During Pregnancy
Severe symptomatic AS + refractory to medical therapy/
life threatening symptomsNon calcified valve may besubjected to BAV/ emergency AVR
Delivery
Vaginal delivery + regional anesthesia in non-sev AS
LSCS in Sev AS
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Aortic Regurgitation
Root dilatation (Marfan syndrome ),BicuspidAortic valve, and RHD are the commonest causes.
The reduced SVR of pregnancy reduces the volume of
regurgitated blood
Women with an abnormal functional capacity or leftventricular dysfunction are predicted to have a high riskof abnormal maternal outcomes, but few data
concerning this population are available
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Tricuspid valve lesions Better tolerated
Maternal risk- HF, Arrhytmias, Progressive worsening of regurgitations
Moderate to severe Regurgitant lesions may undergo exercise testing todecide pre pregnancy intervention
Severe lesions + symptoms/ impaired LV function/ Ventricular
dilatation treated surgically, if possible repair
TV repair if moderate Secondary TR with annular dilatation >40mm,usually during left sided valve surgeries
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PS & PRPS is generally well tolerated
Complications of sev PS- RV failure & Arrhythmias
Pre pregnancy balloon valvuloplasty in severe stenosis(peak Doppler gradient > 64 mmHg)
LSCS is considered in patients with severe PS and inNYHA class III/IV despite medical therapy and bed rest,
in whom percutaneous pulmonary valvotomy cannot beperformed or has failed.
Hameed et al ( JACC 2003 )
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Severe PR with impaired RV function
Pre-pregnancy pulmonary valve replacement (preferablybioprosthesis) should be considered
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Prosthetic valvesMechanical valves
Excellent H.D. Performances
Long term durability
Thrombogenic
Bioprosthetic valves
Good H.D Performances
Much less thrombogenic
High risk of valve
degeneration [~50% women
A,T position
Reoperation mortality risk addl
5%
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Management of valve thrombosis
in pregnancy Presents as embolism or dyspnoea
TTE and then TEE is required. If still not confirmed afluoroscopy is done
Fibrinolysis is recommended
ESC 2010 guidelines - anticoagulation optimisation forsmall clots
Thrombolysis has shown little negative effects on fetus Streptokinase bolus of 250000 IU followed by 100000
iu/hr for 72hrs
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General Management Percutaneous intervention-
After 4thmonth in the second trimester [ organogenesiscomplete, fetal thyroid still inactive, volume of uterus small]
ACT b/w 200-300s
CPBypass-
13th& 28thweek [Fetal malformation - I trim & maternalcomplication - III trim]
3-6% late neurological impairment in children, high fetalmortality hence Sx only when refractory to medical therapy,interventional procedures fail, mothers life threatened
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Peripartum cardiomyopathy
Eur J Heart Fail 2010;12:767
778.
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Etiology
Cathepsin D in response tooxidative stress cleaves
Prolactin into angiostatic &
proapoptotic fragment 16 kDa
Prolactin
Fas/Apo-1, C-reactiveprotein,
IFN-gand IL-6
Viruses
Autoimmune
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Differential diagnosis
Eur J Heart Fail 2010;12:767778.
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Natural history
Am J Obstet Gynecol 2008;199:415.e1-415.e5.
.
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PRESENTATION First 4 months after delivery- most of them(78%)
Last month of pregnancy- 9%
> than 4months after delivery or before 1month of pregnancy 13%
CLINICAL FEATURES Features of right heart or left heart failure or both
Can present as ventricular arrythmia
92% heard a third heart sound (2005 South African study)
LV thrombosis is seen
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INVESTIGATIONS Diagnosis of exclusion
ECG 66% LVH, 96% ST-T changes
Elevated BNP and NT pro BNP Echo Not all have LV dilatation and LVEDD>60
predicts poor recovery
MRI is a better predictor of LV functions and assesses
the chamber volumes better.( Late gadoliniumenhancement)
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FOLLOW UP Repeat echo after 6weeks, 6months and then annually
MRI at 6months and annually for accurate assessmentof LV volumes and function
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MANAGEMENT Similar to HF management
O2 administration to reach saturation of>95%
NIV and PEEP 5-7.5 cm H2O Loop diuretics and NTG
Inotropics when required
Pts after OMT and IABP ,the pt may require assist
device or cardiac transplantationLVAD used as bridge to transplantation or destination
therapy
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Management of stable heart failureACEI and ARB avoided
Hydralazine and nitrates combination used safely
Beta 1 selective agents are preferred LMWH and UFH used in pregnancy
Role of CRT AND ICD- pt with LV dysfunction for 6months post presentation
Bromocriptine- used in acute stage- 2.5mg bd(Denise etal 2007)
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Delivery need not be done in asymptomatics
Encouraged in deteriorating patients
Vaginal delivery encouraged but LSCS in critically illpatients
Left lateral position encouraged
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Prognosis No European studies
Vary geographically
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LV func.returnsto normal in
2341%
SA- 6m &2yrmortalityrates 10% &
28%.Brazil &Haiti 6mrate 1416%Turkey- 4yr
rate 30%
Eur J Heart Fail 2010;12:767778.
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Counselling LVEF
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Hypertensive disordersAccounts for 15% of all pregnancies
BP recordings in lateral recumbent posture
Ambulatory BP monitoring is superior
Investigations LFT, RFT, urine r/e, Uric acid , Hct
Proteinuria >2g/d close monitoring
>3g/d deliveryVMA and plasma metanephrine analysis along with USGabdomen
Doppler USG for uteroplacental perfusion.
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Classification Pre existing hypertension
Gestational hypertension
Pre existing hypertension with superimposedgestational hypertension with proteinuria
Antenatally unclassifiable hypertension
Hypertension defined as SBP> or = 140 & DBP > or = 90
Mild- 140-159/90-109 , Severe ->or = 160/110mmHg
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Hypertensive disordersType Criteria Comments
Pre-existing HTN >140/ 90 mm Hg, eitherprecedes pregnancy or develops
140/ 90 mm Hg, develops >20weeks gestation
Usu resolves within 42 days
PP; 6-7% pregnancy
Pre-eclampsia Gest HTN +proteinuria[>0.3g/day or
>30mg/mmol U. creatinine]
Upto 25% of prev HTN
Eclampsia Pre-eclampsia + seizures Immediate termination ofpregnancy required
Pre-existing HTN +
superimposedgestational HTN with
proteinuria
Pre-existing HTN+ further
worsening of BP+ proteinuria[>0.3g/day] after 20 wks
Antenatally unclassifiable
hypertension
BP first recorded after 20 wks Re- assessment after 42 days
PP
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Management Non pharmacological- salt restriction, calcium
supplementation
Low dose aspirin(75-150mg) at early onset
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Contd
Management of crisis iv Nitroprusside- caution oncyanide toxicity.
Patient with pulmonary edema can be managed withiv Nitroglycerin
Methyldopa should be avoided postpartum because itcauses depression.
Earlier the onset of HT in pregnancy the more thechance of recurrence in next pregnancy
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Recommendations in hypertension
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CAD 3-6 /100000 deliveries.
Coronary artery dissection is a common cause.(LAD is thecommon culprit artery).
Aortic dissection, pulmonary embolism and pre eclampsiaalso to be ruled out in pregnant women with chest pain
Trop I is a useful investigation.
PCI treatment of choice in STEMI.
PCI in high risk NSTEMI only
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Contd
PCI preferred to thrombolysis as it will cover up
dissections as well
BMS Stents are used
CABG carries an extremely high mortality
DRUGS- ASA , beta blockers are safe but safety ofclopidogrel is not known
Vaginal delivery is most appropriate
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Tachyarrhythmia
Premature extra beats / sustained tachyarrhythmias become morefrequent and may even manifest for the first time during pregnancy
PSVT in 20-44% of pregnancy. (Am J Cardiol 2006;97(8):1206-1212)
Immediate electrical cardioversion - a/c Rx of any tachycardia with
haemodynamic instability
For acute conversion of PSVT- vagal manoeuvre followed by I.V.
adenosine is recommended. I.V. metoprolol or propranolol can also be
considered
For long-term management of SVT -oral digoxin or
metoprolol/propranolol is recommended. If not successful oral sotalol
or flecainide may be used
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Arrhythmia Immediate electrical cardioversion of VT is
recommended for sustained, unstable & stable VT . I.V. Sotalol or Procainamide - a/c conversion of
sustained, haemodynamically stable andmonomorphic VT.
Oral metoprolol, propranolol or verapamil - idiopathicsustained VT (Long-term management). Ifunsuccessful oral sotalol, flecainide, propafenone
ICD implantation, recommended prior to pregnancyand during pregnancy also. Implantation of PPI orICDs -considered with echo guidance, especially if thefetus > 8 weeks gestation.
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Bradyarrythmia Rare
Favourable outcome
30% of congenital AV blocks present during pregnancy
Vaginal delivery carries no extra risks
Temporary pacing in patients with CHB withsymptoms
Permanent pacing can be done once fetus is > 8weeksof age.
Echo guidance is used.
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Anticoagulation
No results of RCT to guide the choice of anticoagulanttherapy during pregnancy.
Monitoring to assess whether the antithrombotic effect
is adequate. The effective doses of these drugs change during
pregnancy because of changes in intravascular volumeand body weight.
In a series of 976 women with a total of 1234 pregnanciesthe use of any anticoagulant therapy resulted in majorbleeding in 2.5 % of the pregnancies, with bleeding
usually occurring at the time of delivery.Arch Intern Med
2000;160:191-196
Anticoagulation Strategies
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OAC
UFH
LMWH
OAC
UFH
Anticoagulation Strategies
Maternal outcomes- Chan et al(2000)
OACLMWH
3.9 %
9.2
35
9
3.6
2 %
4
15
Valve thrombosis Maternal mort.
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OAC In women with mechanical valves the use of OAC -Greatest maternal protection.(Risk of thromboembolism-3.9%, risk of death-1.8%).
High rate of fetal loss including spontaneous abortions,stillbirths, and neonatal deaths (30%).
Exposure to warfarin between 6 -12 wks -fetal loss twicethat associated with the use of UFH
Fetopathic effects - (nasal hypoplasia and bone stippling)
occurred in approximately 6 % of cases in doses > 5mg
Vitale et al - J Am Coll Cardio 1999;33:1637-41.
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Heparin
If heparin rather than warfarin was used during the 1st
trimester, the risks of maternal thromboembolism andmaternal death more than doubled (9.2% and 4.2%respectively).
The use of heparin throughout pregnancy was associatedwith the highest risks of maternal thromboembolism andmaternal death (25% and 7 % respectively).
Long-term use of heparin - HIT and osteopenia.
Arch Intern Med 2000;160:191-6.
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LMWH Lower risks of thrombocytopenia and osteopenia than
UFH
There are insufficient data from studies of women withprosthetic heart valves to support the efficacy of thistherapy.
No data regarding the use in AF with valvular disease.
To be monitored with anti X a levels. Target 6 hr post dose0.8 to 1.2 U/ mL.
J CardioPharmacol Ther 2004;9:107-15.
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Anticoagulation Strategies
OAC throughout pregnancy best strategy [esp. if warf
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Differences In strategy
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BOOK REFERENCES BRAUNWALD`S HEART DISEASE
HURST`S THE HEART
VALVULAR HEART DISEASE WANG VALVULARHEART DISEASE IN PREGNANCY
TOPOL TEXTBOOK OF CARDIOVASCULARMEDICINE
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ARTICLES AND REVIEWSCARPREG study (Circulation.2001;104:515-21.)
Am J Obstet Gynecol 1998;179:16431653Am J Cardiol 2006;97(8):1206-1212Am J Obstet Gynecol 2008;199:415
Circulation 2001;104:515-521
Eur J Heart Fail 2008;10:855-860Eur J Heart Fail 2010;12:767778
N Engl J Med 2001;344:1567-71Arch Intern Med 2000;160:191-196
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