ACQUIRED HEART DISEASES IN PREGNANCY ANTICOAGULATION IN PREGNANCY

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Transcript of ACQUIRED HEART DISEASES IN PREGNANCY ANTICOAGULATION IN PREGNANCY

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ACQUIRED HEART DISEASES IN PREGNANCY ANTICOAGULATION IN PREGNANCY Slide 2 INTRODUCTION Prevalence of maternal heart disease -< 1%, its presence increases the risk of adverse maternal, fetal, and neonatal outcomes 0.24% of all pregnancies in western industrialized countries. {Am J Obstet Gynecol 1998;179:16431653.}. In western countries maternal heart disease is now the major cause of maternal death during pregnancy Slide 3 RHD dominates in non-western countries [5689% ] Congenital heart disease [just 919%]. Eur J Heart Fail 2008;10:855-860, Circulation 2001;104:515-521. Slide 4 STUDY A Canadian study analyzed the outcomes of pregnancy in a group of women with congenital or acquired heart disease (562 women and 599 pregnancies) CARPREG study (Circulation.2001;104:515-21.) Slide 5 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 Slide 6 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 risk factors. 2% among those with none of these risk factors. Slide 7 Slide 8 WHO CLASS II Most arrythmias WHO CLASS II/III Mild LV impairment VHD not included in class IV WHO CLASS III Mechanical valve Slide 9 CLASS IV Pulmonary hypertension of any cause Previous PCM with LV impairment Severe MS and severe symptomatic AS Severe LV dysfunction Slide 10 Evaluation The evaluation- Pre conceptional and entail a full cardiac assessment. H/o exercise capacity, current or past evidence of heart failure and associated arrhythmias. Cardiac hemodynamics -PAP and the severity of valve dysfunction - assessed by echo. Exercise testing - Assessment of functional capacity. During pregnancy evaluation of each trimester - Assess any deterioration in maternal cardiac status. Slide 11 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. Slide 12 TMT 80% of predicted heart rate No evidence of spontaneous abortion Dobutamine stress should be avoided Assessment of myocardial reserve pre pregnancy in PPCM & VHD Nuclear stress tests are avoided. Slide 13 Fluoroscopy risks Majority of procedures are < 1mGy to fetus RCR -2009 guidelines During the first 14 days of fertilization -no risk After 14 days major risk occurs if doses > 100mGy Doses Valvular Heart Disease Severity Risk Stenotic lesions > Regurgitant lesion Left sided diseases> Right sided disease Slide 16 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 prior intervention Fetal risks- prematurity 20-30%; IUGR 5-20% ( El Kayam & Hameed 2001) & Silversides JACC 2001: 37:893-899 Slide 17 MS INTERVENTIONS NYHA III or IV patients or valve area less than 1 cm 2, BMV or MVR before pregnancy. BMV - second trimester in NYHA III/ IV or with PAP above 50 mm Hg despite optimal medical therapy. MVR during pregnancy- high fetal loss (30%) hence reserved till all measures fail and mother`s life is in danger. Anticoagulation in AF OR in bed rest. Slide 18 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/s OMC 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 Slide 19 PERIPARTUM MANAGEMENT Vaginal delivery is the usual approach. Avoidance of volume overload and tachycardia is the main hemodynamic goal. In unstable patients, monitoring with arterial line and PCWP aids in optimum hemodynamic management. Slide 20 PERIPARTUM MANAGEMENT Epidural analgesia. Assisted-delivery devices during the second stage of delivery eliminate hemodynamic effects of valsalva maneuver during pushing. Caesarean section for obstetrical indications. Slide 21 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. 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. BMV NYHA class III/IV or sys PAP > 50mm Hg, preferably after 20 weeks POG. [CI in asymptomatic women] BMV NYHA class III/IV or sys PAP > 50mm Hg, preferably after 20 weeks POG. [CI in asymptomatic women] Anticoagulation Paroxysmal or Permanent AF, LA thrombus, prior embolism Considered in mod/sev MS with spontaneous echo contrast, LA > 40ml/m2, low CO, CCF Anticoagulation Paroxysmal or Permanent AF, LA thrombus, prior embolism Considered in mod/sev MS with spontaneous echo contrast, LA > 40ml/m2, low CO, CCF Slide 22 MITRAL REGURGITATION Well tolerated due to reduction in SVR. Women with symptomatic MR may benefit from mitral-valve surgery (preferably repair))before becoming pregnant. Diuretics may be indicated. Outcome data that would help to guide clinical decision making in this area are lacking. Slide 23 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) Slide 24 AORTIC STENOSIS Symptomatic patients - peak outflow gradient > 50 mm Hg are advised to delay conception until after surgical correction. Termination of pregnancy- if patient is symptomatic before the end of the 1 st trimester. Even severe AS may be asymptomatic Aortic-valve replacement and palliative aortic balloon valvuloplasty have been performed during pregnancy with associated maternal and fetal risk. Slide 25 CONTD.. Maternal risk HF 10%, Arrhythmias 3- 25%(Pieper et al 2008) Fetal risk- Preterm Labour, IUGR, LBW Slide 26 PERIPARTUM MANAGEMENT Vaginal 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 positive outcomes. Slide 27 Pharmacological management of symptoms HF- treat with diuretics AF- -blockers, CCB to control HR, Digoxin also may be used Pharmacological management of symptoms HF- treat with diuretics AF- -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 AS Asc. Aorta> 50 MM (27.5mm/m2) During Pregnancy Severe symptomatic AS + refractory to medical therapy/ life threatening symptoms Non calcified valve may be subjected to BAV/ emergency AVR Pre- pregnancy intervention Symptomatic severe AS LVEF 15mm) TMT- symptoms or falling BP Recent progression of AS Asc. Aorta> 50 MM (27.5mm/m2) During Pregnancy Severe symptomatic AS + refractory to medical therapy/ life threatening symptoms Non calcified valve may be subjected to BAV/ emergency AVR Delivery Vaginal delivery + regional anesthesia in non-sev AS LSCS in Sev AS Delivery Vaginal delivery + regional anesthesia in non-sev AS LSCS in Sev AS Slide 28 Aortic Regurgitation Root dilatation (Marfan syndrome ),Bicuspid Aortic 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 left ventricular dysfunction are predicted to have a high risk of abnormal maternal outcomes, but few data concerning this population are available Slide 29 Tricuspid valve lesions Better tolerated Maternal risk- HF, Arrhytmias, Progressive worsening of regurgitations Moderate to severe Regurgitant lesions may undergo exercise testing to decide 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 Slide 30 PS & PR PS 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 in NYHA class III/IV despite medical therapy and bed rest, in whom percutaneous pulmonary valvotomy cannot be performed or has failed. Hameed et al ( JACC 2003 ) Slide 31 Severe PR with impaired RV function Pre-pregnancy pulmonary valve replacement (preferably bioprosthesis) should be considered Slide 32 Prosthetic valves Mechanical valves Excellent H.D. Performances Long term durability Thromboge