Board Review cardiology by niusheng11

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									Internal Medicine Board
Review (from MKSAP 13)
      Cardiology

      June 2006
Congenital Heart Disease
      In the Adult
    Acyanotic Congenital Heart Disease
                   (covered in MKSAP)
• Atrial Septal Defect
• Bicuspid Aortic Valve
    – Most common congenital anomaly
    – More common in men
    – Early systolic ejection click and outflow murmur
    – Diagnosis with echo important because of
      endocarditis risk
    – Coarctation and bicuspid aortic valve are associated
•   Ventricular Septal Defect
•   Patent Ductus Arteriosus
•   Valvular pulmonary stenosis
•   Coarctation of the aorta
Cyanotic Congenital Heart Disease (covered in MKSAP)
• Most patients with unoperated cyanotic heart
    disease have developed Eisenmenger’s
    syndrome.
•   Tetralogy of Fallot
    – most have had complete intracardiac repair,
      occasionally only aortopulmonary shunt.
    – PI leading to right heart dilation is common
    – Yearly mortality increases after 25 years due to
      sudden death, QRS >180ms best predictor, apparent
      interaction between long QRS and right heart dilation,
      general agreement to replace pulmonary valve when
      QRS>180.
• Transposition of Great Arteries
    – most have had been repaired with atrial switch
      (Mustard, Senning) procedure [now doing arterial
      switch]
    – Risk RV failure (survival depends on RV function), sick
      sinus syndrome, atrial arrhythmias
• #70 26 y.o. female. Heart murmur as a child
  did not outgrow it. Married. Would like a child.
  Mild cough and SOB especially at high altitude.
  BP 110/70, HR 86. O2 sat 99%. Nl JVP. Good
  carotid upstroke. Lungs clear. RV lift. S1
  normal S2 wide fixed splitting. 3/6 early to mid
  peaking systolic murmur LUSB. Echo RV
  enlargement, RAE, and high pulm flow but no
  ASD on TTE. PA 45. Valves normal. Next step?
  –   TEE
  –   ABX prophylaxis no other treatment
  –   Have family and then consider closure of the defect
  –   Cardiac cath
  –   Reassurance
# 70 TEE
• Most likely dx is ASD (wide and fixed splitting of S2)
• However partial anomalous pulmonary venous drainage
    is an alternative diagnosis and is suspected when TTE
    does not show ASD. RV enlargement is consistent with
    a hemodynamically significant shunt.
•   Mild elevation of PA pressure is not a contrindication to
    closure
•   TEE is indicated to define the anatomy and exclude
    anomalous pulmonary venous drainage
•   Referral for closure is indicated and if feasible prior to
    pregnancy (CHF sometimes complicates pregnancy, risk
    paradox embolus)
•   Closure percutaneous or sugical depending on anatomy
    and center’s experience
    – Most ostium secundum ASD can be closed percutaneously
    – Others require surgical closure
--Closure of ASD and VSD indicated if pulmonary
to systemic shunt ratio of 1.7:1 or greater with
evidence of right or left ventricular volume
overload respectively.
Location of types of Atrial
Septal Defects                      Majority are secundum



ASD second
Most common
Congenital defect
Encountered in adults
(bicuspid AV #1)
More on ASD’s
• In absence of pulmonary vascular disease shunt
    is left to right resulting in RV volume overload.
•   With advancing age diminished LV compliance
    can lead to increase in shunt fraction with
    consequent right heart failure
•   A.fib is common in older adults with ASD’s.
•   Frequency of A.fib and potential for paradoxical
    embolism lead to high incidence of embolic
    stroke.
•   Before repair prophylaxis for endocarditis is not
    indicated for isolated ASD’s. Following closure 6
    mos of prophylaxis for endocarditis.
• #18 24 y.o. female emigrated from Phillipines
  eval for murmur. HR 82. O2 sat 97%. JVP
  normal. Carotid pulses brisk with rapid upstroke.
  Lungs clear. Sustained apical impulse in 6th
  intercostal space. S1 normal. S2 physiologically
  split with normal P2. A soft S3 is audible.
  Continuous murmur with crescendo-decresendo
  quality is heard throughout, loudest 3rd left
  intercostal space. Diagnosis?
   – Mitral regugitation
   – Mitral stenosis and insufficiency
   – Pulmonary stenosis and insufficiency
   – Patent ducts arteriosus
#18 patent ductus.
• Patent ductus arteriosus
   – In acyanotic adult with patent ductus
     communication is usually small. Murmur soft
     and confined to systole.
   – Most adults with large patent ductus have
     Eisenmenger’s physiology and are not surgical
     candidates.
   – Closure is indicated if associated with a
     murmur to prevent the complications of
     endarteritis.
   – Closure percutaneously with coil.
• PFO —patent foramen ovale.
 – Persist in 20% of people.
 – Can be associated with interatrial septal
   aneurysm.
 – Can be diagnosed by contrast echo.
 – Risk for paradoxical embolism.
 – The specific indications for closure of a
   patent foramen ovale after a cerebral
   embolic event remain unclear
• #43 26 y.o. man diagnosed with heart murmur
 as a baby. Told he would outgrow it.
 Participates in sports without problem. 120/80,
 64. Lungs clear. Nondisplaced apical impulse.
 Normal S1, physio split S2. Thrill in 3rd left
 intercostal space and 4/6 holosystolic murmur
 noted radiating to the right. Echo small
 perimembranous VSD. Normal chamber size
 and normal PA pressures.
  – Refer to surgeon for closure
  – Treat with amoxicillin 2 gm 1 hour before
    dental procedures
  – Refer for percutaneous closure
  – Initiate lisinopril therapy
#43 Treat w/ amoxicillin 2 gm 1 hour before dental procedures

                Ventricular Septal Defect
   • In acyanotic adult VSD usually small
   • Large VSD present in childhood with CHF or pulmonary
     hypertension
   • Most common location in adults is perimembranous near
     tricuspid valve
   • Indications for closure in adulthood are large shunt
     fraction 1.7:1 or greater or left ventricular volume
     overload (LV overload occurs because shunt is primarily
     confined to systole and the RV serves as a reservoir for
     the shunted blood The LV diastolic volume is increased
     because the stroke volume includes both forward flow
     and shunted flow)
   • Exam with hemodynamic sig VSD may reveal displaced
     apical impulse, mitral diastolic rumble, S3.
    Endocarditis Risk and Prophylaxis
             In Congenital Heart Disease
• Risk of endocarditis is substantial except in
    operated patients with pulmonary stenosis, ASD,
    VSD, PDA. If residual VSD or PDA leaks present
    postoperatively, risk persists.
•   Antibiotic prophylaxis is indicated for almost all
    patients with unoperated congenital heart
    disease (except isolated ASD)
•   ASD—before repair no prophylaxis indicated
    unless other coexisting abnormalities.
    Prophylaxis for first 6 mos post repair and
    indefinitely if residual abnormalities.
#59
45 y.o. known Eisenmenger’s b/c of
unrepaired VSD. Increased lethargy, frontal
headache, and difficulty concentrating.
Previous PMD phlebotomized 1 unit every 3
mos. Cyanotic, 95/65, 95, 84%. Clubbing.
Clear lungs, nl JVP. Widely physio split S2,
loud P2. Holosystolic murmur at left
parasternal border. High pitched diastolic
murmur at upper left sternal border. Right
sided S4.
HCT 56%, MCV 72. WBC 5.6. PLT 110.
• Symptoms suggest hyperviscosity, they
 may be caused by iron deficiency.
 Microcytic erythrocytes are rigid and not
 easily deformed. Thus viscosity increases
 paradoxically at lower hematocrit.
Eisenmenger’s Syndrome and Erythrocytosis
• Seconday erythrocytosis is compensatory and
    usually not associated with symptoms.
•   Hyperviscosity syndrome can occur when HCT
    >65. Phlebotomy is indicated only to treat
    symptoms.
•   Be sure not iron deficient and not volume
    depleted.
•   When phlebotomy is necessary, follow by
    isovolumic saline repletion (in presence of CHF
    use 5% dextrose)

• Pregnancy contraindicated. Maternal mortality
    excceds 50% with death usually in early
    postpartum period.
• # 89
• 35 y.o. female hypertensive. Told had
  hypertension at age 20 as well but did not follow
  up. BP 200/100. S1. S2 physio split. An early
  systolic ejection sound is noted and early
  peaking murmur noted in second right
  intercostal space. Short diastolic murmur along
  LSB. U/A normal.
  – Measure TSH
  – Measure BP lower extremities
  – Order Echo
  – Order 24 HR urine test for metanephrine and
    vanillylmandelic acid
  – Obtain CXR
#89 Measure BP lower extremities
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• Coarctation of the aorta
         – Radial femoral delay
         – Lower blood pressure in the legs
         – Rib notching (dilated intercostal arteries that
           provide collateral blood flow)
         – Repair indicated when there is proximal HTN
           and a gradient exceeding 20 mm Hg
         – Discrete coarctation is usually amendable to
           percutaneous repair while longer segments
           may require surgery
Cardiac Disease And
     Pregnancy
• #11 25 y.o. pregnant female presents with heart
  murmur noted second trimester. First
  pregnancy. New murmur. No PMH.
  Asymptomatic. Mild displaced apical impulse
  and lower extrem edema. S1 and S2 normal, S3
  at apex. 2/6 early to mid peaking systolic
  murmur at left sternal border. Likely cause of
  murmur?
   – Bicuspid aortic valve with mild to mod AS
   – Congenitally abnl pulmonary valve with mod
     stenosis
   – Physiologic murmur related to pregnancy
   – Bicuspid aortic valve with moderate
     regurgitation
#11 physiologic murmur
-----------------------------------------------------------------------------------------------------------------------

       – PHYSICAL FINDINGS AND PREGNANCY--
• S3 audible in more than 80% of normal pregnant women
• Early peaking ejection systolic murmur audible in 90%--
  pulmonary outflow murmur
• Increased blood volume during pregnancy
   – (CO increases by 30 to 50% during pregnancy and to
     about 80% above baseline during labor and delivery)
• Apical impulse displaces
• Lower extremity edema common
• Abnormal findings---S4, loud 3/6 systolic
     murmur, diastolic murmur, fixed splitting of S2.
• In general, fixed obstructive lesions (MS, AS) poorly
     tolerated in pregnancy—increased blood volume.
     Regurgitant lesions well tolerated—decreased SVR
• #20 28 y.o. pregnant female referred for eval
  of persistent dyspnea secondary to MS. 30
  weeks pregnant and dyspnea persists after
  metoprolol, lasix, and digoxin. HR 70. Echo
  severe MS, mean grad 14, valve area 1 cm2.
  Trivial MR. RV systolic 50 mmHg. Crackles and
  edema. What do you recommend?
  – Surgical mitral valvotomy
  – Urgent delivery fetus then reassessment of maternal
    cardiac status
  – TEE followed by percutaneous mitral balloon
    valvuloplasty
  – Diagnostic catheterization
  – Fetal Echocardiogram
# 20 TEE followed by percutaneous mitral balloon
valvuloplasty
• Percutaneous valvuloplasty treatment of choice
    in pregnant women with severe MS whose sx
    can’t be controlled with meds.
•   TEE to eval Mitral valve aparatus and eval for LA
    thrombus
•   Abdominal shielding to limit radiation to fetus
    (Avoid during first trimester)
•   Cardiac surgery can be performed during
    pregnancy but should be avoided unless
    absolutely necessary (best time 24-28 weeks)
    (Maternal mortality 1-5%, fetal 15-38%)
• #30 28 y.o. female 29 weeks pregnant referred
    for progressive dyspnea. h/o rheumatic fever
    and mitral stenosis. 4 wk increase dyspnea. No
    palpitations. Elevated JVP. HR 100.
    Parasternal impulse present. Opening snap and
    grade 2 diastolic rumble….EKG sinus tach, LAE,
    RAD.
•   What do you recommend?
    –   Digoxin
    –   Metoprolol
    –   Warfarin
    –   Ramipril
    –   amlodipine
• #30 metoprolol
  – to slow HR, increase diastolic filling time.
  – If sx persist then diuretic
  – Note: ACE I, ARB contraindicated in
    pregnancy
• #38 35 y.o. female 39 weeks pregnant
  comes to office increasing dyspnea. No
  prior PMH. First pregnancy. JVP 13,
  diffuse apical impulse, apical systolic
  murmur. S3 and S4. Crackles. EKG tachy.
• Diagnosis?
  – Severe AS
  – Severe TR
  – ASD
  – Peripartum cardiomyopathy
  – Pulmonary embolism
 #38    Peripartum Cardiomyopathy
• 1:1,300 to 1:15,000 pregancies in US, higher
  in certain parts of Aftrica
• Risk increased in: African Americans,
  multiple gestations, multiparous, women age
  >30 years, h/o peripartum cardiomyopathy
• Usually occurs during last trimester
  pregnancy or in first 6 mos post partum
  (Most commonly diagnosed in first post
  partum month)
• 50% of women with peripartum
  cardiomyopathy will have improvement in LV
  function within 6 mos after delivery.
• Delivery is recommended
• Unless obstetric reasons for c-sec mode of
  delivery should be vaginal because of
  lower hemodynamic burden
• Because risk of recurrence of peripartum
  cardiomyopathy is common repeated
  pregnancy is ―contraindicated‖—pt’s with
  persistent LV dysfunction and pts with h/o
  serious episode should be counseled to
  avoid repeat pregnancy
      Cardiomyopathy and Pregnancy
              Notes on medical therapy
•   NO ACEI, ARB during pregnancy. (in animals
    fetal hypotension and death. Also early delivery,
    low birth weight, oligohydramnios, neonatal
    anuria and renal failure)
•   Digoxin and hydralazine are considered safe
    during pregnancy and breast feeding.
•   Diuretics can be used if sx not controlled by
    decreased salt and central venous pressue
    elevated. Most experience with thiazides and
    lasix. (diuretics impair uterine blood flow and
    placental perfusion).
•   Metoprolol, atenolol, labetalol have been used
    safely in pregnancy—fetal monitoring
    recommended for risk of intrauterine growth
    retardation and fetal bradycardia.
• #58
• 35 y.o. female who has progressive dyspnea
  days after delivery. EF 20%. Treated ACEI,
  diuretic, B-blocker. Sx resolve. 12 mos after
  delivery asymptomatic and EF 50% off meds.
  She comes to you for counseling re: repeat
  pregnancy.
  – Advise her that she may proceed
  – Resume ACE I during pregnancy
  – Advise her not to become pregnant b/c of risk of
    recurrent peripartum cardiomyopathy that may be
    fatal
  – Evaluate for another cause of cardiomyopathy b/c
    diagnosis of peripartum cardiomyopathy is now in
    question
#58 Advise her not to become pregnant b/c of risk of
recurrent peripartum cardiomyopathy that may be fatal

• Because recurrence of peripartum
  cardiomyopathy is common, repeated
  pregnancy is contraindicated.
• Regarding cardiomyopathy in general and
  pregnancy:
   – Avoid pregnancy is LVEF is less than 40% or
     NYHA functional class is higher than II.
   – Bed rest is often required and close cardiac
     and obstetric monitoring mandatory
   – Treating CHF is more difficult in pregnant
     than in nonpregnant women.
• #104 28 y.o. female with aortic and mitral
  mechanical prosthesis. INR therapeutic. Pre-
  pregnancy consult.
  – Discontinue warfarin and treat with ASA and
    dipyridamole during first trimester
  – Continue warfarin through pregnancy and start
    heparin 5000 U SQ TID plus ASA
  – d/c warfarin and treat with enoxaparin 30 mg SQ BID
    through pregnancy
  – d/c warfarin and initiate dose adjusted unfractionated
    heparin SQ during first trimester and resume
    treatment with warfarin for rest of pregnancy until
    shortly before delivery
  – Use clopidogrel and ASA for first trimester and
    warfarin for rest of pregnancy until shortly before
    delivery
 initiate dose adjusted unfractionated heparin SC during first
 trimester and then resume treatment with warfarin
 ---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------



       Anticoagulation and Pregnancy
• During pregnancy increased risk of thombosis
  or embolism
• Pregnant women with mechanical heart valve
  have a 10% risk for development of
  prosthetic valve thrombosis or another life
  threatening complication
• Data are limited on safety of various
  anticoagulation regimens and controversy
  persists
    Anticoagulation and Pregnancy
• Heparin does not cross the placenta
• 12-24% incidence of thromboembolic
     complications including valve thrombosis in high
     risk pregnant patients treated with SQ
     unfractionated heparin
•    Efficacy of dose adjusted SQ heparin not
     established. Dose should be adjusted so that PTT
     is at lesat 2-3 times control value 6 hours after
     adminstered.
•    Heparin may not provide sufficient
     anticoagulation for very high risk patients (caged-
     ball or tilting disk--Bjork Shiley--mechanical
     prosthesis)
•    Prolonged heparin can lead to thrombocytopenia,
     osteoporosis, alopecia
• Warfarin crosses the placentafetal
  anticoagulationrisk of spontaneous
  abortion, prematurity, fetal deformity,
  stillbirth, retroplacental hemorrhage and
  intracranial hemorrhage.
• Historic reports 30% (more recent data 4-
  10%) risk warfarin embryopathy— bone
  and cartilage abnormalities, nasal
  hypoplasia, optic atrophy, blindness,
  retartdation, seizures--with use in first
  trimester.
  – risk highest if exposure during 6th to 12th wk.
  – Low risk if less than 5 mg QD warfarin dose.
• Warfarin does not enter breast milk
                    Current Recommendations
                    for anticoagulation
                    during pregnancy




C-section if labor occurs during warfarin
anticoagulation due to risk of fetal intracranial
hemorrhage.
Anticoagulation and pregnancy …
Low Molecular Weight Heparin

• Currently data insufficient to support use LMWH
    during pregnancy.
•   It does not cross placenta and no teratogenic
    effects reported.
•   6th ACCP conf supports use of LMWH throughout
    pregnancy except 24 hrs before delivery when
    recommendation is IV unfractionated heparin.
•   However FDA changed labeling to state
    enoxaparin not recommended for prosthetic
    valves during pregnancy.
More notes on Anticoagulation and pregnancy…

• Dipyridamole should not be used during
  pregnancy (no data on clopidogrel or
  ticlopidine)
• Information limited on IIbIIIa inhibitors
  during pregnancy
• 81 mg ASA safe during pregnancy—
  recommended for patients with shunts,
  cyanosis, or biologic-valve prosthesis
  – (A low dose of ASA may also decrease the
    incidence of preeclampsia.)
• Thombolytic therapy has been used in
  pregnancy in emergency
• #68 26 y.o. female 30 weeks pregnant
 murmur noted during pregnancy.
 Asymptomatic. Slight elevated JVP.
 Parasternal lift. S1 normal. S2 prominent,
 fixed split. Grade 2 mid peaking ejection
 murmur LSB. Echo secundum ASD with
 RV enlargement. 8 weeks later in labor.
 What do you recommend?
  – Full anticoagulation in postpartum period
  – Hemodynamic monitoring during delivery
  – ABX propylaxis during delivery
  – Early post partum ambulation
  – Delivery by c-section
• #68 Early post partum ambulation
  – Decrease risk of DVT paradoxical
    embolism
• #47 26 y.o. 30 weeks pregnant murmur
 during pregnancy and intermittently in
 past. Asymptomatic. Slight elevation JVP
 with an A wave. Parasternal lift is noted.
 S1 normal S2 prominent, fixed, split.
 Grade 2 mid peaking ejection systolic
 murmur at LSB. What is most likely Dx?
  – Physiologic murmur of pregnancy
  – ASD with volume overload
  – Pulmonary valve stenosis
  – Aortic regurgitation
  – Mitral stenosis
# 47 ASD with volume overload
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• Other notes on congenital heart
         disease in pregnancy
• Congenital heart disease is the most common
         form of structural heart disease that affects
         women of childbearing age in US
•        Pregnant cyanotic women have a high risk of
         fetal loss. Cyanosis is a recognized handicap to
         fetal growth, resulting in low birth weigh infants
•        The incidence of congenital heart disease in
         offspring of women with congenital heart
         disease is about 5 %.
• #91 20 y.o. female in first trimester
 progressive dyspnea. Acyanotic woman
 with parasternal lift and loud P2. No S3 or
 S4. No murmur. EKG tall P waves II, III,
 F and tall R in V1 and RAD. What is most
 likely dx?
  – Severe pulmonic valve stenosis resulting in RV
    pressure overload
  – Primary pulmonary hypertension
  – Large ASD causing RV enlargement and pulm
    HTN
  – Severe mitral stenosis
• #91 Primary pulmonary hypertension.
  – ASD and VSD that result in severe pulm
    HTN cause cyanosis.
  – In pulm stenosis P2 would be
    diminished or absent.
  – Need to exclude secondary causes
    pHTN.
Severe pulmonary
hypertension in pregnancy
• PA pressure >70% systemic
• Whether secondary or primary carries 30-
  50% risk of maternal death.
• If pulmonary hypertension identified
  counsel against pregnancy
• Termination of pregnancy should be
  considered.
• #98 20 y.o. in first trimester of
 pregnancy progressive dyspnea. You
 diagnose severe pulm HTN. TEE excludes
 shunt. What is associated with lowest risk
 of maternal mortality?
  – Termination of pregnancy
  – Initiation of prostacyclin therapy
  – Intiation of bosentan therapy
  – Initiation of anticoagulation
  – Initiation of ACEI therapy
#98—termination of pregnancy
Cardiac contraindications to pregnancy
         “        ”




                         Severe pulmonary HTN
                         is an absolute
                         contraindication to
                         pregnancy . 30-50%
                         risk maternal death.
Indications for C-section in women with
Cardiovascular Disease
• Obstetric reasons
• Anticoagulation with warfarin
• Controversial Reasons
    – Fixed obstructive cardiac lesion
    – Pulmonary hypertension
    – Unstable aortic lesion
____________________________

• Vaginal delivery is the preferred mode of
  delivery in most women with heart
  disease.
Valvular Heart Disease
#15
• 21 y.o. female, murmur on screening exam. No
 PMH. Runs 3-8 miles daily for cross country.
 No syncope. SOB with windsprints. No FH
 sudden death. HR 52. BP 98/60. 2/6 cresendo
 decresendo murmur loudest LUSB. Which would
 suggest need for echo?
  – Murmur decreases in intensity with valsalva
  – SOB with unusual exercise
  – Soft S3
  – Murmur peaks in intensity in the latter half of
    systole
  – A split S1
#15 Murmur peaks in intensity in the latter half of
systole
• Late-peaking suggests LV outflow
    obstructionfurther testing.
•   Murmur of dynamic subvalvular LV outflow
    obsturction (hypertrophic cardiomyopathy)
    increase with valsalva.
•   AS and PS and MR and TR diminish during
    valsalva.
•   Intensity of innocent flow murmurs also diminish
    during valsalva.
•   Flow murmurs peak in the first half of systole
•   An S3 is common in children and young adults
Echo for evaluation of murmurs
Murmurs….
• VSD: pansystolic, palpable thrill may be
    associated
•   PDA: continuous, machinery-like
•   Increase with Inspiration
    – TR, TS, PS (right sided murmurs)
• Increase with Handgrip
    – Mitral regurgitation
• Aortic Stenosis
    – Decrease with handgrip, decrease with standing,
      decrease during valsalva
• Hypertrophic Obstructive Cardiomyopathy
    – Decrease with handgrip, increase with standing,
      increase during valsalva
• 63 y.o. male farmer. 3/6 holosystolic
 murmur at apex heard throughout and
 louder at left sternal border. LV displaced
 laterally. HR 94. BP 136/80.
 ASYMPTOMATIC. Echo--myxomatous
 degeneration MV with partial flail posterior
 leaflet. LV enlarged. LV EF 52%.
  – Surgery if LV dilated 8 weeks after ACEI
  – Surgery if MIBI normal
  – Surgery if TEE shows repairable valve
  – Surgery despite lack of symptoms
  – Surgery contraindicated based on presence of
    LV dysfunction
Chronic severe MR w/ LV dysfunction
--Surgery despite lack of symptoms
--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------


                      • Indications for surgery in chronic
                           severe mitral regurgitation
                               Symptoms
                               Left ventricular systolic dysfunction
                           (EF<60%, endsystolic diameter>45mm)
                               Atrial fibrillation
                               Pulmonary hypertension

                      • Intervention for chronic severe MR should
                           be considered earlier if successful mitral
                           valve repair is likely
  Chronic Mitral regurgitation

• Organic: Myxomatous degeneration,
  rheumatic, infective endocarditis …
• ―Functional‖: Dilated cardiomyopathy,
  ischemic (prior MI)
• Chronic left ventricular volume overload
• Forward CO preserved by LV dilation at
  expense of increased wall stress
        Chronic Mitral regurgitation
• Vasodilators improve hemodynamics in
  acute MR, role in chronic MR not
  adequately studied. Thus routine use in
  asymptomatic pts not recommended. If
  HTN present, then vasodilator. And, in pts
  with functional MR complicating
  cardiomyopathy, afterload reduction is
  indicated.
• In anorectic drug (fenfluramine and
  dexfenfluramine) induced MR (or AR)
  regurgitation appears to regress in the
  first year after discontinuation of
  exposure.
• # 51. 54 y.o. female evaluated for exertional dyspnea.
  Orthopnea for mos. Rheumatic fever as a child. No
  palpitations. HR 86, BP 124/76. JVP 14. Bibasilar rales.
  Regular rhythm, diminished S1, widely split S2. 3/6
  holosystolic murmur at apex radiating to axilla. 2/6
  holosystolic murmur at LLSB increases with inspiration.
  2/6 decresendo diastolic rumble at apex. EKG sinus,
  RVH, BAE. Echo-- BAE, normal LV size and fxn. RVE,
  normal fxn. Mitral leaflets thickened and restricted.
  Minimal leaflet Ca++ and mild to mod subvalvular
  thickening. Mean grad 11 and valve area 0.9 cm2.
  Severe MR and TR noted. RV systolic 62 mmHg. Best
  course of action?
   – Digoxin
   – ASA
   – Anticoagulation INR 2-3
   – Percutaneous balloon mitral valvotomy
   – Refer for mitral valve repair or replacement
# 51 mitral valve repair or replacement
------------------------------------------------------------------------------------------------------------------------------------

               Interventions Mitral Valve
•     Percutaneous balloon mitral valvotomy:
        – Pliable, non-calcified valve, </= 2+ MR, no other
          cardiac intervention required
        – (3 or 4+ MR, LA thrombus contraindications)
• Open commissurotomy
        – Relatively pliable noncalcified valve, any amount MR,
          no other cardiac intervention required
• MVR
        – Calcified nonpliable valves
• In pregnant women, ballon valvotomy
      associated with fewer fetal complications than
      open commussurotomy
                      Mitral Stenosis
• Often due to previous rheumatic heart disease
• Normal MVA 4-5. Mod MS 1-1.5, Sev MS<1cm2.
• MS exacerbated by a.fib, exercise, stress, fever,
    pregnancy (b/c increased HR leads to shorter diastolic filling period)
•   Abx prophylaxis against endocarditis and
    rheumatic fever (at least 10 yrs after last
    episode or until age 40, lifetime in high risk (ie.
    teachers), salt restriction, diuretics, negative
    chronotropic (prolong filling period) agents.
    Anticoagulation if a.fib or prior thomboembolus.
•   Echo if change in symptoms. Mild to mod pHTN
    (PASP >40) may be indication for more frequent
    follow up.
• #80
• 36 y.o. with substernal chest pressure. 2 mos
  progressive fatigue, dysnea, palps. 2 hours
  began CP to jaw, SOB. BP 110/90. HR 110 and
  irregular. Elevated JVP, crackles, irregular,
  accentuated P2. diastolic rumble at apex. EKG
  a.fib, RBBB, RAD, ST elevation V2-5. Cause?
   – CAD plaque rupture
   – Coronary thromboembolism from LV
     thrombus
   – Coronary thromboembolism from LA
     thrombus
   – Coronary arteritis
   – Coronary vasospasm
• # 80 Coronary embolism from LA
 thrombus
• #75 28 y.o. female with palpitations
 (heavy beat then pause) no associated sx.
 HR 72 BP 108/68. Mid systolic
 nonejection click. EKG sinus no
 preexcitation. Echo posterior leaflet
 prolapse with mild late systolic MR. Holter
 multiple PVC’s. Next step?
  – History and PE in 1-2 yrs
  – TEE
  – Lisinopril
  – Echo in 6 mos
  – Propafenone therapy
#75 History and PE in 1-2 years
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           –Mitral Valve prolapse
• Most patients with MVP have a good
  prognosis
• Patients with myxomatous disease are at
  risk for valve degeneration with MR
• Endocarditis prophylaxis in patients with
  MR or leaflet thickening
• MVP syndrome—palpitations and atypical
  chest pain
#23
• 76 y.o. male to your office for yearly exam.
    Over 6 mos decreased exercise tolerance—
    dyspnea and CP uphill. No SOB at rest. No
    syncope. CAD. Lipids. h/o stent. ASA. Lipitor.
    HR 82. BP 142/82. 3/6 cresendo decresendo
    systolic RUSB to carotids. Delayed upstroke of
    pulse. Echo LVH, nl fxn. Peak aortic 86, mean
    44. Mid RCA 70%. 0.7 cm2.
•   What is the best course of action?
    –   Refer AVR and CABG
    –   Refer valvotomy and PTCI
    –   DP MIBI
    –   Exercise testing
    –   No intervention
# 23 AVR plus CABG
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• # 116 71 y.o. male CHF. LV impulse
    enlarged and lateral. Late peaking
    cresendo decresendo systolic murmur.
    Echo global LV dysfunction. EF 20-25%.
    AV calcified decreased opening. Peak
    grad 26 mean 16. What test next?
      – TEE
      – Exercise stress test with EKG
      – Dobutamine stress echo
      – Adenosine MIBI
# 116 Dobutamine stress echo
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         – Low gradient Aortic Stenosis
• Aortic valve gradients depend on flow
• Patients with LV dysfunction have increased
       perioperative risk
•      An increase in aortic gradients in setting systolic
       augmentation of LV suggests AS is severe. (AVR
       better long term survival than med if severe AS and contractile reserve)

• Contractile reserve without an increase in
       gradients suggest that stenosis is not severe.
•      Lack of contractile reserve suggest a poor
       prognosis after AVR. (AVR worse long term survival than meds
       if no contractile reserve)
   More notes on Aortic Stenosis …
• Asymptomatic patients with severe AS
  have a good prognosis
• Severe AS valve area <1.0cm2, mean
  gradient >50 mmHg.
• Consider patient size. Valve area of
  0.45cm2/m2 is severe.
• Echo follow up in asymptomatic AS
  – Every 5 years mild
  – Every 2 years moderate
  – Every year severe (to detect development
    asymptomatic LV dysfunction)
      More notes on Aortic Stenosis …
• AVR in symptomatic patients with severe AS.
• Consider AVR in asymptomatic patients with
    severe stenosis AND left ventricular dysfunction,
    marked LVH, hypotension on exercise testing, or
    moderate or greater valve calcification and a
    rapid increase in aortic jet velocity.
•   Added risk for noncardiac surgery in severe
    symptomatic AS (mortality rate as high as 10%)
    – if elective AVR first,
    – if not surgical (AVR) candidate percutaneous
      valvuloplasty may be considered
• If severe AS but asymptomatic noncardiac
    surgery can be performed with close
    intraoperative monitoring with only slightly
    increased risk.
• # 66 36 y.o. man to ICU with abrupt
 hypotension and hypoxemia. Intubated.
 38.1, 121, 88/30, pulm edema. Regular
 with summation gallop. No murmur. TTE
 inadequate. TEE bicuspid AV partially
 destroyed with vegetations. Severe AI.
 Normal LV fxn. You start abx. Which is
 indicated?
  – B-blocker
  – Nitroprusside
  – Intraaortic balloon pump
  – Cath and coronary arteriography
  – Transfer for surgery for emergent AVR
(#66 Nitroprusside)
• After load reducing therapy with or
  without inotropic support to optimize
  forward cardiac output
• IABP contraindicated in aortic regurg
• Depending on response to intensive
  medical intervention patient may require
  urgent surgery. If surgery can be
  deferred to allow a period of therapy with
  ABX early postop infection after AVR is
  less likely.
Notes on acute valve regurgitation
• Patients with acute severe AR or MR are
    symptomatic and may present with cardiogenic
    shock
•   Many physical findings of chronic severe
    regurgitation are NOT present in patients with
    acute severe regurgitation
•   Diagnosis is with echo
•   IABP useful in acute severe MR but
    contraindicated in AR
•   Urgent or emergent surgical intervention is
    usually indicated in acute mitral or aortic
    regurgitation
• # 85 86 y.o. female evaluated for recent
 abrupt onset dyspnea. She had a
 bioprosthetic AV placed 16 years ago for
 calcific AS. No fever. Harsh cresendo
 decresendo systolic murmur at RUSB to
 carotids. What is cause of SOB?
  – Prosthetic valve failure
  – Paraprosthetic leak
  – Thrombus formation
  – Mitral stenosis and mitral regurgitation
  – Infective endocarditis
• #85 Prosthetic valve failure
 After 16 yrs valve at risk for failure, cuspal
 calcification and then fracture leading to acute
 AR. Intuitively should expect diastolic murmur.
 However murmur of AR may not be prominent
 whereas the increase in stroke volume across
 calcified bioprosthesis is more audible.
 Thombosis not likely in bioprosthetic valve
 placed years earlier.

• KEY POINT—In patients with prosthetic
 valves and new/changed cardiac
 symptoms, need to evaluate valve.
• #100 35 y.o. female for f/up AVR 3 mos
 ago for congenital bicuspid aortic valve.
 No a.fib or thromboembolism. Echo
 shows normal mechanical aortic valve.
  – Coumadin INR 2-3
  – INR 2.5-3.5
  – INR 2-3 plus ASA 100 mg
  – INR 2.5-3.5 plus ASA 100 mg
  – ASA 650 mg QD
#100 INR 2-3. Prosthetic Valves
Preoperative Cardiac
     Evaluation
• ACC/AHA Guidelines.
  – The need for preoperative testing is determined by:
     • 1)Clinical predictors of the patient
       (minor/intermediate/major).
     • 2)Risk of the surgery (low/intermediate/high).
     • 3)Patient’s functional status (</> 4 METS).

  – Remember that all patients requiring emergent
    surgery go to the OR immediately regardless of
    cardiac risk.

• Don’t forget benefit of Beta-blockade to goal HR 60
Patient Clinical Predictors
Risk of Surgery
Functional Capacity
Shortcut to noninvasive testing in
preop patients if any two factors
are present
  – Intermediate clinical predictors (class 1
    or 2 angina, prior MI based on Q’s,
    compensated or prior heart failure, diabetes,
    or renal insufficiency)
  – Poor functional capacity
  – High risk surgery (emergency—may not
    have a choice---,aortic repair, peripheral
    vascular surgery, prolonged surgical
    procedures with large fluid shifts or blood
    loss)

								
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