{"id":43093,"date":"2014-05-19T12:08:41","date_gmt":"2014-05-19T16:08:41","guid":{"rendered":"http:\/\/blogs.nejm.org\/cardioexchange\/?post_type=discussion&p=43093"},"modified":"2014-06-02T15:47:09","modified_gmt":"2014-06-02T19:47:09","slug":"case-a-young-pregnant-woman-with-prior-valve-disease-and-increasing-dyspnea-on-exertion","status":"publish","type":"post","link":"https:\/\/blogs.nejm.org\/cardioexchange\/2014\/05\/19\/case-a-young-pregnant-woman-with-prior-valve-disease-and-increasing-dyspnea-on-exertion\/","title":{"rendered":"Case: A Young Pregnant Woman with Prior Valvular Disease and Increasing Dyspnea on Exertion"},"content":{"rendered":"

A 22-year-old woman is referred for cardiac evaluation during the 35th week of her first pregnancy. She had undergone mechanical aortic and mitral valve replacement for unknown valvular disease after immigrating to the U.S. at age 12. She has had no cardiology follow-up for the past 3 years. She first noticed fatigue and shortness of breath on exertion 2 years ago. Now, in the late stages of pregnancy, she notes a marked increase in dyspnea on exertion (she walks about 3 blocks before needing to rest), trace lower-extremity edema, and no orthopnea. Her current medications include warfarin and prenatal vitamins.<\/p>\n

Transthoracic echocardiography reveals normal LV systolic function, a mean aortic valve gradient of 108 mm Hg, a peak gradient of 158 mm Hg, a peak velocity of 7 m\/sec, and a mean mitral valve gradient of 12 mm Hg. The valve shows no evidence of thrombus. A chest x-ray is normal.<\/p>\n

Questions:<\/b><\/p>\n

    \n
  1. How would you further assess this patient\u2019s current symptoms?<\/li>\n
  2. What additional information, if any, would be helpful in deciding how to manage this patient?<\/li>\n
  3. How would you further evaluate this patient\u2019s valves?<\/li>\n
  4. What recommendations would you make regarding anticoagulation?<\/li>\n
  5. Would you make specific recommendations regarding peripartum management (e.g., method of delivery, anesthesia, hemodynamic monitoring)?<\/li>\n<\/ol>\n

    Response:<\/strong><\/p>\n

    James Fang, MD<\/a><\/strong><\/p>\n

    May 27, 2014<\/p>\n

    1. <\/i>How would you further assess this patient\u2019s current symptoms?<\/i><\/p>\n

    The clinical dilemma is sorting out the cause of the increased velocities through the mitral and aortic valves. Because pregnancy is associated with a 50% increase in circulating blood volume and a subsequent increase in cardiac output, blood velocity through any fixed orifice will rise and result in a transvalvular gradient; anemia also exacerbates this phenomenon. However, in the presence of a mechanical valve, lack of anticoagulation in the hypercoagulable state of pregnancy, and a history of exertional dyspnea, prosthetic valvular stenosis (e.g., from thrombosis, pannus ingrowth, or both) is in the differential diagnosis. The patient should undergo transesophageal echocardiography to further assess function of the valves. If diagnostic uncertainty persists, fluoroscopy or CT imaging may be of use.<\/p>\n

    2. <\/i>What additional information, if any, would be helpful in deciding how to manage this patient?<\/i><\/p>\n

    Measuring B-type natriuretic peptide may be useful in assessing the wall stress, although mitral stenosis may be protecting the LV from volume overload. In this case, there should also be concomitant pulmonary hypertension, which should be assessed on echocardiogram. If not assessable noninvasively, right heart catheterization would be reasonable.<\/p>\n

    3. <\/i>How would you further evaluate this patient\u2019s valves?<\/i><\/p>\n

    In rare instances, direct LV puncture can be used to assess intraventricular pressures when the aortic and mitral valves are both mechanical. In this case, noninvasive means should be sufficient for a diagnosis.<\/p>\n

    4. <\/i>What recommendations would you make regarding anticoagulation?<\/i><\/p>\n

    Anticoagulation should be initiated in the hospital with either low-molecular-weight or unfractionated heparin. Plans for controlled delivery of the baby should be made.<\/p>\n

    5. <\/i>Would you make specific recommendations regarding peripartum management (e.g., method of delivery, anesthesia, hemodynamic monitoring)?<\/i><\/p>\n

    A heart team is critical to this patient\u2019s management. Obstetricians, cardiac surgeons, and cardiologists who specialize in high-risk patients must assess all information in order to make recommendations regarding delivery with or without concomitant surgical approaches to the valvular disease, if any is identified.\u00a0 Because cardiac surgery in the mother poses significant risk to mother and fetus, such an approach is generally recommended only for advanced, medically refractory symptoms. If the valves have significant dysfunction, hemodynamic monitoring should be considered at the time of delivery. In an extreme case of heart failure, immediate postpartum valve replacement may be necessary.\u00a0 Spontaneous vaginal delivery, given the associated extreme hemodynamic changes, is likely to be avoided.<\/p>\n

    Follow-up<\/strong><\/p>\n

    Reva Balakrishnan<\/a><\/p>\n

    June 2, 2014<\/p>\n

    As suggested, this difficult case became a multidisciplinary discussion among OB\/Gyn, anesthesia, CV surgery, and cardiology. Subsequently obtained outside hospital records revealed that the patient had 2 prior echocardiograms showing similarly elevated gradients. Given her unclear adherence to warfarin and symptoms that had started before pregnancy, either pannus ingrowth, chronic thrombosis, or both were assumed to be the cause of the valve dysfunction. As the 2014 ACCF\/AHA valvular heart disease guidelines recommend, the patient was continued on warfarin (class IB) in addition to low-dose aspirin. Heparin and low-molecular-weight heparin (LMWH) are associated with valve thrombosis in pregnancy; LMWH confers a lower risk for thrombosis if anti-Xa levels are monitored closely and is recommended only in the first trimester if the daily dose of warfarin exceeds 5 mg.<\/p>\n

    Before her valve could be evaluated further, the patient began to have contractions and was admitted for preterm labor. Anticoagulation was switched from warfarin to an intravenous unfractionated heparin drip. Monitoring showed fetal distress, and the patient was taken emergently for a C-section with a cardiology team that used general anesthesia in a controlled setting with anesthetics that are associated with a lower risk for hypotension. A pulmonary artery catheter was not used during delivery, as the patient did not appear to be in decompensated heart failure on admission. The baby was delivered without complications, and the mother was monitored postpartum in the CCU, given the expected hemodynamic changes (increase in cardiac output and intravascular volume due to uterine involution).<\/p>\n

    A transthoracic echocardiogram, performed 1 week postpartum, showed improved but still severe gradients across both the aortic and mitral valves. The patient transitioned back to anticoagulation with warfarin. A transesophageal echocardiogram was unable to establish the cause of the valve dysfunction. Postpartum, the patient\u2019s dyspnea improved, but she remained symptomatic with limited exercise tolerance. She underwent double mechanical valve replacement 1 month postpartum; both the aortic and mitral valves showed pannus ingrowth.<\/p>\n","protected":false},"excerpt":{"rendered":"

    Reva Balakrishnan presents the case of a 22-year-old pregnant woman with a history of valvular disease who is experiencing an increase in dyspnea on exertion. <\/p>\n","protected":false},"author":325,"featured_media":0,"comment_status":"open","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[1],"tags":[2141,768,1449,2192],"class_list":["post-43093","post","type-post","status-publish","format-standard","hentry","category-general","tag-aortic-valve-disease","tag-mitral-valve","tag-pregnancy","tag-valvular-heart-disease"],"_links":{"self":[{"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/posts\/43093","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/users\/325"}],"replies":[{"embeddable":true,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/comments?post=43093"}],"version-history":[{"count":0,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/posts\/43093\/revisions"}],"wp:attachment":[{"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/media?parent=43093"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/categories?post=43093"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/tags?post=43093"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}