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Ann Thorac Surg 1999;67:1312-1314
© 1999 The Society of Thoracic Surgeons


Original Articles

Perinatal mitral valve interventions: a report of 10 cases

Cemal Levent Birincioglu, MDa, Seref A. Küçüker, MDa, Elif G. Yapar, MDb, Ülkü Yildiz, MDa, Ahmet T. Ulus, MDa, Birol Yamak, MDa, Salih Fehmi Katircioglu, MDa, Oguz Tasdemir, MDa

a Department of Cardiovascular Surgery, Türkiye Yüksek Ihtisas Hospital, Ankara, Turkey
b Department of Obstetrics and Gynecology, Zekai Tahir Burak Women’s Hospital, Ankara, Turkey

Accepted for publication November 4, 1998.

Address reprint requests to Dr Birincioglu, Cardiovascular Surgery Clinic, Türkiye Yüksek Ihtisas Hospital, 06100 Sihhiye, Ankara, Turkey


    Abstract
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
Background. Rheumatic mitral valve stenosis is still an endemic disease in some parts of the world and may complicate pregnancy and perinatal period. During the 10-year period between January 1988 and December 1997, 10 pregnant women with mitral stenosis were operated on.

Methods. Combined cesarean delivery and closed mitral valvulotomy (CMV) were performed on 6 patients, combined cesarean delivery and Mitral Valve Replacement (MVR) were performed on 1 patient, and 3 patients had CMV during their third trimester.

Results. There was 1 stillbirth. All other patients and delivered babies were healthy. MVR was necessary for mitral restenosis in one patient 5 years after her CMV. Three of the remaining patients had some degree of restenosis but did not require reoperation.

Conclusion. CMV when indicated during pregnancy can be performed with low risk. For symptomatic patients responding to medical therapy, a combined approach of cesarean section and CMV will prevent possible complications that may arise on perinatal period due to hemodynamic fluctuation.


    Introduction
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
Rheumatic fever is still an endemic disease in some parts of the world and mitral stenosis is frequent. In case of pregnancy with mitral stenosis, special problems may arise both for the mother and the fetus. Stroke volume and cardiac output increases during pregnancy and further hemodynamic changes occur during labor and delivery [13]. These physiological changes in the presence of mitral stenosis may lead to cardiac decompensation and end up with the loss of mother and fetus [4]. To prevent such events, careful follow-up and, when indicated, surgical intervention is necessary. We followed 10 pregnant mitral stenosis patients with symptoms of decompensation. Six were medically treated with digitalis and diuretics, had some improvement in their symptoms, and had a combined cesaerean section and Closed Mitral Valvulotomy (CMV) at term. Three patients did not respond to medical therapy at all and CMV was performed during pregnancy. One of these patients had a stillbirth. One other patient with rheumatic calcified mitral disease partially responded to medical therapy and had a combined cesarean section and Mitral Valve Replacement (MVR) at term.


    Patients and methods
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
Between 1988 and 1997, 10 pregnant women (mean ± SD age, 24 ± 5) with rheumatic mitral stenosis underwent perinatal mitral valve intervention at our institution. Surgery was indicated in perinatal period due to clinical deterioration. One patient was in stage II, 4 were in stage III and 5 were in stage IV of the clinical classification of New York Heart Association. In all cases mitral valve pathology was assessed clinically and echocardiographically. Valval leaflets and tension apparatus were analyzed for mobility, chordal shortening, thickening and papillary muscle involvement. There was calcification in only 1 of the 10 patients. In 2 cases mitral stenosis was moderate (mitral area 1.5 cm2), in 5 it was severe (mitral area less than 1.2 cm2) and in 4 it was very severe (less than 0.9 cm2). Pulmonary edema occurred in 6 and hemoptysis occurred in 3.

Surgical intervention during pregnancy
Treatment with digitalis and diuretics did not improve symptoms in 3 cases and CMV was performed during their third trimester as an emergency procedure. These 3 patients received continuos infusion of antispasmodic drugs (isoxsuprine or salbutamol) the day before surgery. Premedication with oral diazepam (10 mg) and intramuscular atropin was given an hour before surgery. Induction of anesthesia was obtained with phenobarbital (5–10 mg per kg) then succinyl choline (1 mg per kg) was administered for endotracheal intubation. Maintenance of anesthesia was provided with fentanyl and pavulon and equal mixtures of oxygen and nitrous oxide. Additional doses of phenobarbital were given when needed during operation.

Commissurotomy was performed through the 4th or 5th left intercostal space while patient was in right lateral decubitis position. A Tubb’s dilator was set to open 3.5 cm. An index finger was introduced through the left atrial appendage and the Tubb’s dilator through the apex of the left ventricle. With the guidance of index finger the dilator was placed in best possible position in the mitral aperture to achieve maximum dilatation without creating mitral regurgitation. At the end of the procedure an index finger was used to assess the adequacy of valvulotomy and the degree of iatrogenic mitral regurgitation. The results were satisfactory in all cases and only mild mitral incompetence was observed in 1 patient.

Combined cesarean section and mitral valve intervention
Some hemodynamic improvement was achieved for the other 7 patients with medical therapy. These patients were then followed up with medications, bed rest and hospitalization when needed until term. Six had combined cesarean section and CMV and 1 with calcific mitral valve had combined cesarean section and MVR. This strategy was adopted to prevent hemodynamic compromises during delivery and immediate postnatal period on these high-risk patients.

Induction of anesthesia for combined surgery of cesarean section and CMV or MVR was with pentotal (4–6 mg per kg) and then lystenon (1 mg per kg) was administered for endotracheal intubation. Following the delivery of the baby maintenance of anesthesia was provided with fentanyl and pavulon. When cesarean section was completed patients were repositioned, repainted and draped. CMV was performed as described above. For the last 2 patients transesophogeal echocardiography was also used for the assessment of mitral valve status before and after the valvulotomy. MVR was performed through midline sternotomy with standard cardiopulmonary bypass and mild hypothermia. A bileaflet mechanical prosthesis (St. Jude Medical, 29 Mitral) was used.

Postoperative care
The 10 patients taken to the intensive care unit were monitored with electrocardiography, arterial and central venous pressures, blood gases and urine output and were extubated within 6 to 10 hours. They were kept in the intensive care unit for 24 hours with uterotonic infusion. Oral warfarin was started on first postoperative day for the patient receiving the mechanical valve.


    Results
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
There were no operative mortalities. All but 1 of the delivered babies were healthy. Three patients with CMV during the third trimester went to term without further decompensation and 2 delivered healthy babies. One patient had a stillbirth. Of the other 7 patients, 6 had combined cesarean section and CMV and 1 calcific mitral stenotic patient had combined cesarean section and MVR. There was no significant morbidity postoperatively and with the exception of the patient receiving warfarin, all patients were able to breast-feed. Patients have been followed for a mean period of 45 months. One patient who had combined cesaerean section and CMV developed restenosis requiring surgical intervention and had MVR with mechanical prosthesis 5 years after the initial operation. Three of the remaining patients had some degree of restenosis but have not required replacement to the present date.


    Discussion
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
The normal cardiovascular response to pregnancy is characterized by a gradual increase in stroke volume and cardiac output. These changes begin during the first trimester and reach a maximum around the 20th week of gestation [48]. Blood volume is also increased by 40% and although the red blood cell volume increases. It is only about 18% and this results in fall of hemotocrit from an average of 40% to 33% for the last 10 weeks of pregnancy. Peripheral edema is a normal occurrence in uncomplicated pregnancy and can occur in the absence of either cardiac or renal disease. Increased tissue hydration is considered universal in normal pregnancy and clinical edema is found in 50% to 80% of healthy gravid women [9]. Estrogen has been found to increase myocardial contractility by what may be a direct effect on the contractile proteins [1012]. Estrogen and progesterone concentrations rise progressively during gestation and by stimulating an increase in circulating levels of aldosterone cause retention of sodium and fluid [13]. The average increase in exchangeable sodium is about 500 mEq to 600 mEq, and in the average pregnant woman total body water increases by about 8.5 L [14].

All these physiological changes may lead to cardiac failure if the heart is diseased. In cases of mitral stenosis, acute or chronic interstitial pulmonary edema and hemoptysis may develop. Some investigators showed that pulmonary edema is the leading cause of maternal death [7,8,15].

Labor and delivery are particularly stressful for women with severe mitral stenosis. Pain, work of labor and anxiety cause tachycardia and increase chances of rate related heart failure. Cardiac output increases 50% during contractions. Labor is associated with a threefold increase in oxygen consumption which is greatly influenced by the form of anesthesia and analgesia used. But no form of anesthesia will prevent the rise of cardiac output during contractions.

Clinical status often deteriorates even more during the immediate post partum period when venous return increases after fetus is removed and caval compression has been relieved. As Clark and coworkers showed, pulmonary capillary wedge pressures usually increase by 20% to 40% in this period [16]. They hypothesized that this is due to loss of the low resistance placental circulation as well as auto transfusion from the lower extremities, pelvic veins, and the now empty uterus.

Additionally a late transient postpartum increase in blood volume has been attributed to the absorption of extracellular fluid accumulated during gestation, in to the circulation. Puerperal diuresis then reduces total body water, and nongravid blood volume is restored but this usually takes 4 to 6 weeks [14]. In case of mitral stenosis, both the abrupt and late elevations in preload may lead to an increase in pulmonary edema and heart failure.

Therapeutic approaches to patients with significant mitral stenosis are designed to reduce the heart rate and to decrease blood volume. Pregnant women with significant mitral stenosis should be followed with limitation of activity, avoidance of hypervolemia, control of arrhythmias and treatment of fluid overload. If these measures cannot prevent decompensation, CMV should be considered. In the early 1950s, Brock [17], Cooley and Chapman [18], Logan and Turner [19], and Mason [20] reported the first cases of CMV during pregnancy. Since then it has gained large acceptance. Szekely and coworkers [21] reported 2 maternal losses and 8 fetal losses in 69 cases of CMV during pregnancy. Vosloo and coworkers [22] reported 41 CMVs performed in 39 pregnant women. There were no maternal deaths and overall fetal survival was 87.8%. Another report from Tunisia [23] of 7 CMVs gave no maternal or fetal loss. Becker described 101 cases of CMV during pregnancy without any maternal death but 3 fetal loses [24].

As one can see from the previous reports, in case of decompensation unresponsive to medical therapy, CMV during gestation is the best option with very low risk for the mother and acceptable risk for the fetus. This was also our strategy for 3 of our cases unresponsive to medical therapy. For the other 7 patients, having some response to medical therapy, we decided to wait until term and combined cesarean section and mitral valve interventions. These patients had a higher risk than the asymptomatic mitral stenotic patients. Normal labor, delivery, and immediate and late postpartum volume changes could risk both the mother and the fetus.

One may advise CMV prior to term but this we believe carries some risk for the fetus. In the literature fetal mortality for CMV during pregnancy fluctuates between 0 and 12.2% [1518]. Besides, it is 2 times more stress for the patient during this short and busy period. As our experience suggests, CMV is safe, easy, and does not add any significant morbidity when combined with cesarean section. Transesophageal echocardiography guidance for CMV may further increase the quality of the procedure as it provides almost direct vision of the mitral valve on beating heart. Transesophageal echocardiography during pregnancy is reported safe [25]. We believe that combining cesarean section and mitral valve intervention is the best option for symptomatic but stabilized mitral stenotic patients.


    References
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 

  1. Oakley C.M. Cardiovascular disease in pregnancy. Can J Cardiol 1990;6(Suppl B):33B.
  2. Longo L.D. Maternal blood volume and cardiac output during pregnancy: A hypothesis of endocrinologic control. Am J Physiol 1983;245:R720.[Abstract/Free Full Text]
  3. Robson S.C., Hunter S., Boys R.J. Serial study of factors influencing changes in cardiac output during human pregnancy. Am J Physiol 1989;256:H1060.[Abstract/Free Full Text]
  4. Gazzangia A. Cardiac surgery during pregnancy. In: Elkayam U., Gleicher N., eds. Cardiac problems in pregnancy, 2nd ed. New York: Alan R Liss Inc, 1990:259.
  5. Rush R.W., Fraser R.C., Commerford P.J. Management of heart disease in pregnancy. S Afr Med J 1986;61:192-195.
  6. Ueland K. Cardiac surgery and pregnancy. Am J Obstet Gynecol 1965;92:148-162.
  7. EI-Maraghy M., Abou Senna I., EI-Tehewy F., Bassiouni M., Ayoub A., EI-Sayed H. Mitral valvotomy in pregnancy. Am J Obstet Gynecol 1983;145:708-710.[Medline]
  8. Harken D.E., Taylor W.J. Cardiac surgery during pregnancy. Clin Obstet Gynecol 1961;4:697-709.
  9. Robertson E.G. The natural history of oedema during pregnancy. J Obstet Gynecol Br Comm 1971;78:520-529.[Medline]
  10. King T.M., Whitehorn W.V., Reeves E. Effect of estrogen on composition and function of cardiac muscle. Am J Physiol 1959;196:1282-1287.[Abstract/Free Full Text]
  11. Ueland K., Parer J.T. Effects of estrogens on the cardiovascular system of the pregnant woman. Am J Obstet Gynecol 1966;96:400-406.[Medline]
  12. Csapo A. Actomyosin formation by estrogen action. Am J Physiol 1950;162:40-44.
  13. Hytten F.E., Thompsan A.M. Water and electrolytes in pregnancy. Br Med Bulletin 1968;24:15-18.[Free Full Text]
  14. Szekely P., Snaith L. Heart disease and pregnancy. Edinburgh: Churchill-Livingstone, 1974.
  15. Szekely P., Snaith L. The place of cardiac surgery in the management of the pregnant woman with heart disease. J Obstet Gynecol 1963;70:69-77.
  16. Clark S.C., Phelan J.P., Greenspoon J. Labor and delivery in the presence of mitral stenosis: central hemodynamic observations. Am J Obstet Gynecol 1985;152:984-988.[Medline]
  17. Brock R.C. Valvotomy in pregnancy. Proc R Soc Med 1952;45:538-543.
  18. Cooley D.A., Chapman D.W. Mitral commissurotomy during pregnancy. JAMA 1952;150:1113-1117.
  19. Logan A., Turner R.W.D. Mitral valvulotomy in pregnancy. Lancet 1952;1:1286-1290.
  20. Mason J. In discussion with Stabler FE, Szekely PJ. Obstet Gynecol Br Emp 1952;59:569–73.
  21. Szekely P., Turner R., Snaith L. Pregnancy and the changing pattern of rheumatic heart disease. Br Heart J 1973;35:1293-1303.[Free Full Text]
  22. Vosloo S., Reichart B. The feasibility of closed mitral valvotomy in pregnancy. J Thorac Cardivasc Surg 1987;53:587-591.[Medline]
  23. Abid A., Abid F., Zargouni N., Khayati A. Closed mitral valvotomy in pregnancy: a study of seven cases. Int J of Cardiol 1990;26:319-321.
  24. Becker R.M. Intracardiac surgery in pregnant woman. Ann Thorac Surg 1983;36:453-457.[Abstract]
  25. Stoddard M.F., Longaker R.A., Vuocolo L.M. Transesophogeal echocardiography in the pregnant patient. Am Heart J 1992;124:785-787.[Medline]




This Article
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Oguz Tasdemir
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