2 The initial core management choices here were reasonable; indeed the prior management was essentially exactly as our center would recommend. She was commenced on Duloxetine, a serotonin/ norepinephrine reuptake inhibitor. During her next clinic visit, she reported marked improvement in symptoms, except for headache and mild cognitive impairment. She was started on Cerefolin to help the memory loss [2]. 3. Discussion Multiple cardiovascular adaptations occur during pregnancy, which are essential for successful completion of pregnancy. These include an increase in cardiac output, sodium, and water retention with increase in expansion of blood volume and a reduction in peripheral vascular resistance and dias- tolic blood pressure [3]. These cardiovascular adaptations continue in the postpartum period and allow for return to a nonpregnant state. These changes in the postpartum period have not been well reported or studied [4]. Our patient developed recurrent episodes of syncope in the postpar- tum period. Postpartum syncope with signiﬁcant maternal morbidity and one infant mortality has been reported previously [1]. There have been reports that patients with POTS can have a favorable outcome during pregnancy and in postpartum period [5, 6]. The joint hypermobility syndrome might have predisposed our patient to symptoms of orthostatic intolerance and made her vulnerable especially as she returned to the prepregnant state with gradual loss of estrogen/progesterone, induced ﬂuid retention in the postpartum period. In patients with POTS, the main mechanism is the con- sistent failure of the peripheral vascular system to increase resistance during upright posture. Patients with joint hyper- mobility syndrome even have more diﬃculty owing to loss of supporting connective tissues in the vessels. Orthostatic intolerance develops in these patients due to the presence of abnormally elastic connective tissue in the vasculature. This results in an increase in vessel distensibility in response to the augmented hydrostatic pressure that occurs during orthostatic stress. Consequently, there is excessive peripheral venous pooling with a resultant compensatory tachycardia. About 70% of patients with hypermobility syndrome may suﬀer from some form of orthostatic intolerance due to sympathetic dys-regulation [7]. Patients with POTS can present with syncope without a substantial fall in blood pressure. Increase in cerebrovascular resistance occurring during orthostatic stress can explain loss of consciousness in these patients [8]. These patients are usually treated with ﬂudrocortisone [9] midodrine [10], methylphenidate [11], and selective serotonin reuptake inhibitors [12, 13]. Combined selective serotonin reuptake inhibitors and selective norepinephrine reuptake inhibitors such as duloxetine are most eﬀective. Duloxetine is postulated to alter serotonin receptor density in brainstem area and thus alter autonomic tone. In our experience, we have found that use of combined selective serotonin reuptake inhibitors and selective nore- Cardiology Research and Practice pinephrine reuptake inhibitors has been more eﬀective in POTS than in neurocardiogenic syncope [14]. 4. Conclusion POTS in the postpartum period can have serious conse- quences; indeed the risks associated with syncope can be life threatening not only to mother but also to the child as well. Early recognition and proper management of these patients are essential to prevent serious morbidity and mortality associated with this clinical entity. Long-term outcomes in patients with postpartum POTS are unknown. References [1] B. P. Grubb, D. Kosinski, D. Samoil, A. Pothoulakis, M. Lorton, and K. Kip, “Postpartum syncope,” Pacing and Clinical Electrophysiology, vol. 18, no. 5, pp. 1028–1031, 1995. [2] K. Nilsson, L. Gustafson, and B. Hultberg, “Improvement of cognitive functions after cobalamine/folate supplementation in elderly patients with dementia and elevated plasma homo- cysteine,” International Journal of Geriatric Psychiatry, vol. 16, pp. 609–614, 2001. [3] K. Ueland, “Maternal cardiovascular dynamics. VII. Intra- partum blood volume changes,” American Journal of Obstetrics and Gynecology, vol. 126, no. 6, pp. 671–677, 1976. [4] W. A. Walters, W. G. MacGregor, and M. Hills, “Cardiac output at rest during pregnancy and the puerperium,” Clinical Science, vol. 30, no. 1, pp. 1–11, 1966. [5] K. A. Glatter, D. Tuteja, N. Chiamvimonvat, M. Hamdan, and J. K. Park, “Pregnancy in postural orthostatic tachycardia syndrome,” Pacing and Clinical Electrophysiology, vol. 28, no. 6, pp. 591–593, 2005. [6] K. Kanjwal, B. Karabin, Y. Kanjwal, and B. P. Grubb, “Outcomes of pregnancy in patients with preexisting postural tachycardia syndrome,” Pacing and Clinical Electrophysiology, vol. 32, no. 8, pp. 1000–1003, 2009. [7] Y. Gazit, A. M. Nahir, R. Grahame, and G. Jacob, “Dysautono- mia in the joint hypermobility syndrome,” American Journal of Medicine, vol. 115, no. 1, pp. 33–40, 2003. [8] J. Jordan, J. R. Shannon, B. K. Black, S. Y. Paranjape, J. Barwise, and D. Robertson, “Raised cerebrovascular resistance in idiopathic orthostatic intolerance: evidence for sympathetic vasoconstriction,” Hypertension, vol. 32, no. 4, pp. 699–704, 1998. [9] J. Freitas, R. Santos, E. Azevedo, O. Costa, M. Carvalho, and A. F. de Freitas, “Clinical improvement in patients with orthostatic intolerance after treatment with bisoprolol and ﬂudrocortisone,” Clinical Autonomic Research, vol. 10, no. 5, pp. 293–299, 2000. [10] B. P. Grubb, B. Karas, D. Kosinski, and K. Boehm, “Prelim- inary observations on the use of midodrine hydrochloride in the treatment of refractory neurocardiogenic syncope,” Journal of Interventional Cardiac Electrophysiology, vol. 3, no. 2, pp. 139–143, 1999. [11] B. P. Grubb, D. Kosinski, A. Mouhaﬀel, and A. Pothoulakis, “The use of methylphenidate in the treatment of refractory neurocardiogenic syncope,” Pacing and Clinical Electrophysi- ology, vol. 19, no. 5, pp. 836–840, 1996. [12] B. P. Grubb, D. Samoil, D. Kosinski, K. Kip, and P. Brewster, “Use of sertraline hydrochloride in the treatment of refractory