CASE REPORT
doi:10.1093/europace/eun075
Incessant right ventricular outflow tract ventricular tachycardia due to subacute postpartum thyroiditis Subbareddy Vanga1, Dimpi Patel2, Huagui Li3, and Dhanunjaya Lakkireddy4* 1
St Luke’s Hospital, Chesterfield, MO, USA; 2Cleveland Clinic, Cleveland, OH, USA; 3Minnesota Heart Center, Minneapolis, MN, USA; and 4Mid America Cardiology at University Kansas Hospitals, Suite G600, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA *Corresponding author. Tel: þ1 913 588 9611; fax: þ1 913 588 9770. E-mail address:
[email protected] Received 28 July 2007; accepted after revision 9 March 2008; online publish-ahead-of-print 9 April 2008
Case report A previously healthy 26-year-old, 4-month postpartum primipara presented with palpitations and pre-syncope and Holter monitoring shows frequent monomorphic ventricular tachycardia (VT). She denies any other symptoms. On admission she was haemodynamically stable and ECG in emergency room showed sustained monomorphic VT (cycle length, 240 ms; left bundle branch abnormality-inferior axis morphology, and right axis deviation) consistent with a right ventricular outflow tract (RVOT) origin. The VT responded initially to intravenous esmolol and diltiazem only to recur. Physical examination, echocardiography, and cardiac MRI were within normal limits. No other arrhythmia was recorded. The patient underwent an electrophysiology (EP) study and attempted ablation on the next day. The mapping/ablation catheter was positioned in the RVOT and mechanical pressure of the catheter on the endocardium led to immediate suppression of the tachycardia and could not be mapped further. Pace mapping from the ablation catheter confirmed a 12/12 match at the free wall. With RF application at this location, there was VT initiation with subsequent resolution. She was then challenged with isoproterenol infusion up to 5 mg/min with no further developed recurrence. However, upon return to the cardiac care unit, she developed incessant right ventricular outflow tract ventricular tachycardia. A repeat radiofrequency ablation of the sustained VT localized to the RVOT free wall with 3-D electroanatomic mapping (CARTO) was attempted (Figure 1) on the next day with short-term success. Patient continued to have symptomatic RVOT-VT of similar morphology with less frequency. Investigations revealed a free T4 to be mildly elevated at 1.7 ng/dL (0.8–1.5 ng/dL), with a markedly elevated free T3 at 11.5 pg/mL (1.8–4.2 pg/mL). Thyroid-stimulating hormone (TSH) levels were low at 0.02 mIU/L (0.4–5.5 mIU/L). Other laboratory tests were within normal limits. A radioiodine uptake scan showed suppressed uptake in the thyroid region suggesting postpartum thyroiditis, but clinically she was euthyroid. Patient was promptly initiated on IV-steroids, methimazole, long-acting b-blocker, and calcium channel blocker. As symptomatic VT episodes continued, she was taken back to the EP laboratory for the third time. Unable to induce sustained or non-sustained RVOT-VT, the outflow tract was pace mapped with 11/12 match and was ablated at the free wall at the previous ablation target sites. Despite repeated ablations she continued to have the clinical VT but less frequently. No further attempts of ablation were made and continued therapy with methimazole resulted in complete resolution of VT over the next few days. Seven days after the initiation of the thyroiditis treatment, repeat TSH and free T3 levels were with in the normal range. The patient was discharged on the 7th day with no further clinical evidence of VT. Later, an outpatient event recorder for 3 months did not reveal any recurrence of VT. Repeat thyroid studies at 1 month were normal and the antithyroid medications and steroids were discontinued. At 6- and 12-month follow-up, the patient remained euthyroid and symptom free. There is no ideal mechanism to explain the origin of this tachycardia. Thyroid hormones can affect the myocardium, and calcium currents at cellular levels that can initiate delay after depolarization. A combination of altered myocardial substrate and hyperthyroidism was probably the inciting factor for this arrhythmia. Atrial fibrillation is the most common arrhythmia associated with hyperthyroidism. This is the first reported case of RVOT-VT related to hyperthryroidism to the best of our knowledge. Hyperthyroid state can rarely cause incessant RVOT-VT, and aggressive medical therapy is warranted prior to attempting ablation. Ablation can be ineffective or incomplete in the management of such arrhythmias with an underlying substrate that requires systemic medical therapy.
Acknowledgements The authors appreciate the input and reviews of David Von Waggoner, Fahmy Tamer, Andrea Natale (Cleveland Clinic, Cleveland, OH, USA). Conflict of interest: none declared. Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2008. For permissions please email:
[email protected].
Downloaded from https://academic.oup.com/europace/article-abstract/10/5/636/596514/Incessant-right-ventricular-outflow-tract by guest on 03 October 2017
Incessant right ventricular outflow tract ventricular tachycardia
637
Figure 1 (A) EP tracing of the patients with right ventricular outflow tract ventricular tachycardia. (B) A CARTO image of the right ventricular outflow tract showing the earliest site of activation of the ventricular tachycardia at the free wall.
Downloaded from https://academic.oup.com/europace/article-abstract/10/5/636/596514/Incessant-right-ventricular-outflow-tract by guest on 03 October 2017
