Letters to the Editor

in morbidity, length of stay and patient comfort. With the growing experience combined with the optimization of transcatheter devices, it appears that SAAs will be soon managed in the catheterization lab even as an outpatient endovascular procedure. References [1] Abbas MA, Stone WM, Fowl RJ, et al. Splenic artery aneurysms: two decades experience at Mayo clinic. Ann Vasc Surg 2002;16(4):442–9. [2] Huang YK, Hsieh HC, Tsai FC, Chang SH, Lu MS, Ko PJ. Visceral artery aneurysm: risk factor analysis and therapeutic opinion. Eur J Vasc Endovasc Surg 2007;33(3):293–301. [3] Lakin RO, Bena JF, Sarac TP, et al. The contemporary management of splenic artery aneurysms. J Vasc Surg 2011;53(4):958–64 [discussion 65]. [4] Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. Circulation 2006;113(11):e463–654. [5] Borioni R, De Persio G, Leporace M, Di Capua C, Boggi U, Garofalo M. Endovascular treatment of multiple anomalous splenic artery aneurysms in a Jehovah witness. G Chir 2013;34(1–2):42–5. [6] Miao YD, Ye B. Intragastric rupture of splenic artery aneurysms: three case reports and literature review. Pak J Med Sci 2013;29(2):656–9. [7] Lee PC, Rhee RY, Gordon RY, Fung JJ, Webster MW. Management of splenic artery aneurysms: the significance of portal and essential hypertension. J Am Coll Surg 1999;189(5):483–90.

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[8] Patel A, Weintraub JL, Nowakowski FS, et al. Single-center experience with elective transcatheter coil embolization of splenic artery aneurysms: technique and midterm follow-up. J Vasc Interv Radiol 2012;23(7):893–9. [9] Kemmeter P, Bonnell B, VanderKolk W, Griggs T, VanErp J. Percutaneous thrombin injection of splanchnic artery aneurysms: two case reports. J Vasc Interv Radiol 2000;11(4):469–72. [10] Zhu X, Tam MD, Pierce G, et al. Utility of the Amplatzer Vascular Plug in splenic artery embolization: a comparison study with conventional coil technique. Cardiovasc Intervent Radiol 2011;34(3):522–31. [11] Carmo M, Mercandalli G, Rampoldi A, et al. Transcatheter thrombin embolization of a giant visceral artery aneurysm. J Cardiovasc Surg (Torino) 2008;49(6):777–82. [12] Carrafiello G, Lagana D, Dizonno M, Mangini M, Fugazzola C. Endovascular ligature of splenic artery aneurysm with Amplatzer Vascular Plug: a case report. Cardiovasc Revasc Med 2007;8(3):203–6. [13] Stella N, Palombo G, Taddeo C, Rizzo L, Taurino M. Stent-assisted coil embolization of a complex wide-neck splenic artery aneurysm. Ann Vasc Surg 2013;27(8):e5–8. [14] Rossi M, Rebonato A, Greco L, Citone M, David V. Endovascular exclusion of visceral artery aneurysms with stent-grafts: technique and long-term follow-up. Cardiovasc Intervent Radiol 2008;31(1):36–42. [15] Schoppe KA, Ciacci J, Bettmann M. Modified stent-supported coil embolization for treatment of a splenic artery pseudoaneurysm. J Vasc Interv Radiol 2010;21(9):1452–6. [16] Aslam MS, Shalev Y. Treatment of splenic artery aneurysm with polytetrafluoroethylene-covered stent. Catheter Cardiovasc Interv 2010;76(2):229–32. [17] Loffroy R, Guiu B, Cercueil JP, et al. Transcatheter arterial embolization of splenic artery aneurysms and pseudoaneurysms: short- and long-term results. Ann Vasc Surg 2008;22(5):618–26. [18] Xin J, Xiao-Ping L, Wei G, et al. The endovascular management of splenic artery aneurysms and pseudoaneurysms. Vascular 2011;19(5):257–61. [19] Pappy R, Sech C, Hennebry TA. Giant splenic artery aneurysm: managed in the cardiovascular catheterization laboratory using the modified neck remodeling technique. Catheter Cardiovasc Interv 2010;76(4):590–4.

http://dx.doi.org/10.1016/j.ijcard.2014.03.158 0167-5273/© 2014 Published by Elsevier Ireland Ltd.

High BNP levels in rheumatoid arthritis may be related with right ventricular functions Cengiz Ozturk a,⁎, Sevket Balta b, Sait Demirkol a, Ahmet Ozturk c, Turgay Celik a, Atila Iyisoy a a b c

Gulhane Medical Faculty, Department of Cardiology, Ankara, Turkey Eskisehir Military Hospital, Department of Cardiology, Eskisehir, Turkey Gulhane Medical Faculty, Department of Geriatric Medicine, Ankara, Turkey

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Article history: Received 8 February 2014 Accepted 22 March 2014 Available online 28 March 2014 Keywords: B-type natriuretic peptide Rheumatoid arthritis Right ventricular functions

Dear Editor, We read the article entitled “High BNP levels in rheumatoid arthritis are related to inflammation but not to left ventricular abnormalities” by George et al. with interest [1]. They concluded that there was a relationship between inflammation and B-type natriuretic peptide (BNP) but not in left ventricular hypertrophy. The value of BNP is well known in the diagnosis of left ventricular dysfunction [2]. But there are some contradictory researches about the

BNP, inflammation and left–right systolic and diastolic dysfunctions [3–5]. In a recent study, no correlations between inflammatory and functional disease parameters of systolic and diastolic function were found [6]. On the other hand, another study revealed that left and right ventricular tissue doppler imaging parameters of rheumatoid arthritis (RA) patients were impaired [7]. It was shown that serum BNP and NT-proBNP levels may be related with elevated pulmonary arterial systolic pressure (PASP) at high altitude in another study [8]. We know that PASP may contribute to the high incidence of cardiovascular events in patients with RA and RA affects the right ventricle via pulmonary hypertension and right ventricular dysfunction [9]. However, the measurement of the degree of left ventricular hypertrophy, PASP, right systolic and diastolic dysfunction parameters were not reported by George et al. [1]. In addition, if rheumatoid arthritis patients with pulmonary hypertension, right heart dilatation and tricuspid regurgitation were included, a comparison could have been made between parameters. The contribution of serum BNP level to RA has not been fully clarified. References

⁎ Corresponding author. Tel.: +90 533 4875060. E-mail address: [email protected] (C. Ozturk).

[1] George J, Mackle G, Manoharan A, Khan F, Struthers AD. High BNP levels in rheumatoid arthritis are related to inflammation but not to left ventricular

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[2]

[3]

[4]

[5]

Letters to the Editor abnormalities: prospective case–control study. Int J Cardiol Mar 1 2014;172(1): e116–8. Januzzi JL, Troughton R. Are serial BNP measurements useful in heart failure management? Serial natriuretic peptide measurements are useful in heart failure management. Circulation Jan 29 2013;127(4):500–7 [discussion 508, Review]. Crowson CS, Myasoedova E, Davis III JM, et al. Use of B-type natriuretic peptide as a screening tool for left ventricular diastolic dysfunction in rheumatoid arthritis patients without clinical cardiovascular disease. Arthritis Care Res (Hoboken) May 2011;63(5):729–34. Armstrong DJ, Gardiner PV, O'Kane MJ. Rheumatoid arthritis patients with active disease and no history of cardiac pathology have higher brain natriuretic peptide (BNP) levels than patients with inactive disease or healthy control subjects. Ulster Med J May 2010;79(2):82–4. Shiina Y, Funabashi N, Lee K, et al. Right atrium contractility and right ventricular diastolic function assessed by pulsed tissue Doppler imaging can predict brain

[6]

[7]

[8]

[9]

natriuretic peptide in adults with acquired pulmonary hypertension. Int J Cardiol Jun 12 2009;135(1):53–9. Vizzardi E, Cavazzana I, Bazzani C, et al. Echocardiographic evaluation of asymptomatic patients affected by rheumatoid arthritis. J Investig Med Dec 2012;60(8):1204–8. Birdane A, Korkmaz C, Ata N, et al. Tissue Doppler imaging in the evaluation of the left and right ventricular diastolic functions in rheumatoid arthritis. Echocardiography May 2007;24(5):485–93. Woods DR, Mellor A, Begley J, et al. Brain natriuretic peptide and NT-proBNP levels reflect pulmonary artery systolic pressure in trekkers at high altitude. Physiol Res Dec 20 2013;62(6):597–603. Keser G, Capar I, Aksu K, et al. Pulmonary hypertension in rheumatoid arthritis. Scand J Rheumatol 2004;33(4):244–5.

http://dx.doi.org/10.1016/j.ijcard.2014.03.157 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.

Clinical profile of Brugada syndrome in Hong Kong Chinese population Christopher B. Wong ⁎, MBBS FACC Cardiology Specialty, Quality Healthcare Medical Service, Hong Kong

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Article history: Received 1 January 2014 Received in revised form 13 March 2014 Accepted 22 March 2014 Available online 29 March 2014 Keywords: Brugada syndrome Sudden cardiac death Electrophysiology studies Arrhythmia Syncope

There has been controversy concerning the optimal management of patients with Brugada ECG patterns. Brugada et al. [1,4] recommended that patients with aborted sudden cardiac death (SCD) be offered an implantable cardiac defibrillator (ICD) (Class 1 indication). Patients who have syncope thought to be related to arrhythmia and type I ECG pattern should receive an ICD (Class 2 indication). Patients with a family history of SCD related to Brugada syndrome and a positive electrophysiology (EP) study should also receive an ICD (Class IIb indication). A positive EP study and a history of syncope were the main predictors of future arrhythmic events. Priori et al. [2] however, did not confirm Brugada's findings. The event rates after diagnosis among asymptomatic patients in Priori's study were significantly lower [3]. We report a retrospective study of Hong Kong patients of Chinese descent with Brugada ECG who were followed for up to 22 years. A total of 68 consecutive patients (mean age 51.4, range 21 to 77, 93% male, from 1989 to 2011) were included in the study. 41% had type I Brugada ECG patterns. 38 patients were asymptomatic (Group A), 25 had syncope presumably arrhythmic in origin (Group B) and five suffered from SCD (Group C). A family history of SCD was not common in our cohort (10.3%). Four patients in Group C received ICD implants. The remaining patient refused ICD and was put on mexilitine for 16 years without any events. One patient in Group C had ventricular fibrillation storm a few months

⁎ Tower 1, 16th floor, Admiralty Center, Hong Kong. Tel.: +852 63135929. E-mail address: [email protected] (C.B. Wong).

after the ICD implant. In Group B, 11 patients underwent EP studies and 8 had positive results (73%). 16 patients underwent flecainide stimulation tests with 31% positive results. Eight patients with a positive EP study had ICD implant. One other patient had an ICD implant despite a negative EP study due to the concern of cardiac syncope related to type I Brugada syndrome. The remaining 16 patients had follow up for 5.5 +/ − 3.2 years (range 1 to 10 years) without any cardiac events. One 43 year old man with a type I Brugada ECG pattern and syncope refused to have an EP study. He was followed for 10 years without cardiac events. No patients had ICD shocks after ICD implantation. No patients had sustained arrhythmia despite positive EP studies. Only one patient with type I Brugada ECG pattern and a positive EP study demonstrated nonsustained ventricular tachycardia on follow up. In Group A, all patients remained asymptomatic during the follow up (mean of five years, range 1 to 14 years). Two patients received ICD implant after positive EP studies. No ICD shocks were recorded. EP studies were performed in six patients in Group A, with three positive studies (50%). One patient (age 23) (Group A) had abnormal EP study but refused ICD and was followed for 9 years without cardiac events. The positive predictive value of EP studies and flecainide stimulation test (Groups A and B) in predicting an arrhythmic event was less than 10% and 1% respectively. From the above findings, it is evident that our local population had a relatively benign course, especially asymptomatic patients or patients with syncope. The management algorithm proposed by Antzelevitch et al. (2005) [1,4] may not work for our population. From an epidemiological standpoint, the overall incidence of SCD (18: 100,000) in Hong Kong is much lower than the western counterpart. The underlying causes are acute myocardial infarction (31%), coronary/hypertensive heart disease (40%), cardiomyopathies (5%), and miscellaneous causes (23%). In less than 1%, channelopathies such as Brugada syndrome, Wolff Parkinson White syndrome and prolonged QT syndrome are the causes. Each year, fewer than 10 patients die of Brugada syndrome in Hong Kong. Over-diagnosing and over-treating the condition with suspicious ECG patterns should be avoided. The prevalence of asymptomatic Brugada ECG pattern was about 1% in Hong Kong Chinese population. Even with the best risk stratifying tool, the positive predictive value of the test in predicting SCD in asymptomatic patients with Brugada ECG pattern would be very low. Conversely, in Western society with an SCD incidence five to six times higher than that of Hong Kong, a risk