186 Correspondence / American Journal of Emergency Medicine 35 (2017) 171–190

showed that plasma BNP level of N 235 pg/mL can predict one-year mortality and N 155 pg/mL can differentiate cardioembolic from non- cardioembolic stroke in patients with first-ever acute ischemic stroke [6]. It would be useful to have data regarding troponin and BNP levels on admission and their relationship with the BUN/Cr ratio in patients with acute ischemic stroke. The effect of BUN/Cr ratio-based saline hydration therapy on early Neurological deterioration would be also valuable in patients with acute ischemic stroke.

Bulent Ozlek ?

Eda Ozlek Murat Biteker

Mugla University, Faculty of Medicine, Department of Cardiology, Turkey

* Corresponding author at: Mugla Sitki Kocman Universitesi Tip Fakultesi Orhaniye Mah, Haluk Ozsoy Cad., 48000 Mugla, Turkey E-mail address: [email protected]

http://dx.doi.org/10.1016/j.ajem.2016.10.044

References

1. Chung JL, Jen TY, Yen CH, Yuan HT, Hsueh LM, Meng L, et al. Favorable outcome of blood urea nitrogen/creatinine-based hydration therapy 3 months after acute ischemic stroke. Am J Emerg Med 2016;34(12):2414-8.
2. Ryu WS, Schellingerhout D, Jeong SW, Nahrendorf M, Kim DE, Warntges S, et al. Association between serum lipid profiles and early neurological deterioration in acute ischemic stroke. J Stroke Cerebrovasc Dis 2016. http://dx.doi.org/10. 1016/j.jstrokecerebrovasdis.2016.05.009 pii: S1052-3057(16)30064-7.
3. Bhatia K, Mohanty SI, Tripathi BK, Gupta B, Mittal MK. Predictors of early neuro- logical deterioration in patients with acute ischaemic stroke with special refer- ence to Blood urea nitrogen /creatinine ratio & urine specific gravity. Indian J Med Res 2015 Mar;141(3):299-307.
4. Kwon HM, Lee YS, Bae HJ, Kang DW. Homocysteine as a predictor of early neuro- logical deterioration in acute ischemic stroke. Stroke 2014 Mar;45(3):871-3. http://dx.doi.org/10.1161/STROKEAHA.113.004099.
5. Llombart V, Antolin-Fontes A, Bustamante A, Giralt D, Rost NS, Furie K, et al. B- Type Natriuretic peptides help in cardioembolic stroke diagnosis: pooled data meta-analysis. Stroke 2015 May;46(5):1187-95.
6. Biteker M, Ozden T, Dayan A, Tekkesin AI, Misirli CH. Aortic stiffness and plasma brain natriuretic peptide predicts mortality in acute ischemic stroke. Int J Stroke 2015;10(5):679-85 Jul.

   serum albumin: a risk of stroke??”>An unusual etiology for acquired long QT syndrome and Torsade de pointes

   

   A 50-year-old woman was admitted to our hospital with chest and back pain after she pulled pin hardly. She had a heart rate of100 bpm and blood pressure of 180/100 mm Hg. Electrocardiogram (ECG) showed an abnormal T-U wave in leads II, III, aVF, V_2-6, as well as a Corrected QT interval (QTc) prolongation of 490 ms and premature ventricular contraction (Fig. 1A). The patient was treated with injection of 50 mg urapidil hydrochloride.

   About 2 h after admission, the patient experienced syncope, and ECG showed torsade de pointes (TdP) (Fig. 1B). Serum K⁺ was 3.25 mmol/L. Administration of potassium chloride and magnesium sulfate led to the disappearance of TdP. Tests for troponin I were negative. Echocardio- gram and cardiac magnetic resonance results ruled out structural heart disease. Abdominal computerized tomography revealed a right adrenal mass of 2.1 x 2.0 cm. It was considered that pheochromocytoma might be the cause of an acquired Long QT syndrome (LQTS).

   The patient agreed to undergo tumor resection. Histopathologic ex- amination of the mass revealed it to be a classical pheochromocytoma, with large polygonal, pleomorphic, and spindly cells arranged in thick nests, and separated from each other by a rich capillary vascular net-

   up, the patient’s blood pressure was 120/80 mm Hg, serum K⁺ was normal without medication, and the QT interval was normal.

   In our presently described case, the patient exhibited QT prolongation and syncope due TdP. TdP is a form of polymorphic ventricular tachycar- dia that occurs in the setting of a prolonged QT interval on surface electro- cardiogram. LQTS can be congenital or acquired, i.e., associated with Environmental factors. Acquired LQTS is typically related to pharmacolog- ical influences, Electrolyte disorders, and Endocrine disorders (such as pheochromocytoma).

   Pheochromocytoma is a rare neuroendocrine tumor that secretes high catecholamine levels and can exert serious metabolic and cardio- vascular effects. Cardiovascular complications of pheochromocytoma can include ischemic heart disease, acute myocardial infarction, and cardiac arrhythmias [1]. QT prolongation and TdP have also been re- ported [2]. With regards to the mechanism underlying our present patient’s QT prolongation, we can only speculate that it may have been related to the presence and relative ratio of the secreted cate- cholamine. Repolarization abnormalities associated with hyper- adrenergic states can cause QT prolongation and Lethal arrhythmia, including TdP [3].

   Lei Wang, MD Chuan-Jun Chen

   Yun-Tao Zhao, MD, PhD?

   Department of Cardiology, Aerospace Center Hospital, 15 Yuquanroad,

   Beijing 100049, People’s Republic of China

   *Corresponding author at: 15 Yuquan Road, Beijing 100049,

   People’s Republic of China.

   E-mail address: [email protected] (Y.-T. Zhao).

   http://dx.doi.org/10.1016/j.ajem.2016.10.048

   References

   Galetta F, Franzoni F, Bernini G, Poupak F, Carpi A, Cini G, et al. Cardiovascular complications in patients with pheochromocytoma: a mini-review. Biomedicine & Pharmacotherapy 2010;64(7):505-9.

7. Shimizu K, Miura Y, Meguro Y, Noshiro T, Ohzeki T, Kusakari T, et al. QT prolongation with torsade de pointes in pheochromocytoma. American Heart Journal 1992;124(1): 235-9.
8. Madias C, Fitzgibbons TP, Alsheikh-Ali AA, Bouchard JL, Kalsmith B, Garlitski AC, et al. Acquired long QT syndrome from stress cardiomyopathy is associated with ventricular arrhythmias and Torsades de pointes. Heart Rhythm 2011;8(4):555-61.

   Serum albumin: a risk of stroke??

   

   To the Editor,

   Recently, one interesting article reported the relationship between serum albumin and the recurrence of acute ischemic stroke [1]. In this study, 753 patients with acute first-ever ischemic stroke were enrolled, and 692 patients completed the measurements of recurrent outcome 1 year after stroke through home interviews. The study indicated that serum Albumin levels of patients with recurrence of stroke were significantly lower than those of patients without recurrence (37.07 +- 4.21 g/L vs 38.91 +- 3.25 g/L, P b .001). It was an interesting study and

   work. The cytoplasm was intensely granular and was stained pink and

   purple with hematoxylin-eosin (Fig. 1C). After three months of follow-

   ? Sources of support: None.

   Correspondence / American Journal of Emergency Medicine 35 (2017) 171–190 187

   

   Figure. Possible mechanisms of relationship between Serum albumin level and stroke.

   testified the value of hypoalbuminemia or low albumin level in predicting 1-year recurrence of acute ischemic stroke. It is a little bit similar to our research result, which was published in International Journal of Cardiology this year. Our research also found that patients with nonvalvular atrial fibrillation with urine albumin greater than or equal to 0.03 g/L were more likely to suffer Thromboembolic events (TEs), especially stroke or transient ischemic attack [2].

   However, it seemed confused in explaining the possible mecha- nisms of the association between serum albumin level and recur- rence of stroke. Serum albumin, as the transporter of hormones, drugs, amino acids, and free fatty acids in the blood and the modu- lator of the colloid osmotic pressure in blood, can improve blood flow perfusion of brain [3], enhance micrangium perfusion [4], re- duce the various cytokines’ adhesion within postcapillary micro- circulation [5], and increase the transport of free fatty acids postischemia [6].

   Several studies in the past have testified the link between serum albumin and the risk of stroke, although the exact pathophysiological mechanisms are still not well understood. In the study of Kato et al [7], they considered that the increased risk of TE in patients with proteinuria resulted from urinary loss of antithrombin, lower free Protein S levels and reduced protein C activity, and activation of the coagulation system. Moreover, the urinary loss of vitamin D-binding protein (by lowing serum vitamin D level) and of the albumin-bound calcium accounts might contribute to TE occurrence, as ionized calcium is the coagulation factor IV and has the crucial role in coagulation system [8]. On the other hand, Ovbiagele [9] indicated that microalbuminuria was a marker of generalized endothelial dysfunction. The elevated urinary leakage of albumin was possibly reflected by greater capillary perme- ability for albumin in the systemic vasculature and probably leading to generalized hemodynamic strain and disequilibrium. What’s more, hypoalbuminemia was generally correlated with severity of albumin- uria. Lionaki et al [10] found that hypoalbuminemia, particularly less than 2.8 g/dL, was significantly associated with vascular thrombotic risk. Possible mechanisms include the following: (1) the hepatic overproduction of coagulation factors V and VIII and fibrinogen as a compensatory response to hypoalbuminemia and (2) decreasing serum albumin level will strengthen coagulation function, as albumin is a cofactor for the binding of plasminogen to fibrin and their interaction with tissue plasminogen activator. Nevertheless, hypoalbuminemia will cause not only loss of fluid from the intravascular compartment because of decreased colloid osmotic pressure but also increase of free arachidonic acid, which normally albumin bound, resulting in high serum level of proaggregatory agent thromboxane A2 in platelets, inducing platelet aggregation [11].

   In summary, most of the current studies have been focused on urinary

   loss of anticoagulation protein and complications of hypoalbuminemia in

   explaining the association between low serum albumin level and stroke. All possible mechanisms of relationship between serum albumin level and stroke are shown in Figure. Future large-sized, multicenter, and prospective studies should include analysis of urine protein composition and assessment of serum albumin level change to delineate the intricate relationship between urine albumin, serum albumin, and stroke. Whatever, the management of serum albumin level cannot be ignored in the patients with acute first-ever stroke.

   Haohui He, MD Jun Guo, MD, PhD?

   Department of Cardiology, the First Affiliated Hospital of Jinan University

   Guangzhou 510630, China

   ?Corresponding author. Department of Cardiology the First Affiliated Hospital of Jinan University, Guangzhou 510630

   China. Tel.: +86 020 38688963

   E-mail address: [email protected]

   http://dx.doi.org/10.1016/j.ajem.2016.10.049

   References

   Zhang Q, Lei YX, Wang Q, et al. Serum albumin level is associated with the recurrence of acute ischemic stroke. Am J Emerg Med 2016;34(9):1812-6.

9. He H, Guo J, Zhang AD. The value of urine albumin in predicting thromboembolic events for patients with non-valvular atrial fibrillation. Int J Cardiol 2016;221: 827-30.
10. Belayev L, Liu Y, Zhao W, et al. Human albumin therapy of acute ischemic stroke: marked neuroprotective efficacy at moderate doses and with a broad therapeutic window. Stroke 2001;32(2):553-60.
11. Park HP, Nimmagadda A, DeFazio RA, et al. Albumin therapy augments the ef- fect of thrombolysis on local vascular dynamics in a rat model of arteriolar thrombosis: a two-photon laser-scanning microscopy study. Stroke 2008; 39(5):1556-62.
12. Belayev L, Pinard E, Nallet H, et al. Albumin therapy of transient focal cerebral ische- mia: in vivo analysis of dynamic microvascular responses. Stroke 2002;33(4): 1077-84.
13. Rodriguez de Turco EB, Belayev L, Liu Y, et al. Systemic fatty acid responses to transient focal cerebral ischemia: influence of neuroprotectant therapy with human albumin. J Neurochem 2002;83(3):515-24.
14. Kato S, Chernyavsky S, Tokita JE, et al. Relationship between proteinuria and venous thromboembolism. J Thromb Thrombolysis 2010;30(3):281-5.
15. Ismail G, Mircescu G, Ditoiu AV, et al. Risk factors for predicting venous thromboembolism in patients with Nephrotic syndrome: focus on haemostasis- related parameters. Int Urol Nephrol 2014;46(4):787-92.
16. Ovbiagele B. Microalbuminuria: risk factor and potential therapeutic target for stroke? J Neurol Sci 2008;271(1):21-8.
17. Lionaki S, Derebail VK, Hogan SL, et al. Venous thromboembolism in patients with membranous nephropathy. Clin J Soc Nephrol 2012;7(1):43-51.
18. Mzayen K, Al-Said J, Nayak-Rao S, et al. Unusual presentation of renal vein thrombosis with pulmonary artery embolism. Saudi J Kidney Dis Transpl 2013; 24(3):566-70.