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The authors report no relationships that could be construed as a conflict of interest. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International of Journal of Cardiology. References [1] Gil RJ, Vassilev D, Formuszewicz R, Rusicka-Piekarz T, Doganov A. The carina anglenew geometrical parameter associated with periprocedural side branch compromise and the long-term results in coronary bifurcation lesions with main vessel stenting only. J Interv Cardiol 2009;22:E1–E10. [2] Novack V, Battaglia L, Popma JJ, Cutlip DE. In-hospital and nine-month outcomes among patients with coronary lesions involving a side branch and treated with bare metal stents. Catheter Cardiovasc Interv 2010;76:951–7. [3] Colombo A, Moses JW, Morice MC, et al. Randomized study to evaluate sirolimuseluting stents implanted at coronary bifurcation lesions. Circulation 2004;109:1244–9. [4] Colombo A, Bramucci E, Saccà S, et al. Randomized study of the crush technique versus provisional side-branch stenting in true coronary bifurcations: the CACTUS (Coronary Bifurcations: Application of the Crushing Technique Using Sirolimuseluting Stents) Study. Circulation 2009;119:71–8. [5] Steigen TK, Maeng M, Wiseth R, et al. Randomized study on simple versus complex stenting of coronary artery bifurcation lesions: the Nordic bifurcation study. Circulation 2006;114:1955–61.

[6] Onuma Y, Dudek D, Thuesen L, et al. Five-year clinical and functional multislice computed tomography angiographic results after coronary implantation of the fully resorbable polymeric everolimus-eluting scaffold in patients with de novo coronary artery disease: the ABSORB cohort A trial. JACC Cardiovasc Interv 2013;6:999–1009. [7] Nakatani S, Onuma Y, Ishibashi Y, et al. Early (before 6 months), late (6– 12 months) and very late (after 12 months) angiographic scaffold restenosis in the ABSORB cohort B trial. EuroIntervention 2014 Feb 27 [pii: 20130829-09. [Epub ahead of print]]. [8] Zhang YJ, Bourantas CV, Muramatsu T, et al. Comparison of acute gain and late lumen loss after PCI with bioresorbable vascular scaffolds versus everolimuseluting stents: an exploratory observational study prior to a randomised trial. EuroIntervention 2014 Jan 30 [pii: 20130822-06]. [9] Jim MH, Ho HH, Miu R, Chow WH. Modified crush technique with double kissing balloon inflation (sleeve technique): a novel technique for coronary bifurcation lesions. Catheter Cardiovasc Interv 2006;67:403–9. [10] Jim MH, Ho HH, Ko RL, Siu CW, Yiu KH, Chow WH. Long-term clinical and angiographic outcomes of the sleeve technique on non-left-main coronary bifurcation lesions. EuroIntervention 2009;5:104–8. [11] Chen SL, Santoso T, Zhang JJ, et al. A randomized clinical study comparing double kissing crush with provisional stenting for treatment of coronary bifurcation lesions: results from the DKCRUSH-II (Double Kissing Crush versus Provisional Stenting Technique for Treatment of Coronary Bifurcation Lesions) trial. J Am Coll Cardiol 2011;57:914–20. [12] Džavík V, Colombo A. The absorb bioresorbable vascular scaffold in coronary bifurcations: insights from bench testing. JACC Cardiovasc Interv 2014;7:81–8. [13] Jim MH. Shoulder technique: a modified sleeve technique devised for treating isolated coronary stenosis at side branch ostium. Int J Cardiol 2014;171:94–5.

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Ischemic stroke in left ventricular noncompaction and celiac disease Claudia Stöllberger ⁎, Josef Finsterer Krankenanstalt Rudolfstiftung, Juchgasse 25, A-1030 Wien, Austria

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Article history: Received 9 May 2014 Accepted 5 July 2014 Available online 12 July 2014 Keywords: Stroke Cardiomyopathy Noncompaction Celiac disease Autoimmunity Folate deficiency

Left ventricular hypertrabeculation/noncompaction (LVHT) is a cardiac abnormality characterized by a hypertrabeculated left ventricular wall with a sponge-like appearance and a two-layered structure with an outer, subepicardially located compacted zone and an inner, subendocardially located noncompacted zone. Cardiac manifestations of LVHT comprise heart failure, thromboembolism and arrhythmias. LVHT is frequently associated with extracardiac diseases and neuromuscular disorders [1,2]. LVHT associated with digestive disorders, so far, has been only reported in a boy with glycogen storage disease type Ib [3]. Celiac disease (CD) is an autoimmune disorder which damages the small intestines and is caused by ingestion of gluten in genetically susceptible individuals [4]. Symptoms of CD comprise chronic diarrhea, abdominal pain and dyspeptic syndromes. Whereas an

⁎ Corresponding author at: Univ. Prof. Dr. Claudia Stöllberger, Steingasse 31/18, A1030 Wien, Austria. Tel.: + 43 676 403 11 87; fax: +43 1 71165 2209. E-mail addresses: [email protected] (C. Stöllberger), fifi[email protected] (J. Finsterer).

association of CD with dilated cardiomyopathy has been described, LVHT in a patient with CD has not been reported [5]. A 51-years old Caucasian male was admitted because of sudden onset of speech disturbance. He was previously healthy except for recurrent epigastric pain, unspecific “digestion” problems, arterial hypertension for unknown time and intolerance for lactose. He smoked 20 cigarettes/day. Clinical cardiologic examination was normal, his body mass index was 19.72. Blood tests revealed macrocytosis (MCV 101.4b fl, normal value 80.0–98.0 fl), decreased serum folic acid (0.80 ng/ml; normal 5.3–14.2 ng/ml), increased homocystein (19.77 μmol/l; normal value b15.00 μmol/l) normal serum vitamin B12, increased cholesterin (207 mg/dl) and LDL cholesterol (143 mg/dl) levels. Immunologic investigations showed no signs indicative for vasculitis. Investigations for thrombophilia were negative and no mutations were found in the GLA gene. Clinical neurologic examination revealed dysarthria, increased speech effort, and absent Achilles tendon reflexes. Cerebral magnetic resonance imaging showed a hyperintense lesion in the left frontal region on diffusion-weighted images, with a corresponding hypointensity on the ADC maps, which was already hyperintense on T2-weighted images. Additionally, there were small lacunas and multiple glial foci in the basal ganglia bilaterally. Carotid ultrasound revealed a nonobstructive plaque in the left internal carotid artery exclusively. The electrocardiogram showed normal sinus rhythm and no arrhythmias were detected during 72 h of monitoring. Echocardiography showed normally sized cardiac cavities, slightly thickened (12 mm) left ventricular walls, good systolic function and LVHT of the left ventricular apex (Figs. 1 and 2). No thrombus was detected within the ventricular trabeculations. He was discharged with the diagnosis of an ischemic, microangiopathic stroke and was put on a medication with acetylsalicylic acid, simvastatin, ramipril, hydrochlorothiazide and folic acid.

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Fig. 1. Echocardiographic parasternal short axis view of the left ventricular apex showing trabeculations and a noncompacted myocardial inner layer which is thicker than the noncompacted outer layer.

Because of digestive troubles and the decreased folic acid levels he was referred to the gastroenterologist. Tissue transglutaminase antibodies IgA and IgG were elevated (N200 U/ml, 188 U/ml, normal b9.99 U/ml). Duodenal biopsy showed marked villous atrophy and crypt hyperplasia, Marsh stage 3b, why the diagnosis of CD was established. After initiation of a gluten-free diet, his digestive problems decreased. After 6 months, the tissue transglutaminase antibodies IgA were only slightly elevated (14.3 U/ml; normal b9.99 U/ml), MCV had normalized (91.3 fl) and folic acid was N45.4 nmol/l (normal 10.4–42.4 nmol/l). Whether our patient's stroke was due to cardiogenic embolization from LVHT or due to CD remains unknown. Whereas left ventricular thrombi are known and acknowledged as occurring in poorly contracting myocardial regions or ventricular aneurysms, thrombi

may also develop in patients with LVHT with good systolic function within the intertrabecular spaces [6,7]. CD has been identified as etiological factor in juvenile strokes [8]. Stroke in CD is believed to be due to malabsorption with consequent deficiency of vitamins known to exert neurotrophic and neuroprotective effects or immunemediated mechanisms. CD affects approximately 1% of the European and North American populations[5]. CD is often associated to other autoimmune diseases including type 1 diabetes, autoimmune thyroid disease, rheumatoid arthritis and Sjögren syndrome [4]. The presented patient, however, did not develop any of these diseases. Although etiology and pathogenesis of LVHT are still unknown no autoimmune mechanisms have been described in association with LVHT. An association of CD with dilated cardiomyopathy has been described, however, the

Fig. 2. Echocardiographic apical four-chamber view of the showing trabeculations in the left ventricular apex.

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pathomechanism of cardiomyopathy in these patients is unknown. The most plausible explanation for the link between CD and cardiomyopathy is that both conditions might be mediated through inflammation and autoimmune mechanisms [5]. Nutritional deficiencies might be a further explanation for the association between cardiomyopathy and CD. Folate deficiency, like in our patient, was found in 20% of adults with newly diagnosed CD [9]. In animal experiments, folate deficiency has been shown to cause myocardial thickening and cardiomyopathy [10]. If folate deficiency plays a role in the development of LVHT is unknown. From our findings we conclude that LVHT may be associated with CD, folate deficiency and stroke. If this association is a pure coincidence or due to a common etiologic factor remains unknown. Since CD is frequently overlooked and is treatable by gluten-free diet, efforts should be made to discover this disease in patients with cardiomyopathies including LVHT. Patients with LVHT and chronic gastrointestinal symptoms should be investigated for CD. The role of folate deficiency in the etiology of cardiomyopathies including LVHT needs to be investigated. The authors report no relationships that could be construed as a conflict of interest.

References [1] Stöllberger C, Finsterer J, Blazek G. Left ventricular hypertrabeculation/noncompaction and association with additional cardiac abnormalities and neuromuscular disorders. Am J Cardiol 2002;90:899–902. [2] Finsterer J. Cardiogenetics, neurogenetics, and pathogenetics of left ventricular hypertrabeculation/noncompaction. Pediatr Cardiol 2009;30:659–81. [3] Goeppert B, Lindner M, Vogel MN, et al. Noncompaction myocardium in association with type Ib glycogen storage disease. Pathol Res Pract 2012;208:620–2. [4] Vives-Pi M, Takasawa S, Pujol-Autonell I, et al. Biomarkers for diagnosis and monitoring of celiac disease. J Clin Gastroenterol 2013;47:308–13. [5] Emilsson L, Andersson B, Elfström P, Green PH, Ludvigsson JF. Risk of idiopathic dilated cardiomyopathy in 29,000 patients with celiac disease. J Am Heart Assoc 2012;1:e001594. [6] Stöllberger C, Blazek G, Dobias C, Hanafin A, Wegner C, Finsterer J. Frequency of stroke and embolism in left ventricular hypertrabeculation/noncompaction. Am J Cardiol 2011;108:1021–3. [7] Baquero GA, Colegrove DJ, Banchs JE. Isolated left ventricular noncompaction causing stroke in a 30-year-old woman: case report and literature review. Tex Heart Inst J 2013;40:331–8. [8] Goodwin FC, Beattie RM, Millar J, Kirkham FJ. Celiac disease and childhood stroke. Pediatr Neurol 2004;31:139–42. [9] Wierdsma NJ, van Bokhorst-de van der Schueren MA, Berkenpas M, Mulder CJ, van Bodegraven AA. Vitamin and mineral deficiencies are highly prevalent in newly diagnosed celiac disease patients. Nutrients 2013;5:3975–92. [10] Garcia MM, Guéant-Rodriguez RM, Pooya S, et al. Methyl donor deficiency induces cardiomyopathy through altered methylation/acetylation of PGC-1α by PRMT1 and SIRT1. J Pathol 2011;225:324–35.

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Iloprost prevents doxorubicin mediated human cardiac progenitor cell depletion☆ Junping Sun a,1, Jia Zhang a,c,1, Wen Yan a, Cai Chen a, Geru Wu a, Shahrzad Abbasi a, Bao Pham a, Steven Lee a, Jie Cheng a,b, Nada B. Memon b, Yutao Xi a,b,⁎ a b c

Texas Heart Institute/St. Luke's Hospital, Houston, TX 77030, USA Section of Cardiology, University of Texas Health Science Center at Houston School of Medicine, Houston, TX 77030, USA Second Department of Thoracic Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an Shaanxi 710061, China

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Article history: Received 17 April 2014 Accepted 5 July 2014 Available online 12 July 2014 Keywords: Doxorubicin Iloprost Cardiac progenitor cells Cardiotoxicity

Doxorubicin (DOX) is one of the most effective antitumor agents against a variety of cancers including lymphoma, leukemia, and solid tumors in both adults and children [1]. However, its clinical use is limited by acute and chronic heart toxicities, which are dose-related, cumulative, and essentially irreversible [2–4]. The DOX-related cardiotoxicities are potent lifelong threats, characterized by progres☆ This work was presented in part at the American Heart Association 2012 Scientific Session in Los Angeles, California. ⁎ Corresponding author at: Texas Heart Institute/St. Luke's Hospital, 6770 Bertner Street, MC 2-255, Houston, TX 77030, USA. Tel.: +1 832 355 4236; fax: +1 832 355 8880. E-mail address: [email protected] (Y. Xi). 1 Dr. Junping Sun and Dr. Jia Zhang contributed equally to this work.

sive left ventricular dysfunction leading to irreversible congestive heart failure [5,6]. So far, there is no effective treatment on DOXrelated cardiotoxicities. Recently studies have been reported that DOX-related cardiotoxicities are not only restricted to cardiomyocytes, but affect cardiac progenitor cells (CPCs) even more dramatically [7,8], which is related to its mechanism of action in anticancer by interacts with DNA and by intercalation and inhibition of DNA macromolecular biosynthesis [9]. The evidence has also shown the high incidence of cardiotoxicities in pediatric cancer patients [10]. One speculation is that the younger population is more susceptible to chemotherapy-induced disruption of cardiac stem cells as evidenced by the finding that cardiomyocytes renew with a gradual decrease from 1% turnover annually at the age of 25, and 0.45% at the age of 75 [11–13]. In juvenile mice model it was directly demonstrated that DOX reduced proliferation and differentiation of the progenitor cells into cardiac lineages [14]. Recently, De Angelis and co-workers reported that DOX-induced cardiomyopathy might be mediated by alterations in rat cardiac progenitor cells and the restoration of progenitor cell function promoted regeneration of cardiomyocytes and vascular structures [15]. However, there is no efficient way to prevent the loss of CPCs. Iloprost (ILO), a stable synthetic analogue of prostacyclin (PGI2), has shown to attenuate DOX-induced cardiac injury and dysfunction without compromising its chemotherapeutic effect [16]. We previously published a hypothesis that prostacyclin administration is a beneficial supplement to the conventional cancer chemotherapy [17].

Ischemic stroke in left ventricular noncompaction and celiac disease.

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