Catheter-induced aorto-coronary artery dissection: Utility and appearance on CT coronary angiogram

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transport systems [5,6]. We recently described the presence of high alkaline phosphatase activity in the rat heart with a myocardial cell localization (striated pattern) reminiscent of the sarcoplasmic reticulum morphology [7]. A functional relationship between alkaline phosphatase and transmembranar transport activity, at different anatomic and cellular levels, had been previously shown [5,6,8–10]. Another interesting observation in our rat heart alkaline phosphatase work was the effect of various drugs used in the treatment of cardiovascular diseases on the activity of this enzyme, namely activation by statins and beta-blockers [7]. So, beyond other known mechanisms of action of these drugs, some of their effects may be due to alkaline phosphatase activation. The report of a relationship between serum alkaline phosphatase and post-Fontan hemodynamics in children [11,12] gives clinical plausibility to our hypothesis. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [13]. References [1] Cheung BM, Ong KL, Wong LY. Elevated serum alkaline phosphatase and peripheral arterial disease in the United States National Health and Nutrition Examination Survey 1999–2004. Int J Cardiol 2009;135: 156–61. [2] Ankle Brachial Index Collaboration, Fowkes FG, Murray GD, et al. Ankle brachial index combined with Framingham Risk Score to predict cardiovascular events and mortality: a meta-analysis. JAMA 2008;300:197–208.

[3] Fernandez NJ, Kidney BA. Alkaline phosphatase: beyond the liver. Vet Clin Pathol 2007;36:223–33. [4] Anderson ME, Mohler PJ. Rescuing a failing heart: think globally, treat locally. Nat Med 2009;15:25–6. [5] Calhau C, Martel F, Soares-da-Silva P, Hipólito-Reis C, Azevedo I. Regulation of [(3)H] MPP(+) transport by phosphorylation/dephosphorylation pathways in RBE4 cells: role of ecto-alkaline phosphatase. Naunyn Schmiedebergs Arch Pharmacol 2002;365:349–56. [6] Martel F, Keating E, Calhau C, Azevedo I. Uptake of (3)H-1-methyl-4phenylpyridinium ((3)H-MPP(+)) by human intestinal Caco-2 cells is regulated by phosphorylation/dephosphorylation mechanisms. Biochem Pharmacol 2002;63:1565–73. [7] Mota A, Silva P, Neves D, et al. Characterization of rat heart alkaline phosphatase isoenzymes and modulation of activity. Braz J Med Biol Res 2008;41:600–9. [8] Martel F, Martins MJ, Calhau C, Hipólito-Reis C, Azevedo I. Postnatal development of organic cation transport in the rat liver. Pharmacol Res 1998;37:131–6. [9] Martel F, Martins MJ, Hipólito-Reis C, Azevedo I. Inward transport of [3H]-1-methyl-4-phenylpyridinium in rat isolated hepatocytes: putative involvement of a P-glycoprotein transporter. Br J Pharmacol 1996;119: 1519–24. [10] Martins MJ, Negrão MR, Hipólito-Reis C, Azevedo I. Putative involvement of alkaline phosphatase in the modulation of taurocholate uptake by rat isolated hepatocytes. Pharmacologist 2002;44(Suppl 1):A41 (Abstr 31.11). [11] Chin AJ, Stephens P, Goldmuntz E, Leonard MB. Serum alkaline phosphatase reflects post-fontan hemodynamics in children. Pediatr Cardiol 2009;30:138–45. [12] Martins MJ, Azevedo I. Cardiac physiopathology and alkaline phosphatase. Pediatr Cardiol 2009;30:91. [13] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131: 149–50.

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Catheter-induced aorto-coronary artery dissection: Utility and appearance on CT coronary angiogram Wee Thong Neo, Uei Pua ⁎, Yeong Shyan Lee Department of Diagnostic Radiology, Tan Tock Seng Hospital, Singapore Received 24 February 2009; accepted 4 March 2009 Available online 29 March 2009

Keywords: Catheter angiography; Dissection; CT angiography

⁎ Corresponding author. Department of Diagnostic Radiology, Tan Tock Seng Hospital, 11 Jalan Tan Tock Seng, 308433, Singapore. Tel.: +65 97547525; fax: +65 67599940. E-mail address: [email protected] (U. Pua).

Dear Editor, We read with great interest the article – “Significant left main coronary artery disease from iatrogenic dissection

Letters to the Editor

during coronary angiography.” by Lee JH and co-workers [1]. We would like to highlight the appearance and potential use of coronary CT angiogram in iatrogenic dissection in the acute setting. Catheter-induced coronary artery dissection with retrograde aortic extension (CCAD) is a rare but feared complication, and occur in up to 0.02% of diagnostic catheterizations and 0.07% of percutaneous coronary interventions [2,3]. Management is dependent on the distal flow status and the extent of propagation of aortic dissection. ECG-gated multidetector coronary CT angiogram (CTA) is well-described in detection of spontaneous coronary artery dissection and in monitoring resolution of CCAD after treatment [4,5]. However, the use of CTA in evaluation of CCAD in the acute setting has not been previously described and we herein report such a case. A 54 year-old man with background history of hypertension and ischemic heart disease underwent coronary angiography for the evaluation of chest pain. Inadvertent CCAD was encountered during catheterization of the right coronary artery (RCA) ostium with a 4F right Judkins catheter (Fig. 1). This was followed by lost of catheter position and subsequent failure to recannulate the RCA, precluding further assessment of the distal flow and endovascular treatment. The patient remained asymptomatic and was hemodynamically stable. CTA was immediately performed to evaluate the extent of retrograde dissection and status of distal flow in the RCA; while awaiting urgent coronary artery bypass grafting (CABG). CTA images were acquired on Somatom Sensation 64 cardiac CT scanner (Siemens Medical Solutions, USA), using a slice thickness of 0.75-mm, 0.5-mm slice overlap and injection rate of 4.5 ml/s. Images were reviewed and multiplanar reconstruction created using Leonardo 3D workstation (Sie-

Fig. 1. Right coronary artery (RCA) angiogram through the 4F Judkins catheter showing a dissection flap in the proximal and mid RCA (black arrow). Loss of catheter position with subsequent failure at cannulation precluded further evaluation of the extent of the dissection and assessment of distal RCA flow.

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mens Medical Solutions, USA). CTA revealed CCAD to be limited to the right sinus of Valsava without propagation to ascending aorta (Fig. 2a, b). Furthermore distal RCA flow limitation is demonstrated correlating well with the catheter angiogram findings (Fig. 1). The CTA appearance is rather striking, with stasis of residual contrast (from catheter angiography) within the false-lumen. The residual contrast being significantly denser than the intravenous contrast within the true vascular channels (cardiac chambers and coronary artery) sharply delineates the extent of the dissection (Figs. 2a– 3a). The patient underwent successful emergency CABG with repair of the sinus of Valsava and made uneventful recovery.

Fig. 2. a) Coronal oblique multiplanar reconstruction b) curved multiplanar reconstruction. Hyperdense residual contrast from the catheter angiography resides in the false lumen and is sharply contrasted against background of less dense contrast in the true vascular channels (e.g. cardiac chambers). As a result, the extent of the dissection; proximal and mid RCA, limited proximally by the sinus of Valsava is well delineated (black arrows). Decreased opacification of the distal RCA (white arrows) alludes to a flow-limiting dissection.

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Fig. 3. a) Coronal oblique multiplanar reconstruction. Axial CT images of the ascending aorta above the sinus of Valsava without ECG gating b) and with ECG-gating c) in our patient. a) Hyperdense contrast is seen within the right sinus of Valsava (black arrow) with no propagation into the ascending aorta. Note the multifocal stenoses in the left anterior descending artery (white arrow). b) Cardiac pulsation artifact in the ascending aorta (curved white arrows) without ECG-gating, equivocal for dissection flaps. c) Such artifact is not present with ECG-gating.

Risk factors for CCAD include: left main coronary artery cannulation, use of Amplatz shaped catheters, catheterization during myocardial infarction, catheter manipulation, vigorous

contrast injections and deep intubation of catheter [6,7]. The outcome of CCAD and therefore its management depends on the status of the distal flow and extent of the propagation of the dissection. Closure of the distal vascular bed can result in myocardial infarction and rapid revascularization (endovascular or CABG) is mandatory. Additionally, even in the presence of good distal flow on angiography, hemodynamic instability, new ECG changes or new onset of chest pain demands immediate revascularization. Further evaluation (e.g. CTA) has no place in these settings as any delay with the risk of myocardial loss cannot be justifiable. The urgency and treatment of clinically stable and asymptomatic patients with CCAD, however, is less clear, with some operators adopting a conservative approach, while others (including our center) advocating early revascularization [7]. Nevertheless, due to the current limited experience of using CTA in the acute setting of CCAD, we would suggest that CTA (if at all) be limited to selected scenarios and should be considered only if it can be performed in a expeditious manner (perhaps opportunistic), that does not delay the time to definitive treatment. In cases such as that experienced by the authors [1], CTA has the potential to confirm suspicion of CCAD, noninvasively. Knowledge of the extent of retrograde aortic dissection is also an important determinant for surgery and greatly aids surgical planning. Although conservative treatment of limited retrograde dissection (e.g. sinus of Valsava) has been reported, the progression of these dissections is unpredictable and can be life-threatening [8]. Rapid progression of the dissection down to the aortic bifurcation has also been described [9]. Both conventional CT and transoesophageal echocardiography (TEE) are commonly used to evaluate the extent of aortic dissection in CCAD. While conventional CT aortography has the advantage of being non-invasive compared to TEE, CT aortography without ECG-gating is prone to cardiac pulsation artifact that can mimic dissection flaps in ascending aorta [10] (Fig. 3b,c) and accurate assessment of the aortic root – the critical region of interest in CCAD is often not possible. CTA is a therefore a superior tool, able to depict distal coronary artery run-off and the extent of the aortic dissection in the same sitting. Furthermore, CTA serve as a convenient baseline for followup studies in both treated and conservatively managed patients. To conclude, within the confines of clinically permissive and selected scenarios, CTA can play a useful role in the management of CCAD. I hereby declare that the manuscript, including related data, figures and tables, has not been published previously and that the manuscript is not under consideration elsewhere. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [11].

Letters to the Editor

References [1] Lee JH, Kim EM, Ahn KT, Kim MS, Kim KS, Jung IS, et al. Significant left main coronary artery disease from iatrogenic dissection during coronary angiography. Int J Cardiol 2010;138:e35–7. [2] Perez-Castellano N, GarcÌa-Fernandez MA, GarcÌa EJ, Delcan JL. Dissection of the aortic sinus of valsalva complicating coronary catheterization: cause, mechanism, evolution, and management. Catheter Cardiovasc Diagn 1998;43:273–9. [3] Carter AJ, Brinker JA. Dissection of the ascending aorta associated with coronary angiography. Am J Cardiol 1994;73:922–3. [4] Kantarci M, Ogul H, Bayraktutan U, Gundogdu F, Bayram E. Spontaneous coronary artery dissection: noninvasive diagnosis with multidetector CT angiography. J Vasc Interv Radiol 2007 May;18 (5):687–8. [5] Kim JY, Yoon J, Jung HS, Yoo BS, Lee SH. Percutaneous coronary stenting in guide-induced aortocoronary dissection: angiographic and CT findings. Int J Cardiovasc Imaging 2005 Aug;21(4):375–8.

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[6] Dunning DW, Kahn JK, Hawkins ET, O'Neill WW. Iatrogenic coronary artery dissections extending into and involving the aortic root. Catheter Cardiovasc Interv 2000;51:387–93. [7] Awadalla H, Sabet S, El Sebaie A, Rosales O, Smalling R. Catheterinduced left main dissection incidence, predisposition and therapeutic strategies: Experience from two sides of the hemisphere. J Invasive Cardiol 2005;17:233–6. [8] Yip HK, Wu CJ, Yeh KH, Hang CL, Fang CY, Hsieh KY, et al. Unusual complication of retrograde dissection to the coronary sinus of valsalva during percutaneous revascularization: a single-center experience and literature review. Chest 2001 Feb;119(2):493–501. [9] Moles VP, Chappuis F, Simonet F, Urban P, De La Serna F, Pande AK, et al. Aortic dissection as complication of percutaneous transluminal coronary angioplasty. Catheter Cardiovasc Diagn 1992;26:8–11. [10] Ko SF, Hsieh MJ, Chen MC, Ng SH, Fang FM, Huang CC, et al. Effects of heart rate on motion artifacts of the aorta on non-ECG-assisted 0.5sec thoracic MDCT. AJR Am J Roentgenol 2005 Apr;184(4):1225–30. [11] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131: 149–50.

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Association between cardiac energy metabolism and gain of left ventricular mass in Fabry disease Tomas Palecek a,⁎, Jan Bultas b , Milan Hajek c , Debora Karetova a , Petr Kuchynka a , Josef Kautzner d , Milan Elleder e , Ales Linhart a a

Charles University of Prague, 1st Medical Faculty, 2nd Medical Department-Clinical Department of Cardiology and Angiology, Prague, Czech Republic b Charles University of Prague, 3rd Medical Faculty, Department of Pharmacology, Prague, Czech Republic c Institute for Clinical and Experimental Medicine, Magnetic Resonance Unit, Prague, Czech Republic d Institute for Clinical and Experimental Medicine, Department of Cardiology, Prague, Czech Republic e Charles University of Prague, 1st Medical Faculty, Institute of Inherited Metabolic Disorders, Prague, Czech Republic Received 24 February 2009; accepted 4 March 2009 Available online 2 April 2009

Keywords: Fabry disease; Cardiomyopathy; Echocardiography; Magnetic resonance spectroscopy; Myocardial energy metabolism

Fabry disease (FD) is an X-linked genetic disorder of glycosphingolipid metabolism caused by deficient activity of lysosomal enzyme α-galactosidase A. The disease is characterized by progressive intracellular accumulation of neutral ⁎ Corresponding author. 2nd Medical Department - Clinical Department of Cardiology and Angiology, General University Hospital, U Nemocnice 2, 128 08 Prague 2, Czech Republic. Tel.: +4202 24962634; fax: +4202 24912154. E-mail address: [email protected] (T. Palecek).

glycosphingolipids, mainly globotriaosylceramide, in different tissues throughout the body including the heart [1]. Left ventricular (LV) hypertrophy is the hallmark of cardiac involvement in FD [2]. However, the pathophysiology of FD-related cardiomyopathy is still poorly understood. Globotriaosylceramide accumulation represents only 1–2% of the total cardiac mass [3,4]. Other histological features, such as myocyte hypertrophy and fibrosis, are also important [2]. This suggests that other processes and signaling pathways also contribute to the development of cardiomyopathy in FD.