- Email: [email protected]
Cardiac amyloidosis and Brugada-like ECG pattern
Letters to the Editor
249
Cardiac amyloidosis and Brugada-like ECG pattern☆ Dimitrios Bramos ⁎, Konstantinos Koutras, George Kollias, Eustathia Prappa, Konstantinos P. Letsas, Antonios Sideris Second Department of Cardiology, Evangelismos General Hospital of Athens, 10676, Athens, Greece
a r t i c l e
i n f o
Article history: Received 10 August 2009 Accepted 20 August 2009 Available online 9 September 2009 Keywords: Brugada syndrome Amyloidosis
Amyloidosis is a systemic disease, which is characterized by protein fibrils deposition in different organs [7]. Rhythm and conduction abnormalities including atrial fibrillation, complex ventricular arrhythmias and atrio-ventricular (AV) block are commonly found in cardiac amyloidosis, and generally represent the terminal event [9]. Pre-syncope or syncope is not uncommon in cardiac amyloidosis, and is mainly attributed to arrhythmic events or to the autonomic nervous system dysfunction [1,9]. The Brugada syndrome is an inherited channelopathy associated with a high propensity of ventricular tachyarrhythmias and sudden cardiac death in individuals with structurally normal hearts. Recent data are indicative of mild structural changes, mainly involving the right ventricle, in patients with Brugada syndrome. Agents including sodium channel blocker, beta blockers, tricyclic antidepressants and many others, or electrolytes disturbances (hyperkalemia, hypokalemia, hypercalcemia), hypothermia, fever, alcohol and recreational drugs may precipitate Brugada ECG pattern [10]. Although by definition there are no apparent evidences of structural heart disease in patients with BS, recent data are indicative of mild structural changes [2,3]. We describe a case of a patient with many episodes of pre-syncope and a new diagnosed heart amyloidosis, which presented in the emergency department with a Brugada pattern ECG. A 72-year-old Caucasian female was admitted to our hospital complaining of short episodes of palpitations and lightheadedness without loss of consciousness. She reported many similar episodes, initiated 10 years ago, but with increased frequency the last 2 years. From her past medical history, AL-type amyloidosis due to multiple myeloma was diagnosed 2 years ago, without indications of heart involvement according to a recent echocardiographic study. Her family history was negative for sudden cardiac death. ECG on admission revealed the diagnostic type 1 pattern of BS (Fig. 1). The patient underwent a comprehensive echocardiographic examination, which showed normal dimensions of left ventricle, with
☆ All authors have read and approved the manuscript. We declare that no one author has any commercial associations that might pose a conflict of interest in connection with the submitted article. ⁎ Corresponding author. Second Department of Cardiology, Division of Cardiac Electrophysiology, Evangelismos General Hospital of Athens, 10676, Athens, Greece. Tel./fax: +30 210 7201466. E-mail addresses: [email protected] (D. Bramos), [email protected] (K. Koutras), [email protected] (G. Kollias), [email protected] (E. Prappa), [email protected] (K.P. Letsas), [email protected] (A. Sideris).
concentric hypertrophy and characteristic “sparkling” on intraventricular septum with low tissue Doppler imaging (TDI) velocity. The ejection fraction was normal and right ventricle had normal size and contractility (Fig. 2). The next days the ECG was normalized. The fourth day of her hospitalization, she complained of palpitations and pre-syncope. The ECG revealed a narrow complex tachycardia (possibly AV nodal reentry tachycardia), terminated following intravenous administration of adenosine (6 mg). After arrhythmia termination, the ECG had the initial Brugada ECG morphology. The patient denied any further investigation and discharged from the hospital the next day. To the best of our knowledge, this is the first case implicating cardiac amyloidosis with a type 1 ECG pattern of BS. Our patient displayed two different entities that may lead to palpitations and pre-syncope and/or syncope. However, the cause of these symptoms was a commonly observed supraventricular tachycardia. The complexity of the diagnosis raised the question that instead of the three different entities there was a unique disease able to generate these episodes. The Brugada syndrome (BS) is an inherited channelopathy associated with a high propensity of polymorphic ventricular tachycardia, ventricular fibrillation and sudden cardiac death in individuals with structurally normal hearts [6]. The characteristic (ECG) pattern referred as Brugada sign consists of complete or incomplete right bundle branch block (RBBB) and ST-segment elevation in leads V1 through V3 [5,6]. The ECG features of BS could be intermittent, requiring a pharmacological challenge with a class I antiarrhythmic agent to unmask the characteristic ST-segment elevation in right precordial leads [5,12]. The BS has been associated with many supraventricular arrhythmias, including atrial fibrillation and AV nodal reentry tachycardia [11]. Although, an apparently normal heart at non-invasive evaluation is prerequisite for the diagnosis of BS, an increasing body of evidences supports the presence of a mild structural heart disease. Frustaci et al., using endomyocardial biopsy, have demonstated structural alterations, mainly prevalent or localized right ventricular myocarditis in patients with BS [3]. Interstitial fibrosis has been additionally detected in a patient with BS ECG phenotype [4]. In a recent study using magnetic resonance imaging, Catalano et al. have shown that patients with BS display right ventricular wall motion abnormalities, segmental reduction of contractility and enlargement of the inflow tract [2]. The progress in imaging techniques may approach a new relation between a pathological substrate and arrhythmic events. Brugada-like ECG pattern is much more common than BS in the general population without structural disease, and is not correlated with fatal arrhythmic events [6]. In contrast with BS, there are no references associating this type of ECG with supraventricular arrhythmias. Multiple myeloma is a malignant plasma cell disorder characterized by monoclonal immunoglobulin production. Almost 15% of myeloma patients present deposition of amyloid in tissues [7]. Cardiac amyloidosis is a structural disease which may disturb the normal electrophysiologic properties of myocardium, producing the substrate for an arrhythmogenic activity. Deposition of fibrils should usually induce left ventricular wall thickening, bi-atrial enlargement, diastolic dysfunction, increase wall echogenicity, right ventricular wall thickening or enlargement and severe impairment of longitudinal TDI and strain of the myocardium contractile function. [8] The infiltration of the myocardium may affect not
250
Letters to the Editor
Fig. 1. Brugada-like ECG pattern.
only the contractility, but the conduction system of the heart. There was a prolongation of infra-His conduction times and H–V interval, which was found to be an independent predictor of sudden cardiac death. It is also exists a ventricular conduction delay, leading to ventricular arrhythmias [9].
Although a clear correlation between Brugada syndrome or Brugada ECG-like pattern and stuctural heart disease has not established yet, it is not impossible in the near future to become a new relationship especially with diseases with right ventricular involvement, such as amyloidosis.
Fig. 2. Concentric left ventricular hypertrophy with enhanced myocardial echogenicity.
Letters to the Editor
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] Falk RH, Rubinow A, Cohen AS. Cardiac arrhythmias in systemic amyloidosis: correlation with echocardiographic abnormalities. J Am Coll Cardiol 1984;3:107–13. [2] Catalano O, Antonaci S, Moro G, et al. Magnetic resonance investigations in Brugada syndrome reveal unexpectedly high rate of structural abnormalities. Eur Heart J 2009;30:2241–8. [3] Frustaci A, Priori SG, Pieroni M, et al. Cardiac histological substrate in patients with clinical phenotype of Brugada syndrome. Circulation 2005;112:3680–7. [4] Coronel R, Casini S, Koopmann TT, et al. Right ventricular fibrosis and conduction delay in a patient with clinical signs of Brugada syndrome: a combined electrophysiological, genetic, histopathologic, and computational study. Circulation 2005;112:2769–77. [5] Corrado D, Nava A, Buja G, et al. Familial cardiomyopathy underlies syndrome of right bundle branch block, ST segment elevation and sudden death. J Am Coll Cardiol 1996;27:443–8.
251
[6] Letsas KP, Gavrielatos G, Efremidis M, et al. Prevalence of Brugada sign in a Greek tertiary hospital population. Europace 2007 Nov;9(11):1077–80. [7] Bahlis NJ, Lazarus HM. Multiple myeloma-associated AL amyloidosis: is a distinctive therapeutic approach warranted? Bone Marrow Transplant 2006 Jul;38:7–15. [8] Rahman JE, Helou EF, Gelzer-Bell R, et al. Noninvasive diagnosis of biopsy-proven cardiac amyloidosis. J Am Coll Cardiol 2004;43:410–5. [9] Reisinger J, Dubrey SW, Lavalley M, et al. Electrophysiologic abnormalities in AL (primary) amyloidosis with cardiac involvement. J Am Coll Cardiol 1997;30:1046–51. [10] Yap YG, Behr ER, Camm AJ. Drug-induced Brugada syndrome. Europace 2009;29:114–9. [11] Eckardt L, Kirchhof P, Loh P, et al. Brugada syndrome and supraventricular tachyarrhythmias: a novel association? J Cardiovasc Electrophysiol 2001;12:680–5. [12] Gavrielatos G, Letsas KP, Pappas LK, Efremidis M, Sideris A, Kardaras F. Sensitivity and specificity of sodium channel blocking test in the diagnosis of Brugada syndrome. Int J Cardiol 2010;141:e31–3. [13] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131:149–50.
0167-5273/$ – see front matter © 2009 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2009.08.045
Crossing of a calcified “balloon uncrossable” coronary chronic total occlusion facilitated by a laser catheter A case report and review recent four years' experience at the Thoraxcenter Zhu Jun Shen, Hector M. García-García, Carl Schultz, Martin van der Ent, Patrick W. Serruys ⁎ Department of Interventional Cardiology, Thoraxcenter, Erasmus MC, Rotterdam, The Netherlands
a r t i c l e
i n f o
Article history: Received 12 August 2009 Accepted 20 August 2009 Available online 13 September 2009 Keywords: Coronary angioplasty Total occlusion Excimer laser
Chronic total occlusions (CTO) are one of the last frontiers in coronary intervention [1,2]. The procedural success rate for this lesion subset is around 60% to 80% in comparison to 99% for other lesions [3– 6]. The rates still remain relatively low despite patient selection due to the fact that difficult CTOs would often not be attempted in many centers, although the success rates of CTO have improved due to improved techniques, equipment and the emergence of CTO specialists [7–9]. One technique that is infrequently used is excimer laser assisted coronary intervention, although it has been available for many years. The laser catheter is currently almost exclusively used to treat undilatable lesions [10]. We report a patient with CTO in whom three previous attempts of recanalisation failed. Finally in the fourth attempt, the operators succeeded by using a laser catheter. Also, we review the cases treated with laser catheter in our institution during these recent 4 years.
⁎ Corresponding author. E-mail address: [email protected] (P.W. Serruys).
A 64-year-old man was admitted in June 2009 in our department due to debilitating stable angina in Canadian cardiovascular society (CCS) function class III. Due to previously recurrent symptoms the patient has undergone 3 previous attempts to open a CTO of the right coronary artery in our department (2001, 2006 and Feb 2009). The patient underwent aortic valve replacement with a bioprosthesis (March 2006) and CABG with vein graft from aorta to obtuse marginal and right descending posterior (MO-RDP) but the graft suffered early failure. Previous medical history also included cerebrovascular ischaemic events, severe chronic obstructive pulmonary disease (COPD) (FEV1 1.0 l) and paroxysmal atrial fibrillation, diet controlled diabetes mellitus, dyslipidemia. Physical and laboratory examination were in keeping with above history without additional relevant findings. ECG was normal. Myocardial scintigraphy showed lateral wall ischemia. Left ventricular function was good without regional wall motion abnormalities on echocardiography. Coronary MSCT showed heavy calcification within the whole coronary artery tree and in particular in the right coronary artery (RCA) occlusion (Fig. 1). Coronary angiography after the previous PCI (February 2009) demonstrated no significant stenosis in left anterior descending artery, instent restenosis in the left circumflex which was successfully treated at that time, and a totally occluded mid-RCA with bridging collaterals (Fig. 2). The logistic Euroscore was 27.34%. The Syntax score was 18. Due to his persistent and debilitating symptoms, a further attempt was made to re-open the RCA. After engagement of the ostium of the RCA with a Vista Brite AL3.0 SH guiding catheter (Cordis Corporation, Warren, NJ, USA), a Pilot 50 guidewire was used (Abbott Vascular, Santa Clara, CA, USA) in combination with Asahi Corsair microcatheter (also called channel dilator, Asahi Intecc Co. Ltd), but the guidewire could not cross the lesion and a Asahi Confianza pro, also did not pass. Then a Pilot 150 guidewire, with the support of a Corsair
249
Cardiac amyloidosis and Brugada-like ECG pattern☆ Dimitrios Bramos ⁎, Konstantinos Koutras, George Kollias, Eustathia Prappa, Konstantinos P. Letsas, Antonios Sideris Second Department of Cardiology, Evangelismos General Hospital of Athens, 10676, Athens, Greece
a r t i c l e
i n f o
Article history: Received 10 August 2009 Accepted 20 August 2009 Available online 9 September 2009 Keywords: Brugada syndrome Amyloidosis
Amyloidosis is a systemic disease, which is characterized by protein fibrils deposition in different organs [7]. Rhythm and conduction abnormalities including atrial fibrillation, complex ventricular arrhythmias and atrio-ventricular (AV) block are commonly found in cardiac amyloidosis, and generally represent the terminal event [9]. Pre-syncope or syncope is not uncommon in cardiac amyloidosis, and is mainly attributed to arrhythmic events or to the autonomic nervous system dysfunction [1,9]. The Brugada syndrome is an inherited channelopathy associated with a high propensity of ventricular tachyarrhythmias and sudden cardiac death in individuals with structurally normal hearts. Recent data are indicative of mild structural changes, mainly involving the right ventricle, in patients with Brugada syndrome. Agents including sodium channel blocker, beta blockers, tricyclic antidepressants and many others, or electrolytes disturbances (hyperkalemia, hypokalemia, hypercalcemia), hypothermia, fever, alcohol and recreational drugs may precipitate Brugada ECG pattern [10]. Although by definition there are no apparent evidences of structural heart disease in patients with BS, recent data are indicative of mild structural changes [2,3]. We describe a case of a patient with many episodes of pre-syncope and a new diagnosed heart amyloidosis, which presented in the emergency department with a Brugada pattern ECG. A 72-year-old Caucasian female was admitted to our hospital complaining of short episodes of palpitations and lightheadedness without loss of consciousness. She reported many similar episodes, initiated 10 years ago, but with increased frequency the last 2 years. From her past medical history, AL-type amyloidosis due to multiple myeloma was diagnosed 2 years ago, without indications of heart involvement according to a recent echocardiographic study. Her family history was negative for sudden cardiac death. ECG on admission revealed the diagnostic type 1 pattern of BS (Fig. 1). The patient underwent a comprehensive echocardiographic examination, which showed normal dimensions of left ventricle, with
☆ All authors have read and approved the manuscript. We declare that no one author has any commercial associations that might pose a conflict of interest in connection with the submitted article. ⁎ Corresponding author. Second Department of Cardiology, Division of Cardiac Electrophysiology, Evangelismos General Hospital of Athens, 10676, Athens, Greece. Tel./fax: +30 210 7201466. E-mail addresses: [email protected] (D. Bramos), [email protected] (K. Koutras), [email protected] (G. Kollias), [email protected] (E. Prappa), [email protected] (K.P. Letsas), [email protected] (A. Sideris).
concentric hypertrophy and characteristic “sparkling” on intraventricular septum with low tissue Doppler imaging (TDI) velocity. The ejection fraction was normal and right ventricle had normal size and contractility (Fig. 2). The next days the ECG was normalized. The fourth day of her hospitalization, she complained of palpitations and pre-syncope. The ECG revealed a narrow complex tachycardia (possibly AV nodal reentry tachycardia), terminated following intravenous administration of adenosine (6 mg). After arrhythmia termination, the ECG had the initial Brugada ECG morphology. The patient denied any further investigation and discharged from the hospital the next day. To the best of our knowledge, this is the first case implicating cardiac amyloidosis with a type 1 ECG pattern of BS. Our patient displayed two different entities that may lead to palpitations and pre-syncope and/or syncope. However, the cause of these symptoms was a commonly observed supraventricular tachycardia. The complexity of the diagnosis raised the question that instead of the three different entities there was a unique disease able to generate these episodes. The Brugada syndrome (BS) is an inherited channelopathy associated with a high propensity of polymorphic ventricular tachycardia, ventricular fibrillation and sudden cardiac death in individuals with structurally normal hearts [6]. The characteristic (ECG) pattern referred as Brugada sign consists of complete or incomplete right bundle branch block (RBBB) and ST-segment elevation in leads V1 through V3 [5,6]. The ECG features of BS could be intermittent, requiring a pharmacological challenge with a class I antiarrhythmic agent to unmask the characteristic ST-segment elevation in right precordial leads [5,12]. The BS has been associated with many supraventricular arrhythmias, including atrial fibrillation and AV nodal reentry tachycardia [11]. Although, an apparently normal heart at non-invasive evaluation is prerequisite for the diagnosis of BS, an increasing body of evidences supports the presence of a mild structural heart disease. Frustaci et al., using endomyocardial biopsy, have demonstated structural alterations, mainly prevalent or localized right ventricular myocarditis in patients with BS [3]. Interstitial fibrosis has been additionally detected in a patient with BS ECG phenotype [4]. In a recent study using magnetic resonance imaging, Catalano et al. have shown that patients with BS display right ventricular wall motion abnormalities, segmental reduction of contractility and enlargement of the inflow tract [2]. The progress in imaging techniques may approach a new relation between a pathological substrate and arrhythmic events. Brugada-like ECG pattern is much more common than BS in the general population without structural disease, and is not correlated with fatal arrhythmic events [6]. In contrast with BS, there are no references associating this type of ECG with supraventricular arrhythmias. Multiple myeloma is a malignant plasma cell disorder characterized by monoclonal immunoglobulin production. Almost 15% of myeloma patients present deposition of amyloid in tissues [7]. Cardiac amyloidosis is a structural disease which may disturb the normal electrophysiologic properties of myocardium, producing the substrate for an arrhythmogenic activity. Deposition of fibrils should usually induce left ventricular wall thickening, bi-atrial enlargement, diastolic dysfunction, increase wall echogenicity, right ventricular wall thickening or enlargement and severe impairment of longitudinal TDI and strain of the myocardium contractile function. [8] The infiltration of the myocardium may affect not
250
Letters to the Editor
Fig. 1. Brugada-like ECG pattern.
only the contractility, but the conduction system of the heart. There was a prolongation of infra-His conduction times and H–V interval, which was found to be an independent predictor of sudden cardiac death. It is also exists a ventricular conduction delay, leading to ventricular arrhythmias [9].
Although a clear correlation between Brugada syndrome or Brugada ECG-like pattern and stuctural heart disease has not established yet, it is not impossible in the near future to become a new relationship especially with diseases with right ventricular involvement, such as amyloidosis.
Fig. 2. Concentric left ventricular hypertrophy with enhanced myocardial echogenicity.
Letters to the Editor
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] Falk RH, Rubinow A, Cohen AS. Cardiac arrhythmias in systemic amyloidosis: correlation with echocardiographic abnormalities. J Am Coll Cardiol 1984;3:107–13. [2] Catalano O, Antonaci S, Moro G, et al. Magnetic resonance investigations in Brugada syndrome reveal unexpectedly high rate of structural abnormalities. Eur Heart J 2009;30:2241–8. [3] Frustaci A, Priori SG, Pieroni M, et al. Cardiac histological substrate in patients with clinical phenotype of Brugada syndrome. Circulation 2005;112:3680–7. [4] Coronel R, Casini S, Koopmann TT, et al. Right ventricular fibrosis and conduction delay in a patient with clinical signs of Brugada syndrome: a combined electrophysiological, genetic, histopathologic, and computational study. Circulation 2005;112:2769–77. [5] Corrado D, Nava A, Buja G, et al. Familial cardiomyopathy underlies syndrome of right bundle branch block, ST segment elevation and sudden death. J Am Coll Cardiol 1996;27:443–8.
251
[6] Letsas KP, Gavrielatos G, Efremidis M, et al. Prevalence of Brugada sign in a Greek tertiary hospital population. Europace 2007 Nov;9(11):1077–80. [7] Bahlis NJ, Lazarus HM. Multiple myeloma-associated AL amyloidosis: is a distinctive therapeutic approach warranted? Bone Marrow Transplant 2006 Jul;38:7–15. [8] Rahman JE, Helou EF, Gelzer-Bell R, et al. Noninvasive diagnosis of biopsy-proven cardiac amyloidosis. J Am Coll Cardiol 2004;43:410–5. [9] Reisinger J, Dubrey SW, Lavalley M, et al. Electrophysiologic abnormalities in AL (primary) amyloidosis with cardiac involvement. J Am Coll Cardiol 1997;30:1046–51. [10] Yap YG, Behr ER, Camm AJ. Drug-induced Brugada syndrome. Europace 2009;29:114–9. [11] Eckardt L, Kirchhof P, Loh P, et al. Brugada syndrome and supraventricular tachyarrhythmias: a novel association? J Cardiovasc Electrophysiol 2001;12:680–5. [12] Gavrielatos G, Letsas KP, Pappas LK, Efremidis M, Sideris A, Kardaras F. Sensitivity and specificity of sodium channel blocking test in the diagnosis of Brugada syndrome. Int J Cardiol 2010;141:e31–3. [13] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131:149–50.
0167-5273/$ – see front matter © 2009 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2009.08.045
Crossing of a calcified “balloon uncrossable” coronary chronic total occlusion facilitated by a laser catheter A case report and review recent four years' experience at the Thoraxcenter Zhu Jun Shen, Hector M. García-García, Carl Schultz, Martin van der Ent, Patrick W. Serruys ⁎ Department of Interventional Cardiology, Thoraxcenter, Erasmus MC, Rotterdam, The Netherlands
a r t i c l e
i n f o
Article history: Received 12 August 2009 Accepted 20 August 2009 Available online 13 September 2009 Keywords: Coronary angioplasty Total occlusion Excimer laser
Chronic total occlusions (CTO) are one of the last frontiers in coronary intervention [1,2]. The procedural success rate for this lesion subset is around 60% to 80% in comparison to 99% for other lesions [3– 6]. The rates still remain relatively low despite patient selection due to the fact that difficult CTOs would often not be attempted in many centers, although the success rates of CTO have improved due to improved techniques, equipment and the emergence of CTO specialists [7–9]. One technique that is infrequently used is excimer laser assisted coronary intervention, although it has been available for many years. The laser catheter is currently almost exclusively used to treat undilatable lesions [10]. We report a patient with CTO in whom three previous attempts of recanalisation failed. Finally in the fourth attempt, the operators succeeded by using a laser catheter. Also, we review the cases treated with laser catheter in our institution during these recent 4 years.
⁎ Corresponding author. E-mail address: [email protected] (P.W. Serruys).
A 64-year-old man was admitted in June 2009 in our department due to debilitating stable angina in Canadian cardiovascular society (CCS) function class III. Due to previously recurrent symptoms the patient has undergone 3 previous attempts to open a CTO of the right coronary artery in our department (2001, 2006 and Feb 2009). The patient underwent aortic valve replacement with a bioprosthesis (March 2006) and CABG with vein graft from aorta to obtuse marginal and right descending posterior (MO-RDP) but the graft suffered early failure. Previous medical history also included cerebrovascular ischaemic events, severe chronic obstructive pulmonary disease (COPD) (FEV1 1.0 l) and paroxysmal atrial fibrillation, diet controlled diabetes mellitus, dyslipidemia. Physical and laboratory examination were in keeping with above history without additional relevant findings. ECG was normal. Myocardial scintigraphy showed lateral wall ischemia. Left ventricular function was good without regional wall motion abnormalities on echocardiography. Coronary MSCT showed heavy calcification within the whole coronary artery tree and in particular in the right coronary artery (RCA) occlusion (Fig. 1). Coronary angiography after the previous PCI (February 2009) demonstrated no significant stenosis in left anterior descending artery, instent restenosis in the left circumflex which was successfully treated at that time, and a totally occluded mid-RCA with bridging collaterals (Fig. 2). The logistic Euroscore was 27.34%. The Syntax score was 18. Due to his persistent and debilitating symptoms, a further attempt was made to re-open the RCA. After engagement of the ostium of the RCA with a Vista Brite AL3.0 SH guiding catheter (Cordis Corporation, Warren, NJ, USA), a Pilot 50 guidewire was used (Abbott Vascular, Santa Clara, CA, USA) in combination with Asahi Corsair microcatheter (also called channel dilator, Asahi Intecc Co. Ltd), but the guidewire could not cross the lesion and a Asahi Confianza pro, also did not pass. Then a Pilot 150 guidewire, with the support of a Corsair