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101. Genetic suppression of atrial fibrillation using a dominant-negative ether-a-go-go-related gene mutant.

Author

Soucek R, Thomas D, Kelemen K, Bikou O, Seyler C, Voss F, Becker R, Koenen M, Katus HA, Bauer A, Soucek, Radim, Thomas, Dierk, Kelemen, Kamilla, Bikou, Olympia, Seyler, Claudia, Voss, Frederik, Becker, Rüdiger, Koenen, Michael, Katus, Hugo A, and Bauer, Alexander

Abstract

Background: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. Gene therapy-dependent modulation of atrial electrophysiology may provide a more specific alternative to pharmacological and ablative treatment strategies.Objective: We hypothesized that genetic inactivation of atrial repolarizing ether-a-go-go-related gene (ERG) K(+) currents using a dominant-negative mutant would provide rhythm control in AF.Methods: Ten domestic swine underwent pacemaker implantation and were subjected to atrial burst pacing to induce persistent AF. Animals were then randomized to receive either AdCERG-G627S to suppress ERG/I(Kr) currents or green fluorescent protein (AdGFP) as control. Adenoviruses were applied using a novel hybrid technique combining atrial virus injection and epicardial electroporation to increase transgene expression.Results: In pigs treated with AdCERG-G627S, the onset of persistent AF was prevented (n = 2) or significantly delayed compared with AdGFP controls (12 ± 2.1 vs. 6.2 ± 1.3 days; P < .001) during 14-day follow-up. Effective refractory periods were prolonged in the AdCERG-G627S group compared with AdGFP animals (221.5 ± 4.7 ms vs. 197.0 ± 4.7 ms; P < .006). Impairment of left ventricular ejection fraction (LVEF) during AF was prevented by AdCERG-G627S application (LVEF(CERG-G627S) = 62.1% ± 4.0% vs. LVEF(GFP) = 30.3% ± 9.1%; P < .001).Conclusion: Inhibition of ERG function using atrial AdCERG-G627S gene transfer suppresses or delays the onset of persistent AF by prolongation of atrial refractoriness in a porcine model. Targeted gene therapy represents an alternative to pharmacological or ablative treatment of AF. [ABSTRACT FROM AUTHOR]

Published
2012
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102. Carvedilol targets human K2P 3.1 (TASK1) K+ leak channels.

Author

Staudacher, K, Staudacher, I, Ficker, E, Seyler, C, Gierten, J, Kisselbach, J, Rahm, A-K, Trappe, K, Schweizer, PA, Becker, R, Katus, HA, Thomas, D, Schweizer, P A, and Katus, H A

Subjects
TARGETED drug delivery, ATRIAL fibrillation treatment, MYOCARDIAL depressants, CARDIAC surgery, MUSCLE cells, POTASSIUM channels, PHARMACOLOGY
Abstract

Background and Purpose: Human K(2P) 3.1 (TASK1) channels represent potential targets for pharmacological management of atrial fibrillation. K(2P) channels control excitability by stabilizing membrane potential and by expediting repolarization. In the heart, inhibition of K(2P) currents by class III antiarrhythmic drugs results in action potential prolongation and suppression of electrical automaticity. Carvedilol exerts antiarrhythmic activity and suppresses atrial fibrillation following cardiac surgery or cardioversion. The objective of this study was to investigate acute effects of carvedilol on human K(2P) 3.1 (hK(2P) 3.1) channels.Experimental Approach: Two-electrode voltage clamp and whole-cell patch clamp electrophysiology was used to record hK(2P) 3.1 currents from Xenopus oocytes, Chinese hamster ovary (CHO) cells and human pulmonary artery smooth muscle cells (hPASMC).Key Results: Carvedilol concentration-dependently inhibited hK(2P) 3.1 currents in Xenopus oocytes (IC(50) = 3.8 µM) and in mammalian CHO cells (IC(50) = 0.83 µM). In addition, carvedilol sensitivity of native I(K2P3.1) was demonstrated in hPASMC. Channels were blocked in open and closed states in frequency-dependent fashion, resulting in resting membrane potential depolarization by 7.7 mV. Carvedilol shifted the current-voltage (I-V) relationship by -6.9 mV towards hyperpolarized potentials. Open rectification, characteristic of K(2P) currents, was not affected.Conclusions and Implications: The antiarrhythmic drug carvedilol targets hK(2P) 3.1 background channels. We propose that cardiac hK(2P) 3.1 current blockade may suppress electrical automaticity, prolong atrial refractoriness and contribute to the class III antiarrhythmic action in patients treated with the drug. [ABSTRACT FROM AUTHOR]

Published
2011
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103. Use of cardiovascular magnetic resonance for risk stratification in chronic heart failure: prognostic value of late gadolinium enhancement in patients with non-ischaemic dilated cardiomyopathy.

Author

Lehrke S, Lossnitzer D, Schöb M, Steen H, Merten C, Kemmling H, Pribe R, Ehlermann P, Zugck C, Korosoglou G, Giannitsis E, and Katus HA

Abstract

Objective Owing to its variable clinical course, risk stratification is of paramount importance in non-ischaemic dilated cardiomyopathy (DCM). The goal of this study was to investigate the long-term prognostic significance of late gadolinium enhancement (LGE) as detected by contrast-enhanced cardiovascular magnetic resonance (CE-CMR) in patients with DCM. Design Observational cohort study. Setting University hospital. Patients 184 consecutive patients with DCM. Measurements CE-CMR was performed on a 1.5 T clinical scanner. Presence, extent and patterns of LGE were determined by two independent observers. Outcome measures Patients were followed for the composite end point of cardiac death, hospitalisation for decompensated heart failure, or appropriate implantable cardioverter defibrillator discharge for a mean±SEM of 685±30days. Results LGE was detected in 72/184 patients (39%) and was associated with a lower left ventricular (LV) ejection fraction (31% (20.9-42.2%) vs 44% (33.1-50.9%), p<0.001), higher LV end-diastolic volume index (133 (116-161)ml/m(2) vs 109 (92.7-137.6)ml/m(2), p<0.001) and higher LV mass (80 (67.1-94.8)g/m(2) vs 65.8 (55.2-82.9)g/m(2), p<0.001). Patients in whom LGE was present were more likely to experience the composite end point (15/72 vs 6/112, p=0.002). Receiver operating characteristic curve analysis revealed a LGE of >4.4% of LV mass as optimal discriminator for the composite end point. When entered into multivariate Cox regression analysis, LGE retained its independent predictive value, yielding an associated HR of 3.4 (95% CI 1.26 to 9). Conclusion The presence of LGE in this large DCM patient cohort is associated with pronounced LV remodelling, functional impairment and an adverse outcome. Further research is necessary to determine whether these findings will aid the clinical management of DCM patients. [ABSTRACT FROM AUTHOR]

Published
2011

104. Quantitative assessment of stenosis severity and atherosclerotic plaque composition using 256-slice computed tomography.

Author

Korosoglou G, Mueller D, Lehrke S, Steen H, Hosch W, Heye T, Kauczor HU, Giannitsis E, Katus HA, Korosoglou, Grigorios, Mueller, Dirk, Lehrke, Stephanie, Steen, Henning, Hosch, Waldemar, Heye, Tobias, Kauczor, Hans-Ulrich, Giannitsis, Evangelos, and Katus, Hugo A

Abstract

Objective: To quantitatively estimate lumen narrowing and to assess the volume and composition of atherosclerotic plaque with 256-slice computed tomography angiography (CTA), using conventional quantitative coronary angiography (QCA) as the gold standard.Methods: Twenty-seven consecutive patients with suspected coronary artery disease (CAD) underwent 256-slice CTA and subsequent coronary angiography within 4 weeks. Quantification of lumen narrowing was performed on curved multiplanar reformatted CTA images, in identical projections to those used for QCA. Atherosclerotic plaque volume and composition were assessed by using commercially available software.Results: The overall correlation between the stenosis severity by QCA compared with CTA was high (r(2) = 0.79, p < 0.001). For the detection of >or=50% and >or=75% diameter lesions, CTA yielded high sensitivity, specificity and accuracy (86%, 95% and 90%; and 89%, 100% and 96%, respectively), using QCA as the standard reference. Furthermore, assessment of atherosclerotic plaque yielded highly reproducible results (inter-observer and intra-variability of 13% and 9%, respectively, for the assessment of plaque volume, and high agreement between observers (kappa = 0.86) for the differentiation between non-calcified, mixed and calcified plaque).Conclusions: Clinically indicated 256-slice CT angiography in symptomatic patients can aid both quantification of lumen narrowing and evaluation of atherosclerotic plaque, with high reproducibility. [ABSTRACT FROM AUTHOR]

Published
2010
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107. Universal definition of myocardial infarction.

Author

Thygesen K, Alpert JS, White HD, Jaffe AS, Apple FS, Galvani M, Katus HA, Newby LK, Ravkilde J, Chaitman B, Clemmensen PM, Dellborg M, Hod H, Porela P, Underwood R, Bax JJ, Beller GA, Bonow R, Van der Wall EE, and Bassand JP

Published
2007

108. Treatment of iatrogenic femoral pseudoaneurysm by ultrasound-guided compression therapy and thrombin injection.

Author

Luedde M, Krumsdorf U, Zehelein J, Ivandic B, Dengler T, Katus HA, and Tiefenbacher C

Abstract

Development of an arterial pseudoaneurysm is a common complication following cardiac catheterization. We analyzed data from 6,300 patients who received left heart catheterization at our institution. One day after the procedure, approximately 10% of the patients were examined with duplex sonography. In 204 patients (3.0%), a pseudoaneurysm of the femoral artery was diagnosed. All patients underwent compression therapy. Thereby, 159 of the pseudoaneurysms could be treated successfully. The remaining 45 pseudoaneurysms had a maximal diameter of more than 1.5 cm. Forty-two patients underwent ultrasound and biopsy-line-guided thrombin injection without complications. This strategy resulted in a successful occlusion in 41 cases. Pseudoaneurysms smaller than 2 cm can be treated with compression therapy. Larger pseudoaneurysms can be occluded by thrombin injection using ultrasound guidance. Patients with a pseudoaneurysm with a wide 'neck' should be treated surgically, because the risk of an arterial occlusion following thrombin injection cannot be excluded. [ABSTRACT FROM AUTHOR]

Published
2007
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112. Usefulness of myocardial parametric imaging to evaluate myocardial viability in experimental and in clinical studies.

Author

Korosoglou G, Hansen A, Bekeredjian R, Filusch A, Hardt S, Wolf D, Schellberg D, Katus HA, and Kuecherer H

Abstract

OBJECTIVE: To evaluate whether myocardial parametric imaging (MPI) is superior to visual assessment for the evaluation of myocardial viability. METHODS AND RESULTS: Myocardial contrast echocardiography (MCE) was assessed in 11 pigs before, during, and after left anterior descending coronary artery occlusion and in 32 patients with ischaemic heart disease by using intravenous SonoVue administration. In experimental studies perfusion defect area assessment by MPI was compared with visually guided perfusion defect planimetry. Histological assessment of necrotic tissue was the standard reference. In clinical studies viability was assessed on a segmental level by (1) visual analysis of myocardial opacification; (2) quantitative estimation of myocardial blood flow in regions of interest; and (3) MPI. Functional recovery between three and six months after revascularisation was the standard reference. In experimental studies, compared with visually guided perfusion defect planimetry, planimetric assessment of infarct size by MPI correlated more significantly with histology (r2 = 0.92 versus r2 = 0.56) and had a lower intraobserver variability (4% v 15%, p < 0.05). In clinical studies, MPI had higher specificity (66% v 43%, p < 0.05) than visual MCE and good accuracy (81%) for viability detection. It was less time consuming (3.4 (1.6) v 9.2 (2.4) minutes per image, p < 0.05) than quantitative blood flow estimation by regions of interest and increased the agreement between observers interpreting myocardial perfusion (kappa = 0.87 v kappa = 0.75, p < 0.05). CONCLUSION: MPI is useful for the evaluation of myocardial viability both in animals and in patients. It is less time consuming than quantification analysis by regions of interest and less observer dependent than visual analysis. Thus, strategies incorporating this technique may be valuable for the evaluation of myocardial viability in clinical routine. [ABSTRACT FROM AUTHOR]

Published
2006

113. Accelerated idioventricular rhythm in the post-thrombolytic era: incidence, prognostic implications, and modulating mechanisms after direct percutaneous coronary intervention.

Author

Bonnemeier H, Ortak J, Wiegand UKH, Eberhardt F, Bode F, Schunkert H, Katus HA, Richardt G, Bonnemeier, Hendrik, Ortak, Jasmin, Wiegand, Uwe K H, Eberhardt, Frank, Bode, Frank, Schunkert, Heribert, Katus, Hugo A, and Richardt, Gert

Abstract

Background: In the thrombolytic era, the occurrence of accelerated idioventricular rhythm (AIR) has been proposed to be a specific marker for successful reperfusion. The incidence, prognostic implications, and potential modulating mechanisms of AIR after successful restoration of antegrade flow by means of modern reperfusion therapy (i.e., direct percutaneous coronary intervention (PCI)) has thus far not been investigated.Methods: We prospectively investigated 125 consecutive patients undergoing direct PCI for a first acute myocardial infarction (AMI). The incidence of AIR was determined from 24-hour Holter monitoring, initiated prior to PCI.Results: AIR appeared in 19 patients (15.2%). There were no significant differences between patients with or without AIR regarding baseline clinical characteristics. The incidence of AIR was not different between patients with TIMI 2 and 3 flow (13% vs 16%). There were no differences in the incidence of major cardiac events within 12-month follow-up in patients with and without AIR. Patients with AIR exhibited higher mean R-R intervals (mean 24-hour R-R interval: 871.3 +/- 121 vs 796.4 +/- 100 ms, P < 0.01), higher hourly mean values of heart rate variability (SDNN, 64.7 +/- 26 vs 49.4 +/- 20 ms, P < 0.01; rMSSD, 29.3 +/- 15 vs 22.0 +/- 12 ms, P < 0.01) and lower serum norepinephrine concentrations (60 minute after PCI, 478.9 +/- 357 vs 649.0 +/- 499 pg/ml, P < 0.05).Conclusions: Our findings indicate that AIR is an nonspecific marker for reperfusion of the infarct-related artery in AMI and thus, predate previous observations of the thrombolytic era. Even though, AIR was associated with higher tonic vagal tone and lower sympathetic activity, the occurrence of AIR had no prognostic impact on the clinical course and was not able to discriminate between complete and incomplete reperfusion. [ABSTRACT FROM AUTHOR]

Published
2005

118. Circadian profile of cardiac autonomic nervous modulation in healthy subjects: differing effects of aging and gender on heart rate variability.

Author

Bonnemeier H, Wiegand EKH, Brandes A, Kluge N, Katus HA, Richardt G, and Potratz J

Abstract

Circadian Profile of Heart Rate Variability. INTRODUCTION: Although heart rate variability (HRV) has been established as a tool to study cardiac autonomic activity, almost no data are available on the circadian patterns of HRV in healthy subjects aged 20 to 70 years. METHODS AND RESULTS: We investigated 166 healthy volunteers (81 women and 85 men; age 42 +/- 15 years, range 20-70) without evidence of cardiac disease. Time-domain HRV parameters were determined from 24-hour Holter monitoring and calculated as hourly mean values and mean 24-hour values. All volunteers were fully mobile, awoke around 7 A.M., and had 6 to 8 hours of sleep. Circadian profiles of vagus-associated HRV parameters revealed a marked day-night pattern, with a peak at nighttime and a plateau at daytime. The characteristic nocturnal peak and the day-night amplitude diminished with aging by decade. Estimates of overall HRV (geometric triangular index [TI], SD of NN intervals [SDNN]) and long-term components of HRV (SD of the averages of NN intervals for all 5-min segments [SDANN]) were low at nighttime and increased in the morning hours. There was a significant decline of 24-hour values of all HRV parameters (P < 0.001) and a strong negative correlation (P < 0.001) with increasing age. Mean 24-hour RR interval (P < 0.001), SDNN, mean SD of NN intervals for all 5-minute intervals (SDNNi), and SDANN (all P < 0.01) were significantly higher in men. Younger men also exhibited significantly higher values for vagus-associated parameters (root mean square successive difference [rMSSD], P < 0.05; SDNNi, P < 0.01); however, gender differences diminished with increasing age. CONCLUSION: Normal aging is associated with a constant decline of cardiac vagal modulation due to a significant decrease of nocturnal parasympathetic activity. The significant gender-related difference of HRV decreases with aging. These findings emphasize the need to determine age-, gender-, and nycthemeral-dependent normal ranges for HRV assessment. [ABSTRACT FROM AUTHOR]

Published
2003
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119. Effect of carvedilol on the morbidity of patients with severe chronic heart failure: results of the carvedilol prospective randomized cumulative survival (COPERNICUS) study.

Author

Packer M, Fowler MB, Roecker EB, Coats AJS, Katus HA, Krum H, Mohacsi P, Rouleau JL, Tendera M, Staiger C, Holcslaw TL, Amann-Zalan I, DeMets DL, Carvedilol Prospective Randomized Cumulative Survival (COPERNICUS) Study Group, Packer, Milton, Fowler, Michael B, Roecker, Ellen B, Coats, Andrew J S, Katus, Hugo A, and Krum, Henry

Published
2002

120. Atrial sensing and av synchrony in single lead vdd pacemakers: a prospective comparison to DDD devices with bipolar atrial leads.

Author

Wiegand UK, Bode F, Schneider R, Taubert G, Brandes A, Peters W, Katus HA, and Potratz J

Abstract

Introduction: Single lead VDD pacing has offered an alternative to DDD .systems in patients with isolated AV block. Up to now, however, the relative performance of these pacemaker systems was not systematically compared. Methods and Results: Three hundred sixty patients who received either a VDD pacemaker (n = 180) or a DDD device (n = 180) with a hipolar atrial lead were investigated prospectively for a mean period of 30 ± 13 months. Pacemaker function was analyzed by telemetry. Holter monitoring, and exercise ECG. Time of implantation and fluoroscopy was significantly lower with VDD devices (44.3 ± 5.1 min vs 74.4 ± 13.5 min and 4.6 ± 2.5 min vs 10.3 ± 5.6 min in DDD pacemakers, respectively). Intermittent atrial undersensing occurred in 23.3% of patients with a VDD pacemaker and in 9.4% with DDD devices (NS). The incidence of atrial tachyarrhythmias did not differ between the VDD (6.7%) and the DDD group (6.1%). Sinus node dysfunction developed in 1.9% of patients, but the vast majority (85.7%) of patients were asymptomatic. There was a tendency for a higher rate of operative revisions in the DDD group (6.1% vs 3.3% in VDD pacemakers, P = 0.15). Cumulative maintenance of AV-.synchronized pacing mode was 94.9% in patients with VDD pacemakers and 92.1% with DDD devices (NS). Conclusion: With the benefit of a simpler implant procedure, long-term outcome of single lead VDD pacing is equivalent to DDD pacing in patients with AV block and preoperative normal sinus node function. [ABSTRACT FROM AUTHOR]

Published
1999

128. Poster session 3

Author

Winter, R, Lindqvist, P, Sheehan, F, Fazlinezhad, A, Vojdanparast, M, Nezafati, P, Martins Fernandes, S, Teixeira, R, Pellegrino, M, Generati, G, Bandera, F, Labate, V, Alfonzetti, E, Guazzi, M, Iriart, X, Dinet, ML, Jalal, Z, Cochet, H, Thambo, JB, Moustafa, S, Ho, TH, Shah, P, Murphy, K, Nelluri, BK, Lee, H, Wilansky, S, Mookadam, F, Stolfo, D, Tonet, E, Merlo, M, Barbati, G, Gigli, M, Pinamonti, B, Ramani, F, Zecchin, M, Sinagra, G, Bieseviciene, M, Vaskelyte, JJ, Mizariene, V, Lesauskaite, V, Verseckaite, R, Karaliute, R, Jonkaitiene, R, Patel, S, Li, L, Craft, M, Danford, D, Kutty, S, Vriz, O, Pellegrinet, M, Zito, C, Carerj, S, Di Bello, V, Cittadini, A, Bossone, E, Antonini-Canterin, F, Sarvari, S I, Rodriguez, M, Sitges, M, Sepulveda-Martinez, A, Gratacos, E, Bijnens, B, Crispi, F, Santos, M, Leite, L, Martins, R, Baptista, R, Barbosa, A, Ribeiro, N, Oliveira, A, Castro, G, Pego, M, Berezin, A, Samura, T, Kremzer, A, Stoebe, S, Tarr, A, Pfeiffer, D, Hagendorff, A, Benyounes Iglesias, N, Van Der Vynckt, C, Gout, O, Devys, JM, Cohen, A, De Chiara, B, Musca, F, D'angelo, L, Cipriani, MG, Parolini, M, Rossi, A, Santambrogio, GM, Russo, C, Giannattasio, C, Moreo, A, Soliman, A, Moharram, M, Gamal, A, Reda, A, Oni, O, Adebiyi, A, Aje, A, Ricci, F, Aquilani, R, Dipace, G, Bucciarelli, V, Bianco, F, Miniero, E, Scipioni, G, De Caterina, R, Gallina, S, Tumasyan, LR, Adamyan, KG, Chilingaryan, AL, Tunyan, LG, Kim, KH, Cho, JY, Yoon, HJ, Ahn, Y, Jeong, MH, Cho, JG, Park, JC, Popa, B A, Popa, A, Cerin, G, Ecocardiografico, Campagna Provinciale di Screening, Yiangou, K, Azina, CH, Yiangou, A, Georgiou, C, Zitti, M, Ioannides, M, Chimonides, S, Olsen, R H, Pedersen, LR, Snoer, M, Christensen, TE, Ghotbi, AA, Hasbak, P, Kjaer, A, Haugaard, SB, Prescott, E, Cacicedo, A, Velasco Del Castillo, S, Gomez Sanchez, V, Anton Ladislao, A, Onaindia Gandarias, J, Rodriguez Sanchez, I, Jimenez Melo, O, Garcia Cuenca, E, Zugazabeitia Irazabal, G, Romero Pereiro, A, Monti, L, Nardi, B, Di Giovine, G, Malanchini, G, Scardino, C, Balzarini, L, Presbitero, P, Gasparini, GL, Holte, E, Orlic, D, Tesic, M, Zamaklar-Trifunovic, D, Vujisic-Tesic, B, Borovic, M, Milasinovic, D, Zivkovic, M, Kostic, J, Belelsin, B, Ostojic, M, investigators, PATA STEMI, Trifunovic, D, Krljanac, G, Savic, L, Asanin, M, Aleksandric, S, Petrovic, M, Zlatic, N, Lasica, R, Mrdovic, I, Nucifora, G, Muser, D, Zanuttini, D, Tioni, C, Bernardi, G, Spedicato, L, Proclemer, A, Casalta, AC, Galli, E, Szymanski, C, Salaun, E, Lavoute, C, Haentjens, J, Tribouilloy, C, Mancini, J, Donal, E, Habib, G, Cavalcante, JL, Delgado-Montero, A, Dahou, A, Caballero, L, Rijal, S, Gorcsan, J, Monin, JL, Pibarot, P, Lancellotti, P, Keramida, K, Kouris, N, Kostopoulos, V, Giannaris, V, Trifou, E, Markos, L, Mihalopoulos, A, Mprempos, G, Olympios, CD, Calin, A, Mateescu, AD, Rosca, M, Beladan, CC, Enache, R, Gurzun, MM, Varga, P, Calin, C, Ginghina, C, Popescu, BA, Almeida Morais, L, Galrinho, A, Branco, L, Gomes, V, Timoteo, A T, Daniel, P, Rodrigues, I, Rosa, S, Fragata, J, Ferreira, R, Bandera, F, Generati, G, Pellegrino, M, Carbone, F, Labate, V, Alfonzetti, E, Guazzi, M, Galli, E, Leclercq, C, Samset, E, Donal, E, Kamal, H M, Oraby, MA, Eleraky, A Z, Yossuef, M A, Leite, L, Baptista, R, Teixeira, R, Ribeiro, N, Oliveira, AP, Barbosa, A, Castro, G, Martins, R, Elvas, L, Pego, M, Polte, CL, Gao, SA, Lagerstrand, KM, Johnsson, AA, Bech-Hanssen, O, Martinez Santos, P, Vilacosta, I, Batlle Lopez, E, Sanchez Sauce, B, Jimenez Valtierra, J, Espana Barrio, E, Campuzano Ruiz, R, De La Rosa Riestra, A, Alonso Bello, J, Perez Gonzalez, F, Jin, CN, Wan, S, Sun, JP, Lee, AP, Generati, G, Bandera, F, Pellegrino, M, Carbone, F, Labate, V, Alfonzetti, E, Guazzi, M, Reali, M, Cimino, S, Salatino, T, Silvetti, E, Mancone, M, Pennacchi, M, Giordano, A, Sardella, G, Agati, L, Kalcik, M, Yesin, M, Gunduz, S, Gursoy, MO, Astarcioglu, MA, Karakoyun, S, Bayam, E, Cersit, S, Ozkan, M, Cacicedo, A, Velasco Del Castillo, S, Gomez Sanchez, V, Anton Ladislao, A, Onaindia Gandarias, J, Rodriguez Sanchez, I, Jimenez Melo, O, Quintana Razcka, O, Romero Pereiro, A, Zugazabeitia Irazabal, G, Nascimento, H, Braga, M, Flores, L, Ribeiro, V, Melao, F, Dias, P, Maciel, MJ, Bettencourt, P, Ferreiro Quero, C, Mesa Rubio, M D, Ruiz Ortiz, M, Delgado Ortega, M, Sanchez Fernandez, J, Duran Jimenez, E, Morenate Navio, C, Romero, M, Pan, M, Suarez De Lezo, J, Kazum, S, Vaturi, M, Weisenberg, D, Monakier, D, Valdman, A, Vaknin- Assa, H, Assali, A, Kornowski, R, Sagie, A, Shapira, Y, Madeira, S, Ribeiras, R, Abecasis, J, Teles, R, Castro, M, Tralhao, A, Horta, E, Brito, J, Andrade, M, Mendes, M, Villagra, JM, Avegliano, G, Ronderos, R, Matta, MG, Camporrotondo, M, Castro, F, Albina, G, Aranda, A, Navia, D, Muraru, D, Siciliano, M, Migliore, F, Cavedon, S, Folino, F, Pedrizzetti, G, Bertaglia, M, Corrado, D, Iliceto, S, Badano, LP, Gobbo, M, Merlo, M, Stolfo, D, Losurdo, P, Ramani, F, Barbati, G, Pivetta, A, Pinamonti, B, Sinagra, GF, Di Lenarda, A, Generati, G, Bandera, F, Pellegrino, M, Labate, V, Carbone, F, Alfonzetti, E, Guazzi, M, D'andrea, A, Di Palma, E, Baldini, L, Verrengia, M, Vastarella, R, Limongelli, G, Bossone, E, Calabro', R, Russo, MG, Pacileo, G, Azevedo, O, Cruz, I, Correia, E, Bento, D, Teles, L, Lourenco, C, Faria, R, Domingues, K, Picarra, B, Marques, N, Group, SUNSHINE, Nucifora, G, Muser, D, Gianfagna, P, Morocutti, G, Proclemer, A, Cruz, I, Gomes, AC, Lopes, LR, Stuart, B, Caldeira, D, Morgado, G, Almeida, AR, Canedo, P, Bagulho, C, Pereira, H, Lozano Granero, VC, Pardo Sanz, A, Marco Del Castillo, A, Monteagudo Ruiz, JM, Rincon Diaz, LM, Ruiz Rejon, F, Casas, E, Hinojar, R, Fernandez-Golfin, C, Zamorano Gomez, JL, Stampfli, S F, Erhart, L, Staehli, BE, Kaufmann, BA, Tanner, FC, Marketou, M, Kontaraki, J, Parthenakis, F, Maragkoudakis, S, Zacharis, E, Patrianakos, A, Vardas, P, Bento, D, Domingues, K, Correia, E, Lopes, L, Teles, L, Picarra, B, Magalhaes, P, Faria, R, Lourenco, C, Azevedo, O, Group, SUNSHINE, Mohty, D, Boulogne, C, Magne, J, Damy, T, Martin, S, Boncoeur, MP, Aboyans, V, Jaccard, A, Hernandez Jimenez, V, Saavedra Falero, J, Alberca Vela, MT, Molina Blazquez, L, Mata Caballero, R, Serrano Rosado, JA, Elviro, R, Gascuena, R, Di Gioia, C, Fernandez Rozas, I, Manzano, MC, Martinez Sanchez, JI, Molina, M, Palma, J, Ingvarsson, A, Werther Evaldsson, A, Radegran, G, Stagmo, M, Waktare, J, Roijer, A, Meurling, CJ, Cameli, M, Righini, FM, Sparla, S, Di Tommaso, C, Focardi, M, D'ascenzi, F, Tacchini, D, Maccherini, M, Henein, M, Mondillo, S, Werther Evaldsson, A, Ingvarsson, A, Waktare, J, Thilen, U, Stagmo, M, Roijer, A, Radegran, G, Meurling, C, Greiner, S, Jud, A, Aurich, M, Katus, HA, Mereles, D, Michelsen, MM, Faber, R, Pena, A, Mygind, ND, Suhrs, HE, Zander, M, Prescott, E, El Eraky, AZZA, Handoka, NESRIN, Ghali, MONA, Eldahshan, NAHED, Ibrahim, AHMED, Kamal, H M, Al-Eraky, A Z, El Attar, M A, Omar, A S, D'ascenzi, F, Pelliccia, A, Alvino, F, Solari, M, Cameli, M, Focardi, M, Bonifazi, M, Mondillo, S, Spinelli, L, Giudice, C A, Assante Di Panzillo, E, Castaldo, D, Riccio, E, Pisani, A, Trimarco, B, Stojanovic, S, Deljanin Ilic, M, Ilic, S, Mincu, RI, Magda, LS, Florescu, M, Velcea, A, Mihalcea, D, Chiru, A, Popescu, BO, Tiu, C, Vinereanu, D, Vindis, D, Hutyra, M, Cechakova, E, Littnerova, S, Taborsky, M, Mantovani, F, Lugli, R, Bursi, F, Fabbri, M, Modena, MG, Stefanelli, G, Mussini, C, Barbieri, A, Yi, JE, Youn, HJ, O, JH, Yoon, HJ, Jung, HO, Shin, GJ, Styczynski, G, Rdzanek, A, Pietrasik, A, Kochman, J, Huczek, Z, Milewska, A, Marczewska, M, Szmigielski, C A, Battah, AHMED, Abd Eldayem, SOHA, El Magd El Bohy, ABO, O'driscoll, J, Slee, A, Peresso, V, Nazir, S, Sharma, R, Generati, G, Bandera, F, Pellegrino, M, Labate, V, Carbone, F, Alfonzetti, E, Guazzi, M, Velasco Del Castillo, S, Anton Ladislao, A, Gomez Sanchez, V, Cacidedo Fernandez Bobadilla, A, Onaindia Gandarias, JJ, Rodriguez Sanchez, I, Romero Pereira, A, Quintana Rackza, O, Jimenez Melo, O, Zugazabeitia Irazabal, G, Voilliot, D, Huttin, O, Venner, C, Deballon, R, Manenti, V, Villemin, T, Olivier, A, Sadoul, N, Juilliere, Y, Selton-Suty, C, Scali, MC, Simioniuc, A, Mandoli, GE, Dini, FL, Marzilli, M, Picano, E, Garcia Campos, A, Martin-Fernandez, M, De La Hera Galarza, JM, Corros-Vicente, C, Leon-Aguero, V, Velasco-Alonso, E, Colunga-Blanco, S, Fidalgo-Arguelles, A, Rozado-Castano, J, Moris De La Tassa, C, Opitz, B, Stelzmueller, ME, Wisser, W, Reichenfelser, W, Mohl, W, Herold, IHF, Saporito, S, Mischi, M, Bouwman, RA, Van Assen, HC, Van Den Bosch, HCM, De Lepper, A, Korsten, HHM, Houthuizen, P, Veiga, CESAR, I, JAVIER. Randulfe Juanjo Andina Jose Fanina Francisco Calvo Emilio Paredes-Galan Pablo Pazos Andres, Ageing, Diseases, Cardiovascular, Santos Furtado, M, Rodrigues, A, Leal, G, Silvestre, O, Andrade, J, Khan, UM, Hjertaas, JJ, Greve, G, Matre, K, Leite, L, Teixeira, R, Baptista, R, Barbosa, A, Ribeiro, N, Castro, G, Martins, R, Cardim, N, Goncalves, L, Pego, M, Leite, L, Teixeira, R, Baptista, R, Barbosa, A, Ribeiro, N, Castro, G, Martins, R, Cardim, N, Goncalves, L, Pego, M, Leite, L, Teixeira, R, Baptista, R, Barbosa, A, Oliveira, AP, Castro, G, Martins, R, Cardim, N, Goncalves, L, Pego, M, Keramida, K, Kouris, N, Kostopoulos, V, Markos, L, Olympios, CD, Molnar, AA, Kovacs, A, Tarnoki, AD, Tarnoki, DL, Kolossvary, M, Apor, A, Maurovich-Horvat, P, Jermendy, G, Sengupta, P, Merkely, B, Rio, P, Viveiros Monteiro, A, Galrinho, A, Pereira-Da-Silva, T, Moura Branco, L, Timoteo, A, Abreu, J, Leal, A, Varela, F, Cruz Ferreira, R, Huang, MS, Yang, LT, Tsai, WC, Papadopoulos, C, Mpaltoumas, K, Fotoglidis, A, Triantafyllou, K, Pagourelias, E, Kassimatis, E, Tzikas, S, Kotsiouros, G, Mantzogeorgou, E, Vassilikos, V, Venneri, L, Calicchio, F, Manivarmane, R, Pareek, N, Baksi, J, Rosen, S, Senior, R, Lyon, AR, Khattar, RS, Onut, R, Marinescu, C, Onciul, S, Zamfir, D, Tautu, O, Dorobantu, M, Casas Rojo, E, Carbonell San Roman, A, Rincon Diez, LM, Gonzalez Gomez, A, Fernandez Santos, S, Lazaro Rivera, C, Moreno Vinues, C, Sanmartin Fernandez, M, Fernandez-Golfin, C, Zamorano Gomez, JL, Bayat, F, Alirezaei, T, Karimi, AS, hospital, cardiovascular research center of shahid beheshti, Aggeli, C, Kakiouzi, V, Felekos, I, Panagopoulou, V, Latsios, G, Karabela, M, Petras, D, Tousoulis, D, Ben Kahla, S, Abid, L, Abid, D, Kammoun, S, Abid, L, Ben Kahla, S, Choi, JH, Lee, JW, Barreiro Perez, M, Martin Fernandez, M, Costilla Garcia, SM, Diaz Pelaez, E, and Moris De La Tassa, C

Abstract

Purpose: We developed a transthoracic echo simulator that can measure psychomotor skill in echo to assist in training as well as for certification of competence. The simulator displays cine loops on a computer in response to the user scanning a mannequin with a mock transducer. The skill metric is the deviation angle between the image acquired by the user and the anatomically correct plane for the specified view. We sought to determine whether the simulator-based test could distinguish levels of expertise. Methods: Attendees at an echo course or at the annual meeting of the Swedish Heart Association were invited to take a 15 min test on the simulator. On the test, the user scanned the mannequin and acquired 4 views: parasternal long axis (pLAX) in patient 1, apical 4 chamber (a4c) and aLAX in patient 2, and pLAX in patient 3. Scan time was limited to 15 min. Attendees were asked regarding current work status, position, and experience with echo assessed from duration in years and procedure volume in the past 12 months. Results: Of the 61 participants there were 22 sonographers, 2 nurses, and 37 doctors who were all in practice except 1 doctor who was a resident. The data of nurses was combined with that of sonographers because their procedure volume was nearer to that of sonographers (850 ± 599 tests/yr) than doctors (312 ± 393, p < 0.001). Doctors and non-doctors had similar duration of experience (9 ± 8 vs. 12 ± 11 yrs, p=NS). The test was not completed by 12 participants (18%) but unfamiliarity with the simulator may have contributed because the deviation angle for pLAX dropped between the first and third patients (23 ± 11 to 18 ± 10 degrees, p<0.020). The average deviation angle over the 4 views was slightly lower for sonographers than for doctors (26 ± 11 vs. 30 ± 14 degrees, p=NS). The deviation angle for pLAX (55 ± 37 degrees) was higher than for a4C (17 ± 22 degrees) or either pLAX view (p<0.00001). pLAX was the only view whose deviation angle correlated significantly with experience and only with procedure volume (r=-0.302, p=0.025). Conclusions: The results of this study demonstrate that the skill metric employed, angle of deviation between the plane of an acquired view and the plane of the anatomically correct image for that view, can distinguish the relative experience of sonographers and doctors in practice. Simulation-based testing provides objective and quantitative assessment of the psychomotor skill of image acquisition and may be of value in certification of trainees and in maintenance of certification examination of practicing sonographers and doctors.

Published
2015
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129. P237 Targeted adeno-associated virus (AAV) vector for efficient gene transfer into endothelial cells in vivo.

Author

Varadi, KH, Katus, HA, and Mueller, OJ

Subjects
*ADENO-associated virus, *GENETIC transformation, *ENDOTHELIAL cells, *GENE therapy, *IMMUNE response, TREATMENT of vascular diseases
Abstract

Background: Gene therapy approaches targeting vascular diseases require an efficient and specific gene transfer to the vascular wall. Previously applied vector systems fail to cover these requirements and induce strong host immune responses. Adeno-associated virus (AAV) vectors enable long-term gene transfer into the myocardium. However, they fail to efficiently transduce endothelial cells. We therefore sought out to develop a targeted AAV vector by modification of the capsid surface and use of a vascular promoter.Methods: In order to restrict transgene expression to endothelium, we used the murine vascular cadherin-5 (mveCad-5) core promoter. For augmentation of expression levels, we generated additionally a chimeric promoter by fusing a CMV-enhancer (CMVenh) to mveCad-5. The constructs were tested in vitro to identify the most efficient promoter for further in vivo studies. For in vivo gene transfer, we compared naturally occurring AAV serotypes 8 and 9 to an AAV9 variant obtained by in vitro selection of a random AAV peptide display library. Vectors carrying a gene encoding the Cre recombinase under control of the CMV or CMVenh-mveCad5 promoters, respectively, were injected intravenously into adult ROSAmT/mG ("Tomato")-mice. The mouse model harbors a cell membrane-targeted, two-color fluorescent Cre-responsive reporter allele enabling expression of green fluorescence in Cre recombinase positive cells. After 3 weeks mice were sacrificed and representative tissues were analyzed by fluorescence microscopy for detection of green fluorescent cells.Results: Our in vitro study showed that replacement of CMV by the mveCad-5 promoter restricted transgene expression to endothelial cells but overall expression was lower than that obtained with the CMV promoter. The CMVenh-mveCad5 promoter instead, resulted in high expression levels in endothelial cells with lower expression in other cells. While AAV8 and AAV9 failed to enable gene expression in endothelial cells in vivo, the peptide-targeted AAV9 vector enabled a highly efficient recombination in endothelial cells of the aorta. While both the CMV and CMVenh-mveCad5 promoter resulted in efficient EGFP expression in the aortic endothelium, unspecific extravascular expression was higher with the CMV-promoter.Conclusion: Taken together, we could show that a targeted AAV-vector can be used for efficient gene transfer into endothelial cells of the aorta in vivo. Besides its use for validation of potentially therapeutic targets for vascular diseases this vector may also be suitable for conditionally knocking out genes in the vascular system. [ABSTRACT FROM AUTHOR]

Published
2014
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130. P107 Role of plasma membrane-associated AKAPs 15/18 and 79 for the regulation of cardiac IK1 current by protein kinase A.

Author

Seyler, C, Scherer, D, Koepple, C, Kulzer, M, Korkmaz, S, Thomas, D, Kaya, Z, Backs, J, Katus, HA, and Zitron, E

Subjects
CELL membranes, POTASSIUM channels, CYCLIC-AMP-dependent protein kinase, HEART cells, CATECHOLAMINES, MYOCARDIAL depressants
Abstract

Background: The cardiac inwardly rectifying potassium current IK1 stabilises the diastolic resting membrane potential of ventricular cardiomyocytes. Protein kinase A (PKA) induces an inhibition of IK1 current which strongly promotes focal arrhythmogenesis under increased catecholamine levels. The molecular mechanisms underlying this regulation have only partially been elucidated to date. Furthermore, the role of A Kinase Anchoring Proteins (AKAPs) in this regulation has not been examined yet. The objective of this project was to elucidate the molecular mechanisms underlying the inhibition of IK1 by PKA and to identify novel molecular targets for antiarrhythmic therapy downstream β-adrenoreceptors.Methods: Cardiac IK1 current was measured in isolated rat ventricular cardiomyocytes using whole-cell patch clamp. Kir2.x channels and AKAPs were expressed in Xenopus oocytes and current recordings were performed using the double-electrode voltage-clamp technique. Association of channels and AKAPs was examined with the use of co-immunoprecipitation and immunofluorescent confocal microscopy in isolated cardiomyocytes and in mammalian cell lines.Results: In patch clamp experiments, activation of PKA inhibited IK1 current in rat ventricular cardiomyocytes. This regulation was markedly attenuated by disrupting PKA-binding to AKAPs with the peptide inhibitor AKAP-IS. In expression systems, we observed functional and spatial coupling of the plasma membrane-associated AKAP15/18 and AKAP79 to Kir2.1 and Kir2.2 channel subunits, but not to Kir2.3 channels, which underly IK1 currents. In contrast, AKAPyotiao had no functional effect on the PKA regulation of Kir channels. AKAP15/18 and AKAP79 co-immunoprecipitated with and co-localized to Kir2.1 and Kir2.2 channel subunits in ventricular cardiomyocytes.Conclusions: In this study, we provide evidence for the functional and spatial coupling of cardiac Kir2.1 and Kir2.2 subunits as molecular components of IK1 current with the plasma membrane-bound AKAPs 15/18 and 79. Cardiac membrane-associated AKAPs are a functionally essential part of the regulatory cascade determining IK1 current function and may be novel molecular targets for antiarrhythmic therapy downstream from β-adrenoreceptors. [ABSTRACT FROM AUTHOR]

Published
2014
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131. P639 Amiodarone and dronedarone inhibit inwardly rectifying Kir2.1 channels, but not Kir2.2 and Kir2.3 channels.

Author

Seyler, C, Xynogalos, P, Scherer, D, Koepple, C, Scholz, EP, Thomas, D, Katus, HA, and Zitron, E

Subjects
AMIODARONE, ION channels, ARRHYTHMIA, TETRAMERS (Oligomers), VOLTAGE-clamp techniques (Electrophysiology), BIOPHYSICS
Abstract

Background: Cardiac inwardly rectifying IK1 current drives terminal repolarisation. Inhibition of IK1 current can suppress re-entry based arrhythmias and has been demonstrated to exert anti-fibrillatory effects. Human IK1 current is mainly formed by heterotetrameric assembly of three subunits: Kir2.1, Kir2.2 and Kir2.3 channels. Amiodarone and dronedarone have been shown to inhibit cardiac IK1 current, but the molecular basis of these effects has not been elucidated to date.Methods: Human Kir2.1 - Kir2.3 channels were expressed in Xenopus oocytes and current recordings were performed using the double-electrode voltage-clamp technique.Results: Amiodarone and dronedarone exerted differential inhibitory effects on Kir2.1, Kir2.2 and Kir2.3 channels, respectively. Both drugs inhibited only Kir2.1 channels without an effect on Kir2.2 and Kir2.3 channels. We analyzed effects of dronedarone in detail. Onset of inhibition was slow, but the effect was completely reversible upon washout. Biophysical current characteristics such as inwardly-rectifying properties and reversal potential of Kir2.1 currents were not modified. The inhibitory effect did not exhibit frequency dependence. Interestingly, dronedarone inhibited Kir2.1 currents mainly at negative potentials.Conclusions: Amiodarone and dronedarone both inhibit only Kir2.1 channels without affecting Kir2.2 and Kir2.3 channels. In view of the functional significance of Kir2.1 channels, this effect probably underlies the observed inhibition of IK1 current by both compounds and may contribute to their anti-fibrillatory efficacy. [ABSTRACT FROM PUBLISHER]

Published
2014
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132. P234 AAV-mediated cardiac transfer of the desmin cDNA ameliorates progression of cardiomyopathy in desmin-deficient mice.

Author

Heckmann, M, Bauer, R, Jungmann, A, Strucksberg, KH, Schroeder, R, Katus, HA, and Mueller, OJ

Subjects
CARDIOMYOPATHIES, DISEASE progression, ANTISENSE DNA, LABORATORY mice, LUCIFERASES, ECHOCARDIOGRAPHY
Abstract

Background: Desmin is a type III intermediate filament which plays a central role in maintaining the structural integrity of cardiac and skeletal muscle cells. Mutations in the desmin coding gene are associated with a heterogeneous phenotype involving cardiomyopathies, cardiac conduction disease and myopathy. Desminopathies are most commonly diagnosed in adults in their mid 30s and show a progressive course, with cardiac involvement as the most important factor limiting prognosis. As of today, only symptomatic treatment is available for patients. Similar to patients with distinct defects in the desmin gene, knockout mice develop dilative cardiomyopathy compared to wildtype littermates.Aim of our study was to determine whether an adeno-associated-viral vector (AAV) mediated gene transfer of the intact desmin cDNA can either prevent or slow-down the development of cardiomyopathy in desmin-deficient (des-KO) mice. Methods: murine desmin cDNA under the control of the TNNT2 promoter was packaged into AAV serotype 9 capsids and were intravenously injected into adult des-KO mice. AAV9-luciferase vectors were used as controls. Left ventricular function was monitored using echocardiography before vector application and 3 months, 6 months and 9 months after treatment. After left heart catheterisation to assess pressure-volume (PV)-loops mice were sacrificed after 10 months for histological and molecular analyses. Results: AAV9-mediated transfer of the desmin cDNA resulted in an efficient reconstitution of desmin with intact intercalated discs. Echocardiographic analyzes revealed a fractional shortening of 38 + 4% (n=10) in desmin deficient mice treated with desmin cDNA compared to 28 + 4% (n=9) in AAV9-luciferase control-treated mice (1-way ANOVA, p < 0.05). PV-loops showed significant improvement in cardiac contractility with increased dp/dtmax in AAV9-desmin-treated mice 7742 + 539 mmHg/sec (n=7) compared to luciferase-treated mice 5901 + 466 mmHg/sec (n=9) suggesting an amelioration of the cardiomyopathy phenotype in AAV9-desmin-treated mice.Conclusion: Our study establishes an approach to specifically treat desmin-related cardiomyopathy by targeting gene expression into the myocardium through systemic application of AAV vectors. [ABSTRACT FROM PUBLISHER]

Published
2014
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133. Poster session 2: Thursday 4 December 2014, 08:30-12:30 * Location: Poster area

Author

Domingos, JS, Augustine, DX, Leeson, P, Noble, JA, Doan, H-L, Boubrit, L, Cheikh-Khalifa, R, Laveau, F, Djebbar, M, Pousset, F, Isnard, R, Hammoudi, N, Lisi, M, Cameli, M, Di Tommaso, C, Curci, V, Reccia, R, Maccherini, M, Henein, M Y, Mondillo, S, Leitman, M, Vered, Z, Rashid, H, Yalcin, M U, Gurses, K M, Kocyigit, D, Evranos, B, Yorgun, H, Sahiner, L, Kaya, B, Aytemir, K, Ozer, N, Bertella, E, Petulla', M, Baggiano, A, Mushtaq, S, Russo, E, Gripari, P, Innocenti, E, Andreini, D, Tondo, C, Pontone, G, Necas, J, Kovalova, S, Hristova, K, Shiue, I, Bogdanva, V, Teixido Tura, G, Sanchez, V, Rodriguez-Palomares, J, Gutierrez, L, Gonzalez-Alujas, T, Garcia-Dorado, D, Forteza, A, Evangelista, A, Timoteo, A T, Aguiar Rosa, S, Cruz Ferreira, R, Campbell, R, Carrick, D, Mccombe, C, Tzemos, N, Berry, C, Sonecki, P, Noda, M, Setoguchi, M, Ikenouchi, T, Nakamura, T, Yamamoto, Y, Murakami, T, Katou, Y, Usui, M, Ichikawa, K, Isobe, M, Kwon, BJ, Roh, JW, Kim, HY, Ihm, SH, Barron, A J, Francis, DP, Mayet, J, Wensel, R, Kosiuk, J, Dinov, B, Bollmann, A, Hindricks, G, Breithardt, OA, Rio, P, Moura Branco, L, Galrinho, A, Cacela, D, Pinto Teixeira, P, Afonso Nogueira, M, Pereira-Da-Silva, T, Abreu, J, Teresa Timoteo, A, Cruz Ferreira, R, Pavlyukova, EN, Tereshenkova, EK, Karpov, RS, Piatkowski, R, Kochanowski, J, Opolski, G, Barbier, P, Mirea, O, Guglielmo, M, Savioli, G, Cefalu, C, Pudil, R, Horakova, L, Rozloznik, M, Balestra, C, P37/03, PRVOUK, Rimbas, RC, Enescu, OA, Calin, S, Vinereanu, D, POSDRU/159/1.5/S/141531, Grant, Karsenty, C, Hascoet, S, Hadeed, K, Semet, F, Dulac, Y, Alacoque, X, Leobon, B, Acar, P, Dharma, S, Sukmawan, R, Soesanto, AM, Vebiona, KPP, Firdaus, I, Danny, SS, Driessen, M M P, Sieswerda, GTJ, Post, MC, Snijder, RJ, Van Dijk, APJ, Leiner, T, Meijboom, FJ, Chrysohoou, C, Tsitsinakis, G, Tsiachris, D, Aggelis, A, Herouvim, E, Vogiatzis, I, Pitsavos, C, Koulouris, G, Stefanadis, C, Erdei, T, Edwards, J, Braim, D, Yousef, Z, Fraser, AG, Cardiff, Investigators, MEDIA, Avenatti, E, Magnino, C, Omede', P, Presutti, D, Moretti, C, Iannaccone, A, Ravera, A, Gaita, F, Milan, A, Veglio, F, Barbier, P, Scali, MC, Simioniuc, A, Guglielmo, M, Savioli, G, Cefalu, C, Mirea, O, Fusini, L, Dini, F, Okura, H, Murata, E, Kataoka, T, Mikaelpoor, A, Ojaghi Haghighi, SH, Ojaghi Haghighi, SZ, Alizadeasl, A, Sharifi-Zarchi, A, Zaroui, A, Ben Halima, M, Mourali, MS, Mechmeche, R, Rodriguez Palomares, J F, Gutierrez, LG, Maldonado, GM, Garcia, GG, Otaegui, IO, Garcia Del Blanco, BGB, Teixido, GT, Gonzalez Alujas, MTGA, Evangelista, AE, Garcia Dorado, DGD, Godinho, A R, Correia, AS, Rangel, I, Rocha, A, Rodrigues, J, Araujo, V, Almeida, PB, Macedo, F, Maciel, MJ, Rekik, B, Mghaieth, F, Aloui, H, Boudiche, S, Jomaa, M, Ayari, J, Tabebi, N, Farhati, A, Mourali, S, Dekleva, M, Markovic-Nikolic, N, Zivkovic, M, Stankovic, A, Boljevic, D, Korac, N, Beleslin, B, Arandjelovic, A, Ostojic, M, Galli, E, Guirette, Y, Auffret, V, Daudin, M, Fournet, M, Mabo, P, Donal, E, Chin, C W L, Luo, E, Hwan, J, White, A, Newby, D, Dweck, M, Carstensen, H G, Larsen, L H, Hassager, C, Kofoed, K F, Jensen, J S, Mogelvang, R, Kowalczyk, M, Debska, M, Kolesnik, A, Dangel, J, Kawalec, W, Migliore, RA, Adaniya, ME, Barranco, MA, Miramont, G, Gonzalez, S, Tamagusuku, H, Davidsen, E S, Kuiper, K K J, Matre, K, Gerdts, E, Igual Munoz, B, Maceira Gonzalez, AMG, Erdociain Perales, MEP, Estornell Erill, JEE, Valera Martinez, FVM, Miro Palau, VMP, Piquer Gil, MPG, Sepulveda Sanchez, PSS, Cervera Zamora, ACZ, Montero Argudo, AMA, Placido, R, Silva Marques, J, Magalhaes, A, Guimaraes, T, Nobre E Menezes, M, Goncalves, S, Ramalho, A, Robalo Martins, S, Almeida, AG, Nunes Diogo, A, Abid, L, Ben Kahla, S, Charfeddine, S, Abid, D, Kammoun, S, Tounsi, A, Abid, LEILA, Abid, DORRA, Charfeddine, SALMA, Hammami, RANIA, Triki, FETEN, Akrout, MALEK, Mallek, SOUAD, Hentati, MOURAD, Kammoun, SAMIR, Sirbu, C F, Berrebi, A, Huber, A, Folliguet, T, Yang, L-T, Shih, JY, Liu, YW, Li, YH, Tsai, 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Abstract

Purpose: 3D echocardiography (3DE) enables fast 3D acquisition but subsequent manual navigation to find 2D diagnostic planes can be time consuming. We have developed and validated an automated machine learning-based technique to find apical 2-, 3- and 4-chamber (A2C, A3C, A4C) views that enables fast volume navigation and analysis. Methods: 3DE volumes were acquired (Philips iE33: X3-1 and X5-1 probes) from 30 healthy volunteers and 36 clinical patients with suspected valve disease and coronary heart disease. 66 end diastolic volumes were used to assess the accuracy of apical standard view finding by our method against manual plane finding. To do this, dedicated software was developed with a machine learning approach and a 3-fold cross validation of results was performed. Results: Automatic A4C view detection was possible in 60/66 (91%) of volumes; detection failures were due to suboptimal myocardium wall integrity or lack of right ventricle in the scan. A2C and A3C views were extracted from the A4C view using the known geometrical relationships between apical standard views (A2C to A3C: 30°~40° and A2C to A4C: 90° of rotation over the left ventricle long axis, as shown in the Figure). In average, our method accurately found the heart apex and mitral valve centre with a 7.1 ± 5.7 mm and 7.2 ± 5.3 mm error, respectively. Conclusions: In order to automate clinical workflow, we have developed a new and fully automatic machine learning strategy for apical standard view finding which performed well (91% detection accuracy) on volunteer and clinical 3D echocardiograms. Figure

Published
2014
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134. Poster session 4: Friday 5 December 2014, 08:30-12:30 * Location: Poster area

Author

Orii, M, Tanimoto, T, Yokoyama, M, Ota, S, Kubo, T, Hirata, K, Tanaka, A, Imanishi, T, Akasaka, T, Michelsen, MM, Pena, A, Mygind, ND, Hoest, NB, Prescott, E, Abd El Dayem, SOHA, Battah, AHMED, Abd El Azzez, FATEN, Ahmed, AZZA, Fattoh, AYA, Ismail, REEM, Andjelkovic, K, Kalimanovska Ostric, D, Nedeljkovic, I, Andjelkovic, I, Rashid, HESHAM, Abuel Enien, HESHAM, Ibraheem, MAHER, work, Tissue Doppler echocardiography research, Vago, H, Toth, A, Csecs, I, Czimbalmos, CS, Suhai, F I, Kecskes, K, Becker, D, Simor, T, Merkely, B, D'ascenzi, F, Pelliccia, A, Natali, BM, Cameli, M, Lisi, M, Focardi, M, Corrado, D, Bonifazi, M, Mondillo, S, Zaha, VG, Kim, GE, Su, KN, Zhang, J, Mikush, N, Ross, J, Palmeri, M, Young, LH, Tadic, M, Ilic, SI, Celic, VC, Jaimes, C, Gonzalez Mirelis, J, Gallego, M, Goirigolzarri, J, Pellegrinet, M, Poli, S, Prati, G, Vriz, O, Di Bello, V, Carerj, S, Zito, C, Mateescu, A, Popescu, BA, Antonini-Canterin, F, Chatzistamatiou, E, Moustakas, G, Memo, G, Konstantinidis, D, 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Sanchez, PSS, Cervera Zamora, ACZ, Piquer Gil Marina, MPG, Montero- Argudo, AMA, Naka, KK, Evangelou, D, Lakkas, L, Kalaitzidis, R, Bechlioulis, A, Gkirdis, I, Tzeltzes, G, Nakas, G, Pappas, K, Michalis, LK, Mansencal, N, Bagate, F, Arslan, M, Siam-Tsieu, V, Deblaise, J, El Mahmoud, R, Dubourg, O, Wierzbowska-Drabik, K, Plewka, M, Kasprzak, JD, Bandera, F, Generati, G, Pellegrino, M, Alfonzetti, E, Labate, V, Villani, S, Gaeta, M, Guazzi, M, Bandera, F, Generati, G, Pellegrino, M, Labate, V, Alfonzetti, E, Guazzi, M, Generati, G, Bandera, F, Pellegrino, M, Labate, V, Alfonzetti, E, Guazzi, M, Grycewicz, T, Szymanska, K, Grabowicz, W, Lubinski, A, Sotaquira, M, Pepi, M, Tamborini, G, Caiani, EG, Bochard Villanueva, B, Chacon-Hernandez, N, Fabregat-Andres, O, Garcia-Gonzalez, P, Cubillos-Arango, A, De La Espriella-Juan, R, Albiach-Montanana, C, Berenguer-Jofresa, A, Perez-Bosca, JL, Paya-Serrano, R, Cheng, H-L, Huang, C-H, Wang, Y-C, Chou, W-H, Kuznetsov, VA, Melnikov, NN, Krinochkin, DV, Kolunin, GV, Enina, TN, Sierraalta, W, Le Bihan, D, Barretto, RBM, Assef, JE, Gospos, M, Buffon, M, Ramos, AIO, Garcia, A, Pinto, IMF, Souza, AGMR, Mueller, H, Reverdin, S, Ehret, G, Conti, L, Dos Santos, S, Abdel Moneim, S S, Nhola, L F, Huang, R, Kohli, M, Longenbach, S, Green, M, Villarraga, H R, Bordun, K A, Jassal, D S, Mulvagh, S L, Evangelista, A, Madeo, A, Piras, P, Giordano, F, Giura, G, Teresi, L, Gabriele, S, Re, F, Puddu, P, Torromeo, C, Suwannaphong, S, Vathesatogkit, P, See, O, Yamwong, S, Katekao, W, Sritara, P, Iliuta, L, Szulik, M, Streb, W, Wozniak, A, Lenarczyk, R, Sliwinska, A, Kalarus, Z, Kukulski, T, Weng, K-P, Lin, C-C, Hein, S, Lehmann, L, Kossack, M, Juergensen, L, Katus, HA, Hassel, D, Turrini, F, Scarlini, S, Giovanardi, P, Messora, R, Mannucci, C, Bondi, M, Olander, R, Sundholm, JKM, Ojala, TH, Andersson, S, Sarkola, T, Karolyi, M, Kocsmar, I, Raaijmakers, R, Kitslaar, PH, Horvath, T, Szilveszter, B, Merkely, B, Maurovich-Horvat, P, Heart, Center, Vascular, University, Semmelweis, Budapest, Hungary, and Group, MTA-SE Lendület Cardiovascular Imaging Research

Abstract

Purpose: Although delayed-enhancement magnetic resonance imaging (DEMRI) is essential for diagnosis of cardiac sarcoidosis (CS), the test was not available when pacemaker was implamted. Recently, MR-conditional pacemaker has become avilable and we hypothesized that this device would be useful for diagnosis and management of CS. The aim of this study was to assess the diagnostic ability of MR-conditional pacemaker about CS in patients with advanced A-V nodal block (AAVB). Methods: Twenty-seven AAVB patients (14 men, 13 women; mean age, 69 ± 11 years) who were implanted MR-conditional pacemaker were studied. DEMRI was performed 6 weeks after implantation of permanent pacemaker. In patients with positive for DE, additional examinations like echocardiography, radioisotope imaging, biopsy, and coronary computed-tomography were performed due to confirm the diagnosis of CS and exclude coronary artery disease. Results: DE was observed in 12 patients (44 %). Out of 12 patients, 2 patients were excluded for having prior myocardial infarction. Seven of 10 (70 %) patients were diagnosed of CS by the consensus criteria. Compared with non-CS group, CS group had significantly lower age (61 ± 12 years vs. 72 ± 9 years p = 0.017). There was no significant difference about sex, angiotensin-converting enzyme, brain natriuretic peptide, and left ventricular ejection fraction between 2 groups. Six patients had started corticosteroid therapy and 5 patients (83%) recovered A-V nodal conduction. Conclusion: MR-conditional pacemaker was useful for diagnosis and management of patients with AAVB caused by CS. Figure Cardiac MRI in patient with AV block

Published
2014
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136. Impact of autonomic neuropathy on left ventricular function in normotensive type 1 diabetic patients: a tissue Doppler echocardiographic study: response to Karamitsos et al.

Author

Humpert PM, Oikonomou D, Morcos M, Kuecherer H, Schilling T, Bierhaus A, Nawroth PP, Katus HA, Korosoglou G, Humpert, Per M, Oikonomou, Dimitrios, Morcos, Michael, Kuecherer, Helmut, Schilling, Tobias, Bierhaus, Angelika, Nawroth, Peter P, Katus, Hugo A, and Korosoglou, Grigorios

Published
2008
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140. Mechanisms of disease: hypertrophic cardiomyopathy.

Author

Frey N, Luedde M, Katus HA, Frey, Norbert, Luedde, Mark, and Katus, Hugo A

Abstract

Hypertrophic cardiomyopathy (HCM) is the most-common monogenically inherited form of heart disease, characterized by thickening of the left ventricular wall, contractile dysfunction, and potentially fatal arrhythmias. HCM is also the most-common cause of sudden cardiac death in individuals younger than 35 years of age. Much progress has been made in the elucidation of the genetic basis of HCM, resulting in the identification of more than 900 individual mutations in over 20 genes. Interestingly, most of these genes encode sarcomeric proteins, such as myosin-7 (also known as cardiac muscle β-myosin heavy chain; MYH7), cardiac myosin-binding protein C (MYBPC3), and cardiac muscle troponin T (TNNT2). However, the molecular events that ultimately lead to the clinical phenotype of HCM are still unclear. We discuss several potential pathways, which include altered calcium cycling and sarcomeric calcium sensitivity, increased fibrosis, disturbed biomechanical stress sensing, and impaired cardiac energy homeostasis. An improved understanding of the pathological mechanisms involved will result in greater specificity and success of therapies for patients with HCM. [ABSTRACT FROM AUTHOR]

Published
2012
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142. Prediction of short‐ and long‐term mortality in takotsubo syndrome: the InterTAK Prognostic Score

Author

Thomas Münzel, Yoshio Kobayashi, Wolfgang Koenig, Hugo A. Katus, Paul Bridgman, Christina Chan, Ioana Sorici-Barb, Eduardo Bossone, Gregor Poglajen, Abhiram Prasad, Fabrizio D'Ascenzo, Jelena R. Ghadri, Monika Budnik, Konrad A. Szawan, Fausto J. Pinto, David E. Winchester, Guido Michels, Carlo Di Mario, Thomas Fischer, Matteo Bianco, Jerold S. Shinbane, Burkert Pieske, Alessandro Candreva, Rodolfo Citro, P. Christian Schulze, Annahita Sarcon, Kan Liu, Christian Ukena, Christoph Kaiser, Martin Borggrefe, Florim Cuculi, Stefan Osswald, Behrouz Kherad, Heribert Schunkert, Jeroen J. Bax, Maike Knorr, Ken Kato, Petr Widimský, Alexandra Shilova, Frank Ruschitzka, Martin Kozel, Victoria L. Cammann, Roman Pfister, Olivier Lairez, Michael Neuhaus, Alessandro Cuneo, Wolfgang Rottbauer, Ibrahim Akin, Lucas Jörg, Christian Hauck, L. Christian Napp, Holger Thiele, Manfred Wischnewsky, K.E. Juhani Airaksinen, Hans Rickli, Tuija Vasankari, Carla Paolini, Lars S. Maier, Philippe Meyer, Adrian P. Banning, Richard Kobza, Beatrice Bacchi, Miłosz Jaguszewski, Rafal Dworakowski, Michael Böhm, Claudio Bilato, Mahir Karakas, Philip MacCarthy, Mikhail Gilyarov, Charanjit S. Rihal, Alexander Pott, Claudius Jacobshagen, Clément Delmas, Jose David Arroja, Ibrahim El-Battrawy, Filippo Crea, Carsten Tschöpe, Pedro Carrilho-Ferreira, Ekaterina Gilyarova, Jennifer Franke, Daniel Beug, Ruediger C. Braun-Dullaeus, John D. Horowitz, Thanh H Nguyen, Sebastiano Gili, Christof Burgdorf, Jan Galuszka, Leonarda Galiuto, Grzegorz Opolski, Susanne Heiner, Johann Bauersachs, Christian Templin, Petr Tousek, Michel Noutsias, Lawrence Rajan, Stephan B. Felix, Wolfgang Dichtl, Thomas F. Lüscher, Gerd Hasenfuß, Wischnewsky, Mb, Candreva, A, Bacchi, B, Cammann, Vl, Kato, K, Szawan, Ka, Gili, S, D'Ascenzo, F, Dichtl, W, Citro, R, Bossone, E, Neuhaus, M, Franke, J, Sorici-Barb, I, Jaguszewski, M, Noutsias, M, Knorr, M, Heiner, S, Burgdorf, C, Kherad, B, Tschope, C, Sarcon, A, Shinbane, J, Rajan, L, Michels, G, Pfister, R, Cuneo, A, Jacobshagen, C, Karakas, M, Koenig, W, Pott, A, Meyer, P, Arroja, Jd, Banning, A, Cuculi, F, Kobza, R, Fischer, Ta, Vasankari, T, Airaksinen, Kej, Napp, Lc, Budnik, M, Dworakowski, R, Maccarthy, P, Kaiser, C, Osswald, S, Galiuto, L, Chan, C, Bridgman, P, Beug, D, Delmas, C, Lairez, O, El-Battrawy, I, Akin, I, Gilyarova, E, Shilova, A, Gilyarov, M, Kozel, M, Tousek, P, Winchester, De, Galuszka, J, Ukena, C, Poglajen, G, Carrilho-Ferreira, P, Hauck, C, Paolini, C, Bilato, C, Prasad, A, Rihal, C, Liu, K, Schulze, Pc, Bianco, M, Jorg, L, Rickli, H, Nguyen, Th, Kobayashi, Y, Bohm, M, Maier, L, Pinto, Fj, Widimsky, P, Borggrefe, M, Felix, Sb, Opolski, G, Braun-Dullaeus, Rc, Rottbauer, W, Hasenfuss, G, Pieske, Bm, Schunkert, H, Thiele, H, Bauersachs, J, Katus, Ha, Horowitz, J, Di Mario, C, Munzel, T, Crea, F, Bax, Jj, Luscher, Tf, Ruschitzka, F, Ghadri, Jr, Templin, C, and Repositório da Universidade de Lisboa

Subjects
Male, Research design, medicine.medical_specialty, MEDLINE, 030204 cardiovascular system & hematology, Prognostic score, 03 medical and health sciences, 0302 clinical medicine, Risk Factors, Takotsubo Cardiomyopathy, Internal medicine, medicine, Humans, 030212 general & internal medicine, Survival analysis, Aged, Aged, 80 and over, Takotsubo syndrome, business.industry, Stroke Volume, Stroke volume, Middle Aged, Prognosis, medicine.disease, Survival Analysis, 3. Good health, Research Design, Heart failure, Cardiology, Female, Long term mortality, Cardiology and Cardiovascular Medicine, business
Abstract

© 2019 The Authors European Journal of Heart Failure © 2019 European Society of Cardiology, Recent evidence suggests comparable in‐hospital and long‐term outcomes between takotsubo syndrome (TTS) and acute coronary syndrome. Medical scoring systems are practical tools for decision making and prognostic assessment. However, TTS‐specific scoring systems for risk stratification have not yet been established. Recently, classification based on triggering conditions proved useful in predicting adverse outcomes in TTS (InterTAK Classification).1 Since clinical parameters other than triggering conditions can be associated with adverse outcomes in TTS, such as systolic blood pressure and heart rate, the present study aimed to establish a scoring system combining triggering factors with other important but easily‐ obtainable clinical parameters of daily clinical practice., C.T. has been supported by the H.H. Sheikh Khalifa bin Hamad Al-Thani Research Programme and the Swiss Heart Foundation. L.S.M. was supported by EU HORIZON 2020 (SILICOFCM ID777204). The InterTAK Registry is supported by the Biss Davies Charitable Trust.

Published
2019

143. Intraventricular thrombus formation and embolism in Takotsubo syndrome insights from the international Takotsubo registry

Author

Alexandra Shilova, Davide Di Vece, Johann Bauersachs, Wolfgang Koenig, Michael Neuhaus, Rodolfo Citro, Jose David Arroja, Adrian P. Banning, Jennifer Franke, Charanjit S. Rihal, Abhiram Prasad, Carlo Di Mario, Michael Böhm, Carsten Tschöpe, Burkhardt Seifert, Filippo Crea, Christian Templin, David E. Winchester, Hugo A. Katus, Clément Delmas, Pedro Carrilho-Ferreira, Paul Bridgman, Petr Tousek, Guido Michels, Fausto J. Pinto, Sebastiano Gili, Jelena R. Ghadri, Petr Widimský, Burkert Pieske, Jeroen J. Bax, Christian Ukena, Christoph Kaiser, Wolfgang Dichtl, Christof Burgdorf, Philippe Meyer, Christina Chan, Gerd Hasenfuß, Philip MacCarthy, Mikhail Gilyarov, Leonarda Galiuto, Grzegorz Opolski, Susanne Heiner, Ruediger C. Braun-Dullaeus, Alexander Pott, Annahita Sarcon, Ekaterina Gilyarova, Michel Noutsias, Lawrence Rajan, Claudius Jacobshagen, Roman Pfister, Behrouz Kherad, John D. Horowitz, Martin Borggrefe, Mahir Karakas, Stefan Osswald, Victoria L. Cammann, Katharina J. Ding, Jan Galuszka, Wolfgang Rottbauer, Ibrahim El-Battrawy, Stephan B. Felix, Martin Kozel, Ibrahim Akin, Thomas F. Lüscher, Frank Ruschitzka, Thomas Fischer, Fabrizio D'Ascenzo, Rafal Dworakowski, Olivier Lairez, L. Christian Napp, Holger Thiele, Eduardo Bossone, Thomas Münzel, Claudio Bilato, Maike Knorr, K.E. Juhani Airaksinen, Florim Cuculi, Carla Paolini, Konrad A. Szawan, Richard Kobza, Alessandro Cuneo, Barbara E. Stähli, Heribert Schunkert, Miłosz Jaguszewski, Manfred Wischnewsky, Tuija Vasankari, Ding, Kj, Cammann, Vl, Szawan, Ka, Stähli, Be, Wischnewsky, M, Di Vece, D, Citro, R, Jaguszewski, M, Seifert, B, Sarcon, A, Knorr, M, Heiner, S, Gili, S, D'Ascenzo, F, Neuhaus, M, Napp, Lc, Franke, J, Noutsias, M, Burgdorf, C, Koenig, W, Kherad, B, Rajan L, Michels, G, Pfister, R, Cuneo, A, Jacobshagen, C, Karakas, M, Pott, A, Meyer, P, Arroja, Jd, Banning, A, Cuculi, F, Kobza, R, Fischer, Ta, Vasankari, T, Airaksinen, Kej, Paolini, C, Bilato, C, Carrilho-Ferreira, P, Opolski, G, Dworakowski, R, Maccarthy, P, Kaiser, C, Osswald, S, Galiuto, L, Dichtl, W, Chan, C, Bridgman, P, Delmas, C, Lairez, O, El-Battrawy, I, Akin, I, Gilyarova, E, Shilova, A, Gilyarov, M, Kozel, M, Tousek, P, Widimský, P, Winchester, De, Galuszka, J, Ukena, C, Horowitz, Jd, Di Mario, C, Prasad A, Rihal, C, Pinto, Fj, Crea, F, Borggrefe, M, Braun-Dullaeus, Rc, Rottbauer, W, Bauersachs, J, Katus, Ha, Hasenfuß, G, Tschöpe, C, Pieske, Bm, Thiele, H, Schunkert, H, Böhm, M, Felix, Sb, Münzel, T, Bax, Jj, Lüscher, Tf, Ruschitzka, F, Ghadri, Jr, Bossone, E, and Templin, C.

Subjects
Male, Coronary angiography, Time Factors, Radionuclide ventriculography, 030204 cardiovascular system & hematology, Coronary Angiography, Electrocardiography, 0302 clinical medicine, Risk Factors, Registries, 030212 general & internal medicine, Framingham Risk Score, medicine.diagnostic_test, Incidence, Incidence (epidemiology), Magnetic Resonance Imaging, 3. Good health, Europe, Survival Rate, Cine, thrombus, cardiovascular system, Cardiology, outcome, Female, Cardiology and Cardiovascular Medicine, Takotsubo syndrome, medicine.medical_specialty, Heart Diseases, Heart Ventricles, Magnetic Resonance Imaging, Cine, risk score, Risk Assessment, embolism, 03 medical and health sciences, Takotsubo Cardiomyopathy, Internal medicine, medicine, Humans, cardiovascular diseases, Thrombus, Radionuclide Ventriculography, Aged, business.industry, Australia, Thrombosis, medicine.disease, United States, Embolism, Settore MED/11 - MALATTIE DELL'APPARATO CARDIOVASCOLARE, business, Follow-Up Studies
Abstract

Objective: Takotsubo syndrome (TTS) is characterized by acute left ventricular dysfunction, which can contribute to intraventricular thrombus and embolism. Still, prevalence and clinical impact of thrombus formation and embolic events on outcome of TTS patients remain unclear. This study aimed to investigate clinical features and outcomes of patients with and without intraventricular thrombus or embolism. Additionally, factors associated with thrombus formation or embolism, as well as predictors for mortality, were identified. Approach and Results: TTS patients enrolled in the International Takotsubo Registry at 28 centers in Australia, Europe, and the United States were dichotomized according to the occurrence/absence of intraventricular thrombus or embolism. Patients with intraventricular thrombus or embolism were defined as the ThrombEmb group. Of 1676 TTS patients, 56 (3.3%) patients developed intraventricular thrombus and/or embolism following TTS diagnosis (median time interval, 2.0 days [range, 0–38 days]). Patients in the ThrombEmb group had a different clinical profile including lower left ventricular ejection fraction, higher prevalence of the apical type, elevated levels of troponin and inflammatory markers, and higher prevalence of vascular disease. In a Firth bias-reduced penalized-likelihood logistic regression model apical type, left ventricular ejection fraction ≤30%, previous vascular disease, and a white blood cell count on admission >10×10 3 cells/μL emerged as independent predictors for thrombus formation or embolism. Conclusions: Intraventricular thrombus or embolism occur in 3.3% of patients in the acute phase of TTS. A simple risk score including clinical parameters associated with intraventricular thrombus formation or embolism identifies patients at increased risk. Clinical Trial Registration: URL: http://www.clinicaltrials.gov . Unique identifier: NCT01947621.

Published
2020

144. Long-Term Prognosis of Patients With Takotsubo Syndrome

Author

John D. Horowitz, Thomas Münzel, David E. Winchester, Guido Michels, Katharina J. Ding, Wolfgang Koenig, Jeroen J. Bax, Burkert Pieske, Mahir Karakas, Christian Ukena, K.E. Juhani Airaksinen, Christoph Kaiser, Sebastiano Gili, Stephan B. Felix, Rafal Dworakowski, Christian Templin, Claudius Jacobshagen, Abhiram Prasad, Fabrizio D'Ascenzo, Lawrence Rajan, Martin Borggrefe, Rena A. Levinson, Christof Burgdorf, Florim Cuculi, Petr Tousek, Thomas F. Lüscher, Alexandra Shilova, Mikhail Gilyarov, Victoria L. Cammann, Roman Pfister, Frank Ruschitzka, Alessandro Candreva, Filippo Crea, Davide Di Vece, Wolfgang Rottbauer, Ruediger C. Braun-Dullaeus, Heribert Schunkert, Carsten Tschöpe, Stefan Osswald, Rodolfo Citro, Burkhardt Seifert, Annahita Sarcon, Ibrahim Akin, Gerd Hasenfuß, Leonarda Galiuto, L. Christian Napp, Holger Thiele, Ekaterina Gilyarova, Grzegorz Opolski, Susanne Heiner, Michel Noutsias, Johann Bauersachs, Miłosz Jaguszewski, Alessandro Cuneo, Hugo A. Katus, Olivier Lairez, Ibrahim El-Battrawy, Wolfgang Dichtl, Jozef Micek, Philip MacCarthy, Rahel Bianchi, Maike Knorr, Ken Kato, Adrian P. Banning, Jelena-R. Ghadri, Martin Kozel, Michael Böhm, Konrad A. Szawan, Jennifer Franke, Manfred Wischnewsky, Klaus Empen, Tuija Vasankari, Eduardo Bossone, Richard Kobza, Beatrice Bacchi, Susanne A. Schlossbauer, Petr Widimský, Stjepan Jurisic, Samir M. Said, Thomas Fischer, Clément Delmas, Ghadri, Jr, Kato, K, Cammann, Vl, Gili, S, Jurisic, S, Di Vece, D, Candreva, A, Ding, Kj, Micek, J, Szawan, Ka, Bacchi, B, Bianchi, R, Levinson, Ra, Wischnewsky, M, Seifert, B, Schlossbauer, Sa, Citro, R, Bossone, E, Munzel, T, Knorr, M, Heiner, S, D'Ascenzo, F, Franke, J, Sarcon, A, Napp, Lc, Jaguszewski, M, Noutsias, M, Katus, Ha, Burgdorf, C, Schunkert, H, Thiele, H, Bauersachs, J, Tschope, C, Pieske, Bm, Rajan, L, Michels, G, Pfister, R, Cuneo, A, Jacobshagen, C, Hasenfuss, G, Karakas, M, Koenig, W, Rottbauer, W, Said, Sm, Braun-Dullaeus, Rc, Banning, A, Cuculi, F, Kobza, R, Fischer, Ta, Vasankari, T, Airaksinen, Kej, Opolski, G, Dworakowski, R, Maccarthy, P, Kaiser, C, Osswald, S, Galiuto, L, Crea, F, Dichtl, W, Empen, K, Felix, Sb, Delmas, C, Lairez, O, El-Battrawy, I, Akin, I, Borggrefe, M, Horowitz, J, Kozel, M, Tousek, P, Widimsky, P, Gilyarova, E, Shilova, A, Gilyarov, M, Winchester, De, Ukena, C, Bax, Jj, Prasad, A, Bohm, M, Luscher, Tf, Ruschitzka, F, and Templin, C

Subjects
Male, Acute coronary syndrome, medicine.medical_specialty, Time Factors, 030204 cardiovascular system & hematology, tako tsubo syndrome, acute coronary syndrome, broken heart syndrome, classification, outcome, stress factor, Broken heart syndrome, 03 medical and health sciences, 0302 clinical medicine, Takotsubo Cardiomyopathy, Internal medicine, medicine, Humans, Registries, 030212 general & internal medicine, Mortality, Aged, Aged, 80 and over, Takotsubo syndrome, business.industry, Mortality rate, Electroencephalography, Emotional stress, Middle Aged, ta3121, Prognosis, Stress factor, medicine.disease, 3. Good health, Physical stress, Cardiology and Cardiovascular Medicine, Cohort, Female, Nervous System Diseases, business, Stress, Psychological, Follow-Up Studies
Abstract

Background Prognosis of Takotsubo syndrome (TTS) remains controversial due to scarcity of available data. Additionally, the effect of the triggering factors remains elusive. Objectives This study compared prognosis between TTS and acute coronary syndrome (ACS) patients and investigated short- and long-term outcomes in TTS based on different triggers. Methods Patients with TTS were enrolled from the International Takotsubo Registry. Long-term mortality of patients with TTS was compared to an age- and sex-matched cohort of patients with ACS. In addition, short- and long-term outcomes were compared between different groups according to triggering conditions. Results Overall, TTS patients had a comparable long-term mortality risk with ACS patients. Of 1,613 TTS patients, an emotional trigger was detected in 485 patients (30%). Of 630 patients (39%) related to physical triggers, 98 patients (6%) had acute neurologic disorders, while in the other 532 patients (33%), physical activities, medical conditions, or procedures were the triggering conditions. The remaining 498 patients (31%) had no identifiable trigger. TTS patients related to physical stress showed higher mortality rates than ACS patients during long-term follow-up, whereas patients related to emotional stress had better outcomes compared with ACS patients. Conclusions Overall, TTS patients had long-term outcomes comparable to age- and sex-matched ACS patients. Also, we demonstrated that TTS can either be benign or a life-threating condition depending on the inciting stress factor. We propose a new classification based on triggers, which can serve as a clinical tool to predict short- and long-term outcomes of TTS. (International Takotsubo Registry [InterTAK Registry]; NCT01947621)

Published
2018

150. A comparison of measured trough levels and abbreviated AUC estimation by limited sampling strategies for monitoring mycophenolic acid exposure in stable heart transplant patients receiving cyclosporin A-containing and cyclosporin A-free immunosuppressive regiments.

Author

Dösch AO, Ehlermann P, Koch A, Remppis A, Katus HA, and Dengler TJ

Abstract

BACKGROUND: Mycophenolate mofetil (NIMF) pharmacokinetics vary widely, and enterohepatic recirculation of the drug and its metabolites may be altered by concurrently administered immunosuppressants, including the widely used agent cyclosporin A (CsA). A reliable method of achieving effective and well-tolerated levels of NIMF-based immunosuppression would be of eminent interest. OBJECTIVE: This study compared the use of measured mycophenolic acid (MPA) trough levels (C0) and abbreviated AUC estimation by limited-sampling strategies for monitoring MPA exposure in stable heart transplant recipients (>1 year after transplantation) receiving a CsA-containing or CsA-free immunosuppressive regimen. METHODS: The treatment groups were receiving chronic maintenance immunosuppressive regimens consisting of either CsA/MMF or rapamycin (RAPA)/MMF. An additional subgroup of patients was switched from the CsA-containing regimen to the RAPA-containing regimen. Fasting venous blood samples were obtained before dosing and at 40, 75, 120, and 240 minutes after administration of the morning dose of MME The validated Emit assay was used to measure MPA plasma concentrations. Dose adjustment of AUCs was performed by dividing the AUC by the morning NIMF dose in grams. Cmax after administration of the morning dose was determined from available MPA data points using curve-fitting analysis. The increase to Cmax (Cmax-C0) was calculated, and dose adjustment was performed as before. Abbreviated 12-hour MPA AUCs were estimated using a limited-sampling strategy (before dosing and 30 and 120 minutes after dosing) based on high-performance liquid chromatography data. Adverse events were monitored during routine follow-up visits. RESULTS: The study included 47 patients receiving CsA/MMF, 15 receiving RAPA/MMF, and 9 who were switched from CsA/MMF to RAPA/MME The population included 55 men and 7 women, with a mean age of 58.94 years and a mean weight of 81.85 kg. The only significant differences in baseline clinical characteristics between groups were the mean number of years since heart transplantation (3.62 CsA/MMF vs 8.53 RAPA/MMF; P<0.01) and the proportions of patients still receiving corticosteroids (44.7% vs 13.3%, respectively; P<0.01). Reported adverse events were generally mild, including leukopenia (8.1%), diarrhea (6.5%), and abdominal pain (4.8%), and did not require drug discontinuation. In patients receiving CsA/MMF, MPA AUCs ranged from 19.67 to 81.80 mg/h.L (mean [SD], 41.92 [14.14] mg/h.L). MPA Co levels were poorly correlated with total AUC (r2=0.36). MPA Co levels of 0.5 and 1.6 mg/L were correlated with AUCs of <30 and <40 mg/h.L, respectively. In patients receiving RAPA/MMF, MPA AUCs ranged from 34.40 to 87.60 mg/h.L (mean, 51.07 [15.80] mg/h.L). The correlation between Co and total AUC was better than in the CsA/MMF group (r2=0.61). MPA C0 levels of 1.0 and 2.3 mg/L were correlated with AUCs of 30 and 40 mg/h.L, respectively. Statistically significant differences between RAPA/MMF and CsA/MMF were noted in the mean MMF dosage (1.90 [0.71] vs 2.87 [0.78] g/d, respectively; P<0.001), the mean dose-adjusted MPA AUC (60.95 [27.42] vs 31.92 [16.12] mg/h.L.g MMF; P<0.001), and mean dose-adjusted MPA C0 levels (5.10 [3.41] vs 1.41 [0.95] mg/L.g; P<0.001). The dose-adjusted increase to Cmax after morning dosing was comparable between groups, and there was no difference in the frequency distribution of Cmax. In the group switched from the CsA-containing regimen to the RAPA-containing regimen, the changes in MMF dose, dose-adjusted AUC, and MPA C0 levels were similar to those in the CsA/MMF and RAPA/MMF groups. CONCLUSIONS: In this comparison of measured MPA C0 levels and 12-hour MPA AUCs estimated by a limited-sampling strategy in stable heart transplant patients receiving chronic maintenance immunosuppressive therapy with CsA/MMF or RAPA/MMF, abbreviated AUC estimation predicted drug exposure more accurately than did measured C0 levels. Thus, MPA AUCs obtained by limited sampling may be useful in guiding clinical management and dosing. However, further study is required, including validation of these findings in clinical outcome studies. [ABSTRACT FROM AUTHOR]

Published
2006
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