Search

Your search keyword '"Cerbai, E"' showing total 473 results
Start Over Author "Cerbai, E"
473 results on '"Cerbai, E"'

3. Minimum Information about a Cardiac Electrophysiology Experiment (MICEE): Standardised reporting for model reproducibility, interoperability, and data sharing

Author

Quinn, TA, Granite, S, Allessie, MA, Antzelevitch, C, Bollensdorff, C, Bub, G, Burton, RAB, Cerbai, E, Chen, PS, Delmar, M, DiFrancesco, D, Earm, YE, Efimov, IR, Egger, M, Entcheva, E, Fink, M, Fischmeister, R, Franz, MR, Garny, A, Giles, WR, Hannes, T, Harding, SE, Hunter, PJ, Iribe, G, Jalife, J, Johnson, CR, Kass, RS, Kodama, I, Koren, G, Lord, P, Markhasin, VS, Matsuoka, S, McCulloch, AD, Mirams, GR, Morley, GE, Nattel, S, Noble, D, Olesen, SP, Panfilov, AV, Trayanova, NA, Ravens, U, Richard, S, Rosenbaum, DS, Rudy, Y, Sachs, F, Sachse, FB, Saint, DA, Schotten, U, Solovyova, O, Taggart, P, Tung, L, Varró, A, Volders, PG, Wang, K, Weiss, JN, Wettwer, E, White, E, Wilders, R, Winslow, RL, and Kohl, P

Subjects
Heart Disease, Cardiovascular, Animals, Electrophysiological Phenomena, Heart, Humans, Information Dissemination, Models, Biological, Reference Standards, Reproducibility of Results, Research Design, Minimum Information Standard, Cardiac electrophysiology, Data sharing, Reproducibility, Integration, Computational modelling, Biochemistry and Cell Biology, Biophysics
Abstract

Cardiac experimental electrophysiology is in need of a well-defined Minimum Information Standard for recording, annotating, and reporting experimental data. As a step towards establishing this, we present a draft standard, called Minimum Information about a Cardiac Electrophysiology Experiment (MICEE). The ultimate goal is to develop a useful tool for cardiac electrophysiologists which facilitates and improves dissemination of the minimum information necessary for reproduction of cardiac electrophysiology research, allowing for easier comparison and utilisation of findings by others. It is hoped that this will enhance the integration of individual results into experimental, computational, and conceptual models. In its present form, this draft is intended for assessment and development by the research community. We invite the reader to join this effort, and, if deemed productive, implement the Minimum Information about a Cardiac Electrophysiology Experiment standard in their own work.

Published
2011

6. Edward Carmeliet (1930-2021) - Channelling scientific curiosity: A tribute from the ESC Working Group on Cardiac Cellular Electrophysiology

Author

Ravens, U, Gomez, A, Heijman, J, Remme, C, Dobrev, D, Smith, G, Volders, P, Cerbai, E, Eisner, D, Casadei, B, Zaza, A, Richard, S, Mugelli, A, Vassort, G, Brown, H, Sipido, K, Ravens U., Gomez A. M., Heijman J., Remme C. A., Dobrev D., Smith G., Volders P. G. A., Cerbai E., Eisner D. A., Casadei B., Zaza A., Richard S., Mugelli A., Vassort G., Brown H. F., Sipido K. R., Ravens, U, Gomez, A, Heijman, J, Remme, C, Dobrev, D, Smith, G, Volders, P, Cerbai, E, Eisner, D, Casadei, B, Zaza, A, Richard, S, Mugelli, A, Vassort, G, Brown, H, Sipido, K, Ravens U., Gomez A. M., Heijman J., Remme C. A., Dobrev D., Smith G., Volders P. G. A., Cerbai E., Eisner D. A., Casadei B., Zaza A., Richard S., Mugelli A., Vassort G., Brown H. F., and Sipido K. R.

Published
2021

8. Paradoxical prolongation of QT interval during exercise in patients with HCM: Cellular mechanisms and implications for diastolic function

Author

Coppini, R, Beltrami, M, Doste, R, Bueno Orovio, A, Ferrantini, C, Vitale, G, Manuel Pioner, J, Santini, L, Argirò, A, Berteotti, M, Mori, F, Marchionni, N, Stefàno, P, Cerbai, E, Poggesi, C, and Olivotto, I

Abstract

Aims Ventricular cardiomyocytes from Hypertrophic Cardiomyopathy (HCM) patient hearts show prolonged action potential duration (APD), impaired intracellular Ca2+ homeostasis and abnormal electrical response to beta -adrenergic stimulation. We sought to determine whether this behavior is associated with abnormal changes of repolarization during exercise and worsening of diastolic function, ultimately explaining the intolerance to exercise experienced by some patients without obstruction. Methods and Results Non-obstructive HCM patients (178) and control subjects (81) underwent standard exercise testing, including exercise echocardiography. Ventricular myocytes were isolated from myocardial samples of 23 HCM and 8 non-failing non-hypertrophic surgical patients. The APD shortening in response to high frequencies was maintained in HCM myocytes, while β-adrenergic stimulation unexpectedly prolonged APDs, ultimately leading to a lesser shortening of APDs in response to exercise. In HCM vs. control subjects, we observed a lesser shortening of QT interval at peak exercise (QTc: +27 ± 52 ms in HCM, -4 ± 50 ms in controls, P 30 ms), the excessive shortening of the electrical diastolic period was linked with a limited increase of heart-rate and deterioration of diastolic function at peak effort. Conclusions Abnormal balance of Ca2+- and K+-currents in HCM cardiomyocytes determines insufficient APD and Ca2+-transient shortening with exercise. In HCM patients, exercise-induced QTc prolongation was associated with impaired diastolic reserve, contributing to the reduced exercise tolerance. Our results support the idea that severe electrical cardiomyocyte abnormalities underlie exercise intolerance in a subgroup of HCM patients without obstruction.

Published
2022

14. Optogenetic manipulation of cardiac electrical dynamics using sub-threshold illumination: dissecting the role of cardiac alternans in terminating rapid rhythms

Author

Biasci, V, primary, Santini, L, additional, Hussaini, S, additional, Ferrantini, C, additional, Coppini, R, additional, Loew, LM, additional, Luther, S, additional, Campione, M, additional, Poggesi, C, additional, Pavone, FS, additional, Cerbai, E, additional, Bub, G, additional, and Sacconi, L, additional

Published
2022
Full Text
View/download PDF

18. Targeting Cyclic Guanosine Monophosphate to Treat Heart Failure: JACC Review Topic of the Week

Author

Emdin, M, Aimo, A, Castiglione, V, Vergaro, G, Georgiopoulos, G, Saccaro, L, Lombardi, C, Passino, C, Cerbai, E, Metra, M, Senni, M, Emdin M, Aimo A, Castiglione V, Vergaro G, Georgiopoulos G, Saccaro LF, Lombardi CM, Passino C, Cerbai E, Metra M, Senni M, Emdin, M, Aimo, A, Castiglione, V, Vergaro, G, Georgiopoulos, G, Saccaro, L, Lombardi, C, Passino, C, Cerbai, E, Metra, M, Senni, M, Emdin M, Aimo A, Castiglione V, Vergaro G, Georgiopoulos G, Saccaro LF, Lombardi CM, Passino C, Cerbai E, Metra M, and Senni M

Abstract

The significant morbidity and mortality associated with heart failure with reduced ejection fraction (HFrEF) or heart failure with preserved ejection fraction (HFpEF) justify the search for novel therapeutic agents. Reduced cyclic guanosine monophosphate levels contribute to HF progression. Among molecules modulating the nitric oxide (NO)–GMP–phosphodiesterase (PDE) pathway, the evaluation of nitrates, synthetic natriuretic peptides (NP), and NP analogs has yielded mixed results. Conversely, sacubitril/valsartan, combining NP degradation inhibition through neprilysin and angiotensin receptor blockade, has led to groundbreaking findings in HFrEF. Other strategies to increase tissue cyclic guanosine monophosphate have been attempted, such as PDE-3 or PDE-5 inhibition (with negative or neutral results), NO-independent soluble guanylate cyclase (sGC) activation, or enhancement of sGC sensitivity to endogenous NO. Following the positive results of the phase 3 VICTORIA (A Study of Vericiguat in Participants With Heart Failure With Reduced Ejection Fraction) trial on the sGC stimulator vericiguat in HFrEF, the main open questions are the efficacy of the sacubitril/valsartan-vericiguat combination in HFrEF and of vericiguat in HFpEF.

Published
2020

28. The genetic architecture of left ventricular non-compaction reveals both substantial overlap with other cardiomyopathies and a distinct aetiology in a subset of cases

Author

Mazzarotto, F, Hawley, M, Beltrami, M, Beekman, L, Boschi, B, Girolami, F, Roberts, A, Lodder, E, Cerbai, E, Cook, S, Ware, J, Funke, B, Olivotto, I, Bezzina, C, Barton, PJR, Walsh, R, and Wellcome Trust

Subjects
cardiovascular system, cardiovascular diseases
Abstract

Rationale: Left ventricular non-compaction (LVNC) is a condition characterised by trabeculations in the myocardial wall and is the subject of considerable conjecture as to whether it represents a distinct pathology or a secondary phenotype associated with other cardiac diseases, particularly cardiomyopathies. Objective: To investigate the genetic architecture of LVNC by identifying genes and variant classes robustly associated with disease and comparing these to other genetically characterised cardiomyopathies. Methods and Results: We performed rare variant association analysis using six different LVNC cohorts comprising 840 cases together with 125,748 gnomAD population controls and compared results to similar analyses with dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM) cases. We observed substantial overlap in genes and variant classes enriched in LVNC and DCM/HCM, indicating that in many cases LVNC belongs to a spectrum of more established cardiomyopathies, with non-compaction representing a phenotypic variation in patients with DCM- or HCM-causing variants. In contrast, five variant classes were uniquely enriched in LVNC cases, of which truncating variants in MYH7, ACTN2 and PRDM16 may represent a distinct LVNC aetiology. MYH7 truncating variants are generally considered as non-pathogenic but were detected in 2% of LVNC cases compared to 0.1% of controls, including a cluster of variants around a single splice region. Additionally, structural variants (exon deletions) in RYR2 and missense variants in the transmembrane region of HCN4 were enriched in LVNC cases, confirming prior reports regarding the association of these variant classes with combined LVNC and arrhythmia phenotypes. Conclusions: We demonstrated that genetic association analysis can clarify the relationship between LVNC and established cardiomyopathies, highlighted substantial overlap with DCM/HCM but also identified variant classes associated with distinct LVNC and with joint LVNC/arrhythmia phenotypes. These results underline the complex genetic landscape of LVNC and inform how genetic testing in LVNC cases should be pursued and interpreted.

Published
2020

30. Optogenetic Manipulation of Cardiac Electrical Dynamics Using Sub-Threshold Illumination: Dissecting the Role of Cardiac Alternans in Terminating Rapid Rhythms

Author

Biasci, V., primary, Santini, L., additional, Hussaini, S., additional, Ferrantini, C., additional, Coppini, R., additional, Loew, L.M., additional, Luther, S., additional, Campione, M., additional, Poggesi, C., additional, Pavone, F.S., additional, Cerbai, E., additional, Bub, G., additional, and Sacconi, Leonardo, additional

Published
2021
Full Text
View/download PDF

31. The genetic architecture of left ventricular non-compaction reveals both substantial overlap with other cardiomyopathies and a distinct aetiology in a subset of cases

Author

Walsh, R, primary, Mazzarotto, F, additional, Hawley, M, additional, Beltrami, M, additional, Beekman, L, additional, Boschi, B, additional, Girolami, F, additional, Roberts, A, additional, Cerbai, E, additional, Cook, S, additional, Ware, J, additional, Funke, B, additional, Olivotto, I, additional, Bezzina, C, additional, and Barton, P, additional

Published
2020
Full Text
View/download PDF

42. Letter to the Editor

Author

Crocini, C., primary, Ferrantini, C., additional, Coppini, R., additional, Pavone, F. S., additional, Poggesi, C., additional, Cerbai, E., additional, and Sacconi, L., additional

Published
2019
Full Text
View/download PDF

43. Real‐time optical manipulation of cardiac conduction in intact hearts

Author

Scardigli, M., primary, Müllenbroich, C., additional, Margoni, E., additional, Cannazzaro, S., additional, Crocini, C., additional, Ferrantini, C., additional, Coppini, R., additional, Yan, P., additional, Loew, L. M., additional, Campione, M., additional, Bocchi, L., additional, Giulietti, D., additional, Cerbai, E., additional, Poggesi, C., additional, Bub, G., additional, Pavone, F. S., additional, and Sacconi, L., additional

Published
2018
Full Text
View/download PDF

50. The efficacy of late sodium current blockers in hypertrophic cardiomyopathy is dependent on genotype: A study on transgenic mouse models with different mutations

Author

Palandri, C., primary, Coppini, R., additional, Mazzoni, L., additional, Ferrantini, C., additional, Gentile, F., additional, Pioner, J.M., additional, Santini, L., additional, Sartiani, L., additional, Bargelli, V., additional, Poggesi, C., additional, Mugelli, A., additional, and Cerbai, E., additional

Published
2018
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results