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154. Quantitative Hybrid Cardiac [18F]FDG-PET-MRI Images for Assessment of Cardiac Repair by Preconditioned Cardiosphere-Derived Cells

Author

Winkler, Johannes, primary, Lukovic, Dominika, additional, Mester-Tonczar, Julia, additional, Zlabinger, Katrin, additional, Gugerell, Alfred, additional, Pavo, Noemi, additional, Jakab, András, additional, Szankai, Zsuzsanna, additional, Traxler, Denise, additional, Müller, Claudia, additional, Spannbauer, Andreas, additional, Riesenhuber, Martin, additional, Hašimbegović, Ena, additional, Dawkins, James, additional, Zimmermann, Matthias, additional, Ankersmit, Hendrik J., additional, Marbán, Eduardo, additional, and Gyöngyösi, Mariann, additional

Published
2020
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155. Intracoronary ALLogeneic heart STem cells to Achieve myocardial Regeneration (ALLSTAR): a randomized, placebo-controlled, double-blinded trial

Author

Makkar, Raj R, primary, Kereiakes, Dean J, additional, Aguirre, Frank, additional, Kowalchuk, Glenn, additional, Chakravarty, Tarun, additional, Malliaras, Konstantinos, additional, Francis, Gary S, additional, Povsic, Thomas J, additional, Schatz, Richard, additional, Traverse, Jay H, additional, Pogoda, Janice M, additional, Smith, Rachel R, additional, Marbán, Linda, additional, Ascheim, Deborah D, additional, Ostovaneh, Mohammad R, additional, Lima, João A C, additional, DeMaria, Anthony, additional, Marbán, Eduardo, additional, and Henry, Timothy D, additional

Published
2020
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156. Allogeneic cardiosphere-derived cells for the treatment of heart failure with reduced ejection fraction: the Dilated cardiomYopathy iNtervention with Allogeneic MyocardIally-regenerative Cells (DYNAMIC) trial

Author

Chakravarty, Tarun, primary, Henry, Timothy D., additional, Kittleson, Michelle, additional, Lima, Joao, additional, Siegel, Robert J., additional, Slipczuk, Leandro, additional, Pogoda, Janice M., additional, Smith, Rachel R., additional, Malliaras, Konstantinos, additional, Marbán, Linda, additional, Ascheim, Deborah D., additional, Marbán, Eduardo, additional, and Makkar, Raj R., additional

Published
2020
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158. Pre-Existing Traits Associated with Covid-19 Illness Severity

Author

Ebinger, Joseph E., primary, Achamallah, Natalie, additional, Ji, Hongwei, additional, Claggett, Brian L., additional, Sun, Nancy, additional, Botting, Patrick, additional, Nguyen, Trevor-Trung, additional, Luong, Eric, additional, Kim, Elizabeth H., additional, Park, Eunice, additional, Liu, Yunxian, additional, Rosenberry, Ryan, additional, Matusov, Yuri, additional, Zhao, Steven, additional, Pedraza, Isabel, additional, Zaman, Tanzira, additional, Thompson, Michael, additional, Raedschelders, Koen, additional, Berg, Anders H., additional, Grein, Jonathan D., additional, Noble, Paul W., additional, Chugh, Sumeet S., additional, Merz, C. Noel Bairey, additional, Marbán, Eduardo, additional, Van Eyk, Jennifer E., additional, Solomon, Scott D., additional, Albert, Christine M., additional, Chen, Peter, additional, and Cheng, Susan, additional

Published
2020
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161. Contributors

Author

ACKERMAN, MICHAEL J., primary, AGUEL, FELIPE, additional, ALBERTE-LISTA, CESAR, additional, ANTZ, MATTHIAS, additional, ANTZELEVITCH, CHARLES, additional, ANUMONWO, JUSTUS M.B., additional, ARORA, RISHI, additional, BACKX, PETER H., additional, BALSER, JEFFREY R., additional, BECKMAN, KAREN, additional, BENDITT, DAVID G., additional, BERBARI, EDWARD J., additional, BERENFELD, OMER, additional, BERS, DONALD M., additional, BEYER, ERIC C., additional, BIEL, MARTIN, additional, BOWLES, NEIL E., additional, BOYETT, MARK R., additional, BRUGADA, JOSEP, additional, BRUGADA, PEDRO, additional, BRUGADA, RAMON, additional, BURSAC, NENAD, additional, BUXTON, ALFRED E., additional, CAIN, MICHAEL E., additional, CALKINS, HUGH, additional, CALLANS, DAVID J., additional, CAPPATO, RICCARDO, additional, CARROLL, SHEILA J., additional, CASTELLANOS, AGUSTIN, additional, CHEN, LAN S., additional, CHEN, PENG-SHENG, additional, CHEN, SHIN-ANN, additional, CHEN, XIONGWEN, additional, CLAPHAM, DAVID E., additional, CLÉMENTY, JACQUES, additional, CRIJNS, HARRY J., additional, DAOUD, EMILE G., additional, DAS, MITHILESH K., additional, DELMAR, MARIO, additional, DIFRANCESCO, DARIO, additional, DIMARCO, JOHN P., additional, DOBRZYNSKI, HALINA, additional, DUFFY, HEATHER S., additional, EFIMOV, IGOR R., additional, EHRLICH, JOACHIM R., additional, EL-SHERIF, NABIL, additional, ELLENBOGEN, KENNETH A., additional, EPSTEIN, ANDREW E., additional, ERMIS, CENGIZ, additional, ERNST, SABINE, additional, ESTES, N. A. MARK, additional, FAST, VLADIMIR G., additional, FEDOROV, VADIM V., additional, FONTAINE, GUY, additional, FORESTI, SARA, additional, FORNES, PAUL, additional, FRANK, ROBERT, additional, FRANZ, MICHAEL R., additional, GALVIN, JOSEPH M., additional, GARFINKEL, ALAN, additional, GILLIS, ANNE M., additional, GOLD, MICHAEL R., additional, GOLDBERGER, JEFFREY, additional, GRAY, RICHARD A., additional, GRIMM, WOLFRAM, additional, GROH, WILLIAM J., additional, HAINES, DAVID E., additional, HAÏSSAGUERRE, MICHEL, additional, HARO, CARLOS, additional, HAYES, DAVID L., additional, HAYRAPETYAN, VOLODYA, additional, HEBERT, JEAN-LOUIS, additional, HENRIQUEZ, CRAIG S., additional, HERRMANN, STEFAN, additional, HINDRICKS, GERHARD, additional, HOCINI, MÉLÈZE, additional, HOFMANN, FRANZ, additional, HOHNLOSER, STEFAN H., additional, HONJO, HARUO, additional, HOUSER, STEVEN R., additional, HRYSHKO, LARRY V., additional, HSU, EDWARD W., additional, HUANG, JIAN, additional, HULOT, JEAN-SÉBASTIEN, additional, HUTCHINS, GARY D., additional, IDEKER, RAYMOND E., additional, INTERIAN, ALBERTO, additional, IWAI, SEI, additional, JACKMAN, WARREN M., additional, JAÏS, PIERRE, additional, JALIFE, JOSÉ, additional, JANUARY, CRAIG T., additional, JOHNSON, CHRISTOPHER R., additional, JOSEPHSON, MARK E., additional, JOUVEN, XAVIER, additional, KADISH, ALAN H., additional, KALMAN, JONATHAN M., additional, KAMP, TIMOTHY J., additional, KASS, ROBERT S., additional, KENNEDY, HAROLD L., additional, KERBER, RICHARD E., additional, KHOSITSETH, ANANT, additional, KILBORN, MICHAEL J., additional, KLÉBER, ANDRÉ G., additional, KLEIN, GEORGE J., additional, KNIGHT, BRADLEY P., additional, KODAMA, ITSUO, additional, KOTTKAMP, HANS, additional, KRAHN, ANDREW D., additional, KUCERA, JAN P., additional, KUCK, KARL-HEINZ, additional, KUGLER, JOHN D., additional, KUO, CHI TAI, additional, KUROKAWA, JUNKO, additional, LAB, MAX J., additional, LAI, WEN TER, additional, LARSON, CLAIRE, additional, LAURITA, KENNETH R., additional, LAZZARA, RALPH, additional, LERMAN, BRUCE B., additional, LERNER, DEBORAH L., additional, LÉVY, SAMUEL, additional, LI, RONALD A., additional, LIN, DAVID, additional, LOCKWOOD, DEBORAH, additional, LONDON, BARRY, additional, LÜ, FEI, additional, LUDWIG, ANDREAS, additional, MAKIELSKI, JONATHAN C., additional, MALIK, MAREK, additional, MARBÁN, EDUARDO, additional, MARCHLINSKI, FRANCIS E., additional, MARKIDES, VIAS, additional, MARKOWITZ, STEVEN M., additional, MARON, BARRY J., additional, MARTÍNEZ, AGUSTÍN D., additional, MCGUIRE, MARK A., additional, MEISSNER, GERHARD, additional, MILES, WILLIAM M., additional, MILLER, JOHN M., additional, MILLER, MICHAEL A., additional, MITTAL, SUNEET, additional, MOLEIRO, FEDERICO, additional, MOOSMANG, SVEN, additional, MORADY, FRED, additional, MORENO, ALONSO P., additional, MOSS, ARTHUR J., additional, MYERBURG, ROBERT J., additional, NAKAGAWA, HIROSHI, additional, NAPOLITANO, CARLO, additional, NATTEL, STANLEY, additional, NERBONNE, JEANNE M., additional, NIKOLSKI, VLADIMIR P., additional, OLGIN, JEFFREY E., additional, ORAL, HAKAN, additional, OTOMO, KENICHIRO, additional, OUDIT, GAVIN Y., additional, OUYANG, FEIFAN, additional, PAGÉ, PIERRE L., additional, PAPPONE, CARLO, additional, PATTERSON, EUGENE, additional, PERTSOV, ARKADY M., additional, PETERS, NICHOLAS S., additional, PETERS, ROBERT W., additional, PRIORI, SILVIA G., additional, PROST-SQUARCIONI, CATHERINE, additional, PRYSTOWSKI, ERIC N., additional, PUNSKE, BONNIE B., additional, QU, ZHILIN, additional, RAMIREZ, RAFAEL J., additional, RIVOLTA, ILARIA, additional, ROBINSON, RICHARD B., additional, RODEN, DAN M., additional, ROHR, STEPHAN, additional, ROSANIO, SALVATORE, additional, ROSEN, MICHAEL R., additional, ROSENBAUM, DAVID S., additional, ROSENSHTRAUKH, LEONID V., additional, ROTH, BRADLEY J., additional, RUDY, YORAM, additional, RUSKIN, JEREMY N., additional, SACHS, FREDERICK, additional, SAFFITZ, JEFFREY E., additional, SANDERS, PRASHANTHAN, additional, SANGUINETTI, MICHAEL C., additional, SAOUDI, NADIR, additional, SCHERLAG, BENJAMIN J., additional, SCHWARTZ, PETER J., additional, SCHWARTZMAN, DAVID, additional, SEGAL, OLIVER R., additional, SHAH, DIPEN C., additional, SHARIFOV, OLEG F., additional, SHIVKUMAR, KALYANAM, additional, SIMMONS, JEFFREY, additional, SINGH, BRAMAH N., additional, SKANES, ALLAN C., additional, SMITH, TIMOTHY W., additional, SOEJIMA, KYOKO, additional, SORGEN, PAUL L., additional, SPRAY, DAVID C., additional, SRINIVAS, MIDUTURU, additional, STEIN, KENNETH M., additional, STEINBERG, SUSAN F., additional, STEVENSON, WILLIAM G., additional, STIEBER, JULIANE, additional, STRAMBA-BADIALE, MARCO, additional, STRICKBERGER, S. ADAM, additional, SUNG, RUEY J., additional, SWEENEY, MICHAEL O., additional, SWERDLOW, CHARLES D., additional, TACCARDI, BRUNO, additional, TAFFET, STEVEN M., additional, TAI, CHING-TAI, additional, THOMAS, DANIEL, additional, TOMASELLI, GORDON F., additional, TONDATO, FERNANDO, additional, TOWBIN, JEFFREY A., additional, TRANQUILLO, JOSEPH V., additional, TRAYANOVA, NATALIA A., additional, TRIEDMAN, JOHN K., additional, TRISTANI-FIROUZI, MARTIN, additional, TSAI, CHIN-FENG, additional, TUNG, LESLIE, additional, TURITTO, GIOIA, additional, VAN HARE, GEORGE F., additional, VAN WAGONER, DAVID R., additional, VOS, MARC A., additional, WALCOTT, GREGORY P., additional, WALDO, ALBERT L., additional, WANG, ZULU, additional, WEINBERG, KENNETH M., additional, WEINSTEIN, DAVID, additional, WELLNER, MARCEL, additional, WILKOFF, BRUCE L., additional, WOOD, MARK A., additional, WU, JIANYI, additional, WU, JIASHIN, additional, WYSE, D. GEORGE, additional, YAMADA, KATHRYN A., additional, YE, BIN, additional, YEE, RAYMOND, additional, ZAITSEV, ALEXEY V., additional, ZAREBA, WOJCIECH, additional, ZHONG, GUOQIANG, additional, and ZIPES, DOUGLAS P., additional

Published
2004
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162. Sodium Channels

Author

Li, Ronald A., primary, Tomaselli, Gordon F., additional, and Marbán, Eduardo, additional

Published
2004
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163. Polhemus.BRC.Repeated cell transplan denervation.2019.pdf

Author

Polhemus, David, Rishi Trivedi, Sharp, Thomas, Li, Zhen, Goodchild, Traci, Scarborough, Amy, Couto, Geoffrey De, Marbán, Eduardo, and Lefer, David J.

Subjects
FOS: Clinical medicine, 110201 Cardiology (incl. Cardiovascular Diseases)
Abstract

Enthusiasm for cell therapy for myocardial injury has waned due to equivocal benefits in clinical trials. In an attempt to improve efficacy, we investigated repeated cell therapy and adjunct renal denervation (RDN) as strategies for augmenting cardioprotection with cardiosphere-derived cells (CDCs). We hypothesized that combining CDC post-conditioning with repeated CDC doses or delayed RDN therapy would result in superior function and remodeling. Wistar–Kyoto (WKY) rats or spontaneously hypertensive rats (SHR) were subjected to 45 min of coronary artery ligation followed by reperfusion for 12–14 weeks. In the first study arm, SHR were treated with CDCs (0.5 × 106 i.c.) or PBS 20 min following reperfusion, or additionally treated with CDCs (1.0 × 106 i.v.) at 2, 4, and 8 weeks. In the second arm, at 4 weeks following myocardial infarction (MI), SHR received CDCs (0.5 × 106 i.c.) or CDCs + RDN. In the third arm, WKY rats were treated with i.c. CDCs administered 20 min following reperfusion and RDN or a sham at 4 weeks. Early i.c. + multiple i.v. dosing, but not single i.c. dosing, of CDCs improved long-term left ventricular (LV) function, but not remodeling. Delayed CDC + RDN therapy was not superior to single-dose delayed CDC therapy. Early CDC + delayed RDN therapy improved LV ejection fraction and remodeling compared to both CDCs alone and RDN alone. Given that both RDN and CDCs are currently in the clinic, our findings motivate further translation targeting a heart failure indication with combined approaches.

Published
2019
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182. Impaired β-Adrenergic Responsiveness in HFpEF Rats

Author

Kilfoil, Peter J., primary, Soetkamp, Daniel, additional, Zhang, Rui, additional, Cho, Jae, additional, Aynaszyan, Stephan, additional, Cingolani, Eugenio, additional, Marbán, Eduardo, additional, and Goldhaber, Joshua I., additional

Published
2019
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183. Corrigendum: Epigenomic Reprogramming of Adult Cardiomyocyte-Derived Cardiac Progenitor Cells

Author

Zhang, Yiqiang, Zhong, Jiang F., Qiu, Hongyu, MacLellan, W. Robb, Marbán, Eduardo, and Wang, Charles

Subjects
Epigenomics, Gene Expression Profiling, Myocardium, Induced Pluripotent Stem Cells, Reproducibility of Results, Cell Dedifferentiation, DNA Methylation, Cellular Reprogramming, Corrigenda, Models, Biological, Epigenesis, Genetic, Mice, Animals, Cluster Analysis, Cellular Reprogramming Techniques, Myocytes, Cardiac, Single-Cell Analysis, Transcriptome, Myoblasts, Cardiac, Stem Cell Transplantation
Abstract

It has been believed that mammalian adult cardiomyocytes (ACMs) are terminally-differentiated and are unable to proliferate. Recently, using a bi-transgenic ACM fate mapping mouse model and an in vitro culture system, we demonstrated that adult mouse cardiomyocytes were able to dedifferentiate into cardiac progenitor-like cells (CPCs). However, little is known about the molecular basis of their intrinsic cellular plasticity. Here we integrate single-cell transcriptome and whole-genome DNA methylation analyses to unravel the molecular mechanisms underlying the dedifferentiation and cell cycle reentry of mouse ACMs. Compared to parental cardiomyocytes, dedifferentiated mouse cardiomyocyte-derived CPCs (mCPCs) display epigenomic reprogramming with many differentially-methylated regions, both hypermethylated and hypomethylated, across the entire genome. Correlated well with the methylome, our transcriptomic data showed that the genes encoding cardiac structure and function proteins are remarkably down-regulated in mCPCs, while those for cell cycle, proliferation, and stemness are significantly up-regulated. In addition, implantation of mCPCs into infarcted mouse myocardium improves cardiac function with augmented left ventricular ejection fraction. Our study demonstrates that the cellular plasticity of mammalian cardiomyocytes is the result of a well-orchestrated epigenomic reprogramming and a subsequent global transcriptomic alteration.

Published
2017

188. Distinct features of calcium handling and β‐adrenergic sensitivity in heart failure with preserved versus reduced ejection fraction.

Author

Kilfoil, Peter J., Lotteau, Sabine, Zhang, Rui, Yue, Xin, Aynaszyan, Stephan, Solymani, Ryan E., Cingolani, Eugenio, Marbán, Eduardo, and Goldhaber, Joshua I.

Subjects
HEART failure, INTRACELLULAR calcium, HIGH-salt diet, CALCIUM, DEVELOPED countries
Abstract

Key points: Heart failure (HF), the leading cause of death in developed countries, occurs in the setting of reduced (HFrEF) or preserved (HFpEF) ejection fraction. Unlike HFrEF, there are no effective treatments for HFpEF, which accounts for ∼50% of heart failure.Abnormal intracellular calcium dynamics in cardiomyocytes have major implications for contractility and rhythm, but compared to HFrEF, very little is known about calcium cycling in HFpEF.We used rat models of HFpEF and HFrEF to reveal distinct differences in intracellular calcium regulation and excitation‐contraction (EC) coupling.While HFrEF is characterized by defective EC coupling at baseline, HFpEF exhibits enhanced coupling fidelity, further aggravated by a reduction in β‐adrenergic sensitivity.These differences in EC coupling and β‐adrenergic sensitivity may help explain why therapies that work in HFrEF are ineffective in HFpEF. Heart failure with reduced or preserved ejection fraction (respectively, HFrEF and HFpEF) is the leading cause of death in developed countries. Although numerous therapies improve outcomes in HFrEF, there are no effective treatments for HFpEF. We studied phenotypically verified rat models of HFrEF and HFpEF to compare excitation‐contraction (EC) coupling and protein expression in these two forms of heart failure. Dahl salt‐sensitive rats were fed a high‐salt diet (8% NaCl) from 7 weeks of age to induce HFpEF. Impaired diastolic relaxation and preserved ejection fraction were confirmed in each animal echocardiographically, and clinical signs of heart failure were documented. To generate HFrEF, Sprague‐Dawley (SD) rats underwent permanent left anterior descending coronary artery ligation which, 8–10 weeks later, led to systolic dysfunction (verified echocardiographically) and clinical signs of heart failure. Calcium (Ca2+) transients were measured in isolated cardiomyocytes under field stimulation or patch clamp. Ultra‐high‐speed laser scanning confocal imaging captured Ca2+ sparks evoked by voltage steps. Western blotting and PCR were used to assay changes in EC coupling protein and RNA expression. Cardiomyocytes from rats with HFrEF exhibited impaired EC coupling, including decreased Ca2+ transient (CaT) amplitude and defective couplon recruitment, associated with transverse (t)‐tubule disruption. In stark contrast, HFpEF cardiomyocytes showed saturated EC coupling (increased ICa, high probability of couplon recruitment with greater Ca2+ release synchrony, increased CaT) and preserved t‐tubule integrity. β‐Adrenergic stimulation of HFpEF myocytes with isoprenaline (isoproterenol) failed to elicit robust increases in ICa or CaT and relaxation kinetics. Fundamental differences in EC coupling distinguish HFrEF from HFpEF. Key points: Heart failure (HF), the leading cause of death in developed countries, occurs in the setting of reduced (HFrEF) or preserved (HFpEF) ejection fraction. Unlike HFrEF, there are no effective treatments for HFpEF, which accounts for ∼50% of heart failure.Abnormal intracellular calcium dynamics in cardiomyocytes have major implications for contractility and rhythm, but compared to HFrEF, very little is known about calcium cycling in HFpEF.We used rat models of HFpEF and HFrEF to reveal distinct differences in intracellular calcium regulation and excitation‐contraction (EC) coupling.While HFrEF is characterized by defective EC coupling at baseline, HFpEF exhibits enhanced coupling fidelity, further aggravated by a reduction in β‐adrenergic sensitivity.These differences in EC coupling and β‐adrenergic sensitivity may help explain why therapies that work in HFrEF are ineffective in HFpEF. [ABSTRACT FROM AUTHOR]

Published
2020
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190. High-Throughput Single-Cell Proteomic Analysis of Organ-Derived Heterogeneous Cell Populations by Nanoflow Dual-Trap Single-Column Liquid Chromatography

Author

Kreimer, Simion, Binek, Aleksandra, Chazarin, Blandine, Cho, Jae Hyung, Haghani, Ali, Hutton, Alexandre, Marbán, Eduardo, Mastali, Mitra, Meyer, Jesse G, Mesquita, Thassio, Song, Yang, Van Eyk, Jennifer, and Parker, Sarah

Abstract

Identification and proteomic characterization of rare cell types within complex organ-derived cell mixtures is best accomplished by label-free quantitative mass spectrometry. High throughput is required to rapidly survey hundreds to thousands of individual cells to adequately represent rare populations. Here we present parallelized nanoflow dual-trap single-column liquid chromatography (nanoDTSC) operating at 15 min of total run time per cell with peptides quantified over 11.5 min using standard commercial components, thus offering an accessible and efficient LC solution to analyze 96 single cells per day. At this throughput, nanoDTSC quantified over 1000 proteins in individual cardiomyocytes and heterogeneous populations of single cells from the aorta.

Published
2024
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191. Allogeneic cardiosphere-derived cells (CAP-1002) in critically ill COVID-19 patients: compassionate-use case series.

Author

Singh, Siddharth, Chakravarty, Tarun, Chen, Peter, Akhmerov, Akbarshakh, Falk, Jeremy, Friedman, Oren, Zaman, Tanzira, Ebinger, Joseph E., Gheorghiu, Mitch, Marbán, Linda, Marbán, Eduardo, and Makkar, Raj R.

Subjects
COVID-19, CRITICALLY ill, HOSPITAL admission & discharge, LYMPHOCYTE count
Abstract

There are no definitive therapies for patients with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection. Therefore, new therapeutic strategies are needed to improve clinical outcomes, particularly in patients with severe disease. This case series explores the safety and effectiveness of intravenous allogeneic cardiosphere-derived cells (CDCs), formulated as CAP-1002, in critically ill patients with confirmed coronavirus disease 2019 (COVID-19). Adverse reactions to CAP-1002, clinical status on the World Health Organization (WHO) ordinal scale, and changes in pro-inflammatory biomarkers and leukocyte counts were analyzed. All patients (n = 6; age range 19–75 years, 1 female) required ventilatory support (invasive mechanical ventilation, n = 5) with PaO2/FiO2 ranging from 69 to 198. No adverse events related to CAP-1002 administration were observed. Four patients (67%) were weaned from respiratory support and discharged from the hospital. One patient remains mechanically ventilated as of April 28th, 2020; all survive. A contemporaneous control group of critically ill COVID-19 patients (n = 34) at our institution showed 18% overall mortality at a similar stage of hospitalization. Ferritin was elevated in all patients at baseline (range of all patients 605.43–2991.52 ng/ml) and decreased in 5/6 patients (range of all patients 252.89–1029.90 ng/ml). Absolute lymphocyte counts were low in 5/6 patients at baseline (range 0.26–0.82 × 103/µl) but had increased in three of these five patients at last follow-up (range 0.23–1.02 × 103/µl). In this series of six critically ill COVID-19 patients, intravenous infusion of CAP-1002 was well tolerated and associated with resolution of critical illness in 4 patients. This series demonstrates the apparent safety of CAP-1002 in COVID-19. While this initial experience is promising, efficacy will need to be further assessed in a randomized controlled trial. [ABSTRACT FROM AUTHOR]

Published
2020
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192. Mechanisms of atrial fibrillation in aged rats with heart failure with preserved ejection fraction.

Author

Mesquita, Thassio Ricardo Ribeiro, Zhang, Rui, de Couto, Geoffrey, Valle, Jackelyn, Sanchez, Lizbeth, Rogers, Russell G., Holm, Kevin, Liu, Weixin, Marbán, Eduardo, Cingolani, Eugenio, and Ribeiro Mesquita, Thassio Ricardo

Abstract

Background: Although ∼20% of the elderly population develops atrial fibrillation (AF), little is known about the mechanisms. Heart failure with preserved ejection fraction (HFpEF), which is associated with AF, is more common in aged women than in men.Objective: The purpose of this study was to identify potential mechanisms of AF in an age-related HFpEF model.Methods: In aged female Fischer F344 rats (21- to 24-month-old), which are prone to HFpEF, we induced AF by atrial pacing. Young Fischer F344 female rats (3- to 4-month-old) and age-matched Sprague Dawley female rats (27-month-old) served as controls. Phenotyping included echocardiography to assess left ventricular structure/function; in vivo electrophysiology and ex vivo high-resolution optical mapping to assess AF vulnerability; systemic and atrial inflammatory profiling; atrial histology; and expression of inflammasome signaling proteins.Results: Aged rats developed left ventricular hypertrophy, left atrial enlargement, diastolic dysfunction, and pulmonary congestion, without ejection fraction impairment, thus meeting the criteria for HFpEF. Increased serum inflammatory markers, hypertension, and obesity further characterize aged females. Sinoatrial and atrioventricular node dysfunction was associated with the high inducibility of AF in aged rats. Ex vivo electrical activation mapping revealed abnormal β-adrenergic responsiveness and slowed conduction velocity. Atrial inflammasome signaling was enhanced in aged rats, which may contribute to fibrotic remodeling and high AF susceptibility.Conclusion: Together, our data demonstrate that aging-related atrial remodeling and HFpEF are associated with atrial enlargement, fibrosis, conduction abnormalities, and nodal dysfunction, favoring a substrate conducive to AF. [ABSTRACT FROM AUTHOR]

Published
2020
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200. van Berlo et al. reply

Author

van Berlo, Jop H., primary, Kanisicak, Onur, additional, Maillet, Marjorie, additional, Vagnozzi, Ronald J., additional, Karch, Jason, additional, Lin, Suh-Chin J., additional, Middleton, Ryan C., additional, Marbán, Eduardo, additional, and Molkentin, Jeffery D., additional

Published
2018
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