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2. Novel Experimental Therapies for Treatment of Pulmonary Arterial Hypertension

Author

Zolty R

Subjects
pulmonary hypertension hypertension/investigational drugs/vascular remodelling/animal models/clinical trials/new drug targets/toxicity, Therapeutics. Pharmacology, RM1-950
Abstract

Ronald Zolty Pulmonary Hypertension Program, University of Nebraska Medical Center, Lied Transplant Center, Omaha, NE, USACorrespondence: Ronald Zolty 982265 Nebraska Medical Center, Room 8712, Omaha, NE, 68198-2265 Tel +1 4025595591Fax +1 4025598355Email ronald.zolty@unmc.eduAbstract: Pulmonary arterial hypertension (PAH) is a progressive and devastating disease characterized by pulmonary artery vasoconstriction and vascular remodeling leading to vascular rarefaction with elevation of pulmonary arterial pressures and pulmonary vascular resistance. Often PAH will cause death from right heart failure. Current PAH-targeted therapies improve functional capacity, pulmonary hemodynamics and reduce hospitalization. Nevertheless, today PAH still remains incurable and is often refractory to medical therapy, underscoring the need for further research. Over the last three decades, PAH has evolved from a disease of unknown pathogenesis devoid of effective therapy to a condition whose cellular, genetic and molecular underpinnings are unfolding. This article provides an update on current knowledge and summarizes the progression in recent advances in pharmacological therapy in PAH.Keywords: pulmonary hypertension, investigational drugs, vascular remodelling, animal models, clinical trials, new drug targets, toxicity

Published
2021

5. Baseline characteristics of patients in the Reduction of Events with Darbepoetin alfa in Heart Failure trial (RED-HF)

Author

McMurray, John J.V., Anand, Inder S., Diaz, Rafael, Maggioni, Aldo P., OʼConnor, Christopher, Pfeffer, Marc A., Solomon, Scott D., Tendera, Michal, van Veldhuisen, Dirk J., Albizem, Moetaz, Cheng, Sunfa, Scarlata, Debra, Swedberg, Karl, Young, James B., Amuchastegui, M., Belziti, C., Bluguermann, J., Caccavo, M., Cartasegna, L., Colque, R., Cuneo, C., Fernandez, A., Gabito, A., Goicochea, R., Gonzalez, M., Gorosito, V., Grinfeld, L., Hominal, M., Kevorkian, R., Litvak Bruno, M., Llanos, J., Mackinnon, I., Manuale, O., Marzetti, E., Nul, D., Perna, E., Riccitelli, M., Sanchez, A., Santos, D., Schygiel, P., Toblli, J., Vogel, D., Aggarwal, A., Amerena, J., De Looze, F., Fletcher, P., Hare, D., Ireland, M., Krum, H., Lattimore, J., Marwick, T., Sindone, A., Thompson, P., Waites, J., Altenberger, J., Ebner, C., Lenz, K., Pacher, R., Poelzl, G., Charlier, F., de Ceuninck, M., De Keulenaer, G., Dendale, P., Maréchal, P., Mullens, W., Thoeng, J., Vanderheyden, M., Vanhaecke, J., Weytjens, C., Wollaert, B., Albuquerque, D., Almeida, D., Aspe y Rosas, J., Bocchi, E., Bordignon, S., Clausell, N., Kaiser, S., Leaes, P., Martins Alves, S., Montera, M., Moura, L., Pereira de Castro, R., Rassi, S., Reis, A., Saraiva, J., Simões, M., Souza Neto, J., Teixeira, M., Benov, H., Chompalova, B., Donova, T., Georgiev, P., Gotchev, D., Goudev, A., Grigorov, M., Guenova, D., Hergeldjieva, V., Ivanov, D., Kostova, E., Manolova, A., Marchev, S., Nikolov, F., Popov, A., Raev, D., Tzekova, M., Czarnecki, W., Giannetti, N., Haddad, H., Heath, J., Huynh, T., Lepage, S., Liu, P., Lonn, E., Ma, P., Manyari, D., Moe, G., Parker, J., Pesant, Y., Rajda, M., Ricci, J., Roth, S., Sestier, F., Sluzar, V., Sussex, B., Vizel, S., Antezana, G., Bugueno, C., Castro, P., Conejeros, C., Manriquez, L., Martinez, D., Potthoff, S., Stockins, B., Vukasovic, J., Gregor, P., Herold, M., Jerabek, O., Jirmar, R., Kuchar, R., Linhart, A., Podzemska, B., Soucek, M., Spac, J., Spacek, R., Vodnansky, P., Bronnum-Schou, J., Clemmensen, K., Egstrup, K., Jensen, G., Kjoller-Hansen, L., Kober, L., Markenvard, J., Rokkedal, J., Skagen, K., Torp-Pedersen, C., Tuxen, C., Videbak, L., Laks, T., Vahula, V., Harjola, V., Kettunen, R., Kotila, M., Bauer, F., Cohen Solal, A., Coisne, D., Davy, J., De Groote, P., Dos Santos, P., Funck, F., Galinier, M., Gibelin, P., Isnard, R., Neuder, Y., Roul, G., Sabatier, R., Trochu, J., Anker, S., Denny, S., Dreykluft, T., Flesch, M., Genth-Zotz, S., Hambrecht, R., Hein, J., Jeserich, M., John, M., Kreider-Stempfle, H., Laufs, U., Muellerleile, K., Natour, M., Sandri, M., Schäufele, T., von Hodenberg, E., Weyland, K., Winkelmann, B., Tse, H., Yan, B., Barsi, B., Csikasz, J., Dezsi, C., Edes, I., Forster, T., Karpati, P., Kerekes, C., Kis, E., Kosa, I., Lupkovics, G., Nagy, A., Preda, I., Ronaszeki, A., Tomcsanyi, J., Zamolyi, K., Agarwal, D., Bahl, V., Bordoloi, A., Chockalingam, K., Chopda, M., Chopra, V., Dugal, J., Ghaisas, N., Ghosh, S., Grant, P., Hiremath, S., Iyengar, S., Jagadeesa Subramania, B., Jain, P., Joshi, A., Khan, A., Mullasari, A., Naik, S., Oomman, A., Pai, V., Pareppally Gopal, R., Parikh, K., Patel, T., Prakash, V., Sastry, B., Sathe, S., Sinha, N., Srikanthan, V., Subburamakrishnan, P., Thacker, H., Wander, G., Admon, D., Katz, A., Klainman, E., Lewis, B., Marmor, A., Moriel, M., Mosseri, M., Shotan, A., Weinstein, J., Zimlichman, R., Agostoni, P., Albanese, M., Alunni, G., Bini, R., Boccanelli, A., Bolognese, L., Campana, C., Carbonieri, E., Carpino, C., Checco, L., Cosmi, F., DʼAngelo, G., De Cristofaro, M., Floresta, A., Fucili, A., Galvani, M., Ivleva, A., Marra, S., Musca, G., Peccerillo, N., Perrone Filardi, P., Picchio, E., Russo, T., Scelsi, L., Senni, M., Tavazzi, L., Erglis, A., Jasinkevica, I., Kakurina, N., Veze, I., Volans, E., Bagdonas, A., Berukstis, E., Celutkiene, J., Dambrauskaite, A., Jarasuniene, D., Luksiene, D., Rudys, A., Sakalyte, G., Sliaziene, S., Aguilar-Romero, R., Cardona-Muñoz, E., Castro-Jimenez, J., Chavez-Herrera, J., Chuquiure Valenzuela, E., De la Pena, G., Herrera, E., Leiva-Pons, J., Lopez Alvarado, A., Mendez Machado, G., Ramos-Lopez, G., Basart, D., Buijs, E., Cornel, J., de Leeuw, M., Dijkgraaf, R., Dunselman, P., Freericks, M., Hamraoui, K., Lenderlink, T., Linssen, G., Lodewick, P., Lodewijks, C., Lok, D., Nierop, P., Ronner, E., Somsen, A., van Dantzig, J., van der Burgh, P., van Kempen, L., van Vlies, B., Voors, A., Wardeh, A., Willems, F., Dickstein, K., Gundersen, T., Hole, T., Thalamus, J., Westheim, A., Dabrowski, M., Gorski, J., Korewicki, J., Kuc, K., Miekus, P., Musial, W., Niegowska, J., Piotrowski, W., Podolec, P., Polonski, L., Ponikowski, P., Rynkiewicz, A., Szelemej, R., Trusz-Gluza, M., Ujda, M., Wojciechowski, D, Wysokinski, A., Camacho, A., Fonseca, C., Monteiro, P., Apetrei, E., Bruckner, I., Carasca, E., Coman, I., Datcu, M., Dragulescu, S., Ionescu, P., Iordachescu-Petica, D., Manitiu, I., Popa, V., Pop-Moldovan, A., Radoi, M., Stamate, S., Tomescu, M., Vita, I., Aroutiounov, G., Ballyuzek, M., Bart, B., Churina, S., Glezer, M., Goloshchekin, B., Ivleva, A., Kobalava, Z., Kostenko, V., Lopatin, Y., Martynov, A., Orlov, V., Semernin, E., Shogenov, Z., Sidorenko, B., Skvortsov, A., Storzhakov, G., Sulimov, V., Talibov, O., Tereshenko, S., Tsyrline, V., Zadionchenko, V., Zateyshchikov, D., Dzupina, A., Hranai, M., Kmec, J., Micko, K., Murin, J., Pella, D., Sojka, G., Spisak, V., Vahala, P., Vinanska, D., Badat, A., Bayat, J., Dawood, S., Delport, E., Ellis, G., Garda, R., Klug, E., Mabin, T., Naidoo, D., Pretorius, M., Ranjith, N., Van Zyl, L., Weich, H., Anguita, M., Berrazueta, J., Bruguera i Cortada, J., de Teresa, E., Gómez Sánchez, M., González Juanatey, J., Gonzalez-Maqueda, I., Jordana, R., Lupon, J., Manzano, L., Pascual Figal, D., Pulpón, L., Recio, J., Ridocci Soriano, F., Rodríguez Lambert, J., Roig Minguell, E., Roig Minguell, E., Romero, J., Valdovinos, P., Klintberg, L., Kronvall, T., Lycksell, M., Morner, S., Rydberg, E., Swedberg, K., Timberg, I., Wikstrom, G., Moccetti, T.4, Ashok, J., Banerjee, P., Carr-White, G., Cleland, J., Connolly, E., Francis, M., Greenbaum, R., Kadr, H., Lindsay, S., McMurray, J., Megarry, S., Memon, A., Murdoch, D., Senior, R., Squire, I., Tan, L., Witte, K., Adams, K., Adamson, P., Adler, A., Altschul, L., Altschuller, A., Amirani, H., Anand, I., Andreou, C., Ansari, M., Antonishen, M., Banchs, H., Banerjee, S., Banish, D., Bank, A., Barbagelata, A., Barnard, D., Bellinger, R., Benn, A., Berk, M., Berry, B., Bethala, V., Bilazarian, S., Bisognano, J., Bleyer, F., Blum, M., Boehmer, J., Bouchard, A., Boyle, A., Bozkurt, B., Brown, C., Burlew, B., Burnham, K., Butler, J., Call, J., Cambier, P., Cappola, T., Carlson, R., Chandler, B., Chandra, R., Chandraratna, P., Chernick, R., Colan, D., Colfer, H., Colucci, W., Connelly, T., Costantini, O., Dadkhah, S., Dauber, I., Davis, J., Davis, S., Denning, S., Drazner, M., Dunlap, S., Egbujiobi, L., Elkayam, U., Elliott, J., El-Shahawy, M., Essandoh, L., Ewald, G., Fang, J., Farhoud, H., Felker, G., Fernandez, J., Festin, R., Fishbein, G., Florea, V., Flores, E., Floro, J., Gabris, M., Garg, M., Gatewood, R., Geller, M., Ghali, J., Ghumman, W., Gibbs, G., Gillespie, E., Gilmore, R., Gogia, H., Goldberg, L., Gradus-Pizlo, I., Grainger, T., Gudmundsson, G., Gunawardena, D., Gupta, D., Hack, T., Hall, S., Hamroff, G., Hankins, S., Hanna, M., Hargrove, J., Haught, W., Hauptman, P., Hazelrigg, M., Herzog, C., Heywood, J., Hill, T., Hilton, T., Hirsch, H., Hunter, J., Ibrahim, H., Imburgia, M., Iteld, B., Jackson, B., Jaffrani, N., Jain, D., Jain, A., James, M., Jimenez, J., Johnson, E., Kale, P., Kaneshige, A., Kapadia, S., Karia, D., Karlsberg, R., Katholi, R., Kerut, E., Khoury, W., Kipperman, R., Klapholz, M., Kosinski, E., Kozinn, M., Kraus, D., Krueger, S., Krum, H., Kumar, S., Lader, E., Lee, C., Levy, W., Lewis, E., Light-McGroary, K., Loh, I., Lombardi, W., Machado, C., Maislos, F., Mancini, D., Markus, T., Mather, P., McCants, K., McGrew, F., McLaurin, B., McMillan, E., McNamara, D., Meyer, T., Meymandi, S., Miller, A., Minami, E., Modi, M., Mody, F., Mohanty, P., Moscoso, R., Moskowitz, R., Moustafa, M., Mullen, M., Naz, T., Noonan, T., OʼBrien, T., Oellerich, W., Oren, R., Pamboukian, S., Pereira, N., Pitt, W., Porter, C., Prabhu, S., Promisloff, S., Ratkovec, R., Richardson, R., Ross, A., Saleh, N., Saltzberg, M., Sarkar, S., Schmedtje, J., Schneider, R., Schuyler, G., Shanes, J., Sharma, A., Siegel, C., Siegel, R., Silber, D., Singh, V., Singh, N., Singh, J., Sklar, J., Small, R., Smith, A., Smith, E., Smith, E., Smull, D., Sotolongo, R., Staniloae, C., Stapleton, D., Steele, P., Stehlik, J., Stein, M., Tang, W., Thadani, U., Torre-Amoine, G., Trichon, B., Tsai, C., Tummala, R., Van Bakel, A., Vicari, R., Vijay, N., Vijayaraghavan, K., Vittorio, T., Vossler, M., Wagoner, L., Wallis, D., Ward, N., Widmer, M., Wight, J., Wilkins, C., Williams, C., Williams, G., Winchester, M., Winkel, E., Wittmer, B., Wood, D., Wormer, D., Wright, R., Xu, Z., Yasin, M., and Zolty, R.

Published
2013
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7. Mutations in cardiac actin appear to be rare in dilated cardiomyopathies

Author

Zolty, R., Passarino, G., Brodsky, G.L., Taylor, M.R.G., Moss, A., Bristow, M.R., Cavalli-Sforza, L., Underhill, P.A., and Mestroni, L.

Subjects
Human genetics -- Research, Genetic disorders -- Research, Cardiomyopathy, Dilated -- Genetic aspects, Biological sciences
Published
2001

8. Incidence of mTORi Associated BOOP in Cardiac Transplant Recipients – A Single Center Perspective.

Author

Brink, H. and Zolty, R.

Subjects
*HEART transplantation, *CRYPTOGENIC organizing pneumonia, *HEART transplant recipients
Abstract

The incidence of mammalian target of rapamycin inhibitor (mTORi) associated bronchiolitis obliterans organizing pneumonia (BOOP) varies in the literature. We have previously reported a 24% incidence of BOOP in patients transitioned to sirolimus. This high rate was believed to be related to the full withdrawal of calcineurin inhibitor (CI) therapy. The aim of this study is to compare those results to our current practice of maintaining a low-dose CI with mTORi-based regimens This was a single-center retrospective review of adult heart transplant recipients initiated on an mTORi at least six months post-transplant. The primary outcome of the study was incidence of BOOP. Secondary outcomes included timing of mTORi conversion post-transplant and associated tacrolimus concentrations. During the study period, none of the 61 included heart transplant patients developed BOOP. Late mTORi transition (>1 year post transplant) was more common (72%) than early conversion (6 months - 1 year post transplant; 28%), and sirolimus was more commonly utilized than everolimus (90% vs 10%). Following our centers mTORi conversion policy, all patients were maintained on low-dose tacrolimus at initiation, with 84% of patients continuing concomitant tacrolimus at one year. Of these patients, 46% had an FK goal < 4 mcg/mL and 38% had an FK goal 4-8 mcg/mL. No patients at our center experienced mTORi related BOOP while maintaining a low dose CI. The results of this study suggest calcineurin inhibitors have a protective effect from BOOP, even at low concentrations. [ABSTRACT FROM AUTHOR]

Published
2022
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9. Safety and Efficacy of SGLT2i Post Orthotopic Heart Transplantation.

Author

Sundaravel, S., Zolty, R., Stoller, D., Lowes, B., and Lundgren, S.

Subjects
*HEART transplantation, *GRAFT rejection, *LIVER transplantation, *DIABETIC acidosis, *BODY mass index, *HYPERGLYCEMIA
Abstract

Diabetes mellitus is common after orthotopic heart transplantation (OHT) due to steroid-induced hyperglycemia. Traditionally, it has been treated using parenteral insulin therapy. The use of sodium-glucose co-transporter 2 inhibitors (SGLT2i) in OHT recipients is not well established. A retrospective chart review was performed on all the patients who underwent OHT at our center to identify patients on SGT2i post OHT. Clinical outcomes pre and post SGLT2i therapy were compared using the student t-test. Out of the 455 patients who had OHT at our single institution, 26 patients were on SGLT2i post OHT (1 patient was dual organ recipient - heart and liver transplant). The baseline characteristics are reported in Table 1. The median days from OHT to initiation of SGLT2i was 780 days (range 40-4986 days), and the median duration of therapy post-OHT was 169 days (range 38-2474 days). There was a statistically significant improvement in the average hemoglobin A1c, weight, and body mass index after starting SGLT2i (Results table). There was a trend towards improving renal function. There was no incidence of systemic infection, hypoglycemia, amputation, or euglycemic diabetic ketoacidosis while on SGLT2i. Two patients were able to discontinue insulin therapy after starting SGLT2i. There was no incidence or progression of cardiac allograft vasculopathy during the therapy. Two patients experienced graft rejection (1Antibody Mediated Rejection and 1 Acute Cellular Rejection) with drop in left ventricular systolic function that recovered after appropriate treatment. SGLT2i can be used safely in OHT recipients. The renal protective mechanism of SGLT2i could be helpful to combat the nephrotoxicity of calcineurin inhibitors (CNI) used for immunosuppression and help prolong the use of CNI. Further randomized studies are required to explore the complete benefits of SGLT2i in OHT recipients [ABSTRACT FROM AUTHOR]

Published
2022
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10. Quality of life and prognosis in heart failure: results of the beta-blocker evaluation of survival trial (best)

Author

Tate CW 3rd, Robertson AD, Zolty R, Shakar SF, Lindenfeld J, Wolfel EE, Bristow MR, and Lowes BD

Abstract

BACKGROUND: Quality of life (QOL) was a prespecified secondary end point in the Beta-Blocker Evaluation of Survival Trial. The Beta-Blocker Evaluation of Survival Trial used four QOL questionnaires to evaluate patient health status over time in response to treatment with placebo or bucindolol. The goal of the current study was to determine the relationship between the different questionnaires, assess the effect of treatment on health status, and evaluate the association between changes in health status and prognosis. METHODS: The San Diego Heart Failure (SDHF), Minnesota Living with Heart Failure (MLHF), Patient Global Assessment (PGA), and Physician Global Assessment (PhyGA) questionnaires were measured at baseline through 48 months of follow-up. For SDHF and MLHF, changes from baseline were calculated. Spearman correlation was used to assess relationships, and Cox Proportional Hazards regression was used to predict time to all-cause mortality, and mortality or heart failure hospitalization, bivariately and multivariately. To determine whether beta-blocker treatment affected QOL, the Wilcoxon rank-sum test was used to compare treatment groups. RESULTS: At 12 months, SDHF (r = +0.56, P = .0001), PGA (r = +0.36, P = .0001), and PhyGA (r = +0.37, P = .0001) correlated with MLHF. SDHF (P = .0001), MLHF (P = .0004), PGA (P = .0001), and PhyGA (P = .0001) were all strongly associated with all-cause mortality, with low values of each associated with a lower hazard. For the combined end point of all-cause mortality or heart failure hospitalization, change in QOL with each instrument had a P value of .0001. At 12 months, bucindolol-treated patients had improvement in both PhyGA and PGA compared with placebo; neither the SDHF nor the MLWF instrument distinguished between the two treatment groups unless a worst-rank assignment was used for patients who died. CONCLUSION: The four instruments correlate with each other and predict clinical end points, suggesting that each is a valid measure of health status. According to the PGA and the PhyGA, bucindolol improves QOL. [ABSTRACT FROM AUTHOR]

Published
2007
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13. Cause of Death and Predictors of All‐Cause Mortality in Anticoagulated Patients With Nonvalvular Atrial Fibrillation: Data From ROCKET AF

Author

Pokorney, Sean D., Piccini, Jonathan P., Stevens, Susanna R., Patel, Manesh R., Pieper, Karen S., Halperin, Jonathan L., Breithardt, Günter, Singer, Daniel E., Hankey, Graeme J., Hacke, Werner, Becker, Richard C., Berkowitz, Scott D., Nessel, Christopher C., Mahaffey, Kenneth W., Fox, Keith A. A., Califf, Robert M., Anderson, J., Bedwell, N., Bilsker, M., Bruce, G., Agah, R., DeSantis, M., Eisenberg, S., Flores, A., Herzog, W., Klein, S., Snyder, H., Krueger, S., Almaguer, E., Lavie, E., Lee, C., Mallis, G., Modi, M., Woodworth, G., Niazi, I., Peart, B., Sundaram, S., Snoddy, B., Sotolongo, R., Moloney, J., Vijayaraghavan, K., Whittier, F., Yellen, L., Banerjee, S., Lustgarten, D., Suresh, D., Gelernt, M., Levinson, L., Ghanekar, R., Kneller, G., Hall, C., Fadl, Y., Pirwitz, M., French, W., Mayer, N., Pugeda, J., Steel, K., Mody, F., Malik, A., Chandna, H., Go, A., Emlein, G., Bowden, W., Moscoso, R., Hodson, R., Berk, M., Pan, D., Pappas, J., Orchard, R., Lynchard, G., Vijay, N., Khan, W., El Khadra, M, Antonishen, M., Cucher, F., Staab, M., Zebrack, J., Borromeo, S, Heilman, J., Chaturvedi, S., Makam, S., Turk, S., Hyers, T., Williams, G., Labroo, A., Gill, S., Myears, D., Weinstein, J., Shanes, J., Chandrashekhar, Y., Shah, S., Reiter, W., Logemann, T., Almquist, A., Bhagwat, R., Tak, T., Shen‐Ling, J., Patel, P., Artis, A., Arouni, A., Lauer, M., Kinney, K., Elsen, J., Roan, P., Villafria, R., Sumpter, M., Ip, J., Welka, S., Schifferdecker, B., Sandoval, R., Speirs, S., Jones, A., Haldis, T., Kazmierski, J., Sutherland, J., Dietrich, D., Telfer, E., Berry, J., McElveen, A., Russell, J., Sackett, M., Antonios, N., Smith, D., Vora, K., Kirby, A., Lui, H., Mego, D., Ziada, K., Navas, J., Taussig, A., Koren, M., Vogel, C., Saba, F., Parrott, C., Schneider, R., Shirwany, A., Rubin, M., Treasure, C, Bertolet, B., Chang, M., Langberg, J., Becker, R., Cohen, Y., McGrew, F., White, J., Arzola, F., Zelenka, J., Tannenbaum, A., Fernandes, V., Jamnadas, P., Agamasu, J., Collins, B., Jauch, W., Sasseen, B., Hotchkiss, D., Abadier, R., Osunkoya, A., Schlau, A., Chappel, C., Foster, M., Braun, E., Mostel, E., Capo, J., Ashchi, M., Howard, V., Albirini, A., Burger, A., Rolston, D., Staniloae, C., Bacon, J., Wiseman, A., McGarvey, J, Sonel, A., Hamroff, G., Chang, D., Daboul, N., Broderick, G., Meholick, A., Corbelli, J., Silverman, R., Raffetto, J., Fishberg, R., Georgeson, S., Held, J., Seidner, M., Saint‐Jacques, H., Heitner, J., Kutalek, S., Friedlander, I., Hutchinson, B., Walia, J., Kondo, N., Smiley, N., Blitz, L., Dale, H., Sulman, S., Szulawski, I., Modares, F., Martin, R., Nahhas, A., Renzi, M., Akyea‐Djamson, A., Alfieri, A., Sandhu, J., Voyce, S., Amaram, S., Meyerrose, G., Shoukfeh, M., Lee, F., Villegas, B., Idowu, O., Khera, A., Sam, C., Vo, A., Lieber, I., Smith, T., Awan, N., Tsai, C., Ganim, R., Alzaghrini, G., Pitt, W., Shepherd, A., Tang, S., Stoltz, S., Nelson, W., Cox, S., Meymandi, S., Melucci, M., Thomas, G., Gogia, H., Machell, C., Chandrasekaran, S., Brown, C., Jetty, P., Miller, G., Dykstra, G., Jaffrani, N., Zakhary, B., Caruso, A., Zolty, R., Fox, D., Jacobs, G., Lebenthal, M., Mukherjee, S., Zimetbaum, P., Kingsley, J., Jones, R., Robinson, V., Kenton, D., Usedom, J., Williams, S., Snipes, C., Wilson, V., Hasty, R., Shoemaker, J., Donahue, M., Al‐Saghir, Y., Thomsen, E., Yarows, S., Chastain, S., McLaughlin, P., Wakham, M., Shrestha, D., Simmons, J., Fisher, D., Seymour, Z., Frandsen, B., First, B., Sharpe, C., Popeil, L., Guthrie, R., Hunter, J., Alvarado, O., Sandberg, J., Gutman, N., Belber, A., Arkhipov, M., Ballyzek, M., Baranov, A., Barbarash, O., Barbarich, V., Belenky, D., Berkovich, O., Bokarev, I., Boyarkin, M., Vaniev, S., Volkova, E., Gratsiansky, N., Demin, A., Zadionchenko, V., Zateyshchikov, D., Zrazhevsky, K., Mazaev, V., Martynov, A., Mikhailov, S., Mkrtchian, V., Novozhenov, V., Raskina, T., Rebrov, A., Sanina, N., Simanekov, V., Sitnikova, M., Smolenskaya, O., Stryuk, R., Storozhakov, G., Tankhilevich, B., Tereschenko, S., Khokhlov, A., Khrustalev, O., Chernov, S., Shvarts, Y., Shubik, Y., Shulman, V., Yakushin, S., Bugrova, O., Ivleva, A., Libis, R., Khozyainova, N., Maslov, S., Baranova, E., Sherenkov, A., Libov, I., Lusov, V., Chumakova, G., Kuznetsov, V., Ryamzina, I., 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Subjects
atrial fibrillation, mortality, rivaroxaban, stroke, warfarin, Atrial Fibrillation, Sudden Cardiac Death, Heart Failure, Ischemic Stroke, Intracranial Hemorrhage
Abstract

Background: Atrial fibrillation is associated with higher mortality. Identification of causes of death and contemporary risk factors for all‐cause mortality may guide interventions. Methods and Results: In the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET AF) study, patients with nonvalvular atrial fibrillation were randomized to rivaroxaban or dose‐adjusted warfarin. Cox proportional hazards regression with backward elimination identified factors at randomization that were independently associated with all‐cause mortality in the 14 171 participants in the intention‐to‐treat population. The median age was 73 years, and the mean CHADS 2 score was 3.5. Over 1.9 years of median follow‐up, 1214 (8.6%) patients died. Kaplan–Meier mortality rates were 4.2% at 1 year and 8.9% at 2 years. The majority of classified deaths (1081) were cardiovascular (72%), whereas only 6% were nonhemorrhagic stroke or systemic embolism. No significant difference in all‐cause mortality was observed between the rivaroxaban and warfarin arms (P=0.15). Heart failure (hazard ratio 1.51, 95% CI 1.33–1.70, P<0.0001) and age ≥75 years (hazard ratio 1.69, 95% CI 1.51–1.90, P<0.0001) were associated with higher all‐cause mortality. Multiple additional characteristics were independently associated with higher mortality, with decreasing creatinine clearance, chronic obstructive pulmonary disease, male sex, peripheral vascular disease, and diabetes being among the most strongly associated (model C‐index 0.677). Conclusions: In a large population of patients anticoagulated for nonvalvular atrial fibrillation, ≈7 in 10 deaths were cardiovascular, whereas <1 in 10 deaths were caused by nonhemorrhagic stroke or systemic embolism. Optimal prevention and treatment of heart failure, renal impairment, chronic obstructive pulmonary disease, and diabetes may improve survival. Clinical Trial Registration URL: https://www.clinicaltrials.gov/. Unique identifier: NCT00403767.

Published
2016
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19. Recurrent Enteroviral Myocarditis in Transplanted Heart from Induced Immune Deficiency.

Author

Azmeen, A., Garvin, R.P., Basheer, A.P., and Zolty, R.

Subjects
*CARDIOGENIC shock, *REVERSE transcriptase polymerase chain reaction, *IMMUNODEFICIENCY, *DIFFUSE large B-cell lymphomas, *MYOCARDITIS, *CARDIAC magnetic resonance imaging
Abstract

Group B enteroviruses are known to cause fulminant myocarditis requiring heart transplantation. We present a case of recurrent enteroviral myocarditis post-transplant posing a diagnostic challenge. A 37-year-old male with a history of Diffuse large B-cell lymphoma (DLBCL) in remission for six years after chimeric antigen receptor T-cell therapy (CAR-T), underwent heart transplant for enteroviral myocarditis. He presented within 2 weeks with worsening left ventricular ejection fraction (LVEF). Cardiac MRI (CMR) demonstrated diffuse, patchy mid myocardial and subepicardial enhancement of multiple segments (Figure) with increased signal on T2 imaging suggestive of edema. Endomyocardial biopsy (EMB) showed mild cellular rejection (grade 1R) with negative C4 complement (C4d) without myocyte necrosis. He developed cardiogenic shock with a decline in his LVEF to 20% and required VA-ECMO support. A repeat EMB showed grade 0R with negative C4d staining. The molecular microscope diagnostic system was negative for B and T-cell-mediated rejection. He received plasma exchange therapy, intravenous immunoglobulin (IVIG), and thymoglobulin. Lymphocyte counts performed on admission showed an absolute count of 31 for CD3 (normal-427 cell/mm3) and no detectable CD19 cells suggesting severe combined immune deficiency. EMB was positive for enterovirus by reverse transcriptase polymerase chain reaction (RT-PCR) thus diagnosing recurrent enteroviral myocarditis. After an extended course of Intravenous Immune globulin (IVIG), he had clinical recovery with an improvement of his LVEF to 55%. This is the first case in literature that highlights recurrence of biopsy-negative enteroviral myocarditis post-transplant, particularly with persistent B cell depletion from past exposure to anti-CD19 CAR-T cell therapy. We hypothesize that the severity of his presentation post-transplant was due to this unforeseen combined immune deficiency in addition to intensive immunosuppression. [ABSTRACT FROM AUTHOR]

Published
2023
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20. Endomyocardial Biopsy Microscopic Molecular Profiling Correlates with Donor Derived Cell Free DNA and Histopathology.

Author

Roberts, S., Stoller, D., Lundgren, S., Zolty, R., Dunbar Matos, C., Hyden, M., Urban, M., and Lowes, B.

Subjects
*CELL-free DNA, *GRAFT rejection, *HEART transplantation, *HISTOPATHOLOGY, *CIRCULATING tumor DNA, *BIOPSY
Abstract

Cardiac allograft rejection (AR) diagnosis has historically relied on endomyocardial biopsy (EMBx) and histopathology (HP). Quantifying donor-derived cell free DNA (ddcfDNA) has recently offered a non-invasive alternative for detecting graft injury. EMBx mRNA analysis via the molecular microscope profiles (MMP) quantifies AR probability not subject to HP interpretation. Our aim was to evaluate the clinical role of MMP in cardiac transplant recipients (HTx) with positive ddcfDNA. We identified 39 patients with ddcfDNA testing and subsequent EMBx for HP (n=36) and MMP (n=39) analysis. MMP was conducted by the molecular microscope diagnostic system (MMDX™). Patients with multi-organ transplantation or coronary allograft vasculopathy were excluded. MMP, HP, echo and ddcfDNA association were assessed using logistical regression (SPSS™). Average time post-transplant was 1585 ±1435 days, average LVEF 55%, and average ddcfDNA 0.81 ± 1.1. Donor specific antibodies were present in 14/39 of patients. MMP was abnormal in 18/39 patients and correlated with ddcfDNA levels (p=0.007) and HP (p=0.05), but not with LVEF (p=0.71). MMP abnormalities included 9 antibody mediated rejection (AMR), 5 acute cellular rejection (ACR), and 4 injury patterns. By HP, biopsies were abnormal in 18/36 patients: 18 ACR (grade 1) and 1 AMR (grade 2). Abnormal HP did not correlate with ddcfDNA levels (p= 0.07). HP and MMP are often discordant, Table 1. Abnormal MMP correlated with both ddcfDNA and HP, but not with LVEF. Large prospective clinical trials are needed to define clinical outcomes from treatment strategies based on biopsy results. Multi-modality testing may be necessary to monitor cardiac transplant patients for rejection and avoid misclassification. [ABSTRACT FROM AUTHOR]

Published
2023
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21. First Results of Soprano: Macitentan in Patients (pts) with Pulmonary Hypertension (PH) Post-Left Ventricular Assist Device (LVAD) Implantation.

Author

Frantz, R.P., Desai, S., Ewald, G., Franco, V., Hage, A., Horn, E.M., LaRue, S.J., Mathier, M.A., Mandras, S.A., Park, M.H., Ravichandran, A., Wang, I., Zolty, R., Rocco, M., Selej, M., Zhao, C., and Rame, J.

Subjects
*HEART assist devices, *PULMONARY hypertension, *AEROBIC capacity, *DRUG efficacy, *PULMONARY artery
Abstract

To assess the efficacy and safety of macitentan in pts with PH post-LVAD. SOPRANO (NCT02554903) was a double-blind, randomized, study of macitentan 10 mg once-daily vs placebo. Pts were ≥18 years with LVAD implanted within 90 days prior to randomization, had mean pulmonary arterial pressure (mPAP) ≥25 mmHg, pulmonary artery wedge pressure (PAWP) ≤18 mmHg and pulmonary vascular resistance (PVR) >3 Wood units (WU). The primary endpoint was change in PVR at week 12 of therapy from baseline. Fifty-seven pts were randomized: macitentan (n=28) or placebo (n=29). Baseline pt demographics and characteristics were well balanced. Baseline PVR (mean [SD]) was 4.3 [0.9] WU (macitentan) and 4.3 [1.3] WU (placebo). At week 12, mean PVR decreased to 58.5% (macitentan) and to 75.5% (placebo) of baseline. Mean placebo-corrected reduction in PVR of macitentan was 26.1% (95% CI: 58.0, 94.3; p=0.0158). Predefined secondary endpoints, notably including changes in PAWP, were not significantly different with macitentan vs placebo (Table). Another relevant hemodynamic parameter, transpulmonary gradient, significantly decreased with macitentan vs placebo (p=0.0499). The incidence of treatment adverse events (TAEs) was 21.4% (macitentan) and 24.1% (placebo); no TAEs occurred in >1 patient in the macitentan arm. AEs of interest included edema, anemia and hypotension: reported in 7 (25.0%), 3 (10.7%), and 4 (14.3%) pts on macitentan (mostly mild-moderate) and in 5 (17.2%), 2 (6.9%) and 1 (3.6%) pts on placebo, respectively. Two pts on macitentan and 1 pt on placebo discontinued for treatment-related AEs. In the first prospective, multicenter, randomized controlled trial of pulmonary vasodilators in the early post-LVAD population, macitentan significantly reduced PVR and was well tolerated. The impact of macitentan on post-LVAD exercise capacity and RV failure warrants further study. [ABSTRACT FROM AUTHOR]

Published
2021
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23. The Effect of Exercise on Endothelin 1 Level in Patients with Pulmonary Hypertension.

Author

Albulushi, A., Dhar, K., Stoller, D., Hyden, M., Burdorf, A., Lowes, B., and Zolty, R.

Subjects
*PREPROENDOTHELIN, *PULMONARY hypertension, *ARM exercises, *EXERCISE, *HEART failure patients
Abstract

Endothelin-1 (ET-1), a potent vasoconstrictor, is elevated in heart failure as well as in pulmonary arterial hypertension (PAH). To our knowledge little is known about ET-1 level in exercise induced pulmonary hypertension when compared to group 1 and 2 pulmonary hypertension. We aim to assess effect of exercise on ET-1 levels in different types of pulmonary hypertension. A prospective study measuring ET-1 level in patient with PAH, heart failure induced pulmonary hypertension (D-PH), exercise induced PAH and exercise induced D-PH both at rest at peak exercise. Demographic and echo data were collected. Right heart cath was done to confirm diagnosis and type of pulmonary hypertension, which was followed by arm lifting exercise for 4 minutes (30 watts and decrease of MVO2 by >10%) using different weights. Exercise induced PAH defined as mean pulmonary pressure (mPA) <20 mmHg at rest, with exercise mPA >30 mmHg and pulmonary wedge (PW) <20 mmHg. Exercise induced D-PH was defined as mPA<20 mmHg at rest, with exercise mPA >30 mmHg and PW >20 mmHg. Blood samples were collected to measure ET-1 level using ET-1 ELISA. A total of 77 patients were included in this study. 5 study groups were divided into: 10 control subjects, 18 patients with D-PH, 22 patients with PAH, 15 patients with Exercise D-PH and 12 patients with Exercise PAH. At rest, ET-1 level was the highest in Exercise-PAH compared to other groups 3.6 +/- 2 with p valule 0.04. Whereas, at peak exercise, ET-1 level was the highest in PAH compared to other groups with, 2.91 +/- 1.8 with p value of 0.05 (figure 1). Patients with D-PH had more evidence of diabetes mellitus, Obesity, smoking, dilated right atrium, right ventricular failure and were more elderly male. At rest, ET-1 level is the highest in patients with exercise induced PAH, whereas at peak exercise, ET-1 is the highest in patients with PAH. Patients with heart failure induced pulmonary hypertension have more cardiac risk factors with evidence of right sided failure. [ABSTRACT FROM AUTHOR]

Published
2020
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24. Trends in Exercise Capacity Following Heart Transplantation.

Author

Lundgren, S., Lyden, E., Hyden, M., Burdorf, A., Zolty, R., Lowes, B., Um, J., and Stoller, D.

Subjects
*HEART transplantation
Abstract

Purpose While exercise capacity has been shown to improve following heart transplantation, transplant patients still have subnormal exercise capacities. We aimed to determine the natural history of exercise capacity post-transplant and whether resting heart rate impacts exercise capacity Methods Retrospective chart review was performed and patients who underwent multiple cardiopulmonary exercise testing (CPET) post-heart transplantation were identified. Fisher's exact test was used to compare categorical data with CPET variables and the Mann-Whitney test was used to compare continuous measures. Measurements over each year were considered repeated measures and fit with a linear mixed effect model. Results A total of 93 patients underwent CPET at 1-year post-transplant, 44 at 2 years, 32 at 3 years, and 17 at 4 years. The average age was 56.1(± 12.6) years, 87 (93.6%) patients were Caucasian, and 64 (68.2%) patients were male sex. There were no significant changes in CPET variables over the first four years following heart transplantation (Table 1). Resting heart rate at 1 year (≤ 95 vs >95) did not significantly impact exercise capacity after heart transplant. Patients with lower peak VO2 (<70% predicted) at 1-year post-transplant exhibited significant improvement in exercise capacity over time (p=0.004) while those with near normal exercise capacity (>70% predicted) remained stable over time. Conclusion While exercise capacity improves following heart transplantation, continued improvement was not observed in our transplant population. Resting heart rate following heart transplantation does not impact exercise capacity. [ABSTRACT FROM AUTHOR]

Published
2019
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25. Pre-Operative Ventilatory Inefficiency is Associated with Gastrointestinal Bleeding in Patients with Continuous-Flow Left Ventricular Assist Devices.

Author

Yu, M.D., Newman, J., Brailovsky, Y., Liebo, M., Zolty, R., Lowes, B., Heroux, A., and Raichlin, E.

Subjects
*HEART assist devices, *EXERCISE tests
Abstract

Purpose Ventilatory efficiency (VE/VCO 2) on cardiopulmonary exercise testing (CPET) has prognostic significance in patients with chronic heart failure; however, its hemodynamic correlates and effect on outcomes following left ventricular assist device (LVAD) implantation has not been evaluated. Aim To explore the association between pre-LVAD VE/VCO 2 and the incidence of post-LVAD gastrointestinal bleeding (GIB). Methods Overall, 159 patients underwent CPET prior to LVAD implantation: 87 had VE/VCO 2 ≥36 and 72 had VE/VCO 2 <36. During 11.75 (median, IQR 4.8-26.2) months of follow up 59 developed GIB. Results Patients with a VE/VCO 2 ≥36 were older (58.4 ± 13.2 vs. 52.5 ± 15.1 years, p=0.02) and had lower BMI (28.8 ± 7.3 vs. 31.0 ± 6.2, p=0.01). On pre-LVAD evaluation, the pulmonary artery pulsatility index (4.1 ± 3.0 vs 2.97 ± 1.8, p=0.01) and echocardiographic E/E' (18.7 ± 7.3 vs. 15.5 ± 7.9, p=0.03) were significantly higher in the VE/VCO 2 ≥36 group (Table 1). Other demographic, clinical, and hemodynamic characteristics did not differ between groups. Freedom from GIB was significantly lower in the VE/VCO 2 ≥36 group (2 years post-LVAD: 47% vs. 76%, p= 0.001, log rank) (Figure 1). There was no association between GIB and other CPET measurements. On Cox proportional regression analysis VE/VCO 2 ≥36 was independently associated with increased GIB (HR 2.1; 95% CI 1.3-3.5, p=0.004). Conclusion VE/VCO 2 ≥36 on pre-LVAD CPET is associated with more frequent GIB after LVAD implantation. The mechanism of this finding requires further evaluation. [ABSTRACT FROM AUTHOR]

Published
2019
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26. Recurrent Pump Thrombosis is Common after Axial Continuous Flow LVAD Exchange.

Author

Macdonald, C., Urban, M., Moulton, M., McCain, N., Stoller, D., Zolty, R., Um, J., and Siddique, A.

Subjects
*AXIAL flow, *THROMBOSIS
Abstract

Purpose LVAD exchange is an accepted treatment for LVAD complications but long-term results are poorly understood. We examined survival and re-thrombosis rate in patients after pump exchange Methods All patients undergoing LVAD exchange at our institution from Jan 2010 to Feb 2018 were retrospectively reviewed. Indications for exchange were pump thrombosis, driveline fracture, and device infection. Survival and freedom from LVAD-related complications were assessed by Kaplan-Meier method. Results Twenty-one patients were included, all underwent axial continuous-flow pump exchange: 14 patients (67%) for pump thrombosis, 5 patients (24%) for driveline fracture, and 2 patients (10%) for device infection. Basic characteristics of patients are presented in Table 1. Survival for all patients was 86±8% at one year and 70±39% at two years (Figure 1A). Amongst patients with pump thrombosis 14.3% died peri-operatively, 43% had recurrent thrombosis after a median of 5.7 months (freedom from hospital death and recurrent thrombosis is shown in Figure 1B). Amongst 6 patients with recurrent thrombosis 2 died during follow up, 1 underwent transplantation, 1 had a second exchange, 1 was defunctionalized and 1 remains on support. Survival at one year in this group was 85±10%, and 55±18% at two years. Conclusion Survival after LVAD exchange compares well with published results after primary LVAD implantation. However, recurrence of thrombosis was common among patients who required a LVAD exchange due to pump thrombosis and survival was less favorable. In this sub-group strong consideration should be given to alternative strategies to avoid recurrent complications. [ABSTRACT FROM AUTHOR]

Published
2019
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27. Pre-Heart Transplant Spirometry Predicts Post-Transplant Survival.

Author

Lundgren, S., Lowes, B., Lyden, E., Zolty, R., Hyden, M., Burdorf, A., Um, J.Y., and Stoller, D.

Subjects
*HEART transplantation, *OBSTRUCTIVE lung diseases, *TRANSPLANTATION of organs, tissues, etc., *PROPORTIONAL hazards models, *LUNG transplantation
Abstract

Lung disease is common in the advanced heart failure population. While pulmonary function testing (PFT) is typically performed as part of a heart transplant evaluation, little is known regarding the prognostic utility of PFTs for outcomes after transplantation. We evaluated whether PFT parameters correlated with survival, length of stay, or time on ventilator following heart transplantation. International Society for Heart and Lung Transplantation (ISHLT) Thoracic Organ Transplant (TTX) registry data was combined with single-center data from the University of Nebraska Medical Center. Cox proportional hazard modeling was used to evaluate univariate and multivariate predictors of survival. A total of 1083 patients (802 from a total of 62,327 from the TTX registry, 281 from the UNMC database) had pre-transplant PFT data available for evaluation. At the time of transplant, the mean age was 50.6 (± 14.5) years, 24.2% were female, 51% had a history of tobacco use, and 8% had a history of chronic obstructive pulmonary disease. Forced expiratory volume in 1 second (FEV1) < 50% of predicted and forced vital capacity (FVC) < 50% of predicted each had significantly higher mortality within the first 5 years post-transplant (p < 0.0001 and p=0.0001, respectively) compared to patients with FEV1 or FVC 50-70% or > 70% (Figure 1). FEV1/FVC < 0.7 and DLCO < 60% predicted were not associated with increased mortality. FEV1 and FVC below 50% of predicted both had longer lengths of stay (p=0.0005 for FEV1 and <0.0001 for FVC), but were not associated with more time on the ventilator. After adjusting for male gender, age, body mass index, smoking history, COPD, creatinine, albumin, and total bilirubin, either FEV1 or FVC < 50% remained independent predictors of mortality with a hazard ratio of 2.65 (p < 0.0001, 95% CI 1.6, 4.3). Abnormal pulmonary function (FEV1 or FVC < 50% prior to transplantation is associated with increased mortality and longer length of stay following transplant. [ABSTRACT FROM AUTHOR]

Published
2020
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28. Impact of Heart Rate and Left Ventricular Mass on Survival Following Heart Transplantation.

Author

Lundgren, S., Lyden, E., Hyden, M., Burdorf, A., Zolty, R., Lowes, B., Um, J., and Stoller, D.

Subjects
*HEART beat, *HEART transplantation
Abstract

Purpose Small studies suggest increased left ventricular (LV) mass and resting heart rate (HR)are associated with increased mortality following heart transplantation. We aimed to validate these prior findings and determine if resting HR is correlated with increased LV mass. Methods Retrospective chart review was conducted on 326 consecutive patients following heart transplantation at a single transplant center. Spearman correlation coefficient was used to evaluate correlation between HR and LV mass. Transplant free survival was estimated using the Kaplan-Meier method and survival was compared between groups using the log rank test. Results A total of 326 consecutive heart transplant patients between September 2005 and July 2018 were identified. The average age was 53.6 (± 14.3) years old, 238 patients (73%) were male, and the median follow-up time was 3.7 years. The average HR was 93 (12) beats per minute (BPM) at 1 month and 95 (12) BPM at 1 year. The average LV mass index was 87.1 g/m2 (21.8) at 1 month and 79.2 g/m2 (17.6) at 1 year. No correlation was present between HR and LV mass at 1 month (r=-0.25) or 1 year (r=-0.07). Stratification by resting HR at 1 year (HR ≥ 90 vs < 90) did reveal a trend toward reduced transplant-free survival in patients with an elevated HR (p=0.08) (Figure). Low LV mass index (<80g/m2) at 1-month post-transplant was associated with significantly reduced transplant-free survival (p=0.024) although this relationship was not present at 1 year. Conclusion Resting HR and LV mass following heart transplant were not correlated in our patient cohort. While a trend toward reduced survival in patients with a HR ≥ 90 bpm at 1 year was present, further research is needed to determine whether treatment targeting HR reduction would result in improved survival. [ABSTRACT FROM AUTHOR]

Published
2019
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29. Comparison of Endothelin-1 Level in Group I Pulmonary Hypertension vs. Group II Pulmonary Hypertension Both at Rest and at Peak Exercise.

Author

Albulushi, A., Patel, A., Stoller, D., Hyden, M., Burdorf, A., Brian, L., and Zolty, R.

Subjects
*PULMONARY hypertension, *EXERCISE
Abstract

Purpose To assess Endothelin-1 (ET-1) level in patients with group I pulmonary hypertension (pulmonary arterial hypertension (PAH)) compared to patients with group II PH (due to heart failure with preserved ejection fraction (HFpEF)), both at rest and at peak exercise Methods We measured ET-1 level in patients with PAH, PH due to HFpEF and normal control both at rest and peak exercise. Right heart cath was done to confirm diagnosis and type of PH. This was followed by arm lifting exercise for 3 minutes (30 watts) and decrease of MVO2 by > 10% using different weights. Blood samples were collected to measure ET-1 level pre and post exercise using ET-1 ELISA. Results A total of 39 patients were included in this study. 18 patients had PH due to HFpEF with a mean ET-1 level of 2.58 fmol/ m +/- 1.12 at rest and 2.62 fmol/ m +/- 1.02 at peak exercise with p value of 0.43. In comparison, there was 16 patients who had PAH with a mean ET-1 level of 2.31 fmol/ m +/- 0.78 at rest and 2.38 fmol/ m +/- 0.87 at peak exercise with p value of 0.25. Higher levels of ET-1 is noted in patients with pulmonary hypertension (especially those due to HFpEF) was significantly higher than normal control. However, exercise didn't effect ET-1 level in the three groups (Figure 1) Conclusion This is the first study to show that ET-1 level is higher in pulmonary hypertension due to HFpEF compared to PAH. However, exercise has no effect on ET-1 level in the two groups [ABSTRACT FROM AUTHOR]

Published
2019
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34. (1043) - Myocarditis Treated with VA-ECMO: A Single Centers Experience.

Author

Burdorf, A., Varnado, S., Balk, J.L., Ryan, T., Raichlin, E., Vongooru, H., Lowes, B., Zolty, R., Um, J., Merritt-Genore, H., Moulton, M., and Siddique, A.

Subjects
*TREATMENT of myocarditis, *EXTRACORPOREAL membrane oxygenation, *CARDIOGENIC shock, *HEART disease related mortality, *HEALTH outcome assessment, *MYOCARDITIS, *PATIENTS
Published
2016
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