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460 results on '"Ramkumar, V."'

3. Diabetes and Risk of Sudden Death in Coronary Artery Disease Patients Without Severe Systolic Dysfunction

Author

Venkateswaran, Ramkumar V, Moorthy, MV, Chatterjee, Neal A, Pester, Julie, Kadish, Alan H, Lee, Daniel C, Cook, Nancy R, and Albert, Christine M

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Heart Disease, Biomedical Imaging, Atherosclerosis, Cardiovascular, Clinical Research, Prevention, Diabetes, Detection, screening and diagnosis, 4.2 Evaluation of markers and technologies, Cohort Studies, Coronary Artery Disease, Death, Sudden, Cardiac, Diabetes Mellitus, Humans, Stroke Volume, Ventricular Function, Left, diabetes mellitus, HbA(1c), risk stratification, sudden cardiac death, Cardiorespiratory Medicine and Haematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract

ObjectivesThis study sought to determine the absolute and relative associations of diabetes mellitus (DM) and hemoglobin A1c (HbA1c) with sudden and/or arrhythmic death (SAD) versus other modes of death in patients with coronary artery disease (CAD) who do not qualify for implantable cardioverter-defibrillators.BackgroundPatients with CAD and DM are at elevated risk for SAD; however, it is unclear whether these patients would benefit from implantable cardioverter-defibrillators given competing causes of death and/or whether HbA1c might augment SAD risk stratification.MethodsIn the PRE-DETERMINE study of 5,764 patients with CAD with left ventricular ejection fraction (LVEF) of >30% to 35%, competing risk analyses were used to compare the absolute and relative risks of SAD versus non-SAD by DM status and HbA1c level and to identify risk factors for SAD among 1,782 patients with DM.ResultsOver a median follow-up of 6.8 years, DM and HbA1c were significantly associated with SAD and non-SAD (P 30% to 35%, patients with DM and/or elevated HbA1c are at much higher absolute risk of dying from non-SAD than SAD. Clinical risk markers, and not HbA1c, were associated with SAD risk in patients with DM. (PRE-DETERMINE: Biologic Markers and MRI SCD Cohort Study; NCT01114269).

Published
2021

11. Cangrelor in cardiogenic shock and after cardiopulmonary resuscitation: A global, multicenter, matched pair analysis with oral P2Y12 inhibition from the IABP-SHOCK II trial

Author

Droppa, Michal, Vaduganathan, Muthiah, Venkateswaran, Ramkumar V., Singh, Abhayjit, Szumita, Paul M., Roberts, Russel J., Qamar, Arman, Hack, Luis, Rath, Dominik, Gawaz, Meinrad, Fuernau, Georg, de Waha-Thiele, Suzanne, Desch, Steffen, Schneider, Steffen, Ouarrak, Taoufik, Jaffer, Farouc A., Zeymer, Uwe, Thiele, Holger, Bhatt, Deepak L., and Geisler, Tobias

Published
2019
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16. Caffeinated Beverage Intake, Dyspnea With Ticagrelor, and Cardiovascular Outcomes: Insights From the PEGASUS‐TIMI 54 Trial

Author

Remo H. M. Furtado, Ramkumar V. Venkateswaran, Jose C. Nicolau, Yared Gurmu, Deepak L. Bhatt, Robert F. Storey, P. Gabriel Steg, Giuglia Magnani, Shinya Goto, Mikael Dellborg, Gabriel Kamensky, Daniel Isaza, Philip Aylward, Per Johanson, and Marc P. Bonaca

Subjects
arrhythmias, caffeine, cardiovascular outcomes, dyspnea, ticagrelor, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Background A proposed cause of dyspnea induced by ticagrelor is an increase in adenosine blood levels. Because caffeine is an adenosine antagonist, it can potentially improve drug tolerability with regard to dyspnea. Furthermore, association between caffeine and cardiovascular events is of clinical interest. Methods and Results This prespecified analysis used data from the PEGASUS TIMI 54 (Prevention of Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin–Thrombolysis in Myocardial Infarction 54) trial, which randomized 21 162 patients with prior myocardial infarction to ticagrelor 60 mg or 90 mg or matching placebo (twice daily). Baseline caffeine intake in cups per week was prospectively collected for 9694 patients. Outcomes of interest included dyspnea, major adverse cardiovascular events (ie, the composite of cardiovascular death, myocardial infarction, or stroke), and arrhythmias. Dyspnea analyses considered the pooled ticagrelor group, whereas cardiovascular outcome analyses included patients from the 3 randomized arms. After adjustment, caffeine intake, compared with no intake, was not associated with lower rates of dyspnea in patients taking ticagrelor (adjusted hazard ratio (HR), 0.91; 95% CI, 0.76–1.10; P=0.34). There was no excess risk with caffeine for major adverse cardiovascular events (adjusted HR, 0.78; 95% CI, 0.63–0.98; P=0.031), sudden cardiac death (adjusted HR, 0.98; 95% CI, 0.57–1.70; P=0.95), or atrial fibrillation (adjusted odds ratio, 1.07; 95% CI, 0.56–2.04; P=0.84). Conclusions In patients taking ticagrelor for secondary prevention after myocardial infarction, caffeine intake at baseline was not associated with lower rates of dyspnea compared with no intake. Otherwise, caffeine appeared to be safe in this population, with no apparent increase in atherothrombotic events or clinically significant arrhythmias. Registration URL: https://www.clini​caltr​ials.gov; Unique identifier: NCT01225562.

Published
2020
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21. Identification of Racial Inequities in Access to Specialized Inpatient Heart Failure Care at an Academic Medical Center

Author

Eberly, Lauren A., Richterman, Aaron, Beckett, Anne G., Wispelwey, Bram, Marsh, Regan H., Cleveland Manchanda, Emily C., Chang, Cindy Y., Glynn, Robert J., Brooks, Katherine C., Boxer, Robert, Kakoza, Rose, Goldsmith, Jennifer, Loscalzo, Joseph, Morse, Michelle, Lewis, Eldrin F., Abel, Samantha, Adams, Ayrenne, Anaya, Joseph, Andrews, Erik H, Atkinson, Benjamin, Avutu, Viswatej, Bachorik, Alexandra, Badri, Omar, Bailey, Mariel, Baird, Katie, Bakshi, Salina, Balaban, Denis, Barshop, Kenneth, Baumrin, Emily, Bayomy, Omar, Beamesderfer, Julia, Becker, Nora, Berg, David D., Berman, Adam N., Blum, Steven M., Boardman, Alexander P., Boden, Kaeleen, Bonacci, Robert A, Brown, Sarah, Campbell, Kirsti, Case, Siobhan, Cetrone, Emily, Charrow, Alexandra, Chiang, David, Clark, Devin, Cohen, Aaron J., Cooper, Alissa, Cordova, Tomas, Cuneo, C. Nicholas, de Feria, Alsina Alejandro, Deffenbacher, Karen, DeFilippis, Ersilia M., DeGregorio, Geneva, Deutsch, Aaron J., Diephuis, Bradford, Divakaran, Sanjay, Dorschner, Peter, Downing, Nicholas, Drescher, Caitlin, D’Silva, Kristin M., Dunbar, Peter, Duong, David, Earp, Sarah, Eckhardt, Christine, Elman, Scott A., England, Ross, Everett, Kay, Fedotova, Natalie, Feingold-Link, Tamara, Ferreira, Mark, Fisher, Herrick, Foo, Patricia, Foote, Michael, Franco, Idalid, Gilliland, Thomas, Greb, Jacqueline, Greco, Katherine, Grewal, Sungat, Grin, Benjamin, Growdon, Matthew E., Guercio, Brendan, Hahn, Cynthia K., Hasselfeld, Brian, Haydu, Erika J, Hermes, Zachary, Hildick-Smith, Gordon, Holcomb, Zachary, Holroyd, Kathryn, Horton, Laura, Huang, George, Jablonski, Stanley, Jacobs, Douglas, Jain, Nina, Japa, Sohan, Joseph, Richard, Kalashnikova, Mariya, Kalwani, Neil, Kang, Daniel, Karan, Abraar, Katz, Joel T, Kellner, Daniel, Kidia, Khameer, Kim, June-Ho, Knowles, Scott M, Kolbe, Laura, Kore, Idil, Koullias, Yiannis, Kuye, Ifedayo, Lang, Joshua, Lawlor, Matthew, Lechner, Melissa G., Lee, Ken, Lee, Scott, Lee, Zachary, Limaye, Neha, Lin-Beckford, Stephanie, Lipsyc, Marla, Little, Jessica, Loewenthal, Julia, Logaraj, Ranjani, Lopez, Diana M, Loriaux, Daniel, Lu, Yi, Ma, Kevin, Marukian, Nareh, Matias, Wilfredo, Mayers, Jared R., McConnell, Ian, McLaughlin, Michael, Meade, Christina, Meador, Catherine, Mehta, Anish, Messenger, Elizabeth, Michaelidis, Constantinos, Mirsky, Jacob, Mitten, Emilie, Mueller, Alisa, Mullur, Jyotsna, Munir, Amir, Murphy, Emily, Nagami, Ellen, Natarajan, Abirami, Nsahlai, Michelle, Nze, Chijioke, Okwara, Noreen, Olds, Peter, Paez, Rafael, Pardo, Michael, Patel, Siddharth, Petersen, Alec, Phelan, Laura, Pimenta, Erica, Pipilas, Daniel, Plovanich, Molly, Pong, Denise, Powers, Brian W., Rao, Anita, Ramirez Batlle, Haiyan, Ramsis, Mattheus, Reichardt, Anna, Reiger, Sheridan, Rengarajan, Michelle, Rico, Stephanie, Rome, Benjamin N., Rosales, Rachael, Rotenstein, Lisa, Roy, Alexis, Royston, Sarah, Rozansky, Hallie, Rudder, Meghan, Ryan, Christine E., Salgado, Sanjay, Sanchez, Pablo, Schulte, Jennifer, Sekar, Aswin, Semenkovich, Nicholas, Shannon, Evan, Shaw, Neil, Shorten, Andrew Ben, Shrauner, William, Sinnenberg, Lauren, Smithy, James W., Snyder, Gregory, Sreekrishnan, Anirudh, Stabenau, Hans, Stavrou, Eleni, Stergachis, Andrew, Stern, Robert, Stone, Alexander, Tabrizi, Shervin, Tanyos, Sam, Thomas, Cristina, Thun, Haley, Torres-Lockhart, Kristine, Tran, An, Treasure, Carolyn, Tsai, Frederick D., Tsaur, Stephen, Tschirhart, Evan, Tuwatananurak, Justin, Venkateswaran, Ramkumar V., Vishnevetsky, Anastasia, Wahl, Lindsay, Wall, April, Wallace, Frances, Walsh, Elisa, Wang, Priscilla, Ward, Heather B., Warner, Lindsay N., Weeks, Lachelle D., Weiskopf, Kipp, Wengrod, Jordan, Williams, Jessica N., Winkler, Marisa, Wong, Jeffrey L., Worster, Devin, Wright, Aileen, Wunsch, Caroline, Wynter, Jamila S., Yarbrough, Chase, Yau, Wai-Ying, Yazdi, Daniel, Yeh, Jennifer, Yialamas, Maria A., Yozamp, Nicholas, Zambrotta, Marina, and Zon, Rebecca

Published
2019
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46. Spontaneous, homeostatic, and inflammation-induced sleep in NF-[kappa]B p50 knockout mice

Author

Jhaveri, K.A., Ramkumar, V., Trammell, R.A., and Toth, L.A.

Subjects
Polysaccharides -- Research, Sleep -- Physiological aspects, Biological sciences
Abstract

The dimeric transcription factor nuclear factor-[kappa]B (NF-[kappa]B) regulates several endogenous sleep-modulatory substances and thereby serves as a pivotal mediator of sleep-wake homeostasis. To further define the role of NF-[kappa]B in sleep regulation, we monitored sleep and temperature in mice that lack the p50 subunit of NF-[kappa]B [p50 knockout (KO) mice]. Compared with the control B6129PF2/J strain, p50 KO mice spend more time in slow-wave sleep (SWS) and rapid eye movement sleep (REMS) under normal conditions and show enhanced homeostatic recovery of sleep after sleep loss. p50 KO mice also show increased SWS and reduced REMS and temperature after the administration of lipopolysaccharide, yet they are behaviorally less responsive to challenge with influenza virus. These data support a role for NF-[kappa]B, and, in particular, for the p50 subunit, in the regulation of sleep in healthy mice and in mice experiencing immune challenge. nuclear factor-[kappa]B; p50 knockout mice; sleep; temperature; lipopolysaccharide; influenza

Published
2006

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