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152. Effect of treatment with rosiglitazone on high-sensitivity cardiac troponin levels among patients with type 2 diabetes mellitus.

Author

Salahuddin, Usman I., Pandey, Ambarish, Ayers, Colby R., See, Raphael, Neeland, Ian J., Gore, M. Odette, Grinsfelder, D. Bennett, Abdullah, Shuaib M., Khera, Amit, de Lemos, James A., and McGuire, Darren K.

Abstract

Objective: To assess the impact of intermediate-term treatment with rosiglitazone on high-sensitivity cardiac troponin T levels among patients with type 2 diabetes mellitus with or at high risk of coronary artery disease. Methods: High-sensitivity cardiac troponin T level was measured at baseline and after 6 months of study treatment in a randomized trial comparing rosiglitazone versus placebo in patients with type 2 diabetes and prevalent cardiovascular disease or multiple cardiovascular disease risk factors. Univariable and multivariable linear regression analyses were performed to assess the effect of rosiglitazone versus placebo on high-sensitivity cardiac troponin T levels. Results: The study included 150 randomized participants, of whom 106 had paired baseline and end-of-study blood samples for analysis (mean age: 56 ± 8 years, 42% women; 8.8 years average type 2 diabetes duration; mean haemoglobin A1c of 7.5). Almost all study participants (93%) had detectable high-sensitivity cardiac troponin T (⩾3 ng/L) at baseline, including 23% with high-sensitivity cardiac troponin T levels exceeding the threshold commonly used to diagnose myocardial infarction (⩾14 ng/L). Change in high-sensitivity cardiac troponin T levels from baseline to follow-up was not significantly different between rosiglitazone and placebo groups (p = 0.316). Conclusion: Rosiglitazone did not impact high-sensitivity cardiac troponin T levels, adding to the growing body of literature suggesting that the incremental heart failure risk associated with rosiglitazone is not mediated by direct myocardial injury. [ABSTRACT FROM AUTHOR]

Published
2016
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153. Relation of Adiponectin to All-Cause Mortality, Cardiovascular Mortality, and Major Adverse Cardiovascular Events (from the Dallas Heart Study).

Author

Witberg, Guy, Ayers, Colby R, Turer, Aslan T, Lev, Eli, Kornowski, Ran, de Lemos, James, and Neeland, Ian J

Subjects
*CARDIOVASCULAR diseases, *COMPARATIVE studies, *CAUSES of death, *DISEASES, *LONGITUDINAL method, *RESEARCH methodology, *MEDICAL cooperation, *RESEARCH, *RESEARCH funding, *SURVIVAL, *TIME, *EVALUATION research, *PROPORTIONAL hazards models, *RETROSPECTIVE studies, *ADIPONECTIN
Abstract

Adiponectin is a key component in multiple metabolic pathways. Studies evaluating associations of adiponectin with clinical outcomes in older adults have reported conflicting results. We investigated the association of adiponectin with mortality and cardiovascular disease (CVD) morbidity in a young, multiethnic adult population. We analyzed data from participants in the Dallas Heart Study without baseline CVD who underwent assessment of total adiponectin from 2000 to 2002. The primary outcome of all-cause mortality was assessed over median 10.4 years of follow-up using multivariable-adjusted Cox proportional hazards models. Secondary outcomes included CVD mortality, major adverse cardiovascular and cerebrovascular events (MACCE), and heart failure (HF). The study cohort included 3,263 participants, mean age 43.4 years, 44% women, and 50% black. There were 184 deaths (63 CVD), 207 MACCE, and 46 HF events. In multivariable models adjusted for age, gender, race, hypertension, diabetes, smoking, high-density lipoprotein cholesterol-C, hyperlipidemia, high-sensitivity C-reactive protein level, estimated glomerular filtration rate, and body mass index, increasing adiponectin quartiles were positively associated with all-cause mortality Q4 versus Q1 (hazard ratio [HR] = 2.27; 95% confidence interval [CI] 1.47, 3.50); CVD mortality Q4 versus Q1 (HR = 2.43; 95% CI 1.15, 5.15); MACCE Q4 versus Q1 (HR = 1.71; 95% CI 1.13, 2.60); and HF Q4 versus Q1 (HR = 2.95; 95% CI 1.14, 7.67). Findings were similar with adiponectin as a continuous variable and consistent across subgroups defined by age, gender, race, obesity, diabetes, metabolic syndrome, or elevated high-sensitivity C-reactive protein. In conclusion, higher adiponectin was associated with increased mortality and CVD morbidity in a young, multiethnic population. These findings may have implications for strategies aimed at lowering adiponectin to prevent adverse outcomes. [ABSTRACT FROM AUTHOR]

Published
2016
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156. Churches as targets for cardiovascular disease prevention: comparison of genes, nutrition, exercise, wellness and spiritual growth (GoodNEWS) and Dallas County populations

Author

Powell-Wiley, Tiffany M., primary, Banks-Richard, Kamakki, additional, Williams-King, Elicia, additional, Tong, Liyue, additional, Ayers, Colby R., additional, de Lemos, James A., additional, Gimpel, Nora, additional, Lee, Jenny J., additional, and DeHaven, Mark J., additional

Published
2012
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166. Multimodality Strategy for Cardiovascular Risk Assessment

Author

de Lemos, James A., Ayers, Colby R., Levine, Benjamin, deFilippi, Christopher R., Wang, Thomas J., Hundley, W. Gregory, Berry, Jarett D., Seliger, Stephen L., McGuire, Darren K., Ouyang, Pamela, Drazner, Mark H., Budoff, Matthew, Greenland, Philip, Ballantyne, Christie M., and Khera, Amit

Abstract

Supplemental Digital Content is available in the text.

Published
2017
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167. Sex-Based Differences in Cardiometabolic Biomarkers

Author

Lew, Jeanney, Sanghavi, Monika, Ayers, Colby R., McGuire, Darren K., Omland, Torbjørn, Atzler, Dorothee, Gore, Maria O., Neeland, Ian, Berry, Jarett D., Khera, Amit, Rohatgi, Anand, and de Lemos, James A.

Abstract

Supplemental Digital Content is available in the text.

Published
2017
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178. Assessment of cardiac structure and function in patients without and with peripheral oedema during rosiglitazone treatment

Author

Narang, Nikhil, primary, Armstead, Sumiko I, additional, Stream, Amanda, additional, Abdullah, Shuaib M, additional, See, Raphael, additional, Snell, Peter G, additional, McGavock, Jonathan, additional, Ayers, Colby R, additional, Gore, M Odette, additional, Khera, Amit, additional, de Lemos, James A, additional, and McGuire, Darren K, additional

Published
2011
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180. Concentric left ventricular hypertrophy as assessed by cardiac magnetic resonance imaging and risk of death in cardiac transplant recipients

Author

Patel, Parag C., primary, Reimold, Sharon C., additional, Araj, Faris G., additional, Ayers, Colby R., additional, Kaiser, Patricia A., additional, Peshock, Ronald M., additional, Yancy, Clyde W., additional, Ring, W. Steves, additional, Gupta, Sachin, additional, Mishkin, Joseph D., additional, Mammen, Pradeep P.A., additional, Markham, David W., additional, and Drazner, Mark H., additional

Published
2010
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182. Health Insurance Is Usually Required for Heart Transplant Recipients but Not Donors; When Informed of this Discrepancy, Public Willingness to Donate May Decrease

Author

Thibodeau, Jennifer T., primary, Rao, Meena P., additional, Gupta, Charu, additional, Ayers, Colby R., additional, Gupta, Sachin, additional, Mammen, Pradeep P.A., additional, Markham, David W., additional, Mishkin, Joseph D., additional, Patel, Parag C., additional, King, Louise P., additional, and Drazner, Mark H., additional

Published
2010
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190. Association of Cystatin C With Left Ventricular Structure and Function

Author

Patel, Parag C., primary, Ayers, Colby R., additional, Murphy, Sabina A., additional, Peshock, Ronald, additional, Khera, Amit, additional, de Lemos, James A., additional, Balko, Jody A., additional, Gupta, Sachin, additional, Mammen, Pradeep P.A., additional, Drazner, Mark H., additional, and Markham, David W., additional

Published
2009
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196. In-hospital cardiopulmonary arrests in patients with left ventricular assist devices.

Author

Garg, Sonia, Ayers, Colby R, Fitzsimmons, Catherine, Meyer, Dan, Peltz, Matthias, Bethea, Brian, Cornwell, William, Araj, Faris, Thibodeau, Jennifer, and Drazner, Mark H

Abstract

Background: Basic and advanced cardiac life support guidelines do not address resuscitation of patients with continuous-flow (CF) left ventricular assist devices (LVADs). As the population of LVAD patients increases, it becomes important to understand how to provide emergency care to such patients. METHODS AND RESULTS: We retrospectively reviewed a consecutive series of patients with an implanted CF-LVAD who had an in-hospital cardiopulmonary arrest at our medical center from January 2011 to October 2013. We compared them with a matched cohort of patients without LVADs who had an inhospital cardiopulmonary arrest during the same time period. Code documentation was used to determine arrest characteristics, perfusion assessment techniques, and time to cardiopulmonary resuscitation (CPR) initiation. There were 415 in-hospital arrests during the study period, and 4% (n 5 16) occurred in patients with CF-LVADs. Response teams used various approaches to assess arterial perfusion, including palpation or Doppler of the arterial pulse and measurement of blood pressure by Doppler or arterial line. Nine of the 16 patients required CPR, but only 5 (56%) received CPR in !2 minutes. In the control group (n 5 32) of patients without an LVAD, 22 received CPR, which was initiated within 2 minutes in all (100%) of the patients. CONCLUSIONS: Cardiopulmonary arrests in LVAD patients accounted for 4% of all arrests in our center. We identified important time delays in CPR initiation, highlighting the need to develop resuscitation guidelines for this patient population. [ABSTRACT FROM AUTHOR]

Published
2014
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198. New-Onset Atrial Fibrillation in Patients Hospitalized With COVID-19: Results From the American Heart Association COVID-19 Cardiovascular Registry.

Author

Rosenblatt, Anna G., Ayers, Colby R., Rao, Anjali, Howell, Stacey J., Hendren, Nicholas S., Zadikany, Ronit H., Ebinger, Joseph E., Daniels, James D., Link, Mark S., de Lemos, James A., and Das, Sandeep R.

Abstract

Background: New-onset atrial fibrillation (AF) in patients hospitalized with COVID-19 has been reported and associated with poor clinical outcomes. We aimed to understand the incidence of and outcomes associated with new-onset AF in a diverse and representative US cohort of patients hospitalized with COVID-19.Methods: We used data from the American Heart Association COVID-19 Cardiovascular Disease Registry. Patients were stratified by the presence versus absence of new-onset AF. The primary and secondary outcomes were in-hospital mortality and major adverse cardiovascular events (MACE; cardiovascular death, myocardial infarction, stroke, cardiogenic shock, and heart failure). The association of new-onset AF and the primary and secondary outcomes was evaluated using Cox proportional-hazards models for the primary time to event analyses.Results: Of the first 30 999 patients from 120 institutions across the United States hospitalized with COVID-19, 27 851 had no history of AF. One thousand five hundred seventeen (5.4%) developed new-onset AF during their index hospitalization. New-onset AF was associated with higher rates of death (45.2% versus 11.9%) and MACE (23.8% versus 6.5%). The unadjusted hazard ratio for mortality was 1.99 (95% CI, 1.81-2.18) and for MACE was 2.23 (95% CI, 1.98-2.53) for patients with versus without new-onset AF. After adjusting for demographics, clinical comorbidities, and severity of disease, the associations with death (hazard ratio, 1.10 [95% CI, 0.99-1.23]) fully attenuated and MACE (hazard ratio, 1.31 [95% CI, 1.14-1.50]) partially attenuated.Conclusions: New-onset AF was common (5.4%) among patients hospitalized with COVID-19. Almost half of patients with new-onset AF died during their index hospitalization. After multivariable adjustment for comorbidities and disease severity, new-onset AF was not statistically significantly associated with death, suggesting that new-onset AF in these patients may primarily be a marker of other adverse clinical factors rather than an independent driver of mortality. Causality between the MACE composites and AF needs to be further evaluated. [ABSTRACT FROM AUTHOR]

Published
2022
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199. Perceived Lifetime Risk for Cardiovascular Disease (from the Dallas Heart Study).

Author

Petr, Elisabeth Joye, Ayers, Colby R., Pandey, Ambarish, de Lemos, James A., Powell-Wiley, Tiffany M., Khera, Amit, Lloyd-Jones, Donald M., and Berry, Jarett D.

Subjects
*CARDIOVASCULAR diseases risk factors, *MYOCARDIAL infarction risk factors, *FAMILY history (Medicine), *LOGISTIC regression analysis, *PHYSIOLOGICAL stress
Abstract

Lifetime risk estimation for cardiovascular disease (CVD) has been proposed as a useful strategy to improve risk communication in the primary prevention setting. However, the perception of lifetime risk for CVD is unknown. We included 2,998 subjects from the Dallas Heart Study. Lifetime risk for developing CVD was classified as high (≥39%) versus low (<39%) according to risk factor burden as described in our previously published algorithm. Perception of lifetime risk for myocardial infarction was assessed by way of a 5-point scale. Baseline characteristics were compared across levels of perceived lifetime risk. Multivariable logistic regression analyses were performed to determine the association of participant characteristics with level of perceived lifetime risk for CVD and with correctness of perceptions. Of the 2,998 participants, 64.8% (n = 1,942) were classified as having high predicted lifetime risk for CVD. There was significant discordance between perceived and predicted lifetime risk. After multivariable adjustment, family history of premature myocardial infarction, high self-reported stress, and low perceived health were all strongly associated with high perceived lifetime risk (odds ratio [OR] 2.37, 95% confidence interval [CI] 1.72 to 3.27; OR 2.17, 95% CI 1.66 to 2.83; and OR 2.71, 95% CI 2.09 to 3.53; respectively). However, the association between traditional CVD risk factors and high perceived lifetime risk was more modest. In conclusion, misperception of lifetime risk for CVD is common and frequently reflects the influence of factors other than traditional risk factor levels. These findings highlight the importance of effectively communicating the significance of traditional risk factors in determining the lifetime risk for CVD. [ABSTRACT FROM AUTHOR]

Published
2014
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