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2. Impaired longitudinal systolic–diastolic coupling and cardiac response to exercise in patients with hypertrophic cardiomyopathy.

Author

MacNamara, James P., Turlington, William M., Dias, Katrin A., Hearon, Christopher M., Ivey, Erika, Delgado, Vincent A., Brazile, Tiffany L., Wakeham, Denis J., Turer, Aslan T., Link, Mark S., Levine, Benjamin D., and Sarma, Satyam

Subjects
LEFT heart ventricle, EXERCISE physiology, RESEARCH funding, EXERCISE therapy, HEART physiology, CARDIAC hypertrophy, TREATMENT effectiveness, DESCRIPTIVE statistics, AEROBIC capacity, CARDIOPULMONARY system, STROKE volume (Cardiac output), EXERCISE tests, OXYGEN consumption, DIASTOLE (Cardiac cycle), LEFT ventricular dysfunction, CARDIAC rehabilitation, REGRESSION analysis, DISEASE complications
Abstract

Background: In patients with hypertrophic cardiomyopathy (HCM), impaired augmentation of stroke volume and diastolic dysfunction contribute to exercise intolerance. Systolic–diastolic (S‐D) coupling characterizes how systolic contraction of the left ventricle (LV) primes efficient elastic recoil during early diastole. Impaired S‐D coupling may contribute to the impaired cardiac response to exercise in patients with HCM. Methods: Patients with HCM (n = 25, age = 47 ± 9 years) and healthy adults (n = 115, age = 49 ± 10 years) underwent a cardiopulmonary exercise testing (CPET) and echocardiogram. S‐D coupling was defined as the ratio of LV longitudinal excursion of the mitral annulus during early diastole (EDexc) and systole (Sexc) and compared between groups. Peak oxygen uptake (peak V̇O2) (Douglas bags), cardiac index (C2H2 rebreathe), and stroke volume index (SVi) were assessed during CPET. Linear regression was performed between S‐D coupling and peak V̇O2, peak cardiac index, and peak SVi. Results: S‐D coupling was lower in HCM (Controls: 0.63 ± 0.08, HCM: 0.56 ± 0.10, p < 0.001). Peak V̇O2 and stroke volume reserve were lower in patients with HCM (Peak VO2 Controls: 28.5 ± 5.5, HCM: 23.7 ± 7.2 mL/kg/min, p < 0.001, SV reserve: Controls 39 ± 16, HCM 30 ± 18 mL, p = 0.008). In patients with HCM, S‐D coupling was associated with peak V̇O2 (r = 0.47, p = 0.018), peak cardiac index (r = 0.60, p = 0.002), and peak SVi (r = 0.63, p < 0.001). Conclusion: Systolic–diastolic coupling was impaired in patients with HCM and was associated with fitness and the cardiac response to exercise. Inefficient S‐D coupling may link insufficient stroke volume generation, diastolic dysfunction, and exercise intolerance in HCM. [ABSTRACT FROM AUTHOR]

Published
2024
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3. Randomized Controlled Trial of Moderate‐ and High‐Intensity Exercise Training in Patients With Hypertrophic Cardiomyopathy: Effects on Fitness and Cardiovascular Response to Exercise

Author

MacNamara, James P., primary, Dias, Katrin A., additional, Hearon, Christopher M., additional, Ivey, Erika, additional, Delgado, Vincent A., additional, Saland, Sophie, additional, Samels, Mitchel, additional, Hieda, Michinari, additional, Turer, Aslan T., additional, Link, Mark S., additional, Sarma, Satyam, additional, and Levine, Benjamin D., additional

Published
2023
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4. Increases in Myocardial Workload Induced by Rapid Atrial Pacing Trigger Alterations in Global Metabolism

Author

Turer, Aslan T, Lewis, Gregory D, O'Sullivan, John F, Elmariah, Sammy, Mega, Jessica L, Addo, Tayo A, Sabatine, Marc S, de Lemos, James A, and Gerszten, Robert E

Subjects
Medical Biochemistry and Metabolomics, Analytical Chemistry, Biomedical and Clinical Sciences, Chemical Sciences, Cardiovascular, Heart Disease, Aetiology, 2.1 Biological and endogenous factors, Amino Acids, Angina Pectoris, Bile Acids and Salts, Carbohydrates, Cardiac Catheterization, Cardiac Pacing, Artificial, Comorbidity, Coronary Sinus, Female, Heart, Heterocyclic Compounds, Humans, Lipolysis, Male, Mass Spectrometry, Metabolic Syndrome, Metabolome, Middle Aged, Myocardial Contraction, Myocardial Ischemia, Smoking, Thyroid Hormones, Tryptophan Hydroxylase, General Science & Technology
Abstract

ObjectiveTo determine whether increases in cardiac work lead to alterations in the plasma metabolome and whether such changes arise from the heart or peripheral organs.BackgroundThere is growing evidence that the heart influences systemic metabolism through endocrine effects and affecting pathways involved in energy homeostasis.MethodsNineteen patients referred for cardiac catheterization were enrolled. Peripheral and selective coronary sinus (CS) blood sampling was performed at serial timepoints following the initiation of pacing, and metabolite profiling was performed by liquid chromatography-mass spectrometry (LC-MS).ResultsPacing-stress resulted in a 225% increase in the median rate·pressure product from baseline. Increased myocardial work induced significant changes in the peripheral concentration of 43 of 125 metabolites assayed, including large changes in purine [adenosine (+99%, p = 0.006), ADP (+42%, p = 0.01), AMP (+79%, p = 0.004), GDP (+69%, p = 0.003), GMP (+58%, p = 0.01), IMP (+50%, p = 0.03), xanthine (+61%, p = 0.0006)], and several bile acid metabolites. The CS changes in metabolites qualitatively mirrored those in the peripheral blood in both timing and magnitude, suggesting the heart was not the major source of the metabolite release.ConclusionsIsolated increases in myocardial work can induce changes in the plasma metabolome, but these changes do not appear to be directly cardiac in origin. A number of these dynamic metabolites have known signaling functions. Our study provides additional evidence to a growing body of literature on metabolic 'cross-talk' between the heart and other organs.

Published
2014

5. Aficamten for Drug-Refractory Severe Obstructive Hypertrophic Cardiomyopathy in Patients Receiving Disopyramide: REDWOOD-HCM Cohort 3

Author

Owens, Anjali T., primary, Masri, Ahmad, additional, Abraham, Theodore P., additional, Choudhury, Lubna, additional, Rader, Florian, additional, Symanski, John D., additional, Turer, Aslan T., additional, Wong, Timothy C., additional, Tower-Rader, Albree, additional, Coats, Caroline J., additional, Fifer, Michael A., additional, Olivotto, Iacopo, additional, Solomon, Scott D., additional, Watkins, Hugh C., additional, Heitner, Stephen B., additional, Jacoby, Daniel L., additional, Kupfer, Stuart, additional, Malik, Fady I., additional, Meng, Lisa, additional, Sohn, Regina, additional, Wohltman, Amy, additional, and Maron, Martin S., additional

Published
2023
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8. Phase 2 Study of Aficamten in Patients With Obstructive Hypertrophic Cardiomyopathy

Author

Maron, Martin S., primary, Masri, Ahmad, additional, Choudhury, Lubna, additional, Olivotto, Iacopo, additional, Saberi, Sara, additional, Wang, Andrew, additional, Garcia-Pavia, Pablo, additional, Lakdawala, Neal K., additional, Nagueh, Sherif F., additional, Rader, Florian, additional, Tower-Rader, Albree, additional, Turer, Aslan T., additional, Coats, Caroline, additional, Fifer, Michael A., additional, Owens, Anjali, additional, Solomon, Scott D., additional, Watkins, Hugh, additional, Barriales-Villa, Roberto, additional, Kramer, Christopher M., additional, Wong, Timothy C., additional, Paige, Sharon L., additional, Heitner, Stephen B., additional, Kupfer, Stuart, additional, Malik, Fady I., additional, Meng, Lisa, additional, Wohltman, Amy, additional, and Abraham, Theodore, additional

Published
2023
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22. Publication or presentation of results from multicenter clinical trials: Evidence from an academic medical center

Author

Turer, Aslan T., Mahaffey, Kenneth W., Compton, Kate L., Califf, Robert M., and Schulman, Kevin A.

Subjects
Medical centers, Clinical trials, Health
Abstract

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ahj.2007.01.005 Byline: Aslan T. Turer (a), Kenneth W. Mahaffey (a), Kate L. Compton (c)(d), Robert M. Califf (a)(d), Kevin A. Schulman (b)(c) Abstract: Nonpublication of research results threatens the integrity of clinical research, but the extent of nonpublication and factors associated with publication remain poorly documented. We sought to examine rates of publication or presentation of research findings from multicenter clinical trials and determine what factors are associated with dissemination of results. Author Affiliation: (a) Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, NC (b) Division of General Internal Medicine, Duke University Medical Center, Durham, NC (c) Center for Clinical and Genetic Economics, Duke University Medical Center, Durham, NC (d) Duke Clinical Research Institute, Duke University Medical Center, Durham, NC Article History: Received 3 October 2006; Accepted 9 January 2007

Published
2007

32. Enzyme estimates of infarct size correlate with functional and clinical outcomes in the setting of ST-segment elevation myocardial infarction

Author

Christenson Robert H, Weaver W Douglas, Gallup Dianne, Mahaffey Kenneth W, Turer Aslan T, Every Nathan R, and Ohman E Magnus

Subjects
Medicine (General), R5-920
Abstract

Abstract Background Cardiac biomarkers are routinely obtained in the setting of suspected myocardial ischemia and infarction. Evidence suggests these markers may correlate with functional and clinical outcomes, but the strength of this correlation is unclear. The relationship between enzyme measures of myocardial necrosis and left ventricular performance and adverse clinical outcomes were explored. Methods Creatine kinase (CK) and CK-MB data were analyzed, as were left ventricular ejection fraction (LVEF) by angiogram, and infarct size by single-photon emission computed tomography (SPECT) imaging in patients in 2 trials: Prompt Reperfusion In Myocardial-infarction Evolution (PRIME), and Efegatran and Streptokinase to Canalize Arteries Like Accelerated Tissue plasminogen activator (ESCALAT). Both trials evaluated efegatran combined with thrombolysis for treating acute ST-segment elevation myocardial infarction (STEMI). Results Peak CK and CK area-under-the-curve (AUC) correlated significantly with SPECT-determined infarct size 5 to 10 days after enrollment. Peak CK had a statistically significant correlation with LVEF, but CK-AUC and LVEF correlation were less robust. Statistically significant correlations exist between SPECT-determined infarct size and peak CK-MB and CK-MB AUC. However, there was no correlation with LVEF for peak CK-MB and CK-MB AUC. The combined outcome of congestive heart failure and death were significantly associated with CK AUC, CK-MB AUC, peak CK, and peak CK-MB measurements. Conclusion Peak CK and CK-MB values and AUC calculations have significant correlation with functional outcomes (LVEF- and SPECT-determined infarct size) and death or CHF outcomes in the setting of STEMI. Cardiac biomarkers provide prognostic information and may serve as valid endpoint measurements for phase II clinical trials.

Published
2005
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35. Myocardial ischemia induced by rapid atrial pacing causes troponin T release detectable by a highly sensitive assay: insights from a coronary sinus sampling study

Author

Turer, Aslan T., Addo, Tayo A., Martin, Justin L., Sabatine, Marc S., Lewis, Gregory D., Gerszten, Robert E., Keeley, Ellen C., Cigarroa, Joaquin E., Lange, Richard A., Hillis, L. David, and de Lemos, James A.

Subjects
Adult, Male, Cardiac Pacing, Artificial, Myocardial Ischemia, Coronary Artery Disease, Middle Aged, Risk Assessment, Sensitivity and Specificity, Severity of Illness Index, Article, Sampling Studies, Angina Pectoris, Troponin T, Humans, Biological Assay, Female, Biomarkers, Follow-Up Studies, Retrospective Studies
Abstract

The purpose of this study was to assess whether: 1) very small increases in troponin T, measured by a new highly sensitive cardiac troponin T (hs-cTnT), may reflect ischemia without necrosis; and 2) serial changes can discriminate ischemia from other causes of cardiac troponin T (cTnT) release.A new hs-cTnT assay offers greater sensitivity than current assays.Nineteen patients referred for diagnostic catheterization underwent cannulation of the coronary sinus (CS). Serial CS and peripheral plasma samples were obtained at multiple time points during and after incremental rapid atrial pacing. cTnT was quantified using both a standard and a pre-commercial highly sensitive assay. Ischemia was determined by the presence of significant coronary artery disease (CAD) and myocardial lactate release with pacing.cTnT concentrations in CS blood increased from a median of 6.8 pg/ml prior to pacing to 15.6 pg/ml 60 min after termination of rapid atrial pacing (p0.0001), changes that were mirrored at 180 min in peripheral blood (5.1 to 11.8 pg/ml, p0.0001). Although peripheral cTnT concentrations tended to be higher at 180 min following pacing for patients with CAD and lactate elution (n = 7) when compared with those without either marker (n = 5) (25.0 pg/ml vs. 10.2 pg/ml, p = 0.10), relative (1.7-fold vs. 5.2-fold) and absolute (6.8 pg/ml vs. 8.8 pg/ml, p = 0.50) changes were not different between groups.Brief periods of ischemia, without frank infarction, cause low-level cTnT release, and small increases are common after periods of increased myocardial work, even among patients without objective evidence of myocardial ischemia or obstructive CAD. Additional research is needed before hs-cTnT assays are widely adopted in the management of subjects with chest pain syndromes.

Published
2010

37. Body Fat Distribution and Incident Cardiovascular Disease in Obese Adults

Author

Neeland, Ian J., primary, Turer, Aslan T., additional, Ayers, Colby R., additional, Berry, Jarett D., additional, Rohatgi, Anand, additional, Das, Sandeep R., additional, Khera, Amit, additional, Vega, Gloria L., additional, McGuire, Darren K., additional, Grundy, Scott M., additional, and de Lemos, James A., additional

Published
2015
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38. Reply

Author

Chandra, Alvin, primary and Turer, Aslan T., additional

Published
2015
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39. Histone Deacetylase Inhibition Blunts Ischemia/Reperfusion Injury by Inducing Cardiomyocyte Autophagy

Author

Xie, Min, primary, Kong, Yongli, additional, Tan, Wei, additional, May, Herman, additional, Battiprolu, Pavan K., additional, Pedrozo, Zully, additional, Wang, Zhao V., additional, Morales, Cyndi, additional, Luo, Xiang, additional, Cho, Geoffrey, additional, Jiang, Nan, additional, Jessen, Michael E., additional, Warner, John J., additional, Lavandero, Sergio, additional, Gillette, Thomas G., additional, Turer, Aslan T., additional, and Hill, Joseph A., additional

Published
2014
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41. Characterization of a Novel Symptom of Advanced Heart Failure: Bendopnea

Author

Thibodeau, Jennifer T., primary, Turer, Aslan T., additional, Gualano, Sarah K., additional, Ayers, Colby R., additional, Velez-Martinez, Mariella, additional, Mishkin, Joseph D., additional, Patel, Parag C., additional, Mammen, Pradeep P.A., additional, Markham, David W., additional, Levine, Benjamin D., additional, and Drazner, Mark H., additional

Published
2014
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42. Inaccuracy of Estimated Resting Oxygen Uptake in the Clinical Setting

Author

Narang, Nikhil, primary, Thibodeau, Jennifer T., additional, Levine, Benjamin D., additional, Gore, M. Odette, additional, Ayers, Colby R., additional, Lange, Richard A., additional, Cigarroa, Joaquin E., additional, Turer, Aslan T., additional, de Lemos, James A., additional, and McGuire, Darren K., additional

Published
2014
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43. Association of prediabetes by fasting glucose and/or haemoglobin A1c levels with subclinical atherosclerosis and impaired renal function: Observations from the Dallas Heart Study

Author

Xing, Frank YF, primary, Neeland, Ian J, additional, Gore, M Odette, additional, Ayers, Colby R, additional, Paixao, Andre RM, additional, Turer, Aslan T, additional, Berry, Jarett D, additional, Khera, Amit, additional, de Lemos, James A, additional, and McGuire, Darren K, additional

Published
2013
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45. Relation of Regional Fat Distribution to Left Ventricular Structure and Function

Author

Neeland, Ian J., primary, Gupta, Sachin, additional, Ayers, Colby R., additional, Turer, Aslan T., additional, Rame, J. Eduardo, additional, Das, Sandeep R., additional, Berry, Jarett D., additional, Khera, Amit, additional, McGuire, Darren K., additional, Vega, Gloria L., additional, Grundy, Scott M., additional, de Lemos, James A., additional, and Drazner, Mark H., additional

Published
2013
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46. Associations of visceral and abdominal subcutaneous adipose tissue with markers of cardiac and metabolic risk in obese adults

Author

Neeland, Ian J., primary, Ayers, Colby R., additional, Rohatgi, Anand K., additional, Turer, Aslan T., additional, Berry, Jarett D., additional, Das, Sandeep R., additional, Vega, Gloria L., additional, Khera, Amit, additional, McGuire, Darren K., additional, Grundy, Scott M., additional, and de Lemos, James A., additional

Published
2013
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