tbuckley/cabot-search huggingface dataset:
Association of Early-Life Stress With Cytomegalovirus Infection in Adults With Major Depressive Disorder
Authors: Bart N. Ford, Robert H. Yolken, Robin L. Aupperle, T. Kent Teague, Michael R. Irwin, Martin P. Paulus, Jonathan Savitz
Journal: JAMA Psychiatry (2019)

Early-life stress is a well-established risk factor in the development of psychiatric disorders.Although the biological processes behind this association are unclear, there is evidence to suggest that early-life stress may lead to immune dysregulation. 1 One possibility is that early-life stress may impair adaptive immunity and, therefore, increase vulnerability to initial infection and subsequent reactivation of herpesviruses.Herpesviruses are potential immune-modifying agents that persist as latent infections and can reactivate during periods of stress.Initially believed to be benign except in cases of immunosuppression, cytomegalovirus (CMV) infection has been found to be associated with a range of negative outcomes, including depression, immunosenescence, neurodegenerative disorders, and reduced lifespan. 2 Given the prevalence of CMV infection (approximately 50% in the United States) and documented pathogenic effects, 2 we focused on CMV as a proof-of-principle test of the association between early-life stress and infectious disease in the context of depression.
MITOCHONDRIAL FISSION INHIBITOR AND FUSION PROMOTER ATTENUATE MYOCARDIAL INFARCTION AND LEFT VENTRICULAR DYSFUNCTION IN OBESE RATS WITH CARDIAC ISCHEMIA-REPERFUSION INJURY
Authors: Chayodom Maneechote, Siripong Palee, Sasiwan Kerdphoo, Thidarat Jaiwongkam, Siriporn Chattipakorn, Nipon Chattipakorn
Journal: Journal of the American College of Cardiology (2019)
Neuro-immune crosstalk and allergic inflammation
Authors: Hiroki Kabata, David Artis
Journal: Journal of Clinical Investigation (2019)

The neuronal and immune systems exhibit bidirectional interactions that play a critical role in tissue homeostasis, infection, and inflammation. Neuron-derived neuropeptides and neurotransmitters regulate immune cell functions, whereas inflammatory mediators produced by immune cells enhance neuronal activation. In recent years, accumulating evidence suggests that peripheral neurons and immune cells are colocalized and affect each other in local tissues. A variety of cytokines, inflammatory mediators, neuropeptides, and neurotransmitters appear to facilitate this crosstalk and positive-feedback loops between multiple types of immune cells and the central, peripheral, sympathetic, parasympathetic, and enteric nervous systems. In this Review, we discuss these recent findings regarding neuro-immune crosstalk that are uncovering molecular mechanisms that regulate inflammation. Finally, neuro-immune crosstalk has a key role in the pathophysiology of allergic diseases, and we present evidence indicating that neuro-immune interactions regulate asthma pathophysiology through both direct and indirect mechanisms.
PROCEDURAL OUTCOMES OF PERCUTANEOUS CORONARY INTERVENTIONS FOR CHRONIC TOTAL OCCLUSIONS IN PATIENTS WITH LOW LEFT VENTRICULAR EJECTION FRACTION: INSIGHTS FROM THE PROGRESS CTO REGISTRY
Authors: Peter Tajti, Dimitrios Karmpaliotis, Khaldoon Alaswad, Farouc Jaffer, Robert Yeh, Mitul Patel, Ehtisham Mahmud, James Choi, M. Nicholas Burke, Anthony Doing, Catalin Toma, Srinivasa Potluri, David Kandzari, Santiago Garcia, Oleg Krestyaninov, Dmitrii Khelimskii, Michalis Koutouzis, Jaikirshan Khatri, Wissam Jaber, Brian Jefferson, Allison Hall, Iosif Xenogiannis, Bavana Rangan, Subhash Banerjee, Emmanouil Brilakis
Journal: Journal of the American College of Cardiology (2019)
Abstract 1415: Activation of Soluble Guanylate Cyclase Regulates Phosphodiesterase 5A Localization and Restores Anti-adrenergic Action of Sildenafil despite Nitric Oxide Synthase Inhibition
Authors: Takahiro Nagayama, Manling Zhang, Eiki Takimoto, David A Kass
Journal: Circulation (2007)

Background: We have shown that inhibition of cyclic GMP-phosphodiesterase 5A (PDE5A) by sildenafil (SIL) blunts cardiomyocyte β-adrenergic stimulation, but this effect depends on the activity of endothelial nitric oxide synthase (eNOS) to generate a specific pool of cyclic GMP. PDE5A normally localizes at Z-bands in myocytes, but localization is more diffuse in cells with eNOS chronically inhibited. Here, we tested whether the influence of eNOS on PDE5A localization and anti-adrenergic action depends upon cyclic GMP. Methods and Results: Mouse in vivo hemodynamics were assessed by pressure-volume analysis. Isoproterenol (ISO: 20 ng/kg/min, iv ) stimulated contractility was inhibited by SIL (100 μg/kg/min, iv ), however this did not occur in mice given N w -nitro-L-arginine methyl ester (L-NAME: 1 mg/mL in drinking water for 1 week) to inhibit NOS. Myocytes transfected with an adenoviral vector encoding a fusion protein (PDE5A-DSred) in vivo were subsequently isolated and examined for PDE5A/α-actinin localization. Normal cells showed strong co-localization, whereas L-NAME-treated cells had diffuse PDE5A distribution. If L-NAME was stopped for 1-wk washout, SIL regained anti-adrenergic activity, and PDE5A z-band localization was restored. If L-NAME was continued but combined with Bay 41– 8543 (BAY: 30 mg/kg/day, po ), a soluble guanylate cyclase (sGC) activator, both PDE5A localization and SIL anti-adrenergic action were also restored. Chronic L-NAME suppressed phosphorylation of vasodilator-stimulated protein (VASP), a marker of protein kinase G (PKG) activity, in hearts acutely exposed to ISO+SIL. After L-NAME washout or L-NAME+BAY, VASP phosphorylation with ISO+SIL was restored. Conclusion: NOS-dependent modulation of both PDE5A sarcomere localization and anti-adrenergic activity depends upon sGC-derived cyclic GMP, and is linked to PKG activation. This suggests sGC activators may have synergistic effects with PDE5A inhibitors.
MODE OF DEATH IN HEART FAILURE WITH PRESERVED, MID-RANGE VERSUS REDUCED EJECTION FRACTION: INSIGHTS FROM KCHF REGISTRY
Authors: Takeshi Kitai, Hidenori Yaku, Takao Kato, Takeshi Morimoto, Neiko Ozasa, Erika Yamamoto, Yodo Tamaki, Yasutaka Inuzuka, Kazuya Nagao, Yutaka Furukawa, Takeshi Kimura
Journal: Journal of the American College of Cardiology (2019)
SHOULD ALL PATIENTS WITH OUT OF HOSPITAL CARDIAC ARREST BE TRANSFERRED TO A 24/7 PRIMARY PERCUTANEOUS CORONARY INTERVENTION CENTRE AND UNDERGO URGENT CORONARY ANGIOGRAPHY? EXPERIENCE OF A BUSY REGIONAL PRIMARY PERCUTANEOUS INTERVENTION CENTRE IN ENGLAND
Authors: Aish Sinha, Lucie Pearce, Chloe Thompson, Jane Fisher, Debkumar Pandit, Mark Snazelle, Paula Mota, Richard Heppell, Keyvan Kamalvand
Journal: Journal of the American College of Cardiology (2019)
IMPACT OF LEFT VENTRICULAR DIASTOLIC DYSFUNCTION ON OUTCOMES AFTER AORTIC VALVE REPLACEMENT
Authors: Rosalyn Adigun, Vidhu Anand, Christopher Kane, Patricia Pellikka, Vuyisile Nkomo, Sorin Pislaru, Kevin Greason, Jeremy Thaden, Cristina Pislaru
Journal: Journal of the American College of Cardiology (2019)
Abstract 15668: Abnormal Sinoatrial Node Pacemaker Activity Persists in Atrial-Specific Na+-Ca2+ Exchanger Knockout Mice
Authors: Angelo G Torrente, Jeffrey Seinfeld, Rui Zhang, Kenneth D Philipson, Joshua I Goldhaber
Journal: Circulation (2012)

Atrial-specific Na+-Ca2+ exchanger (NCX1) KO mice live into adulthood with mild cardiac hypertrophy but have no P waves on the surface electrocardiogram (ECG) and instead depend upon a junctional rhythm. This raises the possibility that the sinoatrial (SA) node relies exclusively upon the “calcium clock” for pacemaker activity. To further test this hypothesis, we used high speed laser scanning confocal microscopy to examine Ca2+ handling in a tissue preparation of either the isolated SA or Atrioventricular (AV) nodes perfused with modified Tyrodes solution at 20oC. Slow and irregular spontaneous Ca2+ transients indicative of depolarization were present in the NCX1 KO SA node (47 ± 14 bpm in KO versus 86 ± 6 bpm in WT). When challenged by isoproterenol (ISO, 100 nM) the NCX1 KO SA node often responded with burst activity indicating an ability to respond to β-adrenergic stimulation despite the absence of NCX1. Surprisingly, we found no evidence of spontaneous transients in AV node tissue isolated from the N...
EFFICACY OF A TECHNOLOGY-ENABLED, HOME-BASED CARDIAC REHABILITATION PROGRAM
Authors: Clare McDermott, Ciara McCormack, Jomme Claes, Luari McDermott, Orlagh O'Shea, Roselien Buys, Noel O'Connor, Noel McCaffrey, Davide Susta, Alison Sheerin, Anne Gallagher, Ivan Casserly, Helen Newton, Brendan Mcadam, Catherine Woods, Veronique Cornelissen, Kieran Moran, Niall Moyna
Journal: Journal of the American College of Cardiology (2019)
Comparison of National Institutes of Health Grant Amounts to First-Time Male and Female Principal Investigators
Authors: Diego F. M. Oliveira, Yifang Ma, Teresa K. Woodruff, Brian Uzzi
Journal: JAMA (2019)

This Research Letter examines differences in the size of National Institutes of Health (NIH) grants awarded to first-time male and female principal investigators at top research institutions, including the Big Ten and Ivy League universities.
Abstract 529: Asporin - Extracellular Matrix Protein Mitigates Pathological Remodeling
Authors: Honit Piplani, Ankush Sharma, Chengqun Huang, Jon Sin, Juliana de Freitas Germano, Robert M Mentzer, Allen M Andres, Roberta A Gottlieb
Journal: Circulation Research (2018)

The cardiac extracellular matrix is a complex network of proteins and plays a key role in cardiac remodeling after myocardial infarction. One of the extracellular matrix proteins, asporin, is a member of the SLRP family and inhibits TGFβ signaling. However, very little is known about the function and regulation of asporin in cardiac remodeling. Using bioinformatics approach, microarray data analysis from publicly available datasets identified asporin as a top candidate showing an increase in left ventricle tissue with ischemic cardiomyopathy as compared to control donor hearts. To confirm, we detected an increase in asporin expression in paired heart biopsies taken before and after cardiopulmonary bypass surgery by western blot analysis. Our group showed that glucagon like receptor 1 agonist (GLP-1Ra) is beneficial for cardiac remodeling and prevents fibrosis. In a permanent coronary artery ligation model, we found increased extracellular asporin expression after 30 days in border zone and scar area with GLP-1Ra treatment compared to vehicle-treatment. To further elucidate the mechanism of asporin secretion, we used H9c2 cells as well as left ventricle tissue from mice and found that asporin was predominantly present in the heavy membrane enriched fraction (8,000xg pellet from postnuclear supernatant). Sequence analysis of asporin protein using SecretomeP 2.0 server predicted asporin might use the non-conventional form of secretion (secretory autophagy). Differentiation of H9c2 cells is accompanied by autophagy and mitochondrial biogenesis, and we found that the abundance of asporin in total lysate and heavy membrane fraction decreased suggesting it could be released via secretory autophagy. Using recombinant human asporin, we demonstrated that asporin stimulates an increase in LC3 and p62 in parallel to a decrease in COX IV and SMAD2 phosphorylation, indicating mitophagy induction and a decrease in TGFβ signaling. Based on our preliminary data and sequence comparison to a previously reported human peptide, we developed a rodent asporin peptide which is predicted to induce mitophagy while decreasing TGFβ signaling to prevent fibrosis. Studies are ongoing to establish the clinical relevance of asporin in animal models of ischemic injury.
SURGICAL CORRECTION OF CHEST WALL DEFORMITY IN PECTUS EXCAVATUM IMPROVES LEFT VENTRICULAR MECHANICAL DYSSYNCHRONY AND RIGHT VENTRICULAR FUNCTION: A TEE SPECKLE TRACKING STRAIN IMAGING STUDY
Authors: Noweeda N. Mirza, Dawn Jaroszewski, Michael B. Gotway, Tasneem Z. Naqvi
Journal: Journal of the American College of Cardiology (2019)
TRENDS AND OUTCOMES OF CARDIAC AMYLOIDOSIS RELATED HOSPITALIZATIONS IN THE UNITED STATES: ANALYSIS OF THE NATIONAL INPATIENT SAMPLE DATABASE FROM 2006 THROUGH 2014
Authors: Abhishek Chaturvedi, Jeanine M. Buchanich, Chenxin Yang, Qi Gao, Parul Chandrika, Tarun Sharma, Mario Castagnaro, Srinivas Murali, Raymond Benza, Azam Hadi, Robert Biederman, Indu Poornima, Craig Alpert
Journal: Journal of the American College of Cardiology (2019)
ABSOLUTE AORTIC SIZE BUT NOT INDEXED AORTIC SIZE PREDICTS LATE OUTCOMES FOR FEMALES UNDERGOING MEDICAL MANAGEMENT OF TYPE B DISSECTION
Authors: Neal Foley, Mark Peterson, Melissa Levack, Raffi Bekeredjian, Alan Braverman, Davide Pacini, Marek Ehrlich, Derek Brinster, Kevin Harris, Stuart Hutchison, Christina Fanola, Firas F. Mussa, Daniel Montgomery, Christoph Nienaber, Eric Isselbacher, Thomas Gleason, Kim Eagle
Journal: Journal of the American College of Cardiology (2019)
PROGNOSTIC POWER OF CARDIOPULMONARY EXERCISE TEST TO PREDICT HEART FAILURE EVENTS IN PATIENTS WITH TRANSPOSITION OF THE GREAT ARTERIES
Authors: António Amadeu Valentim Gonçalves, Tania Mano, Ana Agapito, Lídia de Sousa, Jose Alberto, Andre Viveiros Monteiro, Sílvia Aguiar Rosa, Rui Cruz Ferreira
Journal: Journal of the American College of Cardiology (2019)
Abstract 292: Mitochondrial CLIC4 and CLIC5B Mediate Cardio-protection From Ischemia/reperfusion Injury
Authors: Devasena Ponnalagu, Neel J Patel, Erhe Gao, Walter J Koch, Andrew R Kohut, Harpreet Singh
Journal: Circulation Research (2018)

Mitochondria are important for regulating myocardial physiology, cardiac function and cardio-protection from ischemia/reperfusion injury (IR). Cation channels like BK Ca and K ATP present in the cardiac mitochondria are important in reducing myocardial infarction (MI) upon IR injury. Mitochondrial anion channels are equally important as they regulate cell volume, maintain ionic homeostasis during ischemia and are considered as potential therapeutics for cardiac diseases. However, molecular identity of cardiac mitochondrial chloride channels is not yet elucidated. In this study we focus on unique class of dimorphic ion channels known as chloride intracellular channels (CLICs). Amongst the six paralogs in mammals, we found that CLIC1, CLIC4 and CLIC5 are abundant in heart isolated from R. norvegicus . CLIC4 and CLIC5 localize to the mitochondria whereas CLIC1 in endoplasmic reticulum. CLIC4 and CLIC5 localized to the outer and inner mitochondrial membrane (IMM), respectively, and modulate mitochondrial calcium retention capacity and reactive oxygen species (ROS) production. Interestingly, a splice variant CLIC5B predominantly present in the heart of R. norvegicus was responsible for IMM localization and its function. We also observed that CLICs are cardioprotective as blocking them with its inhibitor IAA-94 increased MI both in in vitro and in vivo IR injury assays . In addition, we performed left main descending coronary artery (LCA) occlusion in clic -/- and wild type (Wt) mice to induce IR injury. LCA was occluded for 40 min prior to 24 h of reperfusion. MI was significantly higher in clic4 -/- mice as compared to Wt mice (58±6 vs 42±2, n≥4, p≤0.05). Only 75% (3 of 4) of clic4 -/- mice showed significant reduction in left ventricular ejection (LVEF) fraction and fractional shortening (LVFS) after in vivo IR injury. Interestingly, 50% (3 of 6) of clic5 -/- mice showed significant increased MI as well as decreased LVEF and LVFS after in vivo IR injury. Clic1 -/- mice showed similar MI and left ventricular function as Wt mice. In conclusion, we demonstrate that cardiac mitochondrial CLIC4 and CLIC5 are vital for cardioprotection from IR injury likely by maintaining the calcium homeostasis and ROS generation by the mitochondria, respectively.
SUBGROUP ANALYSIS OF LONG-TERM BLOOD PRESSURE REDUCTION IN THE GLOBAL SYMPLICITY REGISTRY
Authors: Felix Mahfoud, Giuseppe Mancia, Roland Schmieder, Krzysztof Narkiewicz, Luis Ruilope, Markus Schlaich, Bryan Williams, Robert Whitbourn, Andreas Zirlik, Thomas Zeller, Martin Fahy, Michael Boehm
Journal: Journal of the American College of Cardiology (2019)
Abstract 361: Analysis of Cardiotoxic Mechanisms Associated With Tyrosine Kinase Inhibitor Ponatinib
Authors: Anand P Singh, Michael S Glennon, Prachi P Umbarkar, Manisha Gupte, Cristi L Galindo, Qinkun Zhang, Thomas Force, Jason R Becker, Hind Lal
Journal: Circulation Research (2018)

Background: Ponatinib, a potent pan-BCR-ABL tyrosine kinase inhibitor (TKI) holds significant promise in the treatment of chronic myelogenous leukemia (CML), although the potential cardiotoxicity of this agent remains a concern. In order to overcome ponatinib associated cardiotoxicity, delineation of linked cardiotoxic mechanisms and potential rescue methods are urgently warranted. Objectives: The objectives of the present study were to delineate the signaling mechanisms responsible for ponatinib-induced cardiotoxicity and to identify the potential rescue strategies. Methods: In this study, we employed direct in vivo drug screening in zebrafish for the prediction of cardiotoxicity. We also exploited neonatal rat ventricular myocytes (NRVMs) to explore cardiotoxic mechanism associated with ponatinib. Results: We observed that ponatinib leads to cardiomyocyte apoptosis, elevation in BNP level, decrease in heart rate and fractional shortening leading to cardiac dysfunction in Zebrafish. Consistently, in cultured rat cardiomyocytes, ponatinib was found most cytotoxic drug among all the approved CML TKIs. Mechanistically, ponatinib inhibits the essential prosurvival AKT and ERK signaling pathway, resulting to cardiomyocyte apoptosis. Interestingly, we evaluated the cardioprotective effects of Neuregulin-1β to limit ponatinib toxicity. Neuregulin-1β treatment significantly protects ponatinib-induced cardiotoxicity by supplementing the essential cardiomyocyte prosurvival AKT/ERK signaling pathways. Additionally, the allosteric tyrosine kinase inhibitor asciminib depicts less pronounced cardiotoxic effects than ponatinib in similar settings. Conclusions: This study will advance our mechanistic understanding of ponatinib-induced cardiotoxicity, accelerate the discovery of cardioprotective strategies to prevent and rescue the ponatinib-induced cardiotoxicity. Furthermore, this study suggests asciminib as an alternate treatment option than ponatinib for patients suffering from CML with T315I “gatekeeper” mutation.
OXIDATIVE STRESS-DIASTOLIC FUNCTION RELATIONSHIPS IN WOMEN WITH ISCHEMIA AND NO OBSTRUCTIVE CORONARY ARTERY DISEASE
Authors: Ahmed AlBadri, Michael D. Nelson, Omeed Elboudwarej, Janet Wei, Puja Mehta, Jenna Maughan, Louise Thomson, Arshed Quyyumi, Carl J. Pepine, C. Noel Bairey Merz
Journal: Journal of the American College of Cardiology (2019)
RISK OF PULMONARY HYPERTENSION IN HIV INFECTED PATIENTS IN A SINGLE CENTER IN MIAMI: A RETROSPECTIVE ANALYSIS
Authors: Gerardo J. Zablah, Fahim Pyarali, Roumen Iordanov, Tahir Haque, Rajiv Parmar, Alexis Powell, Catherine Boulanger, Dushyantha Jayaweera, Barry Hurwitz, Michael Kolber, Claudia Martinez
Journal: Journal of the American College of Cardiology (2019)
Oncolytic viruses: overcoming translational challenges
Authors: Jordi Martinez-Quintanilla, Ivan Seah, Melissa Chua, Khalid Shah
Journal: Journal of Clinical Investigation (2019)

Oncolytic virotherapy (OVT) is a promising approach in which WT or engineered viruses selectively replicate and destroy tumor cells while sparing normal ones. In the last two decades, different oncolytic viruses (OVs) have been modified and tested in a number of preclinical studies, some of which have led to clinical trials in cancer patients. These clinical trials have revealed several critical limitations with regard to viral delivery, spread, resistance, and antiviral immunity. Here, we focus on promising research strategies that have been developed to overcome the aforementioned obstacles. Such strategies include engineering OVs to target a broad spectrum of tumor cells while evading the immune system, developing unique delivery mechanisms, combining other immunotherapeutic agents with OVT, and using clinically translatable mouse tumor models to potentially translate OVT more readily into clinical settings.
Diagnostic accuracy and safety of 16α-[18F]fluoro-17β-oestradiol PET-CT for the assessment of oestrogen receptor status in recurrent or metastatic lesions in patients with breast cancer: a prospective cohort study
Authors: Sun Young Chae, Sei Hyun Ahn, Sung-Bae Kim, Sangwon Han, Suk Hyun Lee, Seung Jun Oh, Sang Ju Lee, Hee Jeong Kim, Beom Seok Ko, Jong Won Lee, Byung Ho Son, Jisun Kim, Jin-Hee Ahn, Kyung Hae Jung, Jeong Eun Kim, Seog-Young Kim, Woo Jung Choi, Hee Jung Shin, Gyungyub Gong, Hyo Sang Lee, Jung Bok Lee, Dae Hyuk Moon
Journal: The Lancet Oncology (2019)
USING THE CHA2DS2-VASC SCORE TO PREDICT ISCHEMIC STROKE IN PATIENTS WITH INTRACEREBRAL HEMORRHAGE: A NATIONWIDE COHORT STUDY
Authors: Peter Brønnum Nielsen, Thure Filskov Overvad, Flemming Skjøth, Søren Due Andersen, Mette Søgaard, Torben Bjerregaard Larsen, Gregory Y.H. Lip
Journal: Journal of the American College of Cardiology (2019)
NOW YOU SEE ME, NOW YOU DON'T: HIGH-DOSE TISSUE PLASMINOGEN ACTIVATOR FOR MECHANICAL MITRAL VALVE THROMBOSIS AND CARDIOEMBOLIC MYOCARDIAL INFARCTION IN THE SETTING OF CATASTROPHIC ANTIPHOSPHOLIPID ANTIBODY SYNDROME
Authors: Michael Hart, Mengistu Simegn, Gautam Shroff, Bradley Bart, Christina Thaler, Charles Herzog, Louis Kohl, Woubeshet Ayenew
Journal: Journal of the American College of Cardiology (2019)
Pediatric LSC3 (pLSC3) Score Derived from DNMT3B-CD34-GPR56 As a Prognostic Tool to Predict AML Patient Outcome: Results from Two Independent Pediatric AML Cohorts
Authors: Abdelrahman H Elsayed, Huiyun Wu, Xueyuan Cao, Susana C. Raimondi, James R. Downing, Raul Ribeiro, Tanja A. Gruber, Jeffrey Rubnitz, Stanley Pounds, Jatinder K Lamba
Journal: Blood (2018)
EPIGENETIC EFFECT OF DIABETES ON CODING AND NON-CODING PLATELET TRANSCRIPTOME IN ACUTE CORONARY SYNDROME
Authors: Maria Chiara Grimaldi, Iacopo Fabiani, Paolo Aretini, Giovanna Liuzzo, Larosa Giulio, Massimo Volpe, Filippo Crea, Luigi Biasucci
Journal: Journal of the American College of Cardiology (2019)
Randomized Trial of a Tailored Cognitive Behavioral Intervention in Type 2 Diabetes With Comorbid Depressive and/or Regimen-Related Distress Symptoms: 12-Month Outcomes From COMRADE
Authors: Doyle M. Cummings, Lesley D. Lutes, Kerry Littlewood, Chelsey Solar, Marissa Carraway, Kari Kirian, Shivajirao Patil, Alyssa Adams, Stefanie Ciszewski, Sheila Edwards, Peggy Gatlin, Bertha Hambidge
Journal: Diabetes Care (2019)

OBJECTIVE This study evaluated the effect of cognitive behavioral therapy (CBT) plus lifestyle counseling in primary care on hemoglobin A1c (HbA1c) in rural adult patients with type 2 diabetes (T2D) and comorbid depressive or regimen-related distress (RRD) symptoms. RESEARCH DESIGN AND METHODS This study was a randomized controlled trial of a 16-session severity-tailored CBT plus lifestyle counseling intervention compared with usual care. Outcomes included changes in HbA1c, RRD, depressive symptoms, self-care behaviors, and medication adherence across 12 months. RESULTS Patients included 139 diverse, rural adults (mean age 52.6 ± 9.5 years; 72% black; BMI 37.0 ± 9.0 kg/m2) with T2D (mean HbA1c 9.6% [81 mmol/mol] ± 2.0%) and comorbid depressive or distress symptoms. Using intent-to-treat analyses, patients in the intervention experienced marginally significant improvements in HbA1c (−0.92 ± 1.81 vs. −0.31 ± 2.04; P = 0.06) compared with usual care. However, intervention patients experienced significantly greater improvements in RRD (−1.12 ± 1.05 vs. −0.31 ± 1.22; P = 0.001), depressive symptoms (−3.39 ± 5.00 vs. −0.90 ± 6.17; P = 0.01), self-care behaviors (1.10 ± 1.30 vs. 0.58 ± 1.45; P = 0.03), and medication adherence (1.00 ± 2.0 vs. 0.17 ± 1.0; P = 0.02) versus usual care. Improvement in HbA1c correlated with improvement in RRD (r = 0.3; P = 0.0001) and adherence (r = −0.23; P = 0.007). CONCLUSIONS Tailored CBT with lifestyle counseling improves behavioral outcomes and may improve HbA1c in rural patients with T2D and comorbid depressive and/or RRD symptoms.