tbuckley/cabot-search huggingface dataset:
Abstract 393: Is High Grade Atrioventricular Block Reversible in Hypothyroidism
Authors: Nnamdi A Nwafo
Journal: Circulation Research (2018)

Background: Hypothyroidism is considered a reversible cause of atrioventricular block (AVB) but rigorous studies to support this are limited. An important consideration in clinical practice is whether pacemaker placement should be deferred in patients with hypothyroidism who present with high degree AV block while awaiting reversal of block. This period of waiting places patients at risk of morbidity and mortality, while extending length of stay and cost of care. Objective: To evaluated if high degree AVB in hypothyroidism is in fact reversible, and therefore justify delaying pacemaker(PM) placement. Method: Retrospective review of all adult admission with high degree (Mobitz type II or type III) AVB admitted to a Regional hospital over a 10 year period. Out of 271 cases identified, 41 had hypothyroidism (either prior history or newly diagnosed), and were matched by age and sex with 41 patients with AVB but without hypothyroidism. Each group of 41 patients had 25 females (61%) and 16 men (39%). Placement of PM is assumed to indicate lack of reversibility of AVB. Statistic analysis for matched pairs was by McNemar’s test with Yates continuity correction. Results: In the hypothyroidism group, 31 of 41 patients(76%) received PM, while 34 of 41 patients (83%) in the group without hypothyroidism received PM. The calculated test statistic was 12.02, and when referred to the Chi-squared distribution table with 1 degree of freedom, gives a probability of &lt; 0.01, which is highly significant. 14 of the 41 patients(34%) with hypothyroidism had thyroid dysfunction based on thyroid hormone levels, with 10(24%) having sub-clinical hypothyroidism, and 4 (10%) having overt disease. The mean duration in days from time of admission to time of PM placement in the hypothyroidism group was 4.35, while that in the group without hypothyroidism was 2.26. Conclusion: The finding rejects the null hypothesis that there is no difference in need for PM (and thus reversibility of AVB) in both groups, suggesting AVB may in fact be reversible in hypothyroidism. Larger and more rigorous studies are therefore warranted to definitively determine if AVB in hypothyroidism is reversible, and adopt delaying PM placement while awaiting reversal, as standard of care.
The motor protein Myo1c regulates transforming growth factor-β–signaling and fibrosis in podocytes
Authors: Ehtesham Arif, Ashish K. Solanki, Pankaj Srivastava, Bushra Rahman, Brian R. Tash, Lawrence B. Holzman, Michael G. Janech, René Martin, Hans-Joachim Knölker, Wayne R. Fitzgibbon, Peifeng Deng, Milos N. Budisavljevic, Wing-Kin Syn, Cindy Wang, Joshua H. Lipschutz, Sang-Ho Kwon, Deepak Nihalani
Journal: Kidney International (2019)
ORBITAL ATHERECTOMY FOR TREATMENT OF SEVERELY CALCIFIED CORONARY ARTERY BIFURCATION LESIONS: A MULTICENTER ANALYSIS
Authors: Robert Sturm, Ehrin Armstrong, Eisha Gupta, Naotaka Okamoto, Yuliya Vengrenyuk, Evan Shlofmitz, George Revtyak, Brad Martinsen, Ann Behrens, Javier Valle, Stephen Waldo, Baran Aksut, Sean Bell, Ryan Gardner, Michael Lee, Ramzan Zakir, Adhir Shroff, Creighton Don, Richard Shlofmitz, Jeffrey Chambers, Annapoorna Kini, Samin Sharma
Journal: Journal of the American College of Cardiology (2019)
Abstract 107: The Mevalonate Pathway Controls Cardiomyocyte Proliferation
Authors: James E Hudson
Journal: Circulation Research (2018)

Induction of cardiomyocyte proliferation is emerging as a promising strategy for heart regeneration. Using a recently developed human cardiac organoid system, we have recently discovered a small molecule (Compound 6.28) that inhibits both GSK3 and MST1 and drives robust proliferation (Mills et al., PNAS, 2017). However, chronic stimulation with this compound also causes a decline in contractile function, which would prevent its use as a therapeutic. We have now performed quantitative proteomics of 50 individual organoids under different conditions to de-convolute the effects of GSK3 and MST1 on the pro-proliferative response. GSK3 inhibition was found to be responsible for a cell cycle network whereas MST1 inhibition activated the mevalonate pathway; the detrimental functional effects were specifically associated with inhibition of GSK3. An additional screen of 105 compounds was performed to identify new compounds that could activate proliferation in human cardiac organoids without detrimental effects on functionality. We identified a compound targeting p38, which activated a similar cell cycle network to GSK3, and another compound targeting TGFBR/ACVR/BMPR, which activated the mevalonate pathway similar to MST1 inhibition. A strong synergistic pro-proliferative response was observed when both of these compounds were combined, without any detrimental effects on cardiac function. The pro-proliferative effect could be blocked by inhibition of β-catenin using ICRT14 or inhibition of the mevalonate pathway using a statin. In addition, we provide RNA-seq data revealing large scale transcriptional changes in the mevalonate pathway during heart maturation in vivo and demonstrate that blocking the mevalonate pathway in immature cardiomyocytes reduces proliferation. By re-supplementing different metabolites in the mevalonate pathway, a specific function for the prenylation branch of this metabolic pathway for proliferation was identified and direct inhibition of a downstream kinase activated by Rho prenylation, ROCK, also lead to a reduction in proliferation. Our results reveal a novel role for the mevalonate pathway in cardiomyocyte proliferation and suggest that inhibition of this pathway occurs during postnatal heart maturation.
PREDICTORS OF INTENSIVE CARE UNIT (ICU) UTILIZATION AMONG PATIENTS WITH ST-SEGMENT MYOCARDIAL INFARCTION: INSIGHTS FROM THE BLUE CROSS BLUE SHIELD OF MICHIGAN CARDIOVASCULAR CONSORTIUM (BMC2)
Authors: Ahmad Abdul-Aziz, Devraj Sukul, Milan Seth, Hitinder Gurm
Journal: Journal of the American College of Cardiology (2019)
IMPACT OF DIABETES MELLITUS ACROSS GENDER AND RACE ON OUTCOMES AFTER EVEROLIMUS-ELUTING STENT IMPLANTATION: FROM THE PLATINUM DIVERSITY AND THE PROMUS ELEMENT PLUS POST-APPROVAL STUDIES
Authors: Ridhima Goel, Wayne Batchelor, Bimmer Claessen, Paul Guedeney, David Kandzari, Melissa Aquino, Scott Davis, Luis Tami, John Wang, Islam Othman, Osvaldo Gigliotti, Amir Haghighat, Sarabjeet Singh, Mario Lopez, Gregory Giugliano, Phillip Horwitz, Paul Underwood, Dominic Allocco, Ian Meredith, Roxana Mehran
Journal: Journal of the American College of Cardiology (2019)
CHARACTERISTICS AND OUTCOMES OF PATIENTS WITH CARDIOGENIC SHOCK COMPLICATED BY ACUTE KIDNEY INJURY REQUIRING HEMODIALYSIS
Authors: Oluwole Adegbala, Chakradhari Inampudi, Emmanuel Akintoye, Razan Elsayed, Christina Jara, Karlene Williams, Dinesh Voruganti, Luis Afonso, Alexandros Briasoulis
Journal: Journal of the American College of Cardiology (2019)
Abstract 559: AMP-Activated Protein Kinase And Estrogen-Dependent Mechanisms Underlying Increased Susceptibility To Cardiovascular Disease During Menopause
Authors: Marissa A Pier, John Konhilas
Journal: Circulation Research (2018)

According to the CDC (2017), more women than men have died from heart disease over the last 20-25 years. Yet, premenopausal women are protected against heart and cardiovascular disease (CVD) compared to age-matched men. The cellular and molecular mechanisms underlying the transition from premenopause/perimenopause (CVD-resistance) to postmenopause (CVD-susceptible) in women is unknown and is the focus of this project. The critical barrier impeding translational progress is the lack of appropriate models to study menopause. Most studies have used surgical removal of ovaries (ovariectomy) as a model of menopause; yet this technique poorly recapitulates the natural, physiological transition to menopause that 90% of women experience. We overcome this barrier with administration of the chemical, 4-vinylcyclohexene diepoxide (VCD), where we can mirror progressive ovarian failure and preserve the critical “perimenopause” transitional period, identical to humans. Using this model, we demonstrate that perimenopausal , like cycling (premenopausal) females, are protected from pathological angiotensin II (Ang II)-induced cardiac remodeling, while menopausal females are not. Our novel finding that perimenopausal females remain protected, despite irregular cycling (prior to complete loss of estrogen), underscores the importance of studying the role of estrogen in CVD, across the transition from perimenopause to menopause. Multiple molecular, genetic and cellular mechanisms have been suggested to underlie protection against CVD in non-cycling females, many of which put estrogen as the key mediator. We discovered that one of these pathways, the adenosine monophosphate-activated kinase (AMPK) signaling axis, is activated by estrogen through direct binding of estrogen receptors to the α-catalytic subunit of AMPK. Taken together with our published and preliminary data, we hypothesis that loss of AMPK signaling is responsible for the exacerbated pathological cardiac remodeling in menopause (see Fig.). To date, there are no studies that have tested the ability of AMPK activation to mitigate menopausal susceptibility to CVD. Aim: Determine if AMPK is necessary and/or sufficient to impart protection against pathological cardiac remodeling in menopausal females. Rationale: We discovered that AMPK signaling is severely disabled during menopause where females are more susceptible to CVD. Using the VCD mouse model of menopause, we will determine if protection against Ang II-induced cardiac remodeling during menopause is AMPK-dependent. Summary: We plan to determine the cellular and molecular mechanisms in premenopausal and perimenopausal females that prevent associated cardiovascular morbidities; and determine the underlying shift that gives rise to increased susceptibility to CVD in menopausal females.
ATRESIA OF THE CORONARY SINUS OSTIUM WITH ANOMALOUS DRAINAGE INTO INNOMINATE VEIN: CARDIAC RESYNCHRONIZATION THERAPY AND IMPLICATIONS
Authors: Syed Rafay Ali Sabzwari, Lohit Garg, Fnu Vikram, Nikhil Mehta, Hiwot Ayele, Nghia Hoang
Journal: Journal of the American College of Cardiology (2019)
1-YEAR RESULTS OF TRANSCATHETER AORTIC VALVE REPLACEMENT IN EXTREMELY LARGE ANNULI &gt;683 MM2 WITH EDWARDS SAPIEN 3 VALVE: A MULTICENTER EXPERIENCE
Authors: Syed Zaid, Norihiko Kamioka, Juan Terre, Masaki Miyasaka, Sameer Hirji, Mark Hensey, Nadim Geloo, George Petrossian, Newell Robinson, Eric Sarin, Sung-Han Yoon, Isaac George, Tsuyoshi Kaneko, Pinak Shah, Kapil Sharma, Molly Szerlip, Creighton Don, Hasan Ahmad, Annapoorna Kini, Michael Mack, John Webb, Vasilis Babaliaros, Susheel Kodali, Raj Makkar, Gilbert Tang
Journal: Journal of the American College of Cardiology (2019)
Risk Factors for Retinopathy in Type 1 Diabetes: The DCCT/EDIC Study
Authors: Dean P. Hainsworth, Ionut Bebu, Lloyd P. Aiello, William Sivitz, Rose Gubitosi-Klug, John Malone, Neil H. White, Ronald Danis, Amisha Wallia, Xiaoyu Gao, Andrew J. Barkmeier, Arup Das, Shriji Patel, Thomas W. Gardner, John M. Lachin
Journal: Diabetes Care (2019)

OBJECTIVE The Diabetes Control and Complications Trial (DCCT) demonstrated that intensive therapy reduced the development and progression of retinopathy in type 1 diabetes (T1D) compared with conventional therapy. The Epidemiology of Diabetes Interventions and Complications (EDIC) study observational follow-up showed persistent benefits. In addition to glycemia, we now examine other potential retinopathy risk factors (modifiable and nonmodifiable) over more than 30 years of follow-up in DCCT/EDIC. RESEARCH DESIGN AND METHODS The retinopathy outcomes were proliferative diabetic retinopathy (PDR), clinically significant macular edema (CSME), and ocular surgery. The survival (event-free) probability was estimated using the Kaplan-Meier method. Cox proportional hazards models assessed the association between risk factors and subsequent risk of retinopathy. Both forward- and backward-selection approaches determined the multivariable models. RESULTS Rate of ocular events per 1,000 person-years was 12 for PDR, 14.5 for CSME, and 7.6 for ocular surgeries. Approximately 65%, 60%, and 70% of participants remained free of PDR, CSME, and ocular surgery, respectively. The greatest risk factors for PDR in descending order were higher mean HbA1c, longer duration of T1D, elevated albumin excretion rate (AER), and higher mean diastolic blood pressure (DBP). For CSME, risk factors, in descending order, were higher mean HbA1c, longer duration of T1D, and greater age and DBP and, for ocular surgeries, were higher mean HbA1c, older age, and longer duration of T1D. CONCLUSIONS Mean HbA1c was the strongest risk factor for the progression of retinopathy. Although glycemic control is important, elevated AER and DBP were other modifiable risk factors associated with the progression of retinopathy.
RIGHT VENTRICULAR PRESSURE IS ASSOCIATED WITH POST-LEFT VENTRICLE ASSIST DEVICE IMPLANTATION CHANGES IN DIFFUSION CAPACITY OF LUNGS FOR CARBON MONOXIDE (DLCO)
Authors: Pavol Sajgalik, Chul-Ho Kim, Saki Ito, Brian Lahr, Courtney Wheatley, Sudhir Kushwaha, John Stulak, Alfredo Clavell, Bruce Johnson, John Schirger
Journal: Journal of the American College of Cardiology (2019)
Placental 11β-HSD2 and Cardiometabolic Health Indicators in Infancy
Authors: Lu Chen, Julie Guilmette, Zhong-Cheng Luo, Anik Cloutier, Wen-Juan Wang, Meng-Nan Yang, William D. Fraser, Josée Dubois, Anne Monique Nuyt
Journal: Diabetes Care (2019)

OBJECTIVE Fetal excessive exposure to glucocorticoids may program cardiometabolic risk. Placental 11 β-hydroxysteroid dehydrogenase 2 (11β-HSD2) serves as a barrier to prevent fetal overexposure to maternal glucocorticoids. It has not been explored whether placental 11β-HSD2 levels are associated with cardiometabolic health in postnatal life. RESEARCH DESIGN AND METHODS In a prospective birth cohort study of 246 mother-infant pairs, we measured placental 11β-HSD2 expression and maternal (32–35 weeks of gestation) and cord plasma cortisol concentrations. The primary outcomes were HOMA of insulin resistance (IR) and blood pressure (BP) in infants at age 1 year. Other outcomes included fasting insulin, HOMA β-cell function, carotid intima-media thickness, weight z score, and skinfold thickness (triceps and subscapular) at age 1 year. RESULTS Placental 11β-HSD2 expression was negatively correlated with HOMA-IR (r = −0.17, P = 0.021) and fasting insulin (r = −0.18, P = 0.017) and marginally negatively correlated with systolic BP (r = −0.16, P = 0.057) but was not correlated with HOMA of β-cell function, diastolic BP, carotid intima-media thickness, and skinfold thickness (all P &amp;gt; 0.1) in infants at age 1 year. Cord plasma cortisol was negatively correlated to skinfold thickness (r = −0.20, P = 0007) but was not correlated with other outcomes at age 1 year. Maternal plasma cortisol was positively correlated with maximal carotid intima-media thickness (r = 0.20, P = 0.03) but was not correlated with other outcomes. Adjusting for maternal and infant characteristics, the associations were similar. CONCLUSIONS The study is the first to show that higher placental 11β-HSD2 expression is associated with lower IR in infancy. Independent cohort studies are required to confirm this novel finding.
INDEX OF MICROCIRCULATORY RESISTANCE AS A PREDICTOR OF CARDIAC OUTCOMES IN PATIENTS WITH ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION UNDERGOING PRIMARY CORONARY INTERVENTION: A VALIDATION STUDY IN REAL-WORLD CLINICAL PRACTICE
Authors: Takayuki Onishi, Yuko Onishi, Isshi Kobayashi, Yasuhiro Sato, Akihiro Niwa
Journal: Journal of the American College of Cardiology (2019)
Abstract 11738: A Genome-wide Association Analysis Identifies PDE1ADNAJC10 Locus on Chromosome 2 Associated With Idiopathic Pulmonary Arterial Hypertension in the Japanese Population
Authors: Mai Kimura, Yuichi Tamura, Makoto Takei, Kenjiro Kosaki, Nobuhiro Tanabe, Koichiro Tatsumi, Tsutomu Saji, Tsutomu Saji, Toru Satoh, Shigeo Kamitsuji, Naoyuki Kamatani, Motoaki Sano, Keiichi Fukuda
Journal: Circulation (2015)

Background: Idiopathic pulmonary arterial hypertension (IPAH) is a rare but fatal disease with a mean survival period estimated to be around 3 years if not treated. Although many familial cases of IPAH exhibit an autosomal dominant mode of inheritance with the majority having mutations in BMPR2, the penetrance is low with an estimated lifetime risk of 20 %. To explain the low penetrance of IPAH associated with BMPR2 mutations, it was hypothesized that other genetic loci as well as environmental factors play roles. Purpose: To identify genetic factors associated with IPAH with/ without BMPR2 mutation, we conducted a genome-wide association study (GWAS) followed by a validation study. Methods and Results: We performed GWAS in the Japanese population comprising a total of 44 individuals with IPAH and 2,993 controls. The IPAH cases were identified at three major pulmonary hypertension centers in Japan. The controls consisted of 2,002 and 991 healthy Japanese individuals, which were collected at two different times by Japan PGx Data Science Consortium (JPDSC). At first, we conducted discovery GWAS to identify SNPs related to the disease, comparing 23 cases with IPAH (first set) and 2,002 controls at 1,347,690 SNPs, and identified 8 loci each of which had more than one SNP with P values under 10-5. We then attempted to validate the associations observed in the discovery phase using 21 patients (second set) and 991 controls who were independent of the samples used in the discovery GWAS. In the validation study, we examined the associations of 9 SNPs at 8 loci, and only 2 SNPs at one locus showed significant association. And finally, we identified a novel susceptibility locus PDE1A
Abstract 437: Tyrosine Phosphorylation: Regulator of Cardiac Contraction
Authors: Elizabeth A Brundage, Brendan Agatisa-Boyle, Vikram Shettigar, Mark Y Jeong, Hussam E Salhi, Jae-Hoon Chung, Ziqing Qian, Paul M Janssen, Dehua Pei, Jonathan P Davis, Mark T Ziolo, Brandon J Biesiadecki
Journal: Circulation Research (2018)

Myocardial contractile function is depressed in heart failure. Contractile function of the normal and failing heart is in part determined by kinase mediated serine/threonine phosphorylation. While non-receptor tyrosine specific kinases are expressed in the heart and their activity is increased in disease, the role of tyrosine kinase signaling to modulate cardiac contraction is unknown. Previous work demonstrated the cardiac contractile regulatory protein troponin I (TnI) is phosphorylated at tyrosine 26 (Tyr26). Subsequently, we demonstrated TnI Tyr26 phosphorylation alters myofilament function thereby identifying the first tyrosine phosphorylation to directly modulate cardiac contraction. The role of TnI Tyr26 phosphorylation in the normal or diseased heart and the signaling pathways responsible for its phosphorylation are unknown. To identify the kinase responsible for TnI Tyr26 phosphorylation and its effect on in vivo heart function, we generated a novel tyrosine kinase activator and a TnI Tyr26 phosphorylation (Tg Y26E) mouse. Biochemical kinase assays and kinase activation in ventricular myocytes identify Src family kinases as sufficient to induce TnI Tyr26 phosphorylation. Tg Y26E mice exhibit decreased myofilament calcium sensitivity and accelerated relaxation. Finally, we demonstrate TnI Tyr26 phosphorylation is increased during in vivo myocardial ischemia when Src family tyrosine kinases are also activated. Together these data support targeting Src family tyrosine kinase and TnI Tyr26 phosphorylation to improve heart function in myocardial ischemia and the failing heart.
MSC-derived sEVs enhance patency and inhibit calcification of synthetic vascular grafts by immunomodulation in a rat model of hyperlipidemia
Authors: Yongzhen Wei, Yifan Wu, Runxia Zhao, Kaiyue Zhang, Adam C. Midgley, Deling Kong, Zongjin Li, Qiang Zhao
Journal: Biomaterials (2019)
A PRAGMATIC APPROACH TO RISK ASSESSMENT IN PULMONARY ARTERIAL HYPERTENSION USING THE ESC/ERS GUIDELINES
Authors: Alessandra Manes, Fabio Dardi, Massimiliano Palazzini, Enrico Gotti, Andrea Rinaldi, Elisa Zuffa, Gerardo Vito Lo Russo, Daniele Guarino, Alessandro De Lorenzis, Filippo Pasca, Ilenia Magnani, Mariangela Rotunno, Nazzareno Galiè
Journal: Journal of the American College of Cardiology (2019)
Abstract 487: Arginine Methylation Through PRMT5 Mediates Energy Stress-Induced Autophagy in the Heart
Authors: Risa Mukai, Toshiro Saito, Peiyong Zhai, Junichi Sadoshima
Journal: Circulation Research (2018)

Autophagy is a mechanism of bulk degradation of organelles and proteins that protects cells against stress by maintaining cellular homeostasis. Although autophagy is known to be an adaptive mechanism against stress, how autophagy is activated in cardiomyocytes (CMs) during stress is not fully understood. The ATG proteins, which are required for autophagy, are modulated by post-translational modifications (PTMs) such as phosphorylation, ubiquitination, and acetylation. The level of arginine methylation, another form of PTM, is altered in the heart in response to stress. However, the role of arginine methylation in regulating autophagy is poorly understood in CMs. We postulated that arginine methylation may play an important role in the regulation of autophagy. The level of arginine methylation was significantly increased (1.52-fold, p&lt;0.05) in CMs subjected to glucose deprivation (GD) for 6 hours compared to those without GD. Expression of protein arginine methyltransferases (PRMTs), including PRMT5, was also increased at both the mRNA and protein levels (1.6- and 1.72-fold, p&lt;0.05) in the mouse heart in response to 48 hours of starvation. Energy stress-induced autophagy, as evaluated with LC3-II and p62, was inhibited when PRMT5 function was downregulated. Increased arginine methylation was also observed in the mouse heart in response to 1 hour of myocardial ischemia (1.87-fold, p&lt;0.01), which was accompanied by upregulation of PRMT5 (1.54-fold, p&lt;0.05). These results suggest that arginine methylation mediated through PRMT5 may play an important role in mediating autophagy during energy stress, such as starvation and ischemia, in the heart.
RELATIONSHIP OF CORONARY ATHEROSCLEROSIS, CORONARY LUMEN, AND CORONARY ISCHEMIA: RESULTS FROM THE PROSPECTIVE, MULTICENTER, INTERNATIONAL CREDENCE TRIAL
Authors: Inge J. van den Hoogen, Alexander van Rosendael, Jung Hyun Choi, So-Yeon Choi, Joon-Hyung Doh, Ae-Young Her, Bon-Kwon Koo, Chang-Wook Nam, Jason Cole, Alessia Gimelli, Muhammad Khan, Faisal Nabi, Ryo Nakazato, U. Joseph Schoepf, Randall Thompson, Hyuk-Jae Chang, Philippe Genereux, Paul Knaapen, Gianluca Pontone, Wijnand Stuijfzand, Fay Lin, Leslee J. Shaw, James Min
Journal: Journal of the American College of Cardiology (2019)
Mutational Landscape of the Transcriptome Offers a Rich Neoantigen Resource for Immunotherapy of Myeloproliferative Neoplasms
Authors: Fiorella Schischlik, Roland Jäger, Felix Rosebrock, Eva Hug, Michael Schuster, Raimund Holly, Elisabeth Fuchs, Jelena D. Milosevic Feenstra, Edith Bogner, Bettina Gisslinger, Martin Schalling, Elisa Rumi, Daniela Pietra, Gottfried Fischer, Ingrid Faé, Vulliard Loan, Jörg Menche, Torsten Haferlach, Manja Meggendorfer, Anna Stengel, Christoph Bock, Mario Cazzola, Heinz Gisslinger, Robert Kralovics
Journal: Blood (2018)
Abstract 15911: Bleeding is a Major Cause of Early Readmission After Percutaneous Coronary Intervention Among Patients on Oral Anticoagulant Therapy
Authors: Mahesh K Vidula, Cian McCarthy, Eric A Secemsky, Kevin F Kennedy, Neel M Butala, Jason H Wasfy, Robert W Yeh
Journal: Circulation (2017)

Introduction: The causes of early readmission after percutaneous coronary intervention (PCI) among patients on oral anticoagulant (OAC) therapy are not well characterized. We hypothesized that pati...
HISTOLOGICAL FEATURES OF THE ATRIA IN PATIENTS WITH MIXED MITRAL VALVULAR HEART IN SINUS RHYTHM AND ATRIAL FIBRILLATION
Authors: Deepak Padmanabhan, Bharat Banavalikar, Maneesh Rai, G. Kamalapurkar, S.R. Kalpana, Jayaprakash Shenthar
Journal: Journal of the American College of Cardiology (2019)