tbuckley/cabot-search huggingface dataset:
Increased Chronic Obstructive Pulmonary Disease Exacerbations of Likely Viral Etiology Follow Elevated Ambient Nitrogen Oxides
Authors: Paul E. Pfeffer, Gavin C. Donaldson, Alex J. Mackay, Jadwiga A. Wedzicha
Journal: American Journal of Respiratory and Critical Care Medicine (2018)

Rationale: Epidemiologic research strongly supports an association between air pollution and chronic obstructive pulmonary disease exacerbations. Numerous mechanisms may underlie any association because pollutants are toxic to pulmonary cells and may increase susceptibility to respiratory infections. The relationship between ambient pollution and exacerbation etiology has not been studied.Objectives: To evaluate the characteristics of pollution-associated exacerbations and whether the association is specific to exacerbations of infective or noninfective etiology.Methods: We analyzed the effect of preceding ambient particulate matter less than or equal to 10 μm in aerodynamic diameter, oxides of nitrogen (NOx), and ozone on characterized chronic obstructive pulmonary disease exacerbations in a regression model adjusted for temperature, seasonality, and long-term trend. We specifically examined associations with exacerbations of suspected viral and/or bacterial, or noninfective etiology. For the associations identified we further examined the characteristics of pollution-associated exacerbations.Measurements and Main Results: A total of 4,173 exacerbations occurred over the 20-year study period. Higher ambient NOx was consistently associated with increased viral-type exacerbations at 2–4 days lag (P = 0.010). Recovery for viral-type exacerbations after higher ambient NOx was significantly prolonged. These findings were consistent in the subset of 2,841 exacerbations treated with oral corticosteroids or antibiotics, with recovery 1.29 (95% confidence interval, 1.17–1.42; P < 0.001) times longer with viral-type exacerbations of onset 3 days after above- versus below-median ambient NOx. A likely bimodal association of particulate matter less than or equal to 10 μm in aerodynamic diameter with infective exacerbations was also evident and supported by a daily time-series analysis.Conclusions: Higher levels of ambient NOx are associated with prolonged exacerbations of likely viral etiology, supporting toxicologic effects of air pollution that increase susceptibility to, and severity of, infection.
IN PATIENTS WITH ATHEROSCLEROTIC CARDIOVASCULAR DISEASE, HIGH STATIN ADHERENCE OVER 5 YEARS OF FOLLOW-UP IS ASSOCIATED WITH IMPROVED CARDIOVASCULAR OUTCOMES: RESULTS FROM THE IMPRES STUDY
Authors: Heidi Thomas May, Kirk Knowlton, Jeffrey Anderson, Donald Lappe, Tami Bair, J. Muhlestein
Journal: Journal of the American College of Cardiology (2019)
Abstract 460: Diabetes Impairs Reparative Property of Bone Marrow-derived Endothelial Progenitor Cells: Role of Mir-499-mediated Hydrogen Sulfide Deficiency
Authors: Zhongjian Cheng, Venkata NS Garikipati, Suresh K Verma, May Trungcao, Chunlin Wang, Maria Cimini, David Goukassian, Raj Kishore
Journal: Circulation Research (2018)

Background: miR-499 has been considered as a potential biomarker for myocardial infarction. Overexpression of miR-499 impaired heart function and induced cardiac hypertrophy in mice. Recent studies suggested miR-499 suppresses tumor growth through the inhibition of vascular endothelial growth factor (VEGF) mediated angiogenesis. Furthermore, emerging evidences indicate that miR-499 is increased in heart of diabetic rodents and patients. Here, we tested the hypotheses that miR-499 impairs angiogenic ability of endothelial cells (ECs) under diabetic conditions. Methods and Results: miR-499 levels were examined in endothelial progenitor cells (EPCs), microvascular endothelial cells (MVECs) and plasma in diabetic db/db mice (8-week, male). Gender- and age-matched non-diabetic db/+ mice served as controls. EPCs were isolated from bone marrow density-gradient centrifugation. MVECs were isolated using collagenase. We found that miR-499 levels were significantly increased in EPCs, MVECs as well as plasma of db/db mice. miR-499 antagomiR rescued high glucose (25 mM D-glucose for 48 h)-impaired tube formation and migration of human cardiac microvascular endothelial cells (HCMVECs). Mechanistically, by luciferase assay, we found that miR-499 directly targets cystathionine γ-lyase (CSE), a major hydrogen sulfide (H 2 S)-synthesizing enzyme in cardiovascular cells. Overexpression of miR-499 by transfection of miR-499 mimics decreased CSE protein levels and intracellular H 2 S production in HCMVECs. Conclusions: Our results suggest that miR-499-induced CSE downregulation/inactivation thus H 2 S reduction may play an important role in diabetes-impaired angiogenic capacity. Silencing miR-499 in diabetic EPCs/ECs may provide a novel tool for the treatment of ischemic tissue injury in patients with diabetes.
PREOPERATIVE RISK FACTOR-BASED CARDIAC CATHETERIZATION IS ASSOCIATED WITH LOW CARDIAC MORBIDITY AND MORTALITY IN LIVER TRANSPLANT PATIENTS
Authors: Issa Kutkut, Rayan Jo Rachwan, Patrick Bourdillon, Lava Timsina, Marwan Ghabril, Chandrashekhar Kubal, Marco Lacera, Richard Mangus
Journal: Journal of the American College of Cardiology (2019)
REDUCTION IN LDL-CHOLESTEROL IS ASSOCIATED WITH REGRESSION OF CORONARY PLAQUE AMONG CHINESE INDIVIDUALS
Authors: Junjie Yang, Xi Wang, Guanhua Dou, Dongkai Shan, Jing Jing, Peter Stone, Yundai Chen, Marcelo Di Carli, Ron Blankstein
Journal: Journal of the American College of Cardiology (2019)
Management of vertebral radiotherapy dose in paediatric patients with cancer: consensus recommendations from the SIOPE radiotherapy working group
Authors: Bianca A Hoeben, Christian Carrie, Beate Timmermann, Henry C Mandeville, Lorenza Gandola, Karin Dieckmann, Monica Ramos Albiac, Henriette Magelssen, Yasmin Lassen-Ramshad, Barbora Ondrová, Thankamma Ajithkumar, Claire Alapetite, Brian V Balgobind, Stephanie Bolle, Alison L Cameron, Raquel Davila Fajardo, Stefan Dietzsch, Delphine Dumont Lecomte, Marry M van den Heuvel-Eibrink, Rolf D Kortmann, Anne Laprie, Patrick Melchior, Laetitia Padovani, Barbara Rombi, Giovanni Scarzello, Rudolf Schwarz, Klaus Seiersen, Enrica Seravalli, Nicola Thorp, Gillian A Whitfield, Tom Boterberg, Geert O Janssens
Journal: The Lancet Oncology (2019)
LONG TERM OUTCOMES OF THE ABSORB BIORESORBABLE VASCULAR SCAFFOLD VERSUS SECOND GENERATION DRUG ELUTING STENT: A META-ANALYSIS
Authors: Sunny Goel, Ravi Teja, Elina Zakin, Srilekha Chava, Abhishek Sharma, Bilal Malik, Sergey Ayzenberg, Robert Frankel, Jacob Shani, Umesh Gidwani
Journal: Journal of the American College of Cardiology (2019)
PREDICTIVE VALUE OF A MULTILEVEL CLASSIFICATION SYSTEM FOR VENTILATORY EFFICIENCY IN PATIENTS WITH PRESERVED LEFT VENTRICULAR EJECTION FRACTION
Authors: Jingyi Gong, Renata R.T. Castro, Jesse P. Caron, Jon Hainer, Alexander Opotowsky, Bradley Maron, Marcelo Di Carli, John Groarke
Journal: Journal of the American College of Cardiology (2019)
TREATMENT-BLINDED MEDICATION TITRATION FOR HYPERTENSION CONTROL FOLLOWING RANDOMIZATION TO ENDOVASCULAR ULTRASOUND RENAL DENERVATION OR A SHAM PROCEDURE
Authors: Michel Azizi, Roland Schmieder, Felix Mahfoud, Michael Weber, Joost Daemen, Melvin Lobo, Andrew Sharp, Jan Basile, Yale Wang, Manish Saxena, Lida Feyz, Florian Rader, Philipp Lurz, Jeremy Sayer, Ajay Kirtane
Journal: Journal of the American College of Cardiology (2019)
Sustained B cell depletion by CD19-targeted CAR T cells is a highly effective treatment for murine lupus
Authors: Rita Kansal, Noah Richardson, Indira Neeli, Saleem Khawaja, Damian Chamberlain, Marium Ghani, Qurat-ul-ain Ghani, Louisa Balazs, Sarka Beranova-Giorgianni, Francesco Giorgianni, James N. Kochenderfer, Tony Marion, Lorraine M. Albritton, Marko Radic
Journal: Science Translational Medicine (2019)

CD19-targeted CAR T cells show sustained CD19 + B cell depletion and profound therapeutic benefit in ameliorating disease in mouse models of lupus.
Parental alcohol misuse has major effects on children’s health and development
Authors: Shabeer Syed, Ruth Gilbert
Journal: BMJ (2019)

The new guidelines on fetal alcohol spectrum disorder by the Scottish Intercollegiate Guidelines Network emphasise the importance of reducing alcohol use during pregnancy.1 But fetal alcohol spectrum disorder is one part of a larger problem. Parental alcohol misuse affects children across the life course. It often goes unnoticed and impairs parenting, with major effects on children’s health and development. …
Abstract 425: A Pro-reductive Redox State Protects the Myocardium From Isoproterenol-Induced Pathological Remodeling in Nrf2 Transgenic Mouse
Authors: Gobinath Shanmugam, Anil Kumar Challa, Silvio H Litovsky, Jolyn Fernandes, Dean P Jones, Rajasekaran Namakkal-Soorappan
Journal: Circulation Research (2018)

Background: Nuclear factor (erythroid-derived 2)-like 2 (NEFL2/Nrf2) is an inducible transcription factor that is crucial to fight against stress caused by various means (i.e. oxidative or xenobiotic stresses). While the Nrf2 has a negligible role on regulating the basal transcription of antioxidant and cytoprotective genes, its activation in response to stress is indispensable. Here, we hypothesize that augmentation of myocardial Nrf2, through transgene expression, will protect the myocardium from isoproterenol-induced pathological remodeling. Methods: Cardiac specific Nrf2 transgenic (Nrf2-Tg) and non-transgenic (NTg) litter mates in the C57/BL6 background were subjected to isoproterenol (ISO) treatment (50 mg/kg bw/day, for 7 days), and assessed the myocardial structure, function (Echocardiography) and Nrf2-dependent defense mechanisms. Results: Severe infarction and fibrosis along with increased inflammation leading to myocardial dysfunction in NTg mice exposed to ISO, but the Nrf2-TG hearts were found to be resistant to ISO insult. Suppression of infarction and protection of myocardial structure and function in the Nrf2-Tg mice could be attributed to a pro-reductive condition displayed in these hearts. In particular, ISO administration resulted in an excessive generation of reactive oxygen species and oxidation of proteins along with significant downregulation of antioxidant genes (p&lt;0.05)and their proteins lead to myocardial damage in NTg mice. Of note, myocardium of ISO-treated TG mice displayed significantly reduced protein oxidation and comparable levels of antioxidant genes and proteins (p&lt;0.05) in relation to PBS-treated NTg mice. Taken together, it is suggested that a pre-existing pro-reductive redox milieu is likely to combat ISO-induced oxidative stress, thereby protecting the myocardium from pathological remodeling. Conclusion: Thus, we conclude that a modest trans-activation of the global antioxidant defense system might have therapeutic potential than either targeting single antioxidant (i.e. SOD or catalase or GPX) or supplementation of antioxidant combos to protect the myocardium in response to stress.
ROUTINE VERSUS SMART PHONE APPLICATION BASED - INTENSE FOLLOW-UP OF PATIENTS WITH ACUTE CORONARY SYNDROME UNDERGOING PERCUTANEOUS CORONARY INTERVENTION: IMPACT ON CLINICAL OUTCOMES AND PATIENT SATISFACTION
Authors: Satyavir Yadav, Rishi Sethi, Akshyaya Pradhan, Pravesh Vishwakarma, Sharad Chandra, Gaurav Chaudhary, Sudhanshu Dwivedi, Varun Narain, Monika Bhandari, Akhil Sharma
Journal: Journal of the American College of Cardiology (2019)
Efficacy of primary treatment with immunoglobulin plus ciclosporin for prevention of coronary artery abnormalities in patients with Kawasaki disease predicted to be at increased risk of non-response to intravenous immunoglobulin (KAICA): a randomised controlled, open-label, blinded-endpoints, phase 3 trial
Authors: Hiromichi Hamada, Hiroyuki Suzuki, Yoshihiro Onouchi, Ryota Ebata, Masaru Terai, Shigeto Fuse, Yoshitomo Okajima, Shunji Kurotobi, Katsuki Hirai, Takashi Soga, Yukiko Ishiguchi, Yoshiaki Okuma, Nobuyuki Takada, Masaaki Yanai, Junichi Sato, Mami Nakayashiro, Mamoru Ayusawa, Eiichi Yamamoto, Yuichi Nomura, Yuya Hashimura, Kazunobu Ouchi, Hiroshi Masuda, Shinichi Takatsuki, Keiichi Hirono, Tadashi Ariga, Takashi Higaki, Akio Otsuki, Moe Terauchi, Reiko Aoyagi, Takatoshi Sato, Yasuhisa Fujii, Tadami Fujiwara, Hideki Hanaoka, Akira Hata, Hiromichi Hamada, Takafumi Honda, Kumi Yasukawa, Katsuki Hirai, Nishihara Takahiro, Takashi Soga, Hideoki Yajima, Hideyasu Ooto, You Umeda, Hiroyuki Suzuki, Takashi Takeuchi, Tomohiro Suenaga, Nobuyuki Kakimoto, Yukiko Ishiguchi, Masahiro Kamada, Yoshiaki Okuma, Nobuyuki Takada, Shinichi Suwabe, Masaaki Yanai, Yasushi Ueno, Natsuko Nishi, Junichi Sato, Yuuko Saito, Yutaka Kitani, Mami Nakayashiro, Taisuke Nabeshima, Kiyotaka Takefuta, Mamoru Ayusawa, Takahiro Nakamura, Akiko Komori, Masataka Kato, Ryota Ebata, Naoki Saito, Kentaro Okunushi, Hironobu Kobayashi, Eiichi Yamamoto, Takeshi Nakano, Yuichi Nomura, Kiminori Masuda, Yuya Hashimura, Hirotaka Minami, Takamichi Uchiyama, You Okizuka, Kazunobu Ouchi, Naoki Ohno, Satoko Ogita, Hiroshi Masuda, Hiroshi Ono, Akira Ishiguro, Shinichi Takatsuki, Tsutomu Saji, Fukiko Ichida, Keiichi Hirono, Sayaka Ozawa, Tadashi Ariga, Atsuhito Takeda, Gaku Izumi, Takashi Higaki, Akio Otsuki, Akira Hata, Hideki Hanaoka, Hiroyuki Suzuki, Masaru Terai, Hiromichi Hamada, Yoshihiro Onouchi, Ryota Ebata, Moe Terauchi, Yasuhisa Fujii, Takatoshi Sato, Reiko Aoyagi, Michiko Hanawa, Tadami Fujiwara, Shigeto Fuse, Yoshitomo Okajima, Shunji Kurotobi
Journal: The Lancet (2019)
ANTITHROMBOTIC THERAPY AND CARDIOVASCULAR RISK IN PATIENTS WITH ATRIAL FIBRILLATION AT HIGH RISK FOR THROMBOEMBOLIC EVENTS AFTER TRANSCATHETER AORTIC VALVE REPLACEMENT: FROM THE PARTNER 2 TRIAL
Authors: Ioanna Kosmidou, Mahesh Madhavan, Yangbo Liu, Maria Alu, Angelo Biviano, Tarun Chakravarty, Raj Makkar, Vinod Thourani, Susheel Kodali, Martin Leon
Journal: Journal of the American College of Cardiology (2019)
COMPUTER-AIDED DETECTION AND IDENTIFICATION OF IMPLANTED CARDIAC DEVICES ON CHEST RADIOGRAPHY UTILIZING DEEP CONVOLUTIONAL NEURAL NETWORKS, A FORM OF MACHINE LEARNING
Authors: Michael Weinreich, Brian Weinreich, Jay J. Chudow, Talia Krumerman, Kusha Rahgozar, Tonusri Nag, Eric Shulman, John Fisher, Kevin J. Ferrick
Journal: Journal of the American College of Cardiology (2019)
Abstract 544: Gja1-20k Uses the Actin Cytoskeleton to Promote Both Mitochondrial Fission and Fusion
Authors: Daisuke Shimura, Rachel Baum, Shaohua Xiao, TingTing Hong, Robin M Shaw
Journal: Circulation Research (2018)

Connexin (Cx) 43 is encoded by the GJA1 gene and GJA1-20k has been identified as an N-terminal truncation of Cx43 generated endogenously by internal translation initiation in heart and other organs. We’ve previously identified that GJA1-20k, which increases with ischemic injury, can organize actin networks and also is strongly co-localized with mitochondria, utilizing the cytoskeleton to preserve mitochondrial distribution during stress. Mitochondrial distribution and morphology are associated with metabolic function, and thus we are interested in how GJA1-20k affects mitochondrial shape and connectivity. We transfected GFP-tagged GJA1-20k plasmids into HEK293T cells and assessed mitochondrial distribution and morphology by fluorescence microscopy. Mitochondria exposed to GJA1-20k are smaller, more circular, and more distributed than mitochondria exposed to a control plasmid. Quantitative image analysis indicates an increase in mitochondrial count but no increase in mitochondrial area, indicating greater mitochondrial fission in the presence of GJA1-20k. Paradoxically, acute disruption of actin with Latrunculin A decreased mitochondrial count, yet increased mitochondrial area, indicating acute fusion. Mitochondrial fusion was also observed by live cell imaging, and with high doses of GJA1-20k. Latrunculin A did not affect mitochondrial morphology in cells without GJA-20k. Together these data suggest that GJA1-20k, a mitochondrial and actin associated scaffold, has multiple effects on mitochondrial morphology. At baseline GJA1-20k promotes mitochondrial-actin association, promoting fission and cellular distribution. Yet, GJA1-20k also promotes mitochondrial membrane-membrane association that, in the presence of actin disruption, resulting in mitochondrial fusion. These data suggest GJA1-20k not only organizes mitochondria under physiologic conditions, but during ischemia, it promotes mitochondrial fusion, enhancing tissue survival during stress.
Abstract 583: Cardiac Compensation In ErbB2-deficient Zebrafish Embryos
Authors: Nicole D Fleming, Leigh A Samsa, David Hassel, Li Qian, Jiandong Liu
Journal: Circulation Research (2018)

Congenital heart diseases are a leading birth defect in infants and often feature structural malformations that arise during embryogenesis. Over the course of development, the cardiac chambers undergo extensive morphogenetic changes to optimize their myoarchitecture for efficient conduction and contraction, most notably is the formation of luminal, muscular protrusions called trabeculae within the ventricle. Altered trabeculation is associated with congenital heart diseases, and failure to form trabeculae is embryonic lethal. We have previously reported that ErbB2 signaling plays a direct and essential role in cardiac trabeculation, and erbb2 mutant hearts develop progressive cardiac dysfunction with reduced fractional shortening, and eventually fail. However, the mechanism underlying this functional deterioration in the absence of trabecular formation is not known. In this study, we found that the trabeculae-deficient erbb2 mutant exhibited increased ventricular cardiomyocyte cross-sectional area and myofibril size, a phenotype reminiscent of that of an adult mammalian heart subjected to mechanical overload. Consistently, inhibition of Target of Rapamycin (TOR) signaling by rapamycin suppressed erbb2 mutant hypertrophic-like (HL) growth phenotype. Additional studies suggest the erbb2 mutant HL phenotypes are due to a loss of cardiac trabeculae. We thus propose that trabeculae serve to enhance contractility and that defects in this process lead to wall-stress induced pathological hypertrophic remodeling.
TAVR DURABILITY AND OUTCOMES IN PATIENTS WITH FAILED SURGICAL BIOPROSTHESES: THREE-YEAR RESULTS FROM THE COREVALVE US EXPANDED USE STUDY
Authors: Harold Dauerman, Jeffrey Popma, G. Michael Deeb, Daniel O'Hair, Ron Waksman, Steven Yakubov, Shuzhen Li, Michael Reardon
Journal: Journal of the American College of Cardiology (2019)
RISK OF DEVELOPING ACUTE KIDNEY INJURY ON THE ECMO CIRCUIT IN PATIENTS WITH ACUTE DECOMPENSATED HEART FAILURE
Authors: Manivannan Veerasamy, Michael G. Dickinson, Sangjin Lee, Stephen Fitch, Greg Marco, Marzia Leacche, Theodore Boeve, David E. Langholz, Stefan Jovinge
Journal: Journal of the American College of Cardiology (2019)
Calpain inhibition down-regulates Akt and induces death of non-cycling breast cancer cells
Authors: Ranjana Mitra, Anjaiah Srirangam, John Hawes, Carter Herndon, Christie Orschell, Edward Srour, Harikrishna Nakshatri, David A. Potter
Journal: Cancer Research (2004)

4834  We have observed that calpain activity is increased in ductal breast cancer, compared to adjacent and terminal ductal epithelia. Calpastatin over-expression in the breast cancer lines MCF7 and MDA-MB-231 results in down-regulation of phospho-Akt and cell cycle arrest and cell death, assayed by Hoechst dye 33342/pyronine and propidum iodide/annexin V flow cytometry methods. The HIV protease inhibitor, ritonavir, which we have demonstrated to block calpain-dependent cytoskeletal remodeling and calpain-dependent cleavage of cell permeant substrates, also down-regulates phospho-Akt by approximately 70%, by lowering total Akt protein levels. Ritonavir induces cell death in the MCF7, T47D, MDA-MB-231, MDA-MB-436, and SKBR3 breast cancer lines and the IC50 values for ritonavir, which range between 10 and 45 μM, are clinically attainable. Hoechst/pyronine staining reveals that ritonavir blocks cell cycle entry at the Go/G1 transition, as well as blocking G1/S in cycling cells. Transient ritonavir exposure at IC90 concentrations induces loss of normal colony formation of Go cells. Sustained exposure to the ritonavir IC50 results in loss of clonogenicity of Go cells. G1 and S/G2M cells are also made non-clonogenic by sustained ritonavir exposure. These findings suggest that ritonavir may induce cell death in non-cycling breast cancer cells independent of EGFR, her2 or p53 status, in part by down-regulating Akt signaling.
Abstract 416: Mnsod Cardiomyocyte-specific Knockout Live Up to Four Months: Role in Heart Failure Development and Progression
Authors: Manikandan Panchatcharam, Susmita Bhattarai, Sudha Sharma, Timothy Michael LaBrie, Hailey D Tupper, Md. Shenuarin Bhuiyan, Mini Chandra, Sumitra Miriyala
Journal: Circulation Research (2018)

In our earlier investigation, we have shown that the manganese superoxide dismutase (MnSOD) mimetic, MnTnBuOE-2-PyP 5+ distributes 3-fold more in mitochondria than in cytosol. The exceptional ability of MnTnBuOE-2-PyP5+ to quench O2 •- parallels its ability to reduce ONOO – and CO3 – . The absence of SOD2 (a gene that encodes MnSOD) knocked out globally is found to be embryonic lethal. We have generated mice that specifically lack MnSOD in cardiomyocytes (Mhy6-SOD2 Δ ). Amazingly, we could prolong the lethality for up to four months in these conditional specific knockout mice (Mhy6-SOD2 Δ ) as compared to global knockout mice. FACS analyses using Mito-Tracker Green indicated that the mass of mitochondria per cell was slightly decreased in the Mhy6-SOD2 Δ to the wild type. We then examined Oxidative phosphorylation (OXPHOS) levels in Mhy6-SOD2 Δ v.s. Wild-Type using a Seahorse XF analyzer. The rate of oxygen consumption per cells was significantly lower in Mhy6-SOD2 Δ cardiomyocytes than that in wild-type. The most noticeable difference in the O 2 consumption was found in the presence of FCCP (H + ionophore/uncoupler). Remarkably, while the FCCP treatment increased O 2 consumption in wild-type, the treatment showed no effect on the O 2 consumption in the Mhy6-SOD2 Δ cardiomyocytes. The result indicated that the low basal OXPHOS activity in Mhy6-SOD2 Δ was due to unusually low OXPHOS potential. We examined glycolysis in these cells by measuring extracellular acidification (ECAR), and the pattern precisely opposite to that of oxygen consumption rate (OCR) was observed for glycolysis rates between Mhy6-SOD2 Δ and wild-type. Herein we present the first study ever done to show the existence of cardiac-specific MnSOD knockout mice and the importance of antioxidant enzyme MnSOD that is guarding/protecting the myocardium from cardiac failures.