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Relevant bibliographies by topics / Cardiovascular diseases; Heart; Cardiac

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Academic literature on the topic 'Cardiovascular diseases; Heart; Cardiac'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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Journal articles on the topic "Cardiovascular diseases; Heart; Cardiac"

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Morciano, Giampaolo, Simone Patergnani, Massimo Bonora, Gaia Pedriali, Anna Tarocco, Esmaa Bouhamida, Saverio Marchi, et al. "Mitophagy in Cardiovascular Diseases." Journal of Clinical Medicine 9, no. 3 (March 24, 2020): 892. http://dx.doi.org/10.3390/jcm9030892.

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Cardiovascular diseases are one of the leading causes of death. Increasing evidence has shown that pharmacological or genetic targeting of mitochondria can ameliorate each stage of these pathologies, which are strongly associated with mitochondrial dysfunction. Removal of inefficient and dysfunctional mitochondria through the process of mitophagy has been reported to be essential for meeting the energetic requirements and maintaining the biochemical homeostasis of cells. This process is useful for counteracting the negative phenotypic changes that occur during cardiovascular diseases, and understanding the molecular players involved might be crucial for the development of potential therapies. Here, we summarize the current knowledge on mitophagy (and autophagy) mechanisms in the context of heart disease with an important focus on atherosclerosis, ischemic heart disease, cardiomyopathies, heart failure, hypertension, arrhythmia, congenital heart disease and peripheral vascular disease. We aim to provide a complete background on the mechanisms of action of this mitochondrial quality control process in cardiology and in cardiac surgery by also reviewing studies on the use of known compounds able to modulate mitophagy for cardioprotective purposes.

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Feiskhanova, L. I., and L. R. Khaliullina. "Cardiac involvement in some rheumatic diseases." Clinical Medicine (Russian Journal) 96, no. 7 (December 15, 2018): 597–603. http://dx.doi.org/10.18821/0023-2149-2018-96-7-597-603.

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The review covers the modern scientific literature about cardiovascular disease in patients with rheumatic diseases. Rheumatic diseases are associated with chronic inflammation, most often joints, skin, eyes, lungs, kidneys and circulatory system. Cardiovascular manifestations of autoimmune diseases can be mild and clinically silent; they can also increase morbidity and mortality. Defeat of cardiovascular system at patients with rheumatoid arthritis: myocarditis, a pericarditis, myocardial fibrosis, ventricular arrhythmias, a syndrome of the extended interval of QT, atrial fibrillation, valvulopathy, development of chronic heart failure, formation of heart disease. Cardiac involvement in systemic lupus erythematosus follows different pathophysiologic mechanisms and covers a wide spectrum of clinical phenotypes including pericarditis, myocarditis, valvular abnormalities, aseptic endocarditis, heartfailure, ischaemic heart disease and pulmonary hypertension. Valvular disease in systemic lupus erythematosus includes valvulitis, aortic and mitral regurgitation, aortic stenosis. For diagnosis of cardiovascular diseases are used clinical laboratory methods, the electrocardiogram, echocardiography, single-photon emission computed tomography, positron emission tomography/ computed tomography, computed coronary angiography, computed tomography, magnetic resonance imaging. The following echocardiographic abnormalities have been reported in ankylosing spondylitis: ascending aortitis, aortic and mitral regurgitation, mitral valve prolapse and diastolic dysfunction. The following echocardiographic abnormalities can be seen in psoriatic arthritis: fibrinous pericarditis, myocarditis and valvular disease.

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Caffarra Malvezzi, Cristina, Aderville Cabassi, and Michele Miragoli. "Mitochondrial mechanosensor in cardiovascular diseases." Vascular Biology 2, no. 1 (July 22, 2020): R85—R92. http://dx.doi.org/10.1530/vb-20-0002.

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The role of mitochondria in cardiac tissue is of utmost importance due to the dynamic nature of the heart and its energetic demands, necessary to assure its proper beating function. Recently, other important mitochondrial roles have been discovered, namely its contribution to intracellular calcium handling in normal and pathological myocardium. Novel investigations support the fact that during the progression toward heart failure, mitochondrial calcium machinery is compromised due to its morphological, structural and biochemical modifications resulting in facilitated arrhythmogenesis and heart failure development. The interaction between mitochondria and sarcomere directly affect cardiomyocyte excitation-contraction and is also involved in mechano-transduction through the cytoskeletal proteins that tether together the mitochondria and the sarcoplasmic reticulum. The focus of this review is to briefly elucidate the role of mitochondria as (mechano) sensors in the heart.

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Prajnamitra, Ray Putra, Hung-Chih Chen, Chen-Ju Lin, Li-Lun Chen, and Patrick Ching-Ho Hsieh. "Nanotechnology Approaches in Tackling Cardiovascular Diseases." Molecules 24, no. 10 (May 27, 2019): 2017. http://dx.doi.org/10.3390/molecules24102017.

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Cardiovascular diseases have continued to remain a leading cause of mortality and morbidity worldwide. Poor proliferation capability of adult cardiomyocytes disables the heart from regenerating new myocardium after a myocardial ischaemia event and therefore weakens the heart in the long term, which may result in heart failure and death. Delivery of cardioprotective therapeutics soon after the event can help to protect the heart from further cell death and improve cardiac function, but delivery methods and potential side effects of these therapeutics may be an issue. Advances in nanotechnology, particularly nanoparticles for drug delivery, have enabled researchers to obtain better drug targeting capability, thus increasing the therapeutic outcome. Detailed study of nanoparticles in vivo is useful as it can provide insight for future treatments. Nanogel can help to create a more favourable environment, not only for a sustained delivery of therapeutics, but also for a better navigation of the therapeutics to the targeted sites. Finally, if the damage to the myocardium is too severe for drug treatment, nanopatch can help to improve cardiac function and healing by becoming a platform for pluripotent stem cell-derived cardiomyocytes to grow for the purpose of cell-based regenerative therapy.

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Cheng, Peng, Fangfang Zhang, Lechu Yu, Xiufei Lin, Luqing He, Xiaokun Li, Xuemian Lu, Xiaoqing Yan, Yi Tan, and Chi Zhang. "Physiological and Pharmacological Roles of FGF21 in Cardiovascular Diseases." Journal of Diabetes Research 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/1540267.

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Cardiovascular disease (CVD) is one of the most severe diseases in clinics. Fibroblast growth factor 21 (FGF21) is regarded as an important metabolic regulator playing a therapeutic role in diabetes and its complications. The heart is a key target as well as a source of FGF21 which is involved in heart development and also induces beneficial effects in CVDs. Our review is to clarify the roles of FGF21 in CVDs. Strong evidence showed that the development of CVDs including atherosclerosis, coronary heart disease, myocardial ischemia, cardiac hypertrophy, and diabetic cardiomyopathy is associated with serum FGF21 levels increase which was regarded as a compensatory response to induced cardiac protection. Furthermore, administration of FGF21 suppressed the above CVDs. Mechanistic studies revealed that FGF21 induced cardiac protection likely by preventing cardiac lipotoxicity and the associated oxidative stress, inflammation, and apoptosis. Normally, FGF21 induced therapeutic effects against CVDs via activation of the above kinases-mediated pathways by directly binding to the FGF receptors of the heart in the presence ofβ-klotho. However, recently, growing evidence showed that FGF21 induced beneficial effects on peripheral organs through an indirect way mediated by adiponectin. Therefore whether adiponectin is also involved in FGF21-induced cardiac protection still needs further investigation.

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Kubler, W. "Treatment of cardiac diseases: evidence based or experience based medicine?" Heart 84, no. 2 (August 1, 2000): 134–36. http://dx.doi.org/10.1136/heart.84.2.134.

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Liu, Xiaolei, and Guillermo Oliver. "New insights about the lymphatic vasculature in cardiovascular diseases." F1000Research 8 (October 29, 2019): 1811. http://dx.doi.org/10.12688/f1000research.20107.1.

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The heart contains a complex network of blood and lymphatic vessels. The coronary blood vessels provide the cardiac tissue with oxygen and nutrients and have been the major focus of research for the past few decades. Cardiac lymphatic vessels, which consist of lymphatic capillaries and collecting lymphatic vessels covering all layers of the heart, transport excess fluid from the interstitium and play important roles in maintaining tissue fluid balance. Unlike for the coronary blood vessels, until a few years ago, not much information was available on the origin and function of the cardiac-associated lymphatic vasculature. A growing body of evidence indicates that cardiac lymphatic vessels (lymphatics) may serve as a therapeutic cardiovascular target.

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Blanda, Valeria, Umberto Marcello Bracale, Maria Donata Di Taranto, and Giuliana Fortunato. "Galectin-3 in Cardiovascular Diseases." International Journal of Molecular Sciences 21, no. 23 (December 3, 2020): 9232. http://dx.doi.org/10.3390/ijms21239232.

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Galectin-3 (Gal-3) is a β-galactoside-binding protein belonging to the lectin family with pleiotropic regulatory activities and several physiological cellular functions, such as cellular growth, proliferation, apoptosis, differentiation, cellular adhesion, and tissue repair. Inflammation, tissue fibrosis and angiogenesis are the main processes in which Gal-3 is involved. It is implicated in the pathogenesis of several diseases, including organ fibrosis, chronic inflammation, cancer, atherosclerosis and other cardiovascular diseases (CVDs). This review aims to explore the connections of Gal-3 with cardiovascular diseases since they represent a major cause of morbidity and mortality. We herein discuss the evidence on the pro-inflammatory role of Gal-3 in the atherogenic process as well as the association with plaque features linked to lesion stability. We report the biological role and molecular mechanisms of Gal-3 in other CVDs, highlighting its involvement in the development of cardiac fibrosis and impaired myocardium remodelling, resulting in heart failure and atrial fibrillation. The role of Gal-3 as a prognostic marker of heart failure is described together with possible diagnostic applications to other CVDs. Finally, we report the tentative use of Gal-3 inhibition as a therapeutic approach to prevent cardiac inflammation and fibrosis.

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Vadivelan Ramachandran, Raju Bairi, Kalirajan Rajagopal, and Manogaran Elumalai. "Isoflavones Protective Mechanisms Against Cardiovascular Diseases." International Journal of Research in Pharmaceutical Sciences 11, no. 3 (August 7, 2020): 4670–75. http://dx.doi.org/10.26452/ijrps.v11i3.2754.

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Isoflavones are polyphenolic compounds and a class of phytoestrogens naturally present in plants belongs to legume family and also quantified in fruits, vegetables and beverages.Soybean is rich source of isoflavones. Their chemical structure is similar to endogenously available female reproductive hormonal substance estradiol,and cellular targets are estrogen receptors. After bind to the estrogen receptors isoflavones exert estrogenic and anti-estrogenic action based upon circulatory levels of estradiol. Cardiovascular diseases are leading cause of death in most of the developing countries and they may occur due to the structural and functional changes in either cardiac muscle or smooth muscle of the vasculature and both. Common cardiac diseases are heart attack, coronary heart disease, hyperlipidaemia, angina pectoris, hypertension. Many epidemiological studies data revealing that consumption of soy protein and soy enriched diet correlate with preventive chances of cardiovascular disease. The United States Food and Drug Administration (USFDA) and other countries declared that everyday consumption of food enriched soy along with low fat may decrease the risk of cardiovascular disease. In this review we attempt the mechanism based cardioprotection of isoflavones in different cardiovascular diseases.

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Sibagatullin, N. G., M. Kh Zakirzyanov, I. R. Yagafarov, I. R. Zakirov, E. V. Tenin, M. G. Khatypov, Z. Sh Ishmuratova, and N. G. Faskhutdinov. "Six-year results of the regional medical center department of cardiac surgery." Kazan medical journal 96, no. 3 (June 15, 2015): 285–94. http://dx.doi.org/10.17750/kmj2015-285.

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Aim. To summarize the experience of the first years of activity in the department of cardiac surgery of the regional medical center.Methods. 5549 patients with cardiovascular diseases were treated from December 2008 to December 2014, including 3041 patients who underwent surgeries, among them - 1585 vascular interventions, 1128 hearts surgeries. The study included patients operated on the heart and aortic arch, 238 of them had surgeries in 2014 [854 male (75.7%), 274 female (24.3%), aged 22 to 81 years (57.8±8.9)].Results. Number of performed surgeries was assessed to find out whether it matches with the population needs. For coronary heart disease, 880 patients underwent surgeries, 10 were operated for coronary heart disease complications, 132 - for heart valve disease, 16 - for congenital heart disease, 56 - for combined heart disease, 18 - for aortic aneurysms, 16 - for cardiac tumors, 3 for pulmonary embolism and aortic dissection (type 1). The number of heart surgery using cardiopulmonary bypass in recalculation per 1 million inhabitants in 2014 was 317. Thanks to the active work of the regional medical-diagnostic center, significant progress was made in timely identification and providing specialized care to patients with cardiovascular diseases to meet the population needs in high-tech medical care in the region.Conclusion. Evaluation of the study results reveals that the introduction of cardiac surgeries for cardiovascular diseases in the regional center promotes approximation of high-tech medical care to the population of remote regions, improves the quality of treatment in patients with cardiovascular conditions.

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Dissertations / Theses on the topic "Cardiovascular diseases; Heart; Cardiac"

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Cho, Jinsoo. "Velocity-based cardiac segmentation and motion-tracking." Diss., Available online, Georgia Institute of Technology, 2004:, 2003. http://etd.gatech.edu/theses/available/etd-04082004-180106/unrestricted/cho%5Fjinsoo%5F200312%5Fphd.pdf.

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Brookes, Carl I. O. "The evaluation and assessment of right ventricular function using conductance catheters." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326042.

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Pandey, Raghav. "MicroRNA Mediated Proliferation of Adult Cardiomyocytes to Regenerate Ischemic Myocardium." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1505124343198575.

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Stewart, Simon. "Optimising therapeutic efficacy in acute and chronic cardiac disease states /." Title page, contents and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phs851.pdf.

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Ye, Yanping. "Designing New Drugs to Treat Cardiac Arrhythmia." PDXScholar, 2012. https://pdxscholar.library.pdx.edu/open_access_etds/638.

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Heart failure resulting from different forms of cardiomyopathy is defined as the inability of the heart to pump sufficient blood to meet the body's metabolic demands. It is a major disease burden worldwide and the statistics show that 50% of the people who have the heart failure will eventually die from sudden cardiac death (SCD) associated with an arrhythmia. The central cause of disability and SCD is because of ventricular arrhythmias. Genetic mutations and acquired modifications to RyR2, the calcium release channel from sarcoplasmic reticulum, can increase the pathologic SR Ca2+ leak during diastole, which leads to defects in SR calcium handling and causes ventricular arrhythmias. The mechanism of RyR2 dysfunction includes abnormal phosphorylation, disrupted interaction with regulatory proteins and ions, or altered RyR2 domain interactions. Many pharmacological strategies have shown promising prospects to modulate the RyR2 as a therapy for treating cardiac arrhythmias. Here, we are trying to establish a novel approach to designing new drugs to treat heart failure and cardiac arrhythmias. Previously, we demonstrated that all pharmacological inhibitors of RyR channels are electron donors while all activators of RyR channels are electron acceptors. This was the first demonstration that an exchange of electrons was a common molecular mechanism involved in modifying the function of the RyR. Moreover, we found that there is a strong correlation between the strength of the electron donor/acceptor, and its potency as a channel inhibitor/activator, which could serve as a basis and direction for developing new drugs targeting the RyR. In this study, two new potent RyR inhibitors, 4-methoxy-3-methyl phenol (4-MmC) and the 1,3 dioxole derivative of K201, were synthesized which are derivatives of the known RyR modulators, 4-chloro-3-methyl phenol (4-CmC) and K201. The ability of K201, 1,3 dioxole derivative of K201 and 4-MmC to inhibit the cardiac calcium channel is examined and compared at the single channel level. All of these compounds inhibited the channel activity at low micromolar concentrations or sub-micromolar concentrations.

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Hsiao, Lien-Cheng. "Cardiac stem cell therapy for heart failure." Thesis, University of Oxford, 2012. https://ora.ox.ac.uk/objects/uuid:c4fcb449-2d05-4dc6-9a8d-f7450c0b200c.

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Cardiovascular disease is a leading cause of death worldwide and becomes increasingly prevalent in the elderly population. Independent of etiopathogenesis, heart failure (HF) is the final common stage of numerous heart diseases. Cardiac stem cell (CSC) therapy has emerged as a promising cell-based strategy for treatment of HF. However, cell replacement is not able to fully restore a structurally damaged myocardium in advanced and end-stage HF. The objective of this project was to test the following hypotheses: that a bioengineered heart extracellular matrix (ECM) with preserved intact geometric structure could be generated using decellularization by coronary perfusion; and that autologous CSCs, to repopulate this ECM, could be isolated and expanded from the adult heart, with the caveat that autologous CSCs are depleted and impaired by both aging and chronic dilated cardiomyopathy. This will help to develop a possible therapeutic approach for advanced HF, using a combination of CSCs and engineering technique. Resident CSCs were isolated from explant-derived cells (EDCs) and expanded into cardiosphere-derived cells (CDCs) via cardiosphere formation. The CDCs expressed CSC markers (c-kit and Sca-1), pluripotent markers (Oct3/4 and Sox2), and the cardiac lineage-committed marker (Nkx2.5), and showed clonal expansion, self-renewal, and cardiomyogenic potential in vitro. In tissue engineering experiments, CDCs survived and proliferated within biomaterial alginate scaffolds for up to 7 weeks. An engineered bioartificial ECM scaffold was successfully produced from a whole rat heart using retrograde coronary perfusion and possessed an intact 3D architecture with functionally perfusable vascular network. Compared with ventricles, cultures derived from atria produced significantly higher number of c-kit+ and Sca-1+ CSCs (c-kit: 13% vs. 3.4%; Sca-1: 82% vs. 53%, respectively) and exhibited greater clonogenic and proliferative capacity. CDCs could be grown from young and aged mice, but the yield of CSCs significantly declined with age, as did cell migration and differentiation potential. In comparison to wild-type mice, atrial-CDCs from dystrophic mice showed no significant differences in CSC subpopulations and characteristics, despite confirmation of cardiac dysfunction using MRI. In conclusion, CDCs could be considered to be a viable cell candidate for cardiac therapy and may be used to treat HF at various stages, in combination with myocardial tissue engineering.

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Rigatto, Claudio. "Cardiac disease in renal transplant recipients /." St. John's, NF : [s.n.], 2001.

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Milstone, Zachary J. "Histone Deacetylase 1 and 2 are Essential for Early Cardiac Development." eScholarship@UMMS, 2019. https://escholarship.umassmed.edu/gsbs_diss/1014.

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Congenital heart disease is the most common congenital anomaly, affecting approximately 1% of all live births each year. Although clinical interventions are improving, many affected infants do not survive to adulthood. Congenital cardiac defects originate from disturbances during development, making the study of mammalian cardiogenesis critical to improving outcomes for infants with congenital heart disease. Development of the mammalian heart involves epigenetically-driven specification and commitment of a diverse landscape of cardiac progenitors. Recent studies determined that chromatin modifying enzymes play a previously underappreciated role in the pathogenesis of congenital heart defects. This thesis investigates the functions of Hdac1 and Hdac2, highly homologous Class I histone deacetylases, during early murine cardiac development. We establish that Hdac1 and Hdac2 cooperatively regulate cardiogenesis in distinct cardiac progenitor populations during development. Together, our findings demonstrate that Hdac1 and Hdac2 are critical mediators of the earliest stages of mammalian cardiogenesis through a variety of spatiotemporally specific, redundant, and dose-sensitive roles and indicate they may play important roles in the pathogenesis of human congenital cardiac defects.

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Smith, Kristin K. "A comparison of objective versus subjective recording of respiratory rates in adult medical cardiac patients." free to MU campus, to others for purchase, 1998. http://wwwlib.umi.com/cr/mo/fullcit?p1392396.

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Shaw, I., BS Shaw, and GA Brown. "Influence of strength training on cardiac risk prevention in individuals without cardiovascular disease." African Journal for Physical, Health Education, Recreation and Dance, 2009. http://encore.tut.ac.za/iii/cpro/DigitalItemViewPage.external?sp=1001650.

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Abstract It has widely been shown that exercise, particularly aerobic exercise, has extensive cardioprotective benefits and is an important tool in the prevention of coronary heart disease (CHD). The present investigation aimed to determine the multivariate impact of strength training, designed to prevent the development of CHD, on the Framingham Risk Assessment (FRA) score. Twenty-eight healthy untrained men with low CHD risk (mean age 28 years and 7 months) participated in an eight-week (3- d/wk) strength training programme. Self-administered smoking records, resting blood pressures, total cholesterol (TC), high-density lipoprotein cholesterol (HDLC), FRA scores and absolute 10-year risks for CHD were determined at the pre-test and post-test. After the eight-week period, no significant (p > 0.05) differences were found in number of cigarettes smoked daily, systolic blood pressure, TC, HDLC, FRA scores and absolute 10-year risks for CHD in both the strength-trained (n = 13) and non-exercising control (n = 15) groups. The data indicate that strength training did not reduce the risk of developing CHD and absolute 10-year risk for CHD as assessed by the FRA score.

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Books on the topic "Cardiovascular diseases; Heart; Cardiac"

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Halliday, Jonathon T. Cardiac rehabilitation. New York: Nova Science Publishers, 2010.

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Harlan, Bradley J. Illustrated handbook of cardiac surgery. New York: Springer, 1996.

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Helping cardiac patients. San Francisco: Jossey-Bass, 1985.

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Cardiac CT imaging: Diagnosis of cardiovascular disease. 2nd ed. Dordecht: Springer, 2010.

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Manual of cardiovascular medicine. 4th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2013.

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Khan, M. Gabriel. Cardiac drug therapy. 3rd ed. London: W.B. Sanders, 1992.

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Canadian Association of Cardiac Rehabilitation. Canadian guidelines for cardiac rehabilitation and cardiovascular disease prevention. Winnipeg: The Association, 1999.

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Cardiac rehabilitation in women. Hauppauge, N.Y: Nova Science, 2010.

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Center, American Nurses Credentialing, ed. Cardiac vascular nursing review and resource manual. 3rd ed. Silver Spring, MD: American Nurses Credentialing Center, 2010.

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Daşkapan, Arzu. Cardiac rehabilitation in women. New York: Nova Science Publishers, 2010.

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Book chapters on the topic "Cardiovascular diseases; Heart; Cardiac"

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Nagano, Makoto. "The Diabetic Heart and Cardiac Glycosides." In Diabetes and Cardiovascular Disease, 303–10. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1321-6_38.

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Imamura, Michiaki, and Robert D. B. Jaquiss. "Pediatric Cardiac Transplantation." In Cardiovascular Surgery for Congenital Heart Disease, 256–60. Tokyo: Springer Japan, 2009. http://dx.doi.org/10.1007/978-4-431-99470-1_41.

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Ogilby, J. David, and Abdulmassih S. Iskandrian. "Cardiac output in valvular heart disease." In Developments in Cardiovascular Medicine, 137–52. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1848-4_13.

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Young, Lawrence H., Raymond R. Russell, and Deborah Chyun. "Heart Failure and Cardiac Dysfunction in Diabetes." In Diabetes and Cardiovascular Disease, 555–78. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-908-7:555.

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Masuda, Munetaka. "Minimum Access Cardiac Surgery." In Cardiovascular Surgery for Congenital Heart Disease, 253–55. Tokyo: Springer Japan, 2009. http://dx.doi.org/10.1007/978-4-431-99470-1_40.

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Liu, Zhi-Ping. "Histone Methylation in Heart Development and Cardiovascular Disease." In Epigenetics in Cardiac Disease, 125–46. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-41457-7_6.

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Green, Jeffrey, and Richard Harrigan. "Cardiac Toxins and Drug-Induced Heart Disease." In Cardiovascular Problems in Emergency Medicine, 237–57. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781119959809.ch17.

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Tokunaga, Shigehiko, Kazuhiro Kurisu, and Toshihide Nakano. "Postoperative Management for Pediatric Cardiac Surgery." In Cardiovascular Surgery for Congenital Heart Disease, 13–21. Tokyo: Springer Japan, 2009. http://dx.doi.org/10.1007/978-4-431-99470-1_2.

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Schneider, Michael D., and Eric N. Olson. "Cardiac Development: Toward a Molecular Basis for Congenital Heart Disease." In Cardiovascular Medicine, 1135–56. London: Springer London, 2007. http://dx.doi.org/10.1007/978-1-84628-715-2_52.

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Babick, Andrea P., Vijayan Elimban, and Naranjan S. Dhalla. "Hormonal Mechanisms of Cardiac Remodeling in Heart Failure." In Molecular Defects in Cardiovascular Disease, 215–29. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-7130-2_16.

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Conference papers on the topic "Cardiovascular diseases; Heart; Cardiac"

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Mesihović-Dinarević, Senka. "WHAT IS NEW IN CARDIOVASCULAR MEDICINE?" In Symposium with International Participation HEART AND … Akademija nauka i umjetnosti Bosne i Hercegovine, 2019. http://dx.doi.org/10.5644/pi2019.181.03.

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The rapid pace of change continues to be a hallmark in cardiovascular medicine and many see that pace accelerating in adult cardiovascular medicine as well as in paediatric cardiology medicine. Cardiovascular medicine is an area of clinical practice with a continually rapid expansion of knowledge, guidelines, best practices and new technology. Cardiovascular diseases are the leading cause of mortality in the world and cause major costs for the health sector and economy. Primary care clinicians are challenged to optimally manage a multitude of diseases including congestive heart failure, coronary artery disease, valvular diseases, arrhythmias, lipid disorders, and hypertension. Multimodality imaging techniques are being used more frequently as their utility is better appreciated. Echocardiography has been the mainstay approach, cardiac computerized tomography and magnetic resonance imaging provide a good imaging alternative for patients with multiple complex surgeries. 3D printing has seen a rapid growth in use for planning treatments for patients with congenital heart disease. Simulation using 3D models is emerging as a fundamental resource for teaching procedural techniques and a new standard of care. Artificial intelligence holds the greatest potential for revolutionizing medicine. Innovative technologies in the world of cardiovascular health are expanding every day: wearable computing technologies, bioresorbable stents, leadless pacemaker, valve-in-valve procedure, protein patch for heart muscle growth and others. As a part of lifelong learning process for all professionals in cardiovascular medicine, the imperative is to have continuity of reviewing novelties, with results data from numerous researches in order to treat patient according to best practices and evidence-based medicine.

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Xiao, Min, Annie Bailey, and Olga Pierrakos. "In-Vitro Modeling of Heart Failure in the Presence of a Prosthetic Heart Valve Using Particle Image Velocimetry." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53788.

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It is well-known that cardiovascular disease, affecting millions of people, is the number one killer in the US and worldwide. Current trends indicate that cardiovascular disease (CVD) will claim approximately 20 million victims in 2020 as the leading cause of death worldwide and will be responsible for over a billion deaths between 2000 and 2050 [1]. According to the American Heart Association, one in three American adults have one or more types of heart disease. Economically, the total and indirect costs due to cardiovascular diseases in 2009 were estimated at $475.3 billion. The spectrum of cardiac disease encompasses a broad range of disorders, varying from myocardial ischemia, valvular disease, diastolic dysfunction, congestive heart failure (which is projected to affect 20 million people by 2020), etc. Most of these disorders initiate and are associated to the left side of the heart, which is the workhorse and also the focus of our research herein.

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Walsh, Peter W., Craig McLachlan, Leigh Ladd, and R. Mark Gillies. "Novel Extra Aortic Counterpulsation Device for Enhancing Cardiac Performance." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53699.

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Heart failure is the fastest growing cardiovascular disorder. Incidence is rising at a rate of approximately 2% to 5% in people over 65 years of age, and 10% in people over 75 years of age [1]. Over 13 Million people suffer from heart failure in the USA, Europe, Canada and Australia, and heart failure is a leading cause of hospital admissions and re-admissions in Americans older than 65 years of age [2]. The secondary heart pump system is the expansion and recoil of the aorta which reduces heart load and drives left coronary artery blood flow. Increases in aortic stiffness are a result of elastin degradation due to ageing and/or cardiovascular diseases such as atherosclerosis [3–5], which increase heart load and pulse pressure [6–10]. Significantly higher aortic stiffness is found in hypertensive and heart failure suffers [6,7,9–11]. Specifically, healthy aged subjects have been found to have aortic stiffness 50% higher relative to subjects in a young and healthy group, while symptomatic hypertensive patients in heart failure have aortic stiffness further increased by approx. 77% relative to the age matched healthy cohort (i.e. by ∼88% relative to the young and healthy group) [11].

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Baross, Stephanie, Simon Williams, Kathryn Hentges, Andrew Sharrocks, and Bernard Keavney. "BS54 Variation in cardiac long non-coding rnas in congenital heart disease." In British Cardiovascular Society Annual Conference ‘Digital Health Revolution’ 3–5 June 2019. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bcs.215.

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Zaidi, Syed Hassan, Imran Akhtar, Syed Imran Majeed, Tahir Zaidi, and Muhammad Saif Ullah Khalid. "Nonlinear Characterization of Heart Rate Variability in Normal Sinus Rhythm, Atrial Fibrillation and Congestive Heart Failure." In ASME 2016 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/imece2016-66836.

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This paper highlights the application of methods and techniques from nonlinear analysis to illustrate their far superior capability in revealing complex cardiac dynamics under various physiological and pathological states. The purpose is to augment conventional (time and frequency based) heart rate variability analysis, and to extract significant prognostic and clinically relevant information for risk stratification and improved diagnosis. In this work, several nonlinear indices are estimated for RR intervals based time series data acquired for Healthy Sinus Rhythm (HSR) and Congestive Heart Failure (CHF), as the two groups represent different cases of Normal Sinus Rhythm (NSR). In addition to this, nonlinear algorithms are also applied to investigate the internal dynamics of Atrial Fibrillation (AFib). Application of nonlinear tools in normal and diseased cardiovascular states manifest their strong ability to support clinical decision support systems and highlights the internal complex properties of physiological time series data such as complexity, irregularity, determinism and recurrence trends in cardiovascular regulation mechanisms.

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Moussa, Heba Adel Mohamed Lotfy, Gawaher Saleh Abbas Mahgoub, Mashael Ali H. I. Al-Badr, and Huseyin Cagatay Yalcin. "Investigating the Cardiac Effects of Sildenafil loaded Nanoparticles on Heart Failure using the Zebrafish Embryo Model." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0217.

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Background: Cardiovascular diseases (CVDs) are the first cause of death worldwide. Vasolidator agents are used to relax cardiac muscle, but their extremely short half-lifes limit their effectiveness. Sildenafil is such an agent used to relax the blood vessels muscles and increase the blood flow. The conventional drug can lead to serious problems in patients duo to the systematic drug delivery. Use of Nanomedicine potentially can enhance delivery of this agent while reducing the systematic effect of the drug. Aim: The purpose of the research is to examine the effectiveness sildenafil loaded nanoparticles in rescuing heart failure using zebrafish embryo model. Methods: There will be five experimental groups. The zebrafish will be treated with Aristolochic Acid (AA) at 24 hour per fertilization (hpf) to create the heart injury group. The treatment groups will be heart injury followed by a dose of either Sildenafil or Sildenafil loaded nanoparticles at 36 hpf. Two control groups will be the negative control (exposed to egg water) and vehicle control (exposed to the Dimethylsulfoxide (DMSO)).To evaluate the drug effects on embryo, toxicity assessment (Survival rate, tail flicking and hatching rate), cardiotoxicity assessment and gene expression of heart injury marker via RT-PCR will be conducted. Results: Preliminary findings demonstrate, loading Sildenafil to nanoparticles enhances its effectiveness dramatically. The experiments are ongoing to confirm the results. Conclusion: Nanomedicine is a powerful approach to enhance cardiovascular therapy. Vasodilator drugs in particular will benefit from this improvement as demonstrated with our findings

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Moreno, Michael, Saurabh Biswas, Lewis D. Harrison, Guillaume Pernelle, Matthew W. Miller, Theresa W. Fossum, David A. Nelson, and John C. Criscione. "Assessment of Minimally Invasive Device That Provides Simultaneous Adjustable Cardiac Support and Active Synchronous Assist in an Acute Heart Failure Model." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53089.

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Congestive heart failure (CHF) is a debilitating disease that is generally initiated by some index cardiac event and ultimately characterized by left ventricular (LV) remodeling which dramatically alters the mechanical environment about the heart. It is well established that mechanical stimuli (e.g., stress or strain) are important epigenetic factors in cardiovascular development, adaptation, and disease.1–3 Interestingly, abnormal cardiac kinematics is often considered a symptom of heart failure when in actuality it is likely a primary contributing factor to the relentless progression of the disease.4 Cellular responses to pathologic mechanical factors lead to further pathologic remodeling and a positive feedback loop emerges such that eventually a threshold is reached wherein the neurohormal compensatory mechanisms activated to maintain homeostasis following the initial cardiac event are no longer sufficient to deter further progression of the disease. Consequently, treatment strategies that fail to remedy the aberrant mechanical environment become increasingly ineffective as the disease progresses.

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Fraser, Katharine H., Tao Zhang, Bartley P. Griffith, and Zhongjun J. Wu. "Differences in Shear Stress, Residence Time and Estimates of Hemolysis Between Different Ventricular Assist Devices." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53316.

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Cardiovascular disease is the leading cause of mortality globally. Among various forms of cardiovascular disease, heart failure (HF) affects 5.7 million patients in the United States1. Despite optimal treatment, some patients still do not improve and the available therapies fail to control their symptoms; for them, cardiac transplantation may be the only option. However, only around 2200 transplants are performed in the US each year1, or only about 6% of the estimated 35,000 US patients who would benefit actually receive a heart. To address the need to support the circulation in patients with end-stage HF a wide variety of mechanical circulatory support devices (MCSDs) have been developed over the past four decades.

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Wang, Jing, Suzie Brown, and Stephen W. Tullis. "Oscillatory Blood Flow in a Deformable Human Aortic Arch." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53676.

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The aorta is the largest artery in humans, stemming from the left ventricle of the heart and stretching down to the abdomen. It is responsible for distributing oxygenated blood to the rest of the body during each cardiac cycle. The pulsatile blood flow is complex in nature and has been previously modeled computationally in an effort to understand its effect on cardiovascular diseases and medical device design interaction [4,8–9]. However, the majority of these models either treat the vessel wall as rigid or have significantly simplified geometries, which from a physiological perspective are not true of large vessels such as the aorta. Here, the complex mechanical interaction between pulsatile blood flow and wall dynamics in the aortic arch is investigated using geometry adopted directly from CT images.

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Mahmoud, Ahmed M., Bunyen Teng, S. Jamal Mustafa, and Osama M. Mukdadi. "High-Frequency Ultrasound Tissue Classification of Atherosclerotic Plaques in an APOE-KO Mouse Model Using Spectral Analysis." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-13061.

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Small animal models have been widely used in cardiovascular research when studying the development and treatment of different diseases. This kind of research has promoted the development of noninvasive techniques to assess cardiac tissue and blood vessels of small animals. Recently, we have developed a high-frequency ultrasound imaging system for small animals, in particular, mouse and rat models. In this work, we aim to elucidate the usefulness of using spectral analysis of the received radiofrequency (RF) ultrasound signals to extract quantitative parameters to assess mechanical properties of cardiac and vascular tissues. A custom system that employs high-frequency single-element ultrasound transducers (30–120 MHz) is used for scanning. Various signal and image processing techniques are applied on the received ultrasound signals to reconstruct high resolution B-mode and spectral images. In vitro imaging of isolated heart and vessels of APOE-KO “knock-out” mouse model with atherosclerosis was performed. Power spectral densities (PSD) of RF signals were evaluated within various regions of interests (ROI) including degassed water, normal cardiac tissue, and cardiac tissue with atheroma. Various parameters were extracted from the power spectrum such as the maximum power (Pmax), the frequency at maximum power (Fpeak), and the variance of power spectrum (Pvar). Results of the preliminary spectral analysis indicated larger values for the Pmax, Fpeak, and Pvar parameters for ROI contains atheroma than other regions. For example using the envelop data, the normalized maximum power (Pmax) value for cardiac tissue with atheroma was 0.0 ± 0.789 (dB), whereas for normal tissues it was about −13.71± 0.267 (dB). These results suggest the use spectral images as a quantitative method when assessing mouse hearts and blood vessels noninvasively.

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Reports on the topic "Cardiovascular diseases; Heart; Cardiac"

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Treadwell, Jonathan R., James T. Reston, Benjamin Rouse, Joann Fontanarosa, Neha Patel, and Nikhil K. Mull. Automated-Entry Patient-Generated Health Data for Chronic Conditions: The Evidence on Health Outcomes. Agency for Healthcare Research and Quality (AHRQ), March 2021. http://dx.doi.org/10.23970/ahrqepctb38.

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Background. Automated-entry consumer devices that collect and transmit patient-generated health data (PGHD) are being evaluated as potential tools to aid in the management of chronic diseases. The need exists to evaluate the evidence regarding consumer PGHD technologies, particularly for devices that have not gone through Food and Drug Administration evaluation. Purpose. To summarize the research related to automated-entry consumer health technologies that provide PGHD for the prevention or management of 11 chronic diseases. Methods. The project scope was determined through discussions with Key Informants. We searched MEDLINE and EMBASE (via EMBASE.com), In-Process MEDLINE and PubMed unique content (via PubMed.gov), and the Cochrane Database of Systematic Reviews for systematic reviews or controlled trials. We also searched ClinicalTrials.gov for ongoing studies. We assessed risk of bias and extracted data on health outcomes, surrogate outcomes, usability, sustainability, cost-effectiveness outcomes (quantifying the tradeoffs between health effects and cost), process outcomes, and other characteristics related to PGHD technologies. For isolated effects on health outcomes, we classified the results in one of four categories: (1) likely no effect, (2) unclear, (3) possible positive effect, or (4) likely positive effect. When we categorized the data as “unclear” based solely on health outcomes, we then examined and classified surrogate outcomes for that particular clinical condition. Findings. We identified 114 unique studies that met inclusion criteria. The largest number of studies addressed patients with hypertension (51 studies) and obesity (43 studies). Eighty-four trials used a single PGHD device, 23 used 2 PGHD devices, and the other 7 used 3 or more PGHD devices. Pedometers, blood pressure (BP) monitors, and scales were commonly used in the same studies. Overall, we found a “possible positive effect” of PGHD interventions on health outcomes for coronary artery disease, heart failure, and asthma. For obesity, we rated the health outcomes as unclear, and the surrogate outcomes (body mass index/weight) as likely no effect. For hypertension, we rated the health outcomes as unclear, and the surrogate outcomes (systolic BP/diastolic BP) as possible positive effect. For cardiac arrhythmias or conduction abnormalities we rated the health outcomes as unclear and the surrogate outcome (time to arrhythmia detection) as likely positive effect. The findings were “unclear” regarding PGHD interventions for diabetes prevention, sleep apnea, stroke, Parkinson’s disease, and chronic obstructive pulmonary disease. Most studies did not report harms related to PGHD interventions; the relatively few harms reported were minor and transient, with event rates usually comparable to harms in the control groups. Few studies reported cost-effectiveness analyses, and only for PGHD interventions for hypertension, coronary artery disease, and chronic obstructive pulmonary disease; the findings were variable across different chronic conditions and devices. Patient adherence to PGHD interventions was highly variable across studies, but patient acceptance/satisfaction and usability was generally fair to good. However, device engineers independently evaluated consumer wearable and handheld BP monitors and considered the user experience to be poor, while their assessment of smartphone-based electrocardiogram monitors found the user experience to be good. Student volunteers involved in device usability testing of the Weight Watchers Online app found it well-designed and relatively easy to use. Implications. Multiple randomized controlled trials (RCTs) have evaluated some PGHD technologies (e.g., pedometers, scales, BP monitors), particularly for obesity and hypertension, but health outcomes were generally underreported. We found evidence suggesting a possible positive effect of PGHD interventions on health outcomes for four chronic conditions. Lack of reporting of health outcomes and insufficient statistical power to assess these outcomes were the main reasons for “unclear” ratings. The majority of studies on PGHD technologies still focus on non-health-related outcomes. Future RCTs should focus on measurement of health outcomes. Furthermore, future RCTs should be designed to isolate the effect of the PGHD intervention from other components in a multicomponent intervention.

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