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1

Collinson, Paul O., and David C. Gaze. "Biomarkers of Cardiovascular Damage." Medical Principles and Practice 16, no. 4 (2007): 247–61. http://dx.doi.org/10.1159/000102146.

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Mayhew, Maren S. "Aspirin for Preventing Cardiovascular Damage." Journal for Nurse Practitioners 6, no. 2 (2010): 147–48. http://dx.doi.org/10.1016/j.nurpra.2009.12.004.

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Funder, John W. "Mineralocorticoid Receptors and Cardiovascular Damage." Hypertension 47, no. 4 (2006): 634–35. http://dx.doi.org/10.1161/01.hyp.0000203732.03784.3b.

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Shakariants, G. A. Shakariants, V. Yu Kaplunova Kaplunova, I. S. Chekneva Chekneva, E. V. Privalova Privalova, and Yu N. Belenkov Belenkov. "Postradiation Damage of the Cardiovascular System." Kardiologiia 12_2014 (December 17, 2014): 97–104. http://dx.doi.org/10.18565/cardio.2014.12.97-104.

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Krüger, Thilo, Stephan Oelenberg, Nadine Kaesler, et al. "Warfarin Induces Cardiovascular Damage in Mice." Arteriosclerosis, Thrombosis, and Vascular Biology 33, no. 11 (2013): 2618–24. http://dx.doi.org/10.1161/atvbaha.113.302244.

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van Schooten, Frederik J., Ad M. Knaapen, and Alberto Izzotti. "DNA damage, mutagenesis and cardiovascular disease." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 621, no. 1-2 (2007): 1–4. http://dx.doi.org/10.1016/j.mrfmmm.2007.02.006.

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Lee, S. "Oxidative DNA Damage and Cardiovascular Disease." Trends in Cardiovascular Medicine 11, no. 3-4 (2001): 148–55. http://dx.doi.org/10.1016/s1050-1738(01)00094-9.

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Shukla, Praphulla C., Krishna K. Singh, Bobby Yanagawa, Hwee Teoh, and Subodh Verma. "DNA damage repair and cardiovascular diseases." Canadian Journal of Cardiology 26 (March 2010): 13A—16A. http://dx.doi.org/10.1016/s0828-282x(10)71055-2.

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Richardson, Kelly, Gregory Engel, Takuya Yamazaki, Sung Chun, and Victor F. Froelicher. "Electrocardiographic damage scores and cardiovascular mortality." American Heart Journal 149, no. 3 (2005): 458–63. http://dx.doi.org/10.1016/j.ahj.2004.06.025.

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Richardson, K., G. Engel, and T. Yamazaki. "Electrocardiographic Damage Scores and Cardiovascular Mortality." ACC Current Journal Review 14, no. 12 (2005): 22. http://dx.doi.org/10.1016/j.accreview.2005.11.035.

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Kumar, Naresh. "Cardiovascular Manifestations of SARS CoV-2: A Review." Journal of Advanced Research in Medicine 07, no. 02 (2020): 1–10. http://dx.doi.org/10.24321/2349.7181.202005.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic is a public health emergency of global concern. Besides the profound severe pulmonary damage, SARS-CoV-2 infection also causes a series of cardiovascular abnormalities, including myocardial injury, myocarditis and pericarditis, arrhythmia and cardiac arrest, cardiomyopathy, heart failure, cardiogenic shock, and coagulation abnormalities. COVID-19 patients with preexisting cardiovascular diseases are often at a much higher risk of increased morbidity and mortality. Number of mechanisms have been postulated for SARS CoV-2-asso
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12

Buffolo, Fabrizio, Martina Tetti, Paolo Mulatero, and Silvia Monticone. "Aldosterone as a Mediator of Cardiovascular Damage." Hypertension 79, no. 9 (2022): 1899–911. http://dx.doi.org/10.1161/hypertensionaha.122.17964.

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Besides the physiological regulation of water, sodium, and potassium homeostasis, aldosterone modulates several physiological and pathological processes in the cardiovascular system. At the vascular level, aldosterone excess stimulates endothelial dysfunction and infiltration of inflammatory cells, enhances the development of the atherosclerotic plaque, and favors plaque instability, arterial stiffness, and calcification. At the cardiac level, aldosterone increases cardiac inflammation, fibrosis, and myocardial hypertrophy. As a clinical consequence, high aldosterone levels are associated with
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Quan, Yue, Yanguo Xin, Geer Tian, Junteng Zhou, and Xiaojing Liu. "Mitochondrial ROS-Modulated mtDNA: A Potential Target for Cardiac Aging." Oxidative Medicine and Cellular Longevity 2020 (March 27, 2020): 1–11. http://dx.doi.org/10.1155/2020/9423593.

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Mitochondrial DNA (mtDNA) damage is associated with the development of cardiovascular diseases. Cardiac aging plays a central role in cardiovascular diseases. There is accumulating evidence linking cardiac aging to mtDNA damage, including mtDNA mutation and decreased mtDNA copy number. Current wisdom indicates that mtDNA is susceptible to damage by mitochondrial reactive oxygen species (mtROS). This review presents the cellular and molecular mechanisms of cardiac aging, including autophagy, chronic inflammation, mtROS, and mtDNA damage, and the effects of mitochondrial biogenesis and oxidative
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14

Baaj, Teim, Ahmed Abu-Awwad, Mircea Botoca, et al. "Biochemical and Paraclinical Evaluation of Organ Damage in Arterial Hypertension with Associated Chronic Kidney Disease." Revista de Chimie 71, no. 6 (2020): 194–204. http://dx.doi.org/10.37358/rc.20.6.8183.

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Organ damages, which contribute to the overall cardiovascular risk of hypertensive patients, should be early detected, prevented and treated. The study evaluated organ damage in a hypertensive study group with chronic kidney disease (CKD), compared with a study group of hypertension without CKD. Albuminuria was present in 41.2% and reduced estimated glomerular filtration rate [60 ml/min/m2 was present in 72.5% of hypertensive with CKD. The comparison of organ damage revealed in the CKD group a statistical significant higher prevalence of organ damage as follows: intima-media thickness ]0.9 mm
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15

Gutan, Inesa, Stela Dodu, Elena Panfile, et al. "Cardiovascular damage in patients with systemic scleroderma." Bulletin of the Academy of Sciences of Moldova. Medical Sciences 72, no. 1 (2022): 164–68. http://dx.doi.org/10.52692/1857-0011.2022.1-72.26.

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Systemic sclerosis is a generalized disease of the connective tissue characterized by the expression of pathological manifestations of the skin, musculoskeletal system with damage to the heart, lungs, kidneys, gastrointestinal tract and diffuse vasospastic disorders caused by damage to the connective tissue and the predominance of fibrosis the type of obliterating microangiopathy. Cardiovascular manifestations occur in about 10% of patients with SSc, being an important predictor of patient mortality and often associated with an unfavorable prognosis.
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16

Armani, Chiara, Nicoletta Botto, Maria Grazia Andreassi, and Emilio Centaro. "Molecular Markers of Cardiovascular Damage in Hypertension." Current Pharmaceutical Design 19, no. 13 (2013): 2341–50. http://dx.doi.org/10.2174/1381612811319130002.

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Cinza Sanjurgo, S., J. E. López Paz, A. Hermida Ameijeiras, et al. "ORGAN DAMAGE AND CARDIOVASCULAR PROGNOSIS IN HYPERTENSION." Journal of Hypertension 29 (June 2011): e256. http://dx.doi.org/10.1097/00004872-201106001-00717.

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Zanchetti, Alberto. "Hypertension-related organ damage and cardiovascular risk." Journal of Hypertension 32, no. 11 (2014): 2107–8. http://dx.doi.org/10.1097/hjh.0000000000000388.

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19

Luft, Friedrich C. "Workshop: Mechanisms and Cardiovascular Damage in Hypertension." Hypertension 37, no. 2 (2001): 594–98. http://dx.doi.org/10.1161/01.hyp.37.2.594.

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20

Sehestedt, Thomas, and Michael H. Olsen. "Subclinical organ damage and cardiovascular risk prediction." Blood Pressure 19, no. 3 (2010): 132–39. http://dx.doi.org/10.3109/08037051.2010.483054.

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21

Maxwell, S. R., R. J. Moots, and M. J. Kendall. "Corticosteroids: do they damage the cardiovascular system?" Postgraduate Medical Journal 70, no. 830 (1994): 863–70. http://dx.doi.org/10.1136/pgmj.70.830.863.

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22

Shimosawa, Tatsuo, Yugo Shibagaki, Kotaro Ishibashi, et al. "Adrenomedullin, an Endogenous Peptide, Counteracts Cardiovascular Damage." Circulation 105, no. 1 (2002): 106–11. http://dx.doi.org/10.1161/hc0102.101399.

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23

CRUICKSHANK, J., and J. SMITH. "The beta-receptor, atheroma and cardiovascular damage." Pharmacology & Therapeutics 42, no. 3 (1989): 385–404. http://dx.doi.org/10.1016/0163-7258(89)90032-6.

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24

Matafonova, К. А., Е. N. Romanova, Е. М. Romanova, and D. V. Malko. "CARDIOVASCULAR SYSTEM DAMAGE DURING POST-COVID SYNDROME." Transbaikalian Medical Bulletin, no. 1 (May 18, 2024): 154–62. http://dx.doi.org/10.52485/19986173_2024_1_154.

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The epidemic of a new coronavirus infection provoked a second pandemic, “post-Covid”, among convalescents with a long-lasting clinical condition. Most patients who have had COVID-19 recover completely after two weeks from the onset of the disease. At the same time, every tenth person faces long-term manifestations from a number of body systems. Symptoms of post-Covid syndrome are numerous, heterogeneous and difficult to interpret. The review examines the development mechanisms and main manifestations of long-term COVID-19. Particular attention is paid to the causes and clinical variants of dam
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25

Altabás-González, Irene, Iñigo Rua-Figueroa, Coral Mouriño, et al. "Damage in a large systemic lupus erythematosus cohort from the Spanish Society of Rheumatology Lupus Registry (RELESSER) with emphasis on the cardiovascular system: a longitudinal analysis." Lupus Science & Medicine 11, no. 2 (2024): e001064. http://dx.doi.org/10.1136/lupus-2023-001064.

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ObjectiveTo assess organ damage, with emphasis on the cardiovascular system, over the different stages of the disease in a large SLE cohort.MethodsMulticentre, longitudinal study of a cohort of 4219 patients with SLE enrolled in the Spanish Society of Rheumatology Lupus Registry. Organ damage was ascertained using the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI). We longitudinally analysed SDI (globally and for each domain) over time only in the 1274 patients whose dates of damage events had been recorded.ResultsDuring the first year af
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26

Safari, Mohammad Reza, Mohsen Rezaee, and Saeid Amiri. "Comparing Plasma Fibrinogen,Homocysteine, Cardiac Troponin I, and C-Reactive Protein Levels Among Smokers and Non-smokers inHamadan Hospitals: A Case-Control Study." Avicenna journal of Care and Health in Operating Room 2, no. 2 (2024): 71–74. http://dx.doi.org/10.34172/ajchor.61.

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Background: Cigarette smoking is one of the main risk factors for cardiovascular damage. Current studies have reported an association between some markers such as homocysteine, plasma fibrinogen, cardiac troponin I (cTnI), and C-reactive protein (CRP) and cardiovascular damages. This study aimed to investigate the relationship between these laboratory markers and smoking intensity. Methods: In this case-control study, 200 male employees from the operating room, laboratory, and administrative departments of Hamadan hospitals were categorized into four groups of 50 based on their smoking status:
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27

Korzh, O. M. "Damage to the cardiovascular system in COVID-19." Shidnoevropejskij zurnal vnutrisnoi ta simejnoi medicini 2021, no. 1 (2021): 10–16. http://dx.doi.org/10.15407/internalmed2021.01.010.

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COVID-19 affects not only the respiratory system, but also the cardiovascular system. The damage to the cardiovascular system in COVID-19 is multifactorial and several mechanisms are involved, including direct invasion, inflammation, thrombosis, autoantibody synthesis, and oxygen imbalance. The inflammation causes the release of cytokines, especially interleukin-6, and damage to cardiomyocytes. The overproduction of cytokines leads to an abnormal inflammatory response called a cytokine storm, which is believed to be the culprit in cardiovascular events in COVID-19 patients. Treatment of COVID-
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28

Leone, Aurelio. "Editorial (Hot Topic: Modifying Cardiovascular Risk Factors: New Markers of Cardiovascular Damage)." Current Pharmaceutical Design 19, no. 13 (2013): 2335–40. http://dx.doi.org/10.2174/1381612811319130001.

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Kuan, WP, EK Li, and L.-S. Tam. "Lupus organ damage: what is damaged in Asian patients?" Lupus 19, no. 12 (2010): 1436–41. http://dx.doi.org/10.1177/0961203310370050.

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Assessment of organ damage has become the standard outcome measure for morbidity and mortality in patients with lupus. Ethnicity is thought to be a marker for genetic, environmental, behavioral, and other variables that may affect disease outcomes. Previous studies suggest that Asians residing in western countries had significantly higher prevalence of damage compared with Whites. In contrast, studies performed in Chinese, Korean and Arab patients showed that the overall prevalence of damage and the most commonly involved organs (neuropsychiatric and musculoskeletal) were similar to Whites. Co
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30

Fedorovych, M., R. Khrustavka, D. Koval, A. Mykolenko, T. Golovata, and I. Smachylo. "MORPHOLOGICAL MANIFESTATIONS OF CARDIOVASCULAR AND NEUROLOGICAL COMPLICATIONS OF COVID-19." Sciences of Europe, no. 131 (December 27, 2023): 36–41. https://doi.org/10.5281/zenodo.10434512.

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<strong>Resume.</strong> Currently, the problem of studying the pathogenetic impact of SARS-COV-2 on the cardiovascular and nervous systems in the human body remains relevant, since damage to the heart, blood vessels, and nervous tissue is the cause of the development of complications that significantly worsen the quality of life. <strong>The </strong><strong>purpose of study</strong> is to investigate the pathogenetic and morphological features of the main cardiovascular and neurological complications in COVID-19 and to describe the most important structural changes. <strong>Materials and met
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Di Tomasso, Nora, Fabrizio Monaco, and Giovanni Landoni. "Renal protection in cardiovascular surgery." F1000Research 5 (March 11, 2016): 331. http://dx.doi.org/10.12688/f1000research.7348.1.

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Acute kidney injury (AKI) is one of the most relevant complications after major surgery and is a predictor of mortality. In Western countries, patients at risk of developing AKI are mainly those undergoing cardiovascular surgical procedures. In this category of patients, AKI depends on a multifactorial etiology, including low ejection fraction, use of contrast media, hemodynamic instability, cardiopulmonary bypass, and bleeding. Despite a growing body of literature, the treatment of renal failure remains mainly supportive (e.g. hemodynamic stability, fluid management, and avoidance of further
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32

Leone, Aurelio. "Biochemical Markers of Cardiovascular Damage from Tobacco Smoke." Current Pharmaceutical Design 11, no. 17 (2005): 2199–208. http://dx.doi.org/10.2174/1381612054367391.

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Pillai, Ajay, and Barbara Lawson. "Coronavirus disease 2019 and cardiovascular diseases: collateral damage?" Current Opinion in Anaesthesiology 35, no. 1 (2021): 5–11. http://dx.doi.org/10.1097/aco.0000000000001076.

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Kravtsiva, A. V., A. A. Gulyaeva, E. D. Golovanova, and K. V. Ayrapetov. "DAMAGE TO THE CARDIOVASCULAR SYSTEM IN COVID-19." Вестник Смоленской государственной медицинской академии 20, no. 4 (2021): 59–65. http://dx.doi.org/10.37903/vsgma.2021.4.8.

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Balykova, L. A., D. O. Vladimirov, A. V. Krasnopolskaya, O. M. Soldatov, N. V. Ivyanskaya, and N. V. Shchekina. "CARDIOVASCULAR SYSTEM DAMAGE IN CHILDREN WITH COVID-19." Pediatria. Journal named after G.N. Speransky 100, no. 5 (2021): 90–98. http://dx.doi.org/10.24110/0031-403x-2021-100-5-90-98.

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Coronavirus infection poses a particular danger in relation to decompensation of existing chronic diseases and specific damage to the cardiovascular system (CVS) both during an acute infection and during convalescence. Objective of the study: to summarize current knowledge about the potential involvement of CVS in the development and progression of acute COVID-19 infection and multisystem inflammatory syndrome (MIS) in children and to form an sense of the predictive value, diagnostic tactics and treatment of cardiac anomalies during the coronavirus pandemic. A search was performed in MEDLINE,
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36

Nadarajah, Ramesh, and Chris P. Gale. "Collateral cardiovascular damage during the COVID-19 pandemic." Nature Reviews Cardiology 19, no. 2 (2021): 81–82. http://dx.doi.org/10.1038/s41569-021-00661-x.

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Moguchaia, E. V., O. P. Rotar, M. A. Boyarinova, et al. "Long-term cardiovascular damage in Leningrad Siege survivors." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 27, no. 2 (2021): 170–79. http://dx.doi.org/10.18705/1607-419x-2021-27-2-170-179.

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Objective. To assess the prevalence of markers of preclinical vascular, kidney and brain damage in the survivors of the Leningrad Siege (SLS) in the long-term period of life, as well as to determine a possible connection with starvation in the prenatal period and early childhood.Design and methods. A prospective cohort study of 305 SLS was initiated in 2009–2011. In a control sex- and age-matched group we recruited people born in the same time period in other regions of the Soviet Union and permanently residing in Leningrad after the World War II (n = 51). At the second visit in 2013–2014, 252
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Liu, Ming, Man Han, and Xiao-Mei Leng. "Research progress in psoriatic arthritis-related cardiovascular damage." Chinese Medical Journal 133, no. 24 (2020): 3001–3. http://dx.doi.org/10.1097/cm9.0000000000001215.

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Bader, Michael. "Molecular Interactions of Vasoactive Systems in Cardiovascular Damage." Journal of Cardiovascular Pharmacology 38 (November 2001): S7—S9. http://dx.doi.org/10.1097/00005344-200111002-00003.

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Guida, Lucio, Rita Iannuzzi, Marina Crivaro, et al. "Clinic-daytime blood pressure difference and cardiovascular damage." Journal of Hypertension 17, no. 3 (1999): 331–37. http://dx.doi.org/10.1097/00004872-199917030-00005.

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Salukhov, V. V. Salukhov, and B. V. Sagun Sagun. "Key aspects of cardiovascular damage in COVID-19." Pharmateca 9-10_2023 (November 17, 2023): 70–78. http://dx.doi.org/10.18565/pharmateca.2023.9-10.70-78.

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NAGATA, Daisuke, and Yasunobu HIRATA. "Molecular Mechanism of Cardiovascular Damage Induced by Aldosterone." YAKUGAKU ZASSHI 127, no. 9 (2007): 1339–46. http://dx.doi.org/10.1248/yakushi.127.1339.

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Matsumori, Akira. "Calcium channel blocker-induced protection against cardiovascular damage." International Journal of Cardiology 62 (December 1997): S39—S46. http://dx.doi.org/10.1016/s0167-5273(97)00240-4.

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Witte, K., A. Schnecko, T. Schmidt, C. Voll, B. Kränzlin, and B. Lemmer. "Cardiovascular risk, renal hypertensive damage, and effects of." General Pharmacology: The Vascular System 33, no. 5 (1999): 423–30. http://dx.doi.org/10.1016/s0306-3623(99)00037-3.

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Levin, A. "Prevalence of cardiovascular damage in early renal disease." Nephrology Dialysis Transplantation 16, suppl 2 (2001): 7–11. http://dx.doi.org/10.1093/ndt/16.suppl_2.7.

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GUIDA, L. "G8 White coat hypertension and early cardiovascular damage." American Journal of Hypertension 10, no. 4 (1997): 61A. http://dx.doi.org/10.1016/s0895-7061(97)88861-9.

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Cingolani, Oscar H. "Cardiovascular Risks and Organ Damage in Secondary Hypertension." Endocrinology and Metabolism Clinics of North America 48, no. 4 (2019): 657–66. http://dx.doi.org/10.1016/j.ecl.2019.08.015.

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48

Collinson, Paul O., and David C. Gaze. "Biomarkers of Cardiovascular Damage and Dysfunction—An Overview." Heart, Lung and Circulation 16 (January 2007): S71—S82. http://dx.doi.org/10.1016/j.hlc.2007.05.006.

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Leone, A. "Cardiovascular damage from smoking: a fact or belief?" International Journal of Cardiology 38, no. 2 (1993): 113–17. http://dx.doi.org/10.1016/0167-5273(93)90169-h.

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50

Seriakova, I. Yu, S. O. Kramarov, V. V. Yevtushenko, et al. "Cardiovascular system damage in children with COVID-19." Modern pediatrics. Ukraine, no. 5(133) (September 28, 2023): 6–16. http://dx.doi.org/10.15574/sp.2023.133.6.

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Purpose - to assess the diagnostic and prognostic value of the E-selectin marker in relation to manifestations of damage to the cardiovascular system in children with COVID-19. Materials and methods. We conducted a cohort, observational, retrospective study involving 88 patients aged 1 month to 18 years with laboratory-confirmed COVID-19 by polymerase chain reaction. The children were hospitalized in Kyiv City Children’s Clinical Infectious Disease Hospital. We divided the examined cohort into two groups according to the course of the disease - the main group, which included 42 patients with a
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