Nauki Medyczne

Folia Medica Cracoviensia

Zawartość

Folia Medica Cracoviensia | 2021 | Vol. 61 | No 3

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Abstrakt

Background: The cause of the increased risk of hypertension in children born prematurely is still unclear. The aim of this study was to analyze the results of blood pressure monitoring and the levels of variety of kidney function markers at the 40–42 weeks postmenstrual age in children born prematurely and to compare them with the values obtained from full-term newborns. The analysis of the differences in the observed parameters could be used to assess the risk of developing hypertension in preterm infants in the following years of life.
Methodology: Prospective cohort study included 37 children born prematurely (<35 weeks of gesta-tion) and 20 full-term newborns. The 24-hour ambulatory blood pressure measurement, serum cystatin C and thrombomodulin levels, urine Neutrophil Gelatinase-Associated Lipocalin (NGAL) concentration, renal ultrasound and bioelectrical impedance were performed.
Results: Analysis of the blood pressure monitoring reveled lower values of diastolic (DBP) and mean blood pressure (MAP) in the preterm group (DBP: 47.69 ± 4.79 vs. 53.96 ± 5.3 mmHg; p <0.01; MAP 64 ± 6.7 vs. 68 ± 6 mmHg; p = 0.02), however the preterm children were significantly smaller at the time of evaluation. Moreover, the pulse pressure was significantly higher in the preterm group (44 ± 7.8 vs. 39.4 ± 5.7 mmHg; p = 0.017). In the preterm group serum cystatin C level was lower (1.397 ± 0.22 vs. 1.617 ± 0.22 mg/l; p <0.01) and NGAL urine concentration was higher (57 ± 84 vs. 15 ± 21 ng/ml; p = 0.04). There was substantial difference in body composition between groups - the total body water was lower in the preterm group (75.6 ± 13 vs. 82 ± 8%; p = 0.015).
Conclusion: At the predicted date of birth, preterm newborns show significant differences in blood pressure profile, body weight composition, and levels of cystatin C and NGAL compared to full-term babies.
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Bibliografia

1. Bayrakci U.S., Schaefer F., Duzova A., Yigit S., Bakkaloglu A.: Abnormal Circadian Blood Pressure Regulation in Children Born Preterm. J Pediatr. 2007. doi: 10.1016/j.jpeds.2007.04.003
2. Keller G., Zimmer G., Mall G., Ritz E., Amann K.: Nephron Number in Patients with Primary Hypertension. N Engl J Med. 2003; 348: 101–108.
3. Cosemans C., Nawrot T.S., Janssen B.G., Vriens A., Smeets K., Baeyens W., et al.: Breastfeeding predicts blood mitochondrial DNA content in adolescents. Sci Rep. 2020; 10: 1–9.
4. Dumeige L., Nehlich M., Viengchareun S., Perrot J., Pussard E., Lombès M.: Preterm birth is associated with epigenetic programming of transgenerational hypertension in mice. Exp Mol Med. 2020; 52: 152–165.
5. Mól N., Kwinta P.: Assesment of body composition using bioelectrical impedance analysis in preterm neonates receiving intensive care. Dev period Med. 2015; 19: 297–304.
6. Dinkel E., Ertel M., Dittrich M., Peters H., Berres M., Schulte-Wissermann H.: Kidney size in childhood sonographical growth charts for kidney length and volume. Pediatric Radiology. 1985; 15: 38–43.
7. Schwartz G.J., Muñoz A., Schneider M.F., Mak R.H., Kaskel F.: New Equations to Estimate GFR in Children with CKD. J Am Soc Nephrol. 2020; 20: 629–637.
8. Keijzer-Veen M.G., Schrevel M., Finken M.J.J., Dekker F.W., Nauta J., Hille E.T.M., et al.: Microalbuminuria and Lower Glomerular Filtration Rate at Young Adult Age in Subjects Born Very Premature and after Intrauterine Growth Retardation. J Am Soc Nephrol. 2005; 16: 2762–2768.
9. Rodríguez M.M., Gómez A.H., Abitbol C.L., Chandar J.J., Duara S.: Histomorphometric Analysis of Postnatal Glomerulogenesis in Extremely Preterm Infants. Pediatr Dev Pathol. 2004; 7. doi: 10.1007/s10024-003-3029-2
10. Faa G., Gerosa C., Fanni D., Nemolato S., Locci A., Cabras T., et al.: Marked interindividual variability in renal maturation of preterm infants: lessons from autopsy. J Matern Neonatal Med. 2010; 23: 129– 133.
11. Sutherland M.R., Gubhaju L., Moore L., Kent A.L., Dahlstrom J.E., Horne R.S., et al.: Accelerated maturation and abnormal morphology in the preterm neonatal kidney. J Am Soc Nephrol. 2011; 22: 1365–1374.
12. Miklaszewska M., Korohoda P., Drożdż D., Zachwieja K., Tomasik T., Moczulska A., et al.: eGFR values and selected renal urine biomarkers in preterm neonates with uncomplicated clinical course. Adv Clin Med. 2019; 28: 1657–1666.
13. Loret de Mola C., de França G.V.A., Quevedo L.A., Horta B.L., Bromet E., Andrade L., et al.: Low birth weight, preterm birth and small for gestational age association with adult depression: systematic review and meta-analysis. Br J Psychiatry. 2014; 205: 340–347.
14. Moledina D.G., Parikh C.R.: Phenotyping of Acute Kidney Injury: Beyond Serum Creatinine. Semin Nephrol. 2018; 38: 3–11.
15. Huen S.C., Parikh C.R.: Molecular phenotyping of clinical AKI with novel urinary biomarkers. Am J Physiol Renal Physiol. 2015; 309: 406–413.
16. Haase M., Kellum J.A., Ronco C.: Subclinical AKI—an emerging syndrome with important consequences. Nat Rev Nephrol. 2012; 8: 735–739.
17. Mori K., Lee H.T., Rapoport D., Drexler I.R., Foster K., Yang J., et al.: Endocytic delivery of lipocalin- siderophore-iron complex rescues the kidney from ischemia-reperfusion injury. J Clin Invest. 2005; 115: 610–621.
18. Ronco C., Kellum J.A., Haase M.: Subclinical AKI is still AKI. Crit Care. 2012; 16: 313.
19. Mól N., Zasada M., Tomasik P., Klimasz K., Kwinta P.: Evaluation of irisin and visfatin levels in very low birth weight preterm newborns compared to full term newborns—A prospective cohort study. PLoS One. 2018; 13: e0204835.
20. Pharoah P.O.D., Stevenson C.J., West C.R.: Association of blood pressure in adolescence with birthweight. Arch Dis Child Fetal Neonatal. 1998; 79: 114–119.
21. Keijzer-veen M.G., Dülger A., Dekker F.W., Nauta J., van der Heijden B.J.: Very preterm birth is a risk factor for increased systolic blood pressure at a young adult age. Pediatr Nephrol. 2010; 25: 509–516.
22. Vohr B.R., Allan W., Katz K.H., Schneider K.C., Ment L.R.: Early predictors of hypertension in prematurely born adolescents. Acta Paediatr. 2010; 99: 1812–1818.
23. Lurbe E., Carvajal E., Torro I., Aguilar F., Alvarez J., Redon J.: Influence of Concurrent Obesity and Low Birth Weight on Blood Pressure Phenotype in Youth. Hypertens. 2009; 75: 211–217.
24. Kistner A., Celsi G., Vanpee M., Jacobson S.H.: Increased blood pressure but normal renal function in adult women born preterm. Pediatr Nephrol. 2000; 15: 215–220.
25. Bayrakci U.S., Schaefer F., Duzova A., Yigit S., Bakkaloglu A.: Abnormal circadian blood pressure regulation in children born preterm. J Pediatr. 2007; 151: 399–403.
26. Hovi P., Andersson S., Räikkönen K., Strang-Karlsson S., Järvenpää A.L., Eriksson J.G., et al.: Ambulatory blood pressure in young adults with very low birth weight. J Pediatr. 2010; 156: 54–59.
27. Doyle L.W., Faber B., Callanan C., Morley R.: Blood pressure in late adolescence and very low birth weight. Pediatrics. 2003; 111: 252–257.
28. Pyhälä R., Räikkönen K., Feldt K., Andersson S., Hovi P., Eriksson J.G., Järvenpää A.L.: Blood pressure responses to psychosocial stress in young adults with very low birth weight: Helsinki study of very low birth weight adults. Pediatrics. 2009; 123: 731–734.
29. Fayos L., Lurbe E., Garcia-Vicent C., Torro I., Aguilar F., Martin J., et al.: First-year blood pressure increase steepest in low birthweight newborns. J Hypertens. 2007; 25: 81–86.
30. Farasat S.M., Morrell C.H., Scuteri A., Ting C.T., Yin F.C.P., Spurgeon H.A., et al.: Pulse pressure is inversely related to aortic root diameter implications for the pathogenesis of systolic hypertension. Hypertens. 2008; 51: 196–202.
31. Thomas F., Blacher J., Benetos A., Safar M.E., Pannier B.: Cardiovascular risk as defined in the 2003 European blood pressure classification: the assessment of an additional predictive value of pulse pressure on mortality. J Hypertens. 2008; 26: 1072–1077.
32. Domanski M.J., Davis B.R., Pfeffer M.A., Kastantin M., Mitchell G.F.: Isolated Systolic Hypertension. Hypertens. 1999; 34: 375–380.
33. O’Rourke M., Frohlich E.D.: Pulse pressure: Is this a clinically useful risk factor? Hypertens. 1999; 34: 372–374.
34. Arulkumaran N., Diwakar R., Tahir Z., Mohamed M., Kaski J.C., Banerjee D.: Pulse pressure and progression of chronic kidney disease. J Nephrol. 2010; 23: 189–193.

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Autorzy i Afiliacje

Maja Gilarska
1
Dagmara Wolińska
2
Przemko Kwinta
1

  1. Department of Pediatrics, Jagiellonian University Medical College, Kraków, Poland
  2. Department of Pediatrics, University Children Hospital, Kraków, Poland
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Abstrakt

Objectives: Accidental exposure to non-fire related carbon monoxide (CO) in young people is largely unquantified. Our aim was to estimate the possibility of exposure to CO and the awareness of intoxication in the population of students living in Kraków, one of the largest academic cities in Poland.
Methods: Anonymous questionnaires about CO poisoning were distributed among medical and non- medical students living in Kraków.
Results: 1081 questionnaires were collected — 16% of study participants knew a person who had been poisoned with carbon monoxide, 51.2% of students using a bathroom water heater believed that they had no risk of CO poisoning. Medical students gained significantly higher scores in the CO-poisoning knowl-edge test than non-medical ones.
Conclusions: There is still unsatisfactory awareness of CO poisoning among non-medical students in Kraków.
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Bibliografia

1. Krzyżanowski M., Seroka W., Skotak K., Wojtyniak B.: Mortality and Hospital Admissions Due to Carbon Monoxide Poisoning in Poland. Saf Fire Tech. 2014; 33 (1): 75–82.
2. Gomółka E., Gawlikowski T.: Estimation of carbon monoxide poisonings frequency, based on carboxyhemoglobin determinations performed in Toxicology Laboratory in Krakow in years 2002– 2010. Przegl Lek. 2011; 68 (8): 413–416.
3. Świderska A., Sein Anand J.: Selected data concerning acute intoxications with xenobiotics in Poland in the year 2010. Przegl Lek. 2012; 69 (8): 409–414.
4. Jakóbik K., Chochorowska A., Czekaj A., et al.: Statistical Yearbook Of Kraków 2015. Statistical Office in Kraków 2015.
5. Czerski G.: Impact Assessment of Selected Factors on the Risk of Poisoning with Combustion Products From Gas Appliances. Saf Fire Tech. 2014; 33 (1): 67–74.
6. Earnest G., Mickelsen R., McCammon J., et al.: Carbon monoxide poisonings from small, gasoline- powered, internal combustion engines: just what is a “well-ventilated area”? Am Ind Hyg Assoc J. 1997; 58 (11): 787–791.
7. Meredith T., Vale A.: Carbon monoxide poisoning. Br Med J Clin Res Ed. 1988; 6615 (296): 77–79.
8. Chang C.: Longitudinal study of carbon monoxide intoxication by diffusion tensor imaging with neuropsychiatric correlation. J Psychiatry Neurosci. 2010; 35 (2): 115–125.
9. Sadovnikoff N., Varon J., Sternbach G.: Carbon monoxide poisoning: An occult epidemic. Postgrad Med. 1992; 92 (4): 86–96.
10. Barret L., Danel V., Faure J.: Carbon Monoxide Poisoning, a Diagnosis Frequently Overlooked. J Toxicol Clin Toxicol. 1985; 23 (4–6): 309–313.
11. Marchewka J., Gawlik I., Dębski G., Popiołek L, Marchewka W., Hydzik P.: Cardiological aspects of carbon monoxide poisoning. Folia Med Cracov. 2017; 57 (1): 75–85.
12. Lehr E.: Carbon monoxide poisoning: a preventable environmental hazard. Am J Public Health Nations Health. 1970; 60 (2): 289–293.
13. Krawczyk P., Cebula G., Drab E., et al.: The impact of the European Resuscitation Council in Poland. Resuscitation. 2008; 77 (2): S60.
14. Pach J., Ogonowska D., Targosz D., Dziuban A., Brzyski P., Pach D.: Students knowledge on carbon monoxide. Przegl Lek. 2010; 67 (8): 583–590.
15. Weaver L.: Carbon Monoxide Poisoning. N Engl J Med. 2009; 360 (12): 1217–1225.
16. Raub J., Mathieu-Nolf M., Hampson N., Thom S.: Carbon monoxide poisoning—a public health perspective. Toxicology. 2000; 145 (1): 1–14.
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Autorzy i Afiliacje

Iwona Popiołek
1 2
Lech Popiołek
3
Jakub Marchewka
4 5
Grzegorz Dębski
6
Justyna Bolech-Gruca
1
Małgorzata Szumińska
7
Piotr Hydzik
1 2

  1. University Hospital in Kraków, Kraków, Poland
  2. Department of Toxicology and Environmental Diseases, Jagiellonian University Medical College, Kraków, Poland
  3. Private practice, Kraków, Poland
  4. Department of Physiotherapy, University of Physical Education, Kraków, Poland
  5. Department of Orthopedics and Trauma Surgery, 5th Military Hospital, Kraków, Poland
  6. Radiology Department, 5th Military Hospital, Kraków, Poland
  7. Department of Endocrinology, Jagiellonian University Medical College, Kraków, Poland
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Abstrakt

Memory trace is an effect of temporary arousal (perception, experience, action) that causes a specific change in the nervous system. Memory allows to record and recall various information, thus enabling to learn new things. It is an extremely active and dynamic process. The influence of emotions on memory is obvious, largely determined by the close cooperation of the amygdala (responsible for emo-tions) and the hippocampus (memory processes).
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Bibliografia

1. Vetulani J.: Mózg: fascynacje, problemy, tajemnice. Homini, Kraków 2010; 183–229.
2. Domżał T.M.: Pamięć w neurologii: zaburzenia, diagnostyka i leczenie. Forum Medycyny Rodzinnej. 2013; 7 (4): 155–164.
3. Gerardin E.: Morphometry of the human hippocampus from MRI and conventional MRI high field. Université Paris Sud-Paris XI, 2012. English. ffNNT: 2012PA112375ff.
4. Bisaz R., Travaglia A., Alberini C.M.: The neurobiological bases of memory formation: from physiological conditions to psychopathology. Psychopathology. 2014; 47: 347–356.
5. Asok A., Leroy F., Rayman J. B.: Molecular mechanisms of the memory trace. Trends in Neurosciences. 2019; 42 (1): 14–22.
6. Antonova I., Fang-Min Lu, Zablow L., Udo H., Hawkins R.D.: Rapid and long-lasting increase in sites for synapse assembly during late-phase potentiation in rat hippocampal neurons. PLoS One. 2009; 4: e7690.
7. Rasch B., Born J.: About Sleep’s Role in Memory. Physiological Review. 2013; 93: 681–766.
8. Holcman D., Schuss Z.: Time scale of diffusion in molecular and cellular biology. Journal of Physics A: Mathematical and Theoretical. 2014; 47 (17): 28.
9. Kennedy M.B.: Synaptic signaling in learning and memory. Cold Spring Harbor Perspectives in Biology. 2016; 8 (2): a016824.
10. Rymarczyk K., Makowska I., Pałka-Szafraniec K.: Plastyczność dorosłej kory mózgowej. Aktualności Neurologiczne. 2015; 15 (2): 80–87.
11. Maguire E.A., Woollett K., Spiers, H.J.: London taxi drivers and bus drivers: a structural MRI and neuropsychological analysis. Hippocampus. 2006; 16: 1091–1101.
12. Richardson F.M., Price C.J.: Structural MRI studies of language function in the undamaged brain. Brain Structure and Function. 2009; 213 (6): 511–523.
13. Giffin F., Mitchell D.E.: The rate of recovery of vision after early monocular deprivation in kittens. The Journal of Physiology (London). 1978; 274: 511–537.
14. Camina E., Güell F.: The Neuroanatomical, Neurophysiological and Psychological Basis of Memory: Current Models and Their Origins. Frontiers in Pharmacology. 2017; 8: 438.
15. Sperling G.: The information available in brief visual presentations. Psychological Monographs. 1960; 74: 1–30.
16. Vandenbroucke A.R.E., Sligte I.G., Barrett A.B., Seth A.K., Fahrenfort J.J., Lamme V.A.F.: Accurate metacognition for visual sensory memory representations. Psychological Science. 2014; 25: 861–873.
17. Haber R.N.: The impending demise of the icon: a critique of the concept of iconic storage in visual information processing. Behavioral and Brain Science. 1983; 6: 1–54.
18. Jonides J., Lewis R.L., Nee D.E., Lustig C.A., Berman M.G., Moore K.S.: The mind and brain of short- term memory. Annual Review of Psychology. 2008; 59: 193–224.
19. Standing L.: Learning 10,000 pictures. Quarterly Journal of Experimental Psychology. 1973; 25: 207–222.
20. Ogmen H., Herzog M.H.: A New Conceptualization of Human Visual Sensory-Memory. Frontiers in Psychology. 2016; 7: 830.
21. Alberini C.M., Ledoux J.E.: Memory reconsolidation. Current Biology. 2013; 23: R746–750.
22. Nader K., Hardt O.: A single standard for memory: the case for reconsolidation. Nature Reviews Neuroscience. 2009; 10: 224–234.
23. Marchetti G.: Attention and working memory: two basic mechanisms for constructing temporal experiences. Frontiers in Psychology. 2014; 5: 880.
24. Morris R.G.: D.O. Hebb: The Organization of Behavior, Wiley: New York; 1949. Brain Res Bull. 1999; 50 (5–6): 437.
25. Norris D.: Short-term memory and long-term memory are still different. Psychological Bulletin. 2017; 143 (9): 992–1009.
26. Nie J., Zhang Z., Wang B., et al.: Different memory patterns of digits: a functional MRI study. Journal of Biomedical Science. 2019; 26 (1): 22.
27. Alberini C.M.: The role of protein synthesis during the labile phases of memory: revisiting the skepticism. Neurobiology of Learning and Memory. 2008; 89: 234–246.
28. Eriksson J., Vogel E.K., Lansner A., Bergström F., Nyberg L.: Neurocognitive Architecture of Working Memory. Neuron. 2015; 88 (1): 33–46.
29. MacKay D.G., Shafto M., Taylor J.K., Marian D.E., Abrams L., Dyer J.R.: Relations between emotion, memory, and attention: Evidence from taboo Stroop, lexical decision, and immediate memory tasks. Memory & Cognition. 2004; 32: 474–487.
30. Burton L., Vardy S.B., Frohlich J., Dimitri D., Wyatt G., Rabin L.: Affective tasks elicit material-specific memory effects in temporal lobectomy patients. Journal of Clinical and Experimental Neuropsychology. 2004; 26: 1021–1030.
31. Döhnel K., Sommer M., Ibach B., Rothmayr C., Meinhardt J., Hajak G.: Neuronal correlates of emotional working memory in patients with mild cognitive impairment. Neuropsychologia. 2008; 46: 37–48.
32. Talmi D., Luk B.T.C., McGarry L.M., Moscovitch M.: The contribution of relatedness and distinct- iveness to emotionally-enhanced memory. Journal of Memory and Language. 2007; 56 (4), 555–574.
33. Rothermund K., Wentura D., Bak P.M.: Automatic attention to stimuli signalling chances and dangers: Moderating effects of positive and negative goal and action contexts. Cognition & Emotion. 2001; 15: 231–248.
34. Neisser U., Harsch N.: Phantom flashbulbs: false recollections of hearing the news about Challenger. In: Winograd E., Neisser U. eds. Affect and accuracy in recall: Studies of ‘flashbulb’ memories. Cambridge University Press, New York 1992; 9–31.
35. Geller E.S., Farris J.C., Post D.S.: Prompting a consumer behavior for pollution control. Journal of Applied Behavior Analysis. 1973; 6 (3): 367–376.
36. Meis J., Kashima Y.: Signage as a tool for behavioral change: Direct and indirect routes to understanding the meaning of a sign. PLOS One. 2017; 12 (8): e0182975.
37. Wirth M.M.: Hormones, stress, and cognition: The effects of glucocorticoids and oxytocin on memory. Adaptive Human Behavior and Physiology. 2015; 1: 177–201.
38. Kim E.J., Pellman B., Kim J.J.: Stress effects on the hippocampus: a critical review. Learning & Memory. 2015; 22 (9): 411–416.
39. Anderson A.K., Yamaguchi Y., Grabski W., Lacka D.: Emotional memories are not all created equal: evidence for selective memory enhancement. Learning & Memory. 2006; 13 (6): 711–718.
40. Zhu J., Nelson K., Toth J., Muscat J.E.: Nicotine dependence as an independent risk factor for atherosclerosis in the National Lung Screening Trial. BMC Public Health. 2019; 19: 103.
41. Lee H.S., Ghetti A., Pinto-Duarte A., Wang X., Dziewczapolski G., Galimi F., Huitron-Resendiz S., Pina-Crespo J.C., Roberts A.J., Verma I.M.: Astrocytes contribute to gamma oscillations and recognition memory. Proccedings of the National Academy of Science of the United States of America. 2014; 111: E3343–E3352.
42. Pinto-Duarte A., Roberts A.J., Ouyang K., Sejnowsk T.J.: Impairments in remote memory caused by the lack of Type 2 IP3 receptors. GLIA. 2019; 67 (10): 1976–1989.
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Autorzy i Afiliacje

Paulina Fałek
1
Artur Fałek
1
Monika Kager
2
Richard Kager
3
Piotr Walkowicz
2
Marcin Kubiak
2
Elżbieta Starosławska
2
Franciszek Burdan
2 4

  1. Independent Public Healthcare, Puławy, Poland
  2. St. John’s Cancer Center, Lublin, Poland
  3. Public Independent Clinical Hospital Number 4, Lublin, Poland
  4. Human Anatomy Department, Medical University of Lublin, Lublin, Poland
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Abstrakt

Background: Cardiovascular diseases are the first cause of death globally. Hypercholester-olemia is the most important factor responsible for atherosclerotic plaque formation and increasing cardiovascular risk. Reduction of LDL-C level is the most relevant goal for reduction of cardiovascular risk.
Aims: Real life adherence to guidelines concerning statin therapy in one center study population. Methods: We analyzed data collected in the Department of Internal Diseases from September 2019 to February 2020, obtained from 238 patients hospitalized in this time period. We assessed application of the new 2019 ESC/EAS Guidelines for the Management of Dyslipidaemias in daily clinical practice and compared effectiveness of LLT according to 2016 and 2019 guidelines.
Results: Only 1 in 5 patients with dyslipideamia achieve the 2019 ESC/EAS guideline-recommended levels of LDL-C with relation to their TCVR. We noticed that 20 of patients who did not achieve proper 2019 LDL level, meet the therapy targets established in year 2016. We observed that higher patient TCVR resulted in better compliance with guidelines and ordination of proper LLT. Most patients were on monotherapy with statins.
Conclusions: It could be beneficial to start treatment with double or even triple therapy especially in group with the highest LDL-C levels.
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Bibliografia

1. Cardiovascular diseases. Available from: https://www.who.int/health-topics/cardiovascular-diseases/ #tab=tab_1
2. Poland | Institute for Health Metrics and Evaluation [Internet]. Available from: http://www.healthdata.org/poland
3. Ference B.A., Ginsberg H.N., Graham I., et al.: Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J. 2017; 38 (32): 2459–2472.
4. Navarese E.P., Robinson J.G., Kowalewski M., et al.: Association between baseline LDL-C level and total and cardiovascular mortality after LDL-C lowering a systematic review and meta-analysis. JAMA. 2018; 319 (15): 1566–1579.
5. Zdrojewski T., Solnica B., Cybulska B., et al.: Prevalence of lipid abnormalities in Poland. the NATPOL 2011 survey. Kardiol Pol. 2016; 74 (3): 213–223.
6. Pająk A., Szafraniec K., Polak M., et al.: Changes in the prevalence, treatment, and control of hypercholesterolemia and other dyslipidemias over 10 years in Poland: The WOBASZ study. Pol Arch Med Wewn. 2016; 126 (9): 642–652.
7. Mach F., Baigent C., Catapano A.L., et al.: 2019 ESC/EAS Guidelines for the management of dyslipidaemias: Lipid modification to reduce cardiovascular risk. Vol. 41, European Heart Journal. 2020. p. 111–188.
8. Catapano A.L., Graham I., De Backer G., et al.: 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias. Eur Heart J. 2016; 37: 2999–3058.
9. Baigent C., Blackwell L., Emberson J., et al.: Efficacy and safety of more intensive lowering of LDL cholesterol: A meta-analysis of data from 170 000 participants in 26 randomised trials. Lancet. 2010; 376 (9753): 1670–1681.
10. Silverman M.G., Ference B.A., Im K., et al.: Association between lowering LDL-C and cardiovascular risk reduction among different therapeutic interventions: A systematic review and meta-analysis. JAMA. 2016; 316 (12): 1289–1297.
11. Giugliano R.P., Pedersen T.R., Park J.G., et al.: Clinical efficacy and safety of achieving very low LDL- cholesterol concentrations with the PCSK9 inhibitor evolocumab: a prespecified secondary analysis of the FOURIER trial. Lancet. 2017 Oct 28; 390 (10106): 1962–1971.
12. Soran H., Dent R., Durrington P.: Evidence-based goals in LDL-C reduction. Clin Res Cardiol. 2017; 106 (4): 237–248.
13. Masana L., Girona J., Ibarretxe D., et al.: Clinical and pathophysiological evidence supporting the safety of extremely low LDL levels — The zero-LDL hypothesis. J Clin Lipidol. 2018; 12 (2): 292–299. e3.
14. Katzmann J.L., Sorio-Vilela F., Dornstauder E., et al.: Non-statin lipid-lowering therapy over time in very-high-risk patients: effectiveness of fixed-dose statin / ezetimibe compared to separate pill combination on LDL-C. Clin Res Cardiol. 2020; (0123456789).
15. Guglielmi V., Bellia A., Pecchioli S., et al.: Effectiveness of adherence to lipid lowering therapy on LDL-cholesterol in patients with very high cardiovascular risk: A real-world evidence study in primary care. Atherosclerosis. 2017; 263: 36–41.
16. Kaddoura R., Orabi B., Salam A.M.: Efficacy and safety of PCSK9 monoclonal antibodies: an evidence-based review and update. J Drug Assess. 2020; 9 (1): 129–144.
17. Saborowski M., Dölle M., Manns M.P., et al.: Lipid-lowering therapy with pcsk9-inhibitors in the management of cardiovascular high-risk patients: Effectiveness, therapy adherence and safety in a real world cohort. Cardiol J. 2018; 25 (1): 32–41.
18. Novel Drug Approvals for 2015 | FDA [Internet]. Available from: https://www.fda.gov/drugs/new-drugs-fda-cders-new-molecular-entities-and-new-therapeutic-biological-products/novel-drug-ap-provals-2015
19. Zodda D., Giammona R., Schifilliti S.: Treatment Strategy for Dyslipidemia in Cardiovascular Disease Prevention: Focus on Old and New Drugs. Pharmacy. 2018; 6 (1): 10.
20. Szymański F.M., Barylski M., Cybulska B., et al.: Recommendation for the management of dyslipidemia in Poland — Third declaration of sopot. Interdisciplinary expert position statement endorsed by the Polish cardiac society working group on cardiovascular pharmacotherapy. Cardiol J. 2018; 25 (6): 655–665.
21. Koskinas K.C., Windecker S., Pedrazzini G., et al.: Evolocumab for Early Reduction of LDL Cholesterol Levels in Patients With Acute Coronary Syndromes (EVOPACS). J Am Coll Cardiol. 2019 Nov 19; 74 (20): 2452–62.
22. Sabatine M.S., Giugliano R.P., Keech A.C., et al.: Evolocumab and clinical outcomes in patients with cardiovascular disease. N Engl J Med. 2017; 376 (18): 1713–1722.
23. Murphy S.A., Pedersen T.R., Gaciong Z.A., et al.: Effect of the PCSK9 Inhibitor Evolocumab on Total Cardiovascular Events in Patients with Cardiovascular Disease: A Prespecified Analysis from the FOURIER Trial. JAMA Cardiol. 2019; 4 (7): 613–619.
24. Bittner V.A., Szarek M., Aylward P.E., et al.: Effect of Alirocumab on Lipoprotein(a) and Cardiovascular Risk After Acute Coronary Syndrome. J Am Coll Cardiol. 2020; 75 (2): 133–144.
25. Schwartz G.G., Steg P.G., Szarek M., et al.: Alirocumab and cardiovascular outcomes after acute coronary syndrome. N Engl J Med. 2018; 379 (22): 2097–2107.
26. Raal F.J., Kallend D., Ray K.K., et al.: Inclisiran for the treatment of heterozygous familial hypercholesterolemia. N Engl J Med. 2020 Apr 16; 382 (16): 1520–1530.
27. Ferri N., Corsini A.: Clinical Pharmacology of Statins: an Update. Curr Atheroscler Rep. 2020 Jun 3; 22 (7): 26.
28. Ballantyne C.M., Banach M., Mancini G.B.J., et al.: Efficacy and safety of bempedoic acid added to ezetimibe in statin-intolerant patients with hypercholesterolemia: A randomized, placebo-controlled study. Atherosclerosis. 2018; 277: 195–203.
29. Banach M., Duell P.B., Gotto A.M., et al.: Association of Bempedoic Acid Administration with Atherogenic Lipid Levels in Phase 3 Randomized Clinical Trials of Patients with Hypercholester-olemia. JAMA Cardiol. 2020; 1–11.
30. Kam N., Perera K., Zomer E., et al.: Inclisiran as Adjunct Lipid-Lowering Therapy for Patients with Cardiovascular Disease: A Cost-Effectiveness Analysis. Pharmacoeconomics. 2020; 38 (9): 1007–1020.
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Autorzy i Afiliacje

Patrycja Cecha
1
Anna Chromik
1
Ilona Piotrowska
1
Michał Zabojszcz
1
Magdalena Dolecka-Ślusarczyk
1
Zbigniew Siudak
1

  1. Collegium Medicum, Jan Kochanowski University, Kielce, Poland
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Abstrakt

White adipose tissue plays an important role in the catabolism of branched chain amino acids (BCAAs). Two initial regulatory steps in BCAAs catabolism are catalyzed by branched chain aminotrans-ferase (BCAT) and branched chain α-keto acid dehydrogenase complex (BCKDH complex), respectively. It has been demonstrated that synthetic ligands for PPARγ receptors increased mRNA levels for enzymes involved in BCAAs catabolism. We hypothesized that feeding rats with diet rich in linoleic acid (LA), a natural PPARγ agonist modifies mRNA levels for enzymes catalyzing BCAAs degradation in adipose tissue. The current pilot study was aimed at the investigation of the effect of diet rich in LA on mRNA levels for BCATm, branched chain α-keto acid dehydrogenase (E1 component of the BCKDH), and mRNA levels for the regulatory enzymes of BCKDH complex, a specific kinase (BDK) and a specific phosphatase (PPM1K) in epididymal white adipose tissue (eWAT). Wistar male rats were fed with high unsaturated fat diet containing mainly linoleic acid (study group) or with the high saturated fat diet (control group). The relative mRNA levels were quantified by reverse transcription PCR. We have found that in rats fed diet rich in LA mRNA level for BCATm decreased, while mRNA amount for BDK increased. There was no difference between mRNA levels for BCKDH E1 and PPM1K. It is con-ceivable that changes in mRNA levels for enzymes involved in BCAAs metabolism in eWAT may lead to modification of BCAAs catabolic rate. Further studies are required to fully elucidate this issue.
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Bibliografia

1. Nie C., He T., Zhang W., Zhang G., Ma X.: Branched chain amino acids: Beyond nutrition metabolism. Int J Mol Sci. 2018; 19 (4): 954. doi: 10.3390/ijms19040954
2. Brosnan J.T., Brosnan M.E.: Branched-chain amino acids: enzyme and substrate regulation. J Nutr. 2006; 136: 207S-11S. doi: 10.1093/jn/136.1.207S
3. Conway M.E., Hutson S.M.: The cytosolic and mitochondrial branched chain aminotransferase. in Branched chain amino acids in clinical nutrition. Ed. R. Rajendram, V.R. Preedy, V.B. Patel. Nutrition and Health. Humana Press, New York, NY. 2015; 25–40. doi: 10.1007/978-1-4939-1923-9_3
4. Cole J.T.: Metabolism of BCAAs. in Branched chain amino acids in clinical nutrition. Ed. R. Rajendram, V.R. Preedy, V.B. Patel. Humana Press, New York, NY. 2015; 13–24. doi: 10.1007/978-1-4939-1923-9_2
5. Yeaman S.J.: The mammalian 2-oxoacid dehydrogenases: a complex family. Trends in Biochemical Sciences. 1986; 11 (7): 293–296.
6. Wynn R.M., Li J., Brautigam C.A., Chuang J.L., Chuang D.T.: Structural and biochemical characterization of human mitochondrial branched-chain α-ketoacid dehydrogenase phosphatase. J Biol Chem. 2012; 287 (12): 9178–9192. doi: 10.1074/jbc.M111.314963
7. Herman M.A., She P., Peroni O.D., Lynch C.J., Kahn B.B.: Adipose tissue branched chain amino acid (BCAA) metabolism modulates circulating BCAA levels. J Biol Chem. 2010; 285 (15): 11348–11356. doi: 10.1074/jbc.M109.075184
8. Sun C., Mao S., Chen S., Zhang W., Liu C.: PPARs-orchestrated metabolic homeostasis in the adipose tissue. Int J Mol Sci. 2021; 22 (16): 8974. doi: 10.3390/ijms22168974
9. Kliewer S.A., Sundseth S.S., Jones S.A., et al.: Fatty acids and eicosanoids regulate gene expression through direct interactions with peroxisome proliferator-activated receptors alpha and gamma. Proc Natl Acad Sci U S A. 1997; 94 (9): 4318–4323. doi: 10.1073/pnas.94.9.4318
10. Rasouli N., Kern P.A., Elbein S.C., Sharma N.K., Das S.K.: Improved insulin sensitivity after treatment with PPARγ and PPARα ligands is mediated by genetically modulated transcripts. Pharmacogenet Genomics. 2012; 22 (7): 484–497. doi: 10.1097/FPC.0b013e328352a72e
11. Popov K.M., Zhao Y., Shimomura Y., Jaskiewicz J., Kedishvilli N.Y., Inwin J., Goodwin G.W., Harris R.A.: Dietary control and tissue expression of branched-chain alpha-ketoacid dehydrogenase kinase. Arch Biochem Biophys. 1995; 316 (1): 148–154. doi: 10.1006/abbi.1995.1022
12. Gillim S.E., Paxton R., Cook G.A., Harris R.A.: Activity state of the branched-chain alpha-ketoacid dehydrogenase complex in heart, liver, and kidney of normal, fasted, diabetic, and protein-starved rats. Bioch Biophys Res Comm. 1983; 111 (1): 74–81. doi: 10.1016/s0006-291x(83)80119-3
13. Blanchard P.G., Moreira R.J., Castro É., et al.: PPARγ is a major regulator of branched-chain amino acid blood levels and catabolism in white and brown adipose tissues. Metabolism. 2018; 89: 27–38. doi: 10.1016/j.metabol.2018.09.007
14. Palou M., Priego T., Sánchez J., Rodríguez A.M., Palou A., Picó C.: Gene expression patterns in visceral and subcutaneous adipose depots in rats are linked to their morphologic features. Cell Physiol Biochem. 2009; 24 (5–6): 547–556. doi: 10.1159/000257511
15. Nellis M.M., Doering C.B., Kasinski A., Danner D.J.: Insulin increases branched-chain alpha-ketoacid dehydrogenase kinase expression in Clone 9 rat cells. Am J Physiol Endocrinol Metab. 2002; 283 (4): E853-E860. doi: 10.1152/ajpendo.00133.2002
16. Lai M.C., Teng T.H., Yang C.: The natural PPAR agonist linoleic acid stimulated insulin release in the rat pancreas. J Vet Med Sci. 2013; 75 (11): 1449–1454. doi: 10.1292/jvms.13-0189
17. Lian K., Du C., Liu Y., et al.: Impaired adiponectin signaling contributes to disturbed catabolism of branched-chain amino acids in diabetic mice. Diabetes. 2015; 64 (1): 49–59. doi: 10.2337/db14-0312
18. Pérez-Matute P., Martínez J.A., Marti A., Moreno-Aliaga M.J.: Linoleic acid decreases leptin and adiponectin secretion from primary rat adipocytes in the presence of insulin. Lipids. 2007; 42 (10): 913–920. doi: 10.1007/s11745-007-3092-y
19. Harris R.A., Joshi M., Jeoung N.H.: Mechanisms responsible for regulation of branched-chain amino acid catabolism. Biochem Biophys Res Commun. 2004; 313 (2): 391–396. doi: 10.1016/j.bbrc.2003.11.007
20. Zhou M., Lu G., Gao C., Wang Y., Sun H.: Tissue-specific and nutrient regulation of the branched- chain α-keto acid dehydrogenase phosphatase, protein phosphatase 2Cm (PP2Cm). J Biol Chem. 2012; 287 (28): 23397–23406. doi: 10.1074/jbc.M112.351031
21. Shimomura Y., Obayashi M., Murakami T., Harris R.A.: Regulation of branched-chain amino acid catabolism: nutritional and hormonal regulation of activity and expression of the branched-chain alpha-keto acid dehydrogenase kinase. Curr Opin Clin Nutr Metab Care. 2001; 4 (5): 419–423. doi: 10.1097/00075197-200109000-00013
22. Harris R.A., Kobayashi R., Murakami T., Shimomura Y.: Regulation of branched-chain alpha-keto acid dehydrogenase kinase expression in rat liver. J Nutr. 2001; 131 (3): 841S–845S. doi: 10.1093/jn/131.3.841S
23. Green C.R., Wallace M., Divakaruni A.S., et al.: Branched-chain amino acid catabolism fuels adipocyte differentiation and lipogenesis. Nat Chem Biol. 2016; 12 (1): 15–21. doi: 10.1038/nchembio.1961
24. Koh P.L., Ho J.P., Pang C., Tan H.C., Kovalik J.P.: PH-10 — The role of leucine in stimulation of adipocyte lipolysis. Diabetes Res Clin Pract. 2016; 120: 181–182. doi: 10.1016/S0168-8227(16)31406-1
25. Liang H., Mokrani A., Chisomo-Kasiya H., et al.: Dietary leucine affects glucose metabolism and lipogenesis involved in TOR/PI3K/Akt signaling pathway for juvenile blunt snout bream Megalobrama amblycephala. Fish Physiol Biochem. 2019; 45 (2): 719–732. doi: 10.1007/s10695-018-0594-x
26. Nilsen M.S., Jersin R.Å., Ulvik A., et al.: 3-Hydroxyisobutyrate, a strong marker of insulin resistance in type 2 diabetes and obesity that modulates white and brown adipocyte metabolism. Diabetes. 2020; 69 (9): 1903–1916. doi: 10.2337/db19-1174
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Autorzy i Afiliacje

Małgorzata Knapik-Czajka
1
Justyna Bieleń
1
Monika Zajonz
1
Anna Gawędzka
1
Jagoda Drąg
1
Małgorzata Belczyk
1

  1. Department of Biochemical Analytics, Jagiellonian University Medical College, Kraków, Poland
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Abstrakt

Background: To assess and compare mid-term outcomes and the quality of life (QoL) in patients with multivessel coronary artery disease (MVD) and moderate ischemic mitral regurgitation (IMR), treated with either coronary artery bypass grafting (CABG; group I) or CABG + mitral annulo-plasty (CABG+MA; group II) in 12-months follow-up after surgery.
Methods: We prospectively analyzed 74 patients (50.7% female, 66 [67–72] years) with at least moderate IMR, 3–24 weeks after myocardial infarction (MI). The effective regurgitation orifice (ERO) was used for a quantitative IMR assessment. To evaluate QoL we used a Short Form-36 (SF-36) questionnaire.
Results: Patients in group II spent more time in the hospital, expired more infection complications and received more often in-hospital complications requiring use amines and intra-aortic balloon pump as compared to those in group I. Analysis of SF-36 showed that all patients treated surgically notable improved their QoL during 12 months of follow-up.
Conclusions: We observed a significant improvement in QoL among patients with MVD in 12 months follow-up after surgery irrespective of treatment type.
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Bibliografia

1. Neumann F.J., Sousa-Uva M., Ahlsson A., Alfonso F., Banning A.P., Benedetto U., et al.: 2018 ESC/ EACTS Guidelines on myocardial revascularization. Eur Heart J. 2019; 40 (2): 87–165.
2. Baumgartner H., Falk V., Bax J.J., De Bonis M., Hamm C., Holm P.J., et al.: 2017 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J. 2017; 38 (36): 2739–2791.
3. Hays R.D.: The Medical Outcomes Study (MOS) Measures of Patient Adherence. Retrieved April 19, 2004, from the RAND Corporation web site: http://www.rand.org/health/surveys/MOS.adherence.measures.pdf.
4. Cerqueira M., Weissman N., Dilsizian V., et al.: Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart. Circulation. 2002; 105 (4): 539–542.
5. Lang R., Bierig M., Devereux R., et al.: Recommendations for Chamber Quantification: A Report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group, Developed in Conjunction with the European Association of Echocardiography, a Branch of the European Society of Cardiology. J Am Soc Echocardiogr. 2005; 18: 1440–1463.
6. Yiu S.F., Enriquez-Sarano M., Tribouilloy C., Seward J.B., Tajik A.J.: Determinants of the degree of functional mitral regurgitation in patients with systolic left ventricular dysfunction: A quantitative clinical study. Circulation 2000; 102: 1400–1406.
7. Srichai M.B., Grimm R.A., Stillman A.E., Gillinov A.M., Rodriguez L.L., Lieber M.L., et al.: Ischemic mitral regurgitation: impact of the left ventricle and mitral valve in patients with left ventricular systolic dysfunction. Ann Thorac Surg. 2005;80 (1): 170–178.
8. Kang D.H., Kim M.J., Kang S.J., Song J.M., Song H., Hong M.K., et al.: Mitral valve repair versus revascularization alone in the treatment of ischemic mitral regurgitation. Circulation. 2006; 114 (1 Suppl): I499–I503.
9. Kim B.J., Kim Y.S., Kim H.J., Ju M.H., Kim J.B., Jung S.H., et al.: Concomitant mitral valve surgery in patients with moderate ischemic mitral regurgitation undergoing coronary artery bypass grafting. J Thorac Dis. 2018; 10 (6): 3632–3642.
10. Bouchard D., Jensen H., Carrier M., Demers P., Pellerin M., Perrault L.P., et al.: Effect of systematic downsizing rigid ring annuloplasty in patients with moderate ischemic mitral regurgitation. J Thorac Cardiovasc Surg. 2014; 147 (5): 1471–1477.
11. Chan K.M., Punjabi P.P., Flather M., Wage R., Symmonds K., Roussin I., et al.: Coronary artery bypass surgery with or without mitral valve annuloplasty in moderate functional ischemic mitral regurgitation: final results of the Randomized Ischemic Mitral Evaluation (RIME) trial. Circulation. 2012; 126 (21): 2502–2510.
12. Fattouch K., Guccione F., Sampognaro R., Panzarella G., Corrado E., Navarra E., et al.: POINT: Efficacy of adding mitral valve restrictive annuloplasty to coronary artery bypass grafting in patients with moderate ischemic mitral valve regurgitation: a randomized trial. J Thorac Cardiovasc Surg. 2009; 138 (2): 278–285.
13. Borger M.A., Alam A., Murphy P.M., Doenst T., David T.E.: Chronic ischemic mitral regurgitation: repair, replace or rethink? Ann Thorac Surg. 2006; 81 (3): 1153–1161.
14. Sundt T.M.: Surgery for ischemic mitral regurgitation. N Engl J Med. 2014; 371 (23): 2228–2289.
15. Wagner A.K., Gandek B., Aaronson N.K., et al.: Cross-cultural comparison of the content of SF-36 translations across 10 countries: result from the IQOLA Project. International Quality of Life Assessment. J Clin Epidemiol 1998; 51: 925–932.
16. Simchen E., Galai N., Braun D., et al.: Sociodemographic and clinical factors associated with low quality of life one year after coronary bypass operations: the Israeli coronary artery bypass study (ISCAB). J Thorac Cardiovasc Surg. 2001; 121: 909–919.
17. Permanyer M., Brotons C., Cascant P., et al.: Assessment of quality of life related health 2 years after coronary surgery. Med Clin (Barc). 1997; 108: 446–451.
18. Al-Ruzzeh S., Athanasiou T., Mangoush O., Wray J., Modine T., George S., Amrani M.: Predictors of poor mid-term health related quality of life after primary isolated coronary artery bypass grafting surgery. Heart. 2005 Dec; 91 (12): 1557–1562.
19. Westlake C., Dracup K., Creaser J., et al.: Correlates of health-related quality of life in patients with heart failure. Heart Lung 2002; 31: 85–93.
20. Smith P.K., Puskas J.D. Ascheim D.D., Voisine P., Gelijns A.C., Moskowitz A.J., et al.: Surgical treatment of moderate ischemia mitral regurgitation. N Engl J Med. 2014; 371: 2178–2188.
21. Baig K., Harling L., Papanikitas J., Attaran S., Ashrafian H., Casula R., et al.: Does coronary artery bypass grafting improve quality of life in elderly patients? Interact Cardiovasc Thorac Surg. 2013; 17 (3): 542–553.
22. Jokinen J.J., Hippeläinen M.J., Turpeinen A.K., Pitkänen O., Hartikainen J.E.: Health-related quality of life after coronary artery bypass grafting: a review of randomized controlled trials. J Card Surg. 2010; 25 (3): 309–317.
23. Dunning J., Waller J.R., Smith B., Pitts S., Kendall S.W., Khan K.: Coronary artery bypass grafting is associated with excellent long-term survival and quality of life: a prospective cohort study. Ann Thorac Surg. 2008; 85: 1988–1993.
24. Rijnhart-de Jong H., Haenen J., Bol Raap G., et al.: Determinants of non-recovery in physical health- related quality of life one year after cardiac surgery: a prospective single Centre observational study. J Cardiothorac Surg. 2020; 15 (1): 234. doi: 10.1186/s13019-020-01273-1
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Autorzy i Afiliacje

Radosław Piątkowski
1
Jakub Kucharz
2
Monika Gawałko
1 3 4
Monika Budnik
1
Katarzyna Wołosiewicz
5
Barbara Kozub
6
Janusz Kochanowski
1
Marcin Grabowski
1
Grzegorz Opolski
1

  1. 1st Department of Cardiology, Medical University of Warsaw, Warsaw, Poland
  2. Department of Uro-Oncology, Maria Skłodowska-Curie, National Research Institute of Oncology, Warsaw, Poland
  3. Department of Cardiology, Maastricht University Medical Centre and Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands
  4. Institute of Pharmacology, West German Heart and Vascular Centre, University Duisburg-Essen, Germany
  5. 1st Department of Pediatrics, Bielanski Hospital, Warsaw, Poland
  6. Department of Ophthalmology, Medical Centre for Postgraduate Education, Warsaw, Poland
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Abstrakt

There are only very few studies on the anatomy of the deep brachial artery — DBA (arteria profunda brachii), both regarding its course, branching pattern and contribution to the cubital rete. Most of the textbooks are based on data which remain unchanged for years. The aim of this article was to summarize the current knowledge on this vessel, based on the anatomical and clinical studies and other sources available including also own cadaveric study. We tried to present also some controversies regarded to the nomenclature of the branches of the DBA.
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Bibliografia

1. Standring S.: Gray’s Anatomy. The Anatomical Basis of Clinical Practice. Churchill Livingstone Elsevier 2008. ISBN 978-0-8089-2371-8.
2. Spodnik J.H.: Polsko angielsko łacińskie mianownictwo anatomiczne. Edra, Urban & Partner, Wrocław 2017. ISBN 978-83-65625-53-3.
3. Aleksandrowicz R., Gołąb B., Narkiewicz O.: Mianownictwo anatomiczne — wydanie V. PZWL Warszawa 1989. ISBN 83-200-1311-9.
4. Kahn C.I., MacNeil M., Fanola C.L., Whitney E.R.: Complex arterial patterning in an anatomical donor. Translational Research in Anatomy. 2018 Sept; 12: 11–19; https://doi.org/10.1016/j.tria.2018.06.001
5. Żytkowski A., Tubbs R.S., Iwanaga J., Clarke E., Polguj M., Wysiadecki G.: Anatomical normality and variability: Historical perspective and methodological consideration. Translational Research in Anatomy. 2021 Jun; 23: 100105. https://doi.org/10.1016/j.tria.2020.100105
6. Tubbs R.S., Parmar A., Noordeh N., Rogers C., Rogers N., Loukas M., Shoja M.M., Cohen Gadol A.A.: Surgical anatomy of the radial nerve and profunda brachii artery within the triangular interval. Ital J Anat Embryol. 2008 Jul–Sep; 113 (3): 129–134. PMID: 19205584.
7. Menck J., Döbler A., Döhler J.R.: Vascularization of the humerus. Langenbecks Arch Chir. 1997; 382 (3): 123–127. PMID: 9324609.
8. Casoli V., Kostopoulos E., Pélissier P., Caix P., Martin D., Baudet J.: The middle collateral artery: anatomic basis for the “extreme” lateral arm flap. Surg Radiol Anat. 2004 Jun; 26 (3): 172–177. https://doi.org/10.1007/s00276-003-0206-y. Epub 2004 Jan 17. PMID: 14730394.
9. Katsaros J., Schusterman M., Beppu M., Banis J.C. Jr, Acland R.D.: The lateral upper arm flap: anatomy and clinical applications. Ann Plast Surg. 1984 Jun; 12 (6): 489–500. https://doi.org/10.1097/00000637-198406000-00001. PMID: 6465806.
10. Hammer H., Bugyi I.: Free transfer of a lateral upper arm flap. Handchir Mikrochir Plast Chir. 1988 Jan; 20 (1): 20–26. PMID: 2895050.
11. Wenig B.L.: The lateral arm free flap for head and neck reconstruction. Otolaryngol Head Neck Surg. 1993 Jul; 109 (1): 116–119. https://doi.org/10.1177/019459989310900121. PMID: 8336957.
12. Lim A.Y., Pereira B.P., Kumar V.P.: The long head of the triceps brachii as a free functioning muscle transfer. Plast Reconstr Surg. 2001 Jun; 107 (7): 1746–1752. https://doi.org/10.1097/00006534-200106000-00016. PMID: 11391194.
13. Piquilloud G., Villani F., Casoli V.: The medial head of the triceps brachii. Anatomy and blood supply of a new muscular free flap: the medial triceps free flap. Surg Radiol Anat. 2011 Jul; 33 (5): 415–420. https://doi.org/10.1007/s00276-010-0739-9. Epub 2010 Oct 26. PMID: 20976453.
14. Naveen K., Jyothsna P., Nayak S.B., Mohandas R.K., Swamy R.S., Deepthinath R., Shetty S.D.: Variant origin of an arterial trunk from axillary artery continuing as profunda brachii artery—a unique arterial variation in the axilla and its clinical implications. Ethiop J Health Sci. 2014 Jan; 24 (1): 93–96. https://doi.org/10.4314/ejhs.v24i1.13. PMID: 24591805.
15. Aastha, Jain A., Kumar M.S.: An unusual variation of axillary artery: a case report. J Clin Diagn Res. 2015 Jan; 9 (1): AD05–7. https://doi.org/10.7860/JCDR/2015/11680.5477. Epub 2015 Jan 1. PMID: 25737968.
16. Celik H.H., Aldur M.M., Tunali S., Ozdemir M.B., Aktekin M.: Multiple variations of the deep artery of arm: double deep artery of arm and deep artery of arm with the superior ulnar collateral artery. A case report. Morphologie. 2004 Dec; 88 (283): 188–190. https://doi.org/10.1016/s1286-0115(04)98147-7. PMID: 15693422.
17. Vitale N., Lucarelli K., Di Bari N., Milano A.D.: Anomalous origin of a grafted left internal mammary artery from the deep brachial artery. Eur Heart J. 2021 Mar 21; 42 (12): 1182. https://doi.org/10.1093/eurheartj/ehab015
18. Iwanaga J., Singh V., Ohtsuka A., et al.: Acknowledging the use of human cadaveric tissues in research papers: Recommendations from anatomical journal editors. Clinical Anat. 2021; 2–4. https://doi.org/10.1002/ca.23671
19. Walocha J.A., Szczepański W., Miodoński A.J., Gorczyca J., Skrzat J., Bereza T., Ceranowicz P., Lorkowski J., Stachura J.: Application of acrylic emulsion Liquitex R (Binney and Smith) for the preparation of injection specimens and immunohistochemical studies — an observation. Folia Morphol. 2003; 62 (2): 157–161.
20. Crocco J.A.: The Classic Collector’s Edition Gray’s Anatomy. Bounty Books, New York 1977. ISBN 0-517-223651.
21. Panagouli E., Tsaraklis A., Gazouli I., Anagnostopoulou S., Venieratos D.: A rare variation of the axillary artery combined contralaterally with an unusual high origin of a superficial ulnar artery: description, review of the literature and embryological analysis. Ital J Anat Embryol. 2009 Oct–Dec; 114 (4): 145–156. PMID: 20578671.
22. Clarke E., Mazurek A., Radek M., Żytkowski A., Twardokęs W., Polguj M., Wysiadecki G.: Superficial brachial artery — A case report with commentaries on the classification. Trans Res in Anat. 2021; 23: 100112. https://doi.org/10.1016/j.tria.2021.100112
23. Yücel A.H.: Unilateral variation of the arterial pattern of the human upper extremity with a muscle variation of the hand. Acta Med Okayama. 1999 Apr; 53 (2): 61–65. https://doi.org/10.18926/AMO/31629. PMID: 10358720
24. Cavdar S., Zeybek A., Bayramiçli M.: Rare variation of the axillary artery. Clin Anat 2000; 13 (1): 66–68. https://doi.org/10.1002/(SICI)1098-2353(2000)13:166::AID-CA8>3.0.CO;2-M.
25. Dalin L., Jingqiang Y., Kun Z., Yunhui C.: Surgical treatment of deep brachial artery aneurysm. Ann Vasc Surg. 2011 Oct; 25 (7): 983.e13–6. https://doi.org/10.1016/j.avsg.2011.05.006.
26. Griffin L., Garland S.J., Ivanova T., Hughson R.L.: Blood flow in the triceps brachii muscle in humans during sustained submaximal isometric contractions. Eur J Appl Physiol. 2001 May; 84 (5): 432–437. https://doi.org/10.1007/s004210100397. PMID: 11417431
27. de Paula R.C., Erthal R., Fernandes R.M.P., Babinski M.A., Silva J.G., Chagas C.A.A.: Alomalous origin of the deep brachial artery (profunda brachii) observed in bilateral arms: case report. J Vasc Bras. 2013; 12 (1): 53–56.
28. Osiak K., Elnazir P., Mazurek A., Pasternak A.: Prevalence of the persistent median artery in patients undergoing surgical open carpal tunnel release: A case series. Trans Res in Anat; 2021; 23: 100113. https://doi.org/10.1016/j.tria.2021.100113
29. Rodriguez-Niedenführ M., Burton G.J., Deu J., Sañudo J.R.: Development of the arterial pattern in the upper limb of staged human embryos: normal development and anatomic variations. J Anat 2001; 199 (4): 407–417. PMID: 11693301.
30. Dubreuil-Chambardel L.: Variations des Arteres du Membre Superieur. Paris: Masson et Cie, 1926.
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Autorzy i Afiliacje

Wojciech Przybycień
1
Michał Zarzecki
1
Agata Musiał
1
Paweł Depukat
1
Bartłomiej Kruszyna
1
Agata Mazurek
1
Julia Jaszczyńska
1
Kinga Glądys
1
Ewa Walocha
2
Ewa Mizia
1
Grzegorz Wysiadecki
3
Jerzy Walocha
1

  1. Department of Anatomy, Jagiellonian University Medical College, Kraków, Poland
  2. Department of Clinical Nursing, Institute of Nursing and Obstetrics, Jagiellonian University Medical College, Kraków, Poland
  3. Department of Normal and Clinical Anatomy, Chair of Anatomy and Histology, Medical University of Łódź, Łódź, Poland

Abstrakt

Microvascular angina (MVA) is a condition characterized by the presence of angina-like chest pain, a positive response to exercise stress tests, and no significant stenosis of coronary arteries in coronary angiography, with absence of any other specific cardiac diseases. The etiology of this syndrome is still not known and it is probably multifactorial. Coronary microvascular dysfunction is proposed as the main pathophysiological mechanism in the development of MVA. Altered somatic and visceral pain perception and autonomic imbalance, in addition to myocardial ischemia, has been observed in subjects with MVA, involving dynamic variations in the vasomotor tone of coronary microcirculation with consequent tran-sient ischemic episodes. Other theories suggest that MVA may be a result of a chronic inflammatory state in the body that can negatively influence the endothelium or a local imbalance of factors regulating its function. This article presents the latest information about the epidemiology, diagnostics, etiopathogen-esis, prognosis, and treatment of patients with MVA.
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Autorzy i Afiliacje

Jarosław Jarczewski
1
Aleksandra Jarczewska
1
Andrzej Boryczko
1
Adrian Poniatowski
1
Agata Furgała
1
ORCID: ORCID
Andrzej Surdacki
2
Krzysztof Gil
1

  1. Department of Pathophysiology, Faculty of Medicine, Jagiellonian University Medical College, Kraków, Poland
  2. Second Department of Cardiology, Institute of Cardiology, Jagiellonian University Medical College, Kraków, Poland
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Abstrakt

With the steady increase in the incidence of breast cancer in women, treatment that includes not only tumor removal but also breast reconstruction is becoming a more relevant issue for oncologic and plastic surgeons. Mastectomy recently evolved as a form of primary prevention of hereditary breast cancer, commonly performed in combination with simultaneous reconstruction. A case of 44-year-old woman who underwent right mastectomy with adjuvant radiotherapy is presented. Due to the patient’s positivity for BRCA1 mutation and her wishes, a risk-reducing mastectomy with nipple-areola complex preservation and bilateral deep inferior epigastric artery perforator flap reconstruction were performed in one-stage. In selected cases this method appears to be the best possible procedure for simultaneous preventative and reconstructive management in patients with genetically determined breast cancer who have undergone mastectomy with radiotherapy.
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Bibliografia

1. Wojciechowska U., Didkowska J., Michałek I., et al.: Cancer in Poland in 2018. Polish National Cancer Registry, Warsaw 2020.
2. Kuchenbaecker K.B., Hopper J.L., Barnes D.R., et al.: Risks of breast, ovarian, and contralateral breast cancer for BRCA1 and BRCA2 mutation carriers. JAMA. 2017; 317: 2402–2416. doi: 10.1001/jama.2017.7112
3. Ulatowski Ł., Kaniewska A.: The Use Of The Diep Flap In The Modern Reconstructive Surgery. Pol J Surg. 2015; 87 (9): 472–481. doi: 10.1515/pjs-2015-0091
4. Bletsis P., Bucknor A., Chattha A., et al.: Evaluation of Contralateral and Bilateral Prophylactic Mastectomy and Reconstruction Outcomes: Comparing Alloplastic and Autologous Reconstruction. Ann Plast Surg. 2018 Apr; 80 (4): 144–149. doi: 10.1097/SAP.0000000000001358
5. Nestle-Krämling C., Kühn T.: Role of Breast Surgery in BRCA Mutation Carriers. Breast Care. 2012; 7: 378–382. doi: 10.1159/000343717
6. Rocco N., Montagna G., Criscitiello C., et al.: Nipple Sparing Mastectomy as a Risk-Reducing Procedure for BRCA-Mutated Patients. Genes. 2021; 12 (2): 253. doi: 10.3390/genes12020253
7. Daar D.A., Abdou S.A., Rosario L., et al.: Is There a Preferred Incision Location for Nipple-Sparing Mastectomy? A Systematic Review and Meta-Analysis. Plast Reconstr Surg. 2019 May; 143 (5): 906e– 919e. doi: 10.1097/PRS.0000000000005502
8. Chirurgiczne leczenie zmian nowotworowych piersi. Konsensus Polskiego Towarzystwa Chirurgii Onkologicznej. Eds. Z.I. Nowecki, A. Jeziorski. Biblioteka chirurga onkologa. Tom 5. Via Medica, Gdańsk 2016.
9. Ulatowski Ł., Noszczyk B.: BREAST-Q questionnaire: tool for evaluation of quality of life following breast reconstruction with DIEP/SIEA flap. Pol J Surg. 2018; 90 (4): 16–20. doi: 10.5604/01.3001.0012.0758
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Autorzy i Afiliacje

Łukasz Ulatowski
1
Piotr Gierej
1
Maria Molska
1

  1. Department of Plastic Surgery, Medical Centre for Postgraduate Education, Professor W. Orlowski Memorial Hospital, 231st Czerniakowska Street, 00-416 Warsaw, Poland
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Abstrakt

Pellagra is a rare disease caused by niacin deficiency or a disruption of its metabolism. Its manifestations are dermatitis with pronounced photosensitivity, gastrointestinal symptoms, and neuropsychiatric ailments. Currently pellagra is developed in people who chronically abuse alcohol or are treated with medications from specific pharmacological groups (immunosuppressive and anti-tuberculosis drugs).
Although the root cause of the disease was established in the mid-twentieth century, a detailed explanation of the processes leading to the development of symptoms has not yet been proposed. They include complex abnormalities at the molecular, metabolic, and immunological levels. Diagnostics is based primarily on the clinical presentation of the disease, while auxiliary tests play secondary role. The low prevalence of the disease, meaning that physicians are unfamiliar with its re-cognition, often leads to delays in diagnosis and appropriate treatment. The therapy is causal and based on administering niacinamide. Failure to implement treatment in the early stages of the disease leads to the patient’s death.
The aim of this literature review is to summarize the current state of knowledge on the pathomechanisms of pellagra, highlighting the clinical implications, and key elements of diagnostic and therapeutic manage-ment that are important in the treatment of pellagra patients.
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Bibliografia

1. Karthikeyan K., Thappa D.M.: Pellagra and skin. Int J Derm. 2002; 41 (8): 476–481.
2. Cao S., Wang X., Cestodio K.: Pellagra, an Almost-Forgotten Differential Diagnosis of Chronic Diarrhea: More Prevalent Than We Think. Nutrition in Clinical Practice. Nutr Clin Pract. 2019; 35 (5): 860–863.
3. Hegyi J., Schwartz R.A., Hegyi V.: Pellagra: Dermatitis, dementia, and diarrhea. Int J Derm. 2004; 43 (1): 1–5.
4. Prinzo Z.W.: Pellagra and its prevention and control in major emergencies. WHO. 2000; NHD/00.01: 1–32.
5. Narasimha V.L., Ganesh S., Reddy S., et al.: Pellagra and Alcohol Dependence Syndrome: Findings From a Tertiary Care Addiction Treatment Centre in India. MCA. 2019; 54 (2): 148–151.
6. Redzic S., Gupta V.: Niacin Deficiency. StatPearls 2021.
7. Elvehjem C.A., Madden R.J., Strong F.M., Woolley D.W.: Relation of Nicotinic Acid And Nicotinic Acid Amide To Canine Black Tongue. J Am Chem Soc. 1937; 59 (9): 1767–1768.
8. Stratigos J.D., Katsambas A.: Pellagra: a still existing disease. Br J Dermatol. 1977; 96 (1): 99–106.
9. Tymoczko J.L., Berg J.M., Stryer L.: Biochemistry. A Short Course. W.H. Freeman Company 2013.
10. Jacobson M.K., Jacobson E.L.: Vitamin B3 in Health and Disease: Toward the Second Century of Discovery. In: Methods in Molecular Biology. Methods Mol Biol. 2018; 1813: 3–8.
11. Horwitt M.K., Harvey C.C., Rothwell W.S., Cutler J.L., Haffron D.: Tryptophan-Niacin Relationships in Man. J Nutr. 1956; 60 (Suppl. 1): 1–43.
12. Badawy A.A.-B.: Pellagra and Alcoholism: A Biochemical Perspective. Alcohol Alcohol. 2014; 49 (3): 238–250.
13. Carpenter K.J.: The Relationship of Pellagra to Corn and the Low Availability of Niacin in Cereals. Experientia Suppl. 1983; 44: 197–222.
14. Judd L.E., Poskitt B.L.: Pellagra in a patient with an eating disorder. Br J Dermatol. 1991; 125 (1): 71–72.
15. Yamaguchi S., Miyagi T., Sogabe Y., et al.: Depletion of Epidermal Langerhans Cells in the Skin Lesions of Pellagra Patients. Am J Dermatopath. 2017; 39 (6): 428–432.
16. Kipsang J.K., Choge J.K., Marinda P.A., Khayeka-Wandabwa C.: Pellagra in isoniazid preventive and antiretroviral therapy. IDCases. 2019; 17: e00550.
17. Chauchan R., Vyas P., Mabena D.: Pellagra in an HIV-infected Individual: a Cause of Chronic Diarrhoea. Med J Armed Forces India. 1997; 53 (4): 303–304.
18. Murray R.K., Granner D.K., Rodwell V.W.: Harper’s Illustrated Biochemistry, Twenty-Seventh Edition. The McGraw-Hill Companies 2012.
19. Shah G.M., Shah R.G., Veillette H., Kirkland J.B., Pasieka J.L., Warner R.R.P.: Biochemical Assessment of Niacin Deficiency Among Carcinoid Cancer Patients. Am J Gastroenterol. 2005; 100 (10): 2307– 2314.
20. Periyasamy S., John S., Padmavati R., et al.: Association of Schizophrenia Risk With Disordered Niacin Metabolism in an Indian Genome-wide Association Study. JAMA Psychiatry. 2019; 76 (10): 1026–1034.
21. Sugita K., Ikenouchi-Sugita A., Nakayama Y., et al.: Prostaglandin E2 is critical for the development of niacin-deficiency-induced photosensitivity via ROS production. Sci Rep. 2013; 3 (1): 2973.
22. Wan P., Moat S., Anstey A.: Pellagra: a review with emphasis on photosensitivity. Br J Dermatol. 2011; 164 (6): 1188–1200.
23. Taylor R.G., Levy H.L., McInnes R.R.: Histidase and histidinemia. Clinical and molecular considerations. Mol Biol Med. 1991; 8 (1): 101–116.
24. Beretich G.R. Jr.: Do high leucine/low tryptophan dieting foods (yogurt, gelatin) with niacin supplementation cause neuropsychiatric symptoms (depression) but not dermatological symptoms of pellagra? Med Hypotheses. 2005; 65 (3): 628–629.
25. Savvidou S.: Pellagra: A Non-Eradicated Old Disease. Clin Pract. 2014; 4 (1): 637.
26. Duncan K.O., Bolognia J.L., Schaffer J.V., Ko C.J.: Dermatology Essentials. Elsevier 2014.
27. Crook M.A.: The importance of recognizing pellagra (niacin deficiency) as it still occurs. Nutrition. 2014; 30 (6): 729–730.
28. Szepietowski J., Wiśnicka B.: Zmiany skórne u chorych z zespołami otępiennymi. Polska Medycyna Paliatywna. 2004; 3 (1): 33–37.
29. Tadil S., Darla R.: Pemphigus Pellagrosus masquerading as cutaneous adverse drug reaction. Int J Derm. 2020; 2 (1): 34–37.
30. Zhang X.-J., Wang A.-P., Shi T.-Y., et al.: The psychosocial adaptation of patients with skin disease: a scoping review. BMC Public Health. 2019; 19: 1404.
31. Roosta N., Black D., Peng D., Riley L.: Skin disease and stigma in emerging adulthood: impact on healthy development. J Cutan Med Surg. 2010; 14 (6): 285–290.
32. Yuksel P.E., Sen. S., Aydin F., Senturk N., Sen N., Cengiz N., et al.: Phenobarbital-induced pellagra resulted in death. Cutan Ocul Toxicol. 2013; 33 (1): 76–78.
33. Mousa T.Y., Mousa O.Y.: Nicotinic Acid Deficiency. StatPearls 2020. 34. Wei W., Bo L.: Case report of mental disorder induced by niacin deficiency. Shanghai Arch Psychiatry. 2012; 24 (6): 352–354.
35. Niacin. Fact Sheet for Health Professionals. https://ods.od.nih.gov/factsheets/Niacin-HealthProfessional/ (access on 1st February 2021).
36. Piqué-Duran E., Pérez-Cejudo J.A., Cameselle D., Palacios-Llopis S., García-Vázquez O.: Pellagra: A Clinical, Histopathological, and Epidemiological Study of 7 Cases. Actas Dermosifiliogr. 2012; 103 (1): 51–58.
37. Frank G.P., Voorend D.M., Chamdula A., van Oosterhout J.J., Koop K.: Pellagra: A non-communicable disease of poverty. Trop Doct. 2012; 42 (3): 182–184.
38. Milovanović D., Djukić A., Stepanović R., Peković D., Vranjesecić D.: [Hatnup disease (report of 2 cases in one family)]. Srp Arh Celok Lek. 2000; 128 (3–4): 97–103.
39. Vanucchi H., Favaro F.M., Cunha D.F., Marchini J.F.: Assessment of zinc nutritional status of pellagra patients. Alcohol Alcohol. 1995; 30 (3): 297–302.
40. Wang S.Q., Balagula Y., Osterwalder U.: Photoprotection: a Review of the Current and future Technologies. Dermatol Ther. 2010; 23 (1): 31–47.
41. Pellagra Treated With Tryptophan. Nutr Rev. 1987; 45 (7): 142–148.
42. Allen J.A., Peterson A., Sufit R., et al.: Post-epidemic eosinophilia-myalgia syndrome associated with L-tryptophan. Arthritis Rheum. 2011; 63 (11): 3633–3639.
43. Burgdorf W.H.C., Plewig G., Wolff H.H., Landthaler M.: Dermatologia Braun-Falco. Wydawnictwo Czelej 2017. 44. Bilgili S.G., Karadag A.S., Calka O., Altun F.: Isoniazid-induced pellagra. Cutan Ocul Toxicol. 2011; 30 (4): 317–319.
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Autorzy i Afiliacje

Przemysław Hałubiec
1
ORCID: ORCID
Monika Leończyk
1
Filip Staszewski
1
Monika Łazarczyk
1
Andrzej Kazimierz Jaworek
1
Anna Wojas-Pelc
1

  1. Department of Dermatology, Jagiellonian University Medical College, Kraków, Poland

Bibliografia

1. Lenfant C.: Chest pain of cardiac and noncardiac origin. Metabolism. 2010; 59 (Suppl. 1): S41–46. doi: 10.1016/j.metabol.2010.07.014
2. Hochman J.S., Tamis J.E., Thompson T.D., et al.: Sex, clinical presentation, and outcome in patients with acute coronary syndromes. N Engl J Med. 1999; 341 (4): 226–232. doi: 10.1056/ NEJM199907223410402
3. Lanza G.A., De Vita A., Kaski J.C.: “Primary” microvascular angina: Clinical characteristics, pathogenesis and management. Interv Cardiol Rev. 2018; 13 (3): 108–111. doi: 10.15420/ icr.2018.15.2
4. Lanza G.A.: Cardiac syndrome X: A critical overview and future perspectives. Heart. 2007; 93 (2): 159–166. doi: 10.1136/hrt.2005.067330
5. Cheng T.O.: Cardiac syndrome X versus metabolic syndrome X. Int J Cardiol. 2007; 119 (2): 137–138. doi: 10.1016/j.ijcard.2006.06.062
6. Lichtlen P.R., Bargheer K., Wenzlaff P.: Long-term prognosis of patients with anginalike chest pain and normal coronary angiographic findings. J Am Coll Cardiol. 1995; 25 (5): 1013–1018. doi: 10.1016/0735-1097 (94)00519-V
7. Lamendola P., Lanza G.A., Spinelli A., et al.: Long-term prognosis of patients with cardiac syndrome X. Int J Cardiol. 2010; 140 (2): 197–199. doi: 10.1016/j.ijcard.2008.11.026
8. Di Monaco A., Lanza G.A., Bruno I., et al.: Usefulness of impairment of cardiac adrenergic nerve function to predict outcome in patients with cardiac syndrome X. Am J Cardiol. 2010; 106 (12): 1813–1818. doi: 10.1016/j.amjcard.2010.07.052
9. Singh M., Singh S., Arora R., Khosla S.: Cardiac syndrome X: Current concepts. Int J Cardiol. 2010; 142 (2): 113–119. doi: 10.1016/j.ijcard.2009.11.021
10. Ryan T.J.: The Coronary Angiogram and Its Seminal Contributions to Cardiovascular Medicine over Five Decades. Circulation. 2002; 106 (6). doi: 10.1161/01.CIR.0000024109.12658.D4
11. Kemp H.G., Vokonas P.S., Cohn P.F., Gorlin R.: The anginal syndrome associated with normal coronary arteriograms. Report of a six year experience. Am J Med. 1973; 54 (6): 735–742. doi: 10.1016/0002-9343 (73)90060-0
12. Cannon R.O., Epstein S.E.: “Microvascular angina” as a cause of chest pain with angiographically normal coronary arteries. Am J Cardiol. 1988; 61 (15): 1338–1343. doi: 10.1016/0002-9149 (88) 91180-0
13. Fox K., Alonso Garcia M.A., Ardissino D., et al.: Guidelines on the management of stable angina pectoris: Executive summary — The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology. Eur Heart J. 2006; 27 (11): 1341–1381. doi: 10.1093/eurheartj/ ehl001
14. Montalescot G., Sechtem U., Achenbach S., et al.: 2013 ESC guidelines on the management of stable coronary artery disease. Eur Heart J. 2013; 34 (38): 2949–3003. doi: 10.1093/eurheartj/eht296
15. Ong P., Camici P.G., Beltrame J.F., et al.: International standardization of diagnostic criteria for microvascular angina. Int J Cardiol. 2018; 250: 16–20. doi: 10.1016/j.ijcard.2017.08.068
16. Knuuti J., Wijns W., Achenbach S., et al.: 2019 ESC guidelines for the diagnosis and management of chronic coronary syndromes. Eur Heart J. 2020; 41 (3): 407–477. doi: 10.1093/eurheartj/ehz425
17. Diver D.J., Bier J.D., Ferreira P.E., et al.: Clinical and arteriographic characterization of patients with unstable angina without critical coronary arterial narrowing (from the TIMI-IIIA trial). Am J Cardiol. 1994; 74 (6): 531–537. doi: 10.1016/0002-9149 (94)90739-0
18. Reis S.E., Holubkov R., Smith A.J.C., et al.: Coronary microvascular dysfunction is highly prevalent in women with chest pain in the absence of coronary artery disease: Results from the NHLBI WISE study. Am Heart J. 2001; 141 (5): 735–741. doi: 10.1067/mhj.2001.114198
19. Noel Bairey Merz C., Eteiba W., Pepine C.J., Johnson B.D., Shaw L.J., Kelsey S.F.: Cardiac syndrome X: Relation to microvascular angina and other conditions. Curr Cardiovasc Risk Rep. 2007; 1 (2): 167–175. doi: 10.1007/s12170-007-0027-3
20. Bugiardini R., Merz C.N.B.: Angina with “normal” coronary arteries: A changing philosophy. J Am Med Assoc. 2005; 293 (4): 477–484. doi: 10.1001/jama.293.4.477
21. Krumholz H.M., Douglas P.S., Lauer M.S., Pasternak R.C.: Selection of patients for coronary angiography and coronary revascularization early after myocardial infarction: Is there evidence for a gender bias? Ann Intern Med. 1992; 116 (10): 785–790. doi: 10.7326/0003-4819-116-10-785
22. Kaski J.C.: Overview of gender aspects of cardiac syndrome X. Cardiovasc Res. 2002; 53 (3): 620–626. doi: 10.1016/s0008-6363 (01)00460-6
23. Pasceri V., Lanza G.A., Buffon A., Montenero A.S., Crea F., Maseri A.: Role of abnormal pain sensitivity and behavioral factors in determining chest pain in syndrome X. J Am Coll Cardiol. 1998; 31 (1): 62–66. doi: 10.1016/s0735-1097 (97)00421-x
24. Ford T.J., Stanley B., Good R., et al.: Stratified Medical Therapy Using Invasive Coronary Function Testing in Angina: The CorMicA Trial. J Am Coll Cardiol. 2018; 72 (23): 2841–2855. doi: 10.1016/j. jacc.2018.09.006
25. Kanatsuka H., Eastham C.L., Marcus M.L., Lamping K.G.: Effects of nitroglycerin on the coronary microcirculation in normal and ischemic myocardium. J Cardiovasc Pharmacol. 1992; 19 (5): 755–763.
26. Russo G., Di Franco A., Lamendola P., et al.: Lack of effect of nitrates on exercise stress test results in patients with microvascular angina. Cardiovasc Drugs Ther. 2013; 27 (3): 229–234. doi: 10.1007/ s10557-013-6439-z
27. Ohba K., Sugiyama S., Sumida H., et al.: Microvascular coronary artery spasm presents distinctive clinical features with endothelial dysfunction as nonobstructive coronary artery disease. J Am Heart Assoc. 2012; 1 (5): e002485. doi: 10.1161/JAHA.112.002485
28. Maseri A., Crea F., Kaski J.C., Crake T.: Mechanisms of angina pectoris in syndrome X. J Am Coll Cardiol. 1991; 17 (2): 499–506. doi: 10.1016/S0735-1097 (10)80122-6
29. Lanza G.A., Crea F.: Primary coronary microvascular dysfunction: Clinical presentation, pathophysiology, and management. Circulation. 2010; 121 (21): 2317–2325. doi: 10.1161/ CIRCULATIONAHA.109.900191
30. Nihoyannopoulos P., Kaski J.C., Crake T., Maseri A.: Absence of myocardial dysfunction during stress in patients with syndrome X. J Am Coll Cardiol. 1991; 18 (6): 1463–1470. doi: 10.1016/0735- 1097 (91)90676-z
31. Panza J.A., Laurienzo J.M., Curiel R. V, et al.: Investigation of the mechanism of chest pain in patients with angiographically normal coronary arteries using transesophageal dobutamine stress echocardiography. J Am Coll Cardiol. 1997; 29 (2): 293–301. doi: 10.1016/s0735-1097 (96)00481-0
32. Ong P., Athanasiadis A., Borgulya G., Mahrholdt H., Kaski J.C., Sechtem U.: High prevalence of a pathological response to acetylcholine testing in patients with stable angina pectoris and unobstructed coronary arteries: The ACOVA study (abnormal coronary vasomotion in patients with stable angina and unobstructed coronary arteries. J Am Coll Cardiol. 2012; 59 (7): 655–662. doi: 10.1016/j.jacc.2011.11.015
33. White C.W., Wright C.B., Doty D.B., et al.: Does Visual Interpretation of the Coronary Arteriogram Predict the Physiologic Importance of a Coronary Stenosis? N Engl J Med. 1984; 310 (13): 819–824. doi: 10.1056/NEJM198403293101304
34. Hulten E., Di Carli M.F.: FFR CT : Solid PLATFORM or Thin Ice? J Am Coll Cardiol. 2015; 66 (21): 2324–2328. doi: 10.1016/j.jacc.2015.09.065
35. Thomson L.E.J., Wei J., Agarwal M., et al.: Cardiac magnetic resonance myocardial perfusion reserve index is reduced in women with coronary microvascular dysfunction: A national heart, lung, and blood institute-sponsored study from the women’s ischemia syndrome evaluation. Circ Cardiovasc Imaging. 2015; 8 (4). doi: 10.1161/CIRCIMAGING.114.002481
36. Gould K.L., Johnson N.P., Bateman T.M., et al.: Anatomic versus physiologic assessment of coronary artery disease: Role of coronary flow reserve, fractional flow reserve, and positron emission tomography imaging in revascularization decision-making. J Am Coll Cardiol. 2013; 62 (18): 1639–1653. doi: 10.1016/j.jacc.2013.07.076
37. Galiuto L., Sestito A., Barchetta S., et al.: Noninvasive Evaluation of Flow Reserve in the Left Anterior Descending Coronary Artery in Patients With Cardiac Syndrome X. Am J Cardiol. 2007; 99 (10): 1378–1383. doi: 10.1016/j.amjcard.2006.12.070
38. Lee B.K., Lim H.S., Fearon W.F., et al.: Invasive evaluation of patients with angina in the absence of obstructive coronary artery disease. Circulation. 2015; 131 (12): 1054–1060. doi: 10.1161/ CIRCULATIONAHA.114.012636
39. Ng M.K.C., Yeung A.C., Fearon W.F.: Invasive assessment of the coronary microcirculation: Superior reproducibility and less hemodynamic dependence of index of microcirculatory resistance compared with coronary flow reserve. Circulation. 2006; 113 (17): 2054–2061. doi: 10.1161/CIRCULATIO-NAHA.105.603522
40. Beltrame J.F.: Defining the coronary slow flow phenomenon. Circ J. 2012; 76 (4): 818–820. doi: 10.1253/circj.CJ-12-0205
41. Gibson C.M., Cannon C.P., Daley W.L., et al.: TIMI frame count: A quantitative method of assessing coronary artery flow. Circulation. 1996; 93 (5): 879–888. doi: 10.1161/01.CIR.93.5.879
42. Odaka Y., Takahashi J., Tsuburaya R., et al.: Plasma concentration of serotonin is a novel biomarker for coronarymicrovascular dysfunction in patients with suspected angina and unobstructive coronary arteries. Eur Heart J. 2017; 38 (7): 489–496. doi: 10.1093/eurheartj/ehw448
43. Rasmi Y., Roshani-Asl E., KhademAnsari M., SeyedMohammadza M., Rostamzadeh A.: Angiopoie-tin-2 as a biomarker for patients with Cardiac Syndrome X. J Am Coll Cardiol. 2016; 68 (16): C24. doi: 10.1016/j.jacc.2016.07.092
44. Uğurlu M., Karahan Z., Sezer F., et al.: OP-024 A Novel Biomarker in Syndrome X Disease: Mr-Proadrenomedullin. Am J Cardiol. 2016; 117: S9. doi: 10.1016/j.amjcard.2016.04.070
45. Cannon R.O. 3rd, Camici P.G., Epstein S.E.: Pathophysiological Dilemma of Syndrome X. Circulation. 1992; 85 (3): 883–892.
46. Rosano G.M., Ponikowski P., Adamopoulos S., et al.: Abnormal autonomic control of the cardiovascular system in syndrome X. Am J Cardiol. 1994; 73 (16): 1174–1179. doi: 10.1016/0002- 9149 (94)90177-5
47. Börjesson M., Albertsson P., Dellborg M., et al.: Esophageal dysfunction in syndrome X. Am J Cardiol. 1998; 82 (10): 1187–1191. doi: 10.1016/s0002-9149 (98)00598-0
48. Kao C.H., Hsieh J.F., Tsai C.S., Ho Y.J., Lee J.K.: Evidence of abnormal esophageal motility in syndrome X by radionuclide esophageal transit test. Digestion. 2000; 62 (1): 26–30. doi: 10.1159/ 000007774
49. Brunelli C., Nobili F., Spallarossa P., et al.: Cerebral blood flow reserve in patients with syndrome X. Coron Artery Dis. 1996; 7 (8): 587–590. doi: 10.1097/00019501-199608000-00005
50. Zeiher A.M., Krause T., Schächinger V., Minners J., Moser E.: Impaired endothelium-dependent vasodilation of coronary resistance vessels is associated with exercise-induced myocardial ischemia. Circulation. 1995; 91 (9): 2345–2352. doi: 10.1161/01.cir.91.9.2345
51. Lin C.-P., Lin W.-T., Leu H.-B., Wu T.-C., Chen J.-W.: Differential mononuclear cell activity and endothelial inflammation in coronary artery disease and cardiac syndrome X. Int J Cardiol. 2003; 89 (1): 53–62. doi: 10.1016/s0167-5273 (02)00428-x
52. Newby D.E., Flint L.L., Fox K.A.A., Boon N.A., Webb D.J.: Reduced responsiveness to endothelin-1 in peripheral resistance vessels of patients with syndrome X. J Am Coll Cardiol. 1998; 31 (7): 1585–1590. doi: 10.1016/S0735-1097 (98)00143-0
53. Kidawa M., Krzeminska-Pakula M., Peruga J.Z., Kasprzak J.D.: Arterial dysfunction in syndrome X: Results of arterial reactivity and pulse wave propagation tests. Heart. 2003; 89 (4): 422–426. doi: 10.1136/heart.89.4.422
54. Shmilovich H., Deutsch V., Roth A., Miller H., Keren G., George J.: Circulating endothelial progenitor cells in patients with cardiac syndrome X. Heart. 2007; 93 (9): 1071–1076. doi: 10.1136/ hrt.2005.077909
55. Trott D.W., Fadel P.J.: Inflammation as a mediator of arterial ageing. Exp Physiol. 2019; 104 (10): 1455–1471. doi: 10.1113/EP087499
56. Dollard J., Kearney P., Clarke G., Moloney G., Cryan J.F., Dinan T.G.: A prospective study of C-reactive protein as a state marker in Cardiac Syndrome X. Brain Behav Immun. 2015; 43: 27–32. doi: 10.1016/j.bbi.2014.07.011
57. Demir B., Önal B., Özyazgan S., et al.: Does Inflammation Have a Role in the Pathogenesis of Cardiac Syndrome X? A Genetic-Based Clinical Study With Assessment of Multiple Cytokine Levels. Angiology. 2015; 67 (4): 355–363. doi: 10.1177/0003319715590057
58. Recio-Mayoral A., Rimoldi O.E., Camici P.G., Kaski J.C.: Inflammation and microvascular dysfunction in cardiac syndrome X patients without conventional risk factors for coronary artery disease. JACC Cardiovasc Imaging. 2013; 6 (6): 660–667. doi: 10.1016/j.jcmg.2012.12.011
59. Recio-Mayoral A., Mason J.C., Kaski J.C., Rubens M.B., Harari O.A., Camici P.G.: Chronic inflammation and coronary microvascular dysfunction in patients without risk factors for coronary artery disease. Eur Heart J. 2009; 30 (15): 1837–1843. doi: 10.1093/eurheartj/ehp205
60. Konst R.E., Guzik T.J., Kaski J.C., Maas A.H.E.M., Elias-Smale S.E.: The pathogenic role of coronary microvascular dysfunction in the setting of other cardiac or systemic conditions. Cardiovasc Res. 2020; 116 (4): 817–828. doi: 10.1093/cvr/cvaa009
61. Ahmed A., Hollan I., Curran S.A., et al.: Brief Report: Proatherogenic Cytokine Microenvironment in the Aortic Adventitia of Patients with Rheumatoid Arthritis. Arthritis Rheumatol. 2016; 68 (6): 1361–1366. doi: 10.1002/art.39574
62. Karbalaei M., Sahebkar A., Keikha M.: Helicobacter pylori infection and susceptibility to cardiac syndrome X: A systematic review and meta-analysis. World J Meta-Analysis. 2021; 9 (2): 208–219. doi: 10.13105/wjma.v9.i2.208
63. Li J.J., Zhu C.G., Nan J.L., et al.: Elevated circulating inflammatory markers in female patients with cardiac syndrome X. Cytokine. 2007; 40 (3): 172–176. doi: 10.1016/j.cyto.2007.09.005
64. Tenekecioglu E., Yilmaz M., Demir S., et al.: HDL-cholesterol is associated with systemic inflammation in cardiac syndrome X. Minerva Med. 2015; 106 (3): 133–141.
65. Aslan G., Polat V., Bozcali E., Opan S., Çetin N., Ural D.: Evaluation of serum sST2 and sCD40L values in patients with microvascular angina. Microvasc Res. 2019; 122: 85–93. doi: 10.1016/j. mvr.2018.11.009
66. Akasaka T., Sueta D., Arima Y., et al.: CYP2C19 variants and epoxyeicosatrienoic acids in patients with microvascular angina. IJC Hear Vasc. 2017; 15: 15–20. doi: 10.1016/j.ijcha.2017.03.001
67. Akasaka T., Sueta D., Arima Y., et al.: Association of CYP2C19 variants and epoxyeicosatrienoic acids on patients with microvascular angina. Am J Physiol — Hear Circ Physiol. 2016; 311 (6): H1409–H1415. doi: 10.1152/ajpheart.00473.2016
68. Güler G.B., Güler E., Hatipoğlu S., et al.: Assessment of 25-OH vitamin D levels and abnormal blood pressure response in female patients with cardiac syndrome X. Anatol J Cardiol. 2016; 16 (12): 961–966. doi: 10.14744/AnatolJCardiol.2016.6862
69. Horváth Z., Csuka D., Vargova K., et al.: Elevated C1rC1sC1inh levels independently predict atherosclerotic coronary heart disease. Mol Immunol. 2013; 54 (1): 8–13. doi: 10.1016/j. molimm.2012.10.033
70. Horváth Z., Csuka D., Vargova K., et al.: Association of Low Ficolin-Lectin Pathway Parameters with Cardiac Syndrome X. Scand J Immunol. 2016; 84 (3): 174–181. doi: 10.1111/sji.12454
71. Cenko E., Amaduzzi P.L., Bugiardini R.: Microvascular angina as a cause of ischemia: An update. In: Gender Differences in the Pathogenesis and Management of Heart Disease. Springer International Publishing; 2018: 135–163. doi: 10.1007/978-3-319-71135-5_9
72. Kaski J.C.: Cardiac syndrome X in women: The role of oestrogen deficiency. Heart. 2006; 92 (Suppl. 3): 5–9. doi: 10.1136/hrt.2005.070318
73. Gilligan D.M., Badar D.M., Panza J.A., Quyyumi A.A., Cannon R.O.: Acute vascular effects of estrogen in postmenopausal women. Circulation. 1994; 90 (2): 786–791. doi: 10.1161/01. CIR.90.2.786
74. Lim T.K., Choy A.J., Khan F., Belch J.J., Struthers A.D., Lang C.C.: Therapeutic development in cardiac syndrome X: A Need to target the underlying pathophysiology: REVIEW. Cardiovasc Ther. 2009; 27 (1): 49–58. doi: 10.1111/j.1755-5922.2008.00070.x
75. Opherk D., Mall G., Zebe H., et al.: Reduction of coronary reserve: a mechanism for angina pectoris in patients with arterial hypertension and normal coronary arteries. Circulation. 1984; 69 (1): 1–7. doi: 10.1161/01.CIR.69.1.1
76. Meeder J.G., Blanksma P.K., Crijns H.J.G.M., et al.: Mechanisms of angina pectoris in syndrome X assessed by myocardial perfusion dynamics and heart rate variability. Eur Heart J. 1995; 16 (11): 1571–1577. doi: 10.1093/oxfordjournals.eurheartj.a060780
77. Saghari M., Assadi M., Eftekhari M., et al.: Frequency and severity of myocardial perfusion abnormalities using Tc-99m MIBI SPECT in cardiac syndrome X. BMC Nucl Med. 2006; 6: 1–8. doi: 10.1186/1471-2385-6-1
78. Kaski J.C., Rosano G.M.C., Collins P., Nihoyannopoulos P., Maseri A., Poole-Wilson P.A.: Cardiac syndrome X: Clinical characteristics and left ventricular function. Long-term follow-up study. J Am Coll Cardiol. 1995; 25 (4): 807–814. doi: 10.1016/0735-1097 (94)00507-M
79. Furgała A., Kolasińska-Kloch W., Kloch M., Laskiewicz J., Thor P.J.: Heart rate variability in cardiological syndrome X patients | Zmienność rytmu serca u chorych z kardiologicznym zespołem X. Folia Cardiol. 2003; 10 (4).
80. Adamopoulos S., Rosano G.M., Ponikowski P., et al.: Impaired baroreflex sensitivity and sympathovagal balance in syndrome X. Am J Cardiol. 1998; 82 (7): 862–868. doi: 10.1016/s0002- 9149 (98)00493-7
81. Crea F., Camici P.G., Merz C.N.B.: Coronary microvascular dysfunction: An update. Eur Heart J. 2014; 35 (17): 1101–1111. doi: 10.1093/eurheartj/eht513
82. Chen J.W., Hsu N.W., Ting C.T., Lin S.J., Chang M.S.: Differential coronary hemodynamics and left ventricular contractility in patients with syndrome X. Int J Cardiol. 2000; 75 (1): 49–57. doi: 10.1016/ s0167-5273 (00)00285-0
83. Mammana C., Salomone O.A., Kautzner J., Schwartzman R.A., Kaski J.C.: Heart rate-independent prolongation of QTc interval in women with syndrome X. Clin Cardiol. 1997; 20 (4): 357–360. doi: 10.1002/clc.4960200411
84. Gulli G., Cemin R., Pancera P., Menegatti G., Vassanelli C., Cevese A.: Evidence of parasympathetic impairment in some patients with cardiac syndrome X. Cardiovasc Res. 2001; 52 (2): 208–216. doi: 10.1016/S0008-6363 (01)00369-8
85. Antonio L.G., Alessandro G., Christian P., et al.: Abnormal Cardiac Adrenergic Nerve Function in Patients With Syndrome X Detected By [123I]Metaiodobenzylguanidine Myocardial Scintigraphy. Circulation. 1997; 96 (3): 821–826. doi: 10.1161/01.CIR.96.3.821
86. Lee W.L., Chen J.-W.W., Kong C.W., et al.: Changes in Cardiac Autonomic Activities in Patients with Syndrome X: A Study of Spectral Analysis of Heart Rate Variability. Angiology. 1996; 47 (10): 929–939. doi: 10.1177/000331979604701001
87. Eriksson B., Jansson E., Kaijser L., Sylvan C.: Exercise performance, autonomic control and skeletal muscle function in syndrome X. Circulation. 1997; 96 (8S).
88. Rosano G.M., Kaski J.C., Arie S., et al.: Failure to demonstrate myocardial ischaemia in patients with angina and normal coronary arteries. Evaluation by continuous coronary sinus pH monitoring and lactate metabolism. Eur Heart J. 1996; 17 (8): 1175–1180. doi: 10.1093/oxfordjournals.eurheartj. a015034
89. Bøtker H.E., Sonne H.S., Frøbert O., Andreasen F.: Enhanced exercise-induced hyperkalemia in patients with syndrome X. J Am Coll Cardiol. 1999; 33 (4): 1056–1061. doi: 10.1016/S0735-1097(98) 00683-4
90. Villasante Fricke A.C., Iacobellis G.: Epicardial Adipose Tissue: Clinical Biomarker of Cardio- Metabolic Risk. Int J Mol Sci. 2019; 20 (23). doi: 10.3390/ijms20235989
91. Kalçik M., Yesin M., Güner A., et al.: Echocardiographic measurement of epicardial adipose tissue thickness in patients with microvascular angina. Interv Med Appl Sci. 2019; 11 (2): 106–111. doi: 10.1556/1646.11.2019.12
92. Lanza G.A., Colonna G., Pasceri V., Maseri A.: Atenolol versus amlodipine versus isosorbide-5- mononitrate on anginal symptoms in syndrome X. Am J Cardiol. 1999; 84 (7): 854–856. doi: 10.1016/S0002-9149 (99)00450-6
93. Leonardo F., Fragasso G., Rossetti E., et al.: Comparison of trimetazidine with atenolol in patients with syndrome X: effects on diastolic function and exercise tolerance. Cardiologia. 1999; 44 (12): 1065–1069.
94. Erdamar H., Sen N., Tavil Y., et al.: The effect of nebivolol treatment on oxidative stress and antioxidant status in patients with cardiac syndrome-X. Coron Artery Dis. 2009; 20 (3): 238–244. doi: 10.1097/MCA.0b013e32830936bb
95. Ozçelik F., Altun A., Ozbay G.: Antianginal and anti-ischemic effects of nisoldipine and ramipril in patients with syndrome X. Clin Cardiol. 1999; 22 (5): 361–365. doi: 10.1002/clc.4960220513
96. Zhang X., Li Q., Zhao J., et al.: Effects of combination of statin and calcium channel blocker in patients with cardiac syndrome X. Coron Artery Dis. 2014; 25 (1): 40–44. doi: 10.1097/ MCA.0000000000000054
97. Ong P., Athanasiadis A., Sechtem U.: Pharmacotherapy for coronary microvascular dysfunction. Eur Hear J — Cardiovasc Pharmacother. 2015; 1 (1): 65–71. doi: 10.1093/ehjcvp/pvu020
98. Pizzi C., Manfrini O., Fontana F., Bugiardini R.: Angiotensin-converting enzyme inhibitors and 3-hydroxy-3-methylglutaryl coenzyme A reductase in cardiac Syndrome X: role of superoxide dismutase activity. Circulation. 2004; 109 (1): 53–58. doi: 10.1161/01.CIR.0000100722.34034.E4
99. Chen J.W., Hsu N.W., Wu T.C., Lin S.J., Chang M.S.: Long-term angiotensin-converting enzyme inhibition reduces plasma asymmetric dimethylarginine and improves endothelial nitric oxide bioavailability and coronary microvascular function in patients with syndrome X. Am J Cardiol. 2002; 90 (9): 974–982. doi: 10.1016/S0002-9149 (02)02664-4
100. Pauly D.F., Johnson B.D., Anderson R.D., et al.: In women with symptoms of cardiac ischemia, nonobstructive coronary arteries, and microvascular dysfunction, angiotensin-converting enzyme inhibition is associated with improved microvascular function. Am Heart J. 2011; 162 (4): 678–684. doi: 10.1016/j.ahj.2011.07.011
101. Kayikcioglu M., Payzin S., Yavuzgil O., Kultursay H., Can L.H., Soydan I.: Benefits of statin treatment in cardiac syndrome-X1. Eur Heart J. 2003; 24 (22): 1999–2005. doi: 10.1016/S0195-668X (03)00478-0
102. Fábián E., Varga A., Picano E., Vajo Z., Rónaszéki A., Csanády M.: Effect of simvastatin on endothelial function in cardiac syndrome X patients. Am J Cardiol. 2004; 94 (5): 652–655. doi: 10.1016/j.amjcard.2004.05.035
103. Mehta P.K., Goykhman P., Thomson L.E.J., et al.: Ranolazine improves angina in women with evidence of myocardial ischemia but no obstructive coronary artery disease. JACC Cardiovasc Imaging. 2011; 4 (5): 514–522. doi: 10.1016/j.jcmg.2011.03.007
104. Tagliamonte E., Rigo F., Cirillo T., et al.: Effects of ranolazine on noninvasive coronary flow reserve in patients with myocardial ischemia but without obstructive coronary artery disease. Echocardiography. 2015; 32 (3): 516–521. doi: 10.1111/echo.12674
105. Villano A., Di Franco A., Nerla R., et al.: Effects of ivabradine and ranolazine in patients with microvascular angina pectoris. Am J Cardiol. 2013; 112 (1): 8–13. doi: 10.1016/j.amjcard.2013.02.045
106. Chen J.W., Lee W.L., Hsu N.W., et al.: Effects of short-term treatment of Nicorandil on exercise- induced myocardial ischemia and abnormal cardiac autonomic activity in microvascular angina. Am J Cardiol. 1997; 80 (1): 32–38. doi: 10.1016/S0002-9149 (97)00279-8
107. Nalbantgil S., Altintiğ A., Yilmaz H., Nalbantgil I., Önder R.: The effect of trimetazidine in the treatment of microvascular angina. Int J Angiol. 1999; 8 (1): 40–43. doi: 10.1007/BF01616842
108. Adamson D.L., Webb C.M., Collins P.: Esterified estrogens combined with methyltestosterone improve emotional well-being in postmenopausal women with chest pain and normal coronary angiograms. Menopause. 2001; 8 (4): 233–238. doi: 10.1097/00042192-200107000-00003
109. Emdin M., Picano E., Lattanzi F., l’Abbate A.: Improved exercise capacity with acute aminophylline administration in patients with syndrome X. J Am Coll Cardiol. 1989; 14 (6): 1450–1453. doi: 10.1016/0735-1097 (89)90380-X
110. Yoshio H., Shimizu M., Kita Y., et al.: Effects of short-term aminophylline administration on cardiac functional reserve in patients with syndrome X. J Am Coll Cardiol. 1995; 25 (7): 1547–1551. doi: 10.1016/0735-1097 (95)00097-N
111. Elliott P.M., Krzyzowska-Dickinson K., Calvino R., Hann C., Kaski J.C.: Effect of oral aminophylline in patients with angina and normal coronary arteriograms (cardiac syndrome X). Heart. 1997; 77 (6): 523–526. doi: 10.1136/hrt.77.6.523
112. Fukumoto Y., Mohri M., Inokuchi K., et al.: Anti-ischemic effects of fasudil, a specific Rho-kinase inhibitor, in patients with stable effort angina. J Cardiovasc Pharmacol. 2007; 49 (3): 117–121. doi: 10.1097/FJC.0b013e31802ef532
113. Mohri M., Shimokawa H., Hirakawa Y., Masumoto A., Takeshita A.: Rho-kinase inhibition with intracoronary fasudil prevents myocardial ischemia in patients with coronary microvascular spasm. J Am Coll Cardiol. 2003; 41 (1): 15–19. doi: 10.1016/S0735-1097 (02)02632-3
114. Olgin J.E., Takahashi T., Wilson E., Vereckei A., Steinberg H., Zipes D.P.: Effects of Thoracic Spinal Cord Stimulation on Cardiac Autonomic Regulation of the Sinus and Atrioventricular Nodes. J Cardiovasc Electrophysiol. 2002; 13: 475–481.
115. Hautvast R.W.M., Blanksma P.K., DeJongste M.J.L., et al.: Effect of spinal cord stimulation on myocardial blood flow assessed by positron emission tomography in patients with refractory angina pectoris. Am J Cardiol. 1996; 77 (7): 462–467. doi: 10.1016/S0002-9149 (97)89338-1
116. Murray S., Carson K.G.S., Ewings P.D., Collins P.D., James M.A.: Spinal cord stimulation significantly decreases the need for acute hospital admission for chest pain in patients with refractory angina pectoris. Heart. 1999; 82 (1): 89 LP-92. doi: 10.1136/hrt.82.1.89
117. Sharma U., Ramsey H.K., Tak T.: The role of enhanced external counter pulsation therapy in clinical practice. Clin Med Res. 2013; 11 (4): 226–232. doi: 10.3121/cmr.2013.1169
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