Цель: изучить и сопоставить уровень гомоцистеина с результатами коронарографии у больных инфарктом миокарда (ИМ) на фоне хронической обструктивной болезни легких (ХОБЛ). Материалы и методы. Обследовано 246 больных ИМ. У 137 (55,7%) человек ИМ развился на фоне ХОБЛ, 109 (44,3%) пациентов имели ИМ в качестве мононозологии. Группы сравнения составили 55 соматически здоровых лиц и 50 больных ХОБЛ. Определение содержания уровня гомоцистеина в образцах плазмы осуществлялось методом иммуноферментного анализа.Результаты. Стенозы только одной коронарной артерии (КА) при гипергомоцистеинемии встречались редко в обеих группах больных (3,5% у больных ИМ и 3% у больных ИМ на фоне ХОБЛ), статистически значимо преобладали многососудистые поражения КА. Поражение 3 сосудов и более обнаруживали статистически значимо чаще у больных с гипергомоцистеинемией при ИМ на фоне ХОБЛ. Среди больных ИМ с гипергомоцистеинемией преобладали пациенты со степенью сужения КА на 50-75%, а среди больных ИМ на фоне ХОБЛ с гипергомоцистеинемией статистически значимо чаще встречались пациенты со степенью сужения КА на 75-99% и полной окклюзией. То есть у больных с ИМ на фоне ХОБЛ с гипергомоцистеинемией отмечалось более выраженное поражение КА, что проявлялось многососудистым поражением, большей выраженностью окклюзии и более частой регистрацией полного стеноза КА.
Objective. To create a personalized mathematical model of the development of complications – cardiogenic shock and pulmonary edema in patients with myocardial infarction (MI) with chronic obstructive pulmonary disease (COPD) depending of the homocysteine (HCY) level and the COPD phenotype.Materials and methods. The study included 88 patients with MI and COPD with various phenotypes: 25 patients with emphysematous phenotype, 22 patients with a mixed phenotype, 20 patients with chronic bronchitis phenotype, 21 patients with eosinophilia and bronchial asthma (BA). As a control group, 50 somatically healthy individuals were examined. Gender anamnestic, clinical, and laboratory – instrumental indicators were studied and analyzed to develop a predictive mathematical model. The level of HCY was determined by enzyme-linked immunosorbent assay in all patients.Results. It was found that in patients with MI and COPD with different COPD phenotypes, the level of HCY was statistically significantly higher than in the control group. The highest level of HCY was in patients with the chronic bronchitis phenotype and was 45 [14.1; 51.9] mmol/l, which was statistically significantly higher than in patients with the phenotype with eosinophilia and BA, with emphysematous and mixed phenotypes. Predictor factors were selected using the logit regression method from gender-anamnestic, clinical, and laboratory – instrumental indicators to create a mathematical model with the highest prediction accuracy. HCY level and COPD phenotype were predictors of the mathematical model for predicting the development of complications – cardiogenic shock and pulmonary edema in patients with MI and COPD. It was also found that the threshold value of HCY for predicting the development of cardiogenic shock and pulmonary edema in patients with MI and COPD was 0.82 ± 0.51 confidence interval [0.72–0.91] mmol/l (p < 0.001).Conclusion. The personalized mathematical model initiated for predicting the development of complications-cardiogenic shock and pulmonary edema in patients with MI and COPD, depending of the HCY level and the COPD phenotype, has a high sensitivity (85%) and prognostic significance (92%), which allows us to recommend it for use in clinical practice.
Objective. To identify clinical and functional correlations in patients with myocardial infarction against the background of the chronic obstructive pulmonary disease with various phenotypes.Materials and methods. 188 patients were examined, from which the following groups were formed: control group – 50 patients, group 1–50 patients with myocardial infarction (MI), group 2–25 patients with MI against the background of the chronic obstructive pulmonary disease (COPD) with emphysematous phenotype, group 3–20 patients with MI + COPD with chronic bronchitis phenotype, group 4–22 patients with MI + COPD with mixed phenotype and group 5–21 patients with MI + COPD with the phenotype with eosinophilia and bronchial asthma. Clinical examination of patients included assessment of complaints, medical history and history of life. Spirography on apparatus SP-100 Schiller (Switzerland) was used for the assessment of respiratory function. Echocardiography was performed on Acuson-Sequoia 512 echo scanner (Siemens). Statistical analyses were performed using Statistica 12.0 (Stat Soft).Results. The highest frequency of symptoms such as chest pain, nausea/vomiting, fatigue, tachycardia, cough with sputum was observed among patients with MI + COPD with chronic bronchitis phenotype. In this group of patients, the level of systolic blood pressure in the pulmonary artery and the left ventricular ejection fraction were the lowest.Conclusion. Chronic bronchitis phenotype of COPD in patients with MI is the most prognostically unfavorable. It is associated with the severity of clinical manifestations, with signs of pulmonary hypertension and dysfunction of the left heart, that makes necessary to take into account the phenotypes of COPD in the care of patients with MI against the background of COPD and the allocation of chronic bronchitis phenotype as a criterion for an unfavorable prognosis of MI.
Introduction: Chronic obstructive pulmonary disease (COPD) is the leading cause of mortality. Using the evidence obtained about various clinical phenotypes of patients with the same disease allowed us to expand our understanding of the treatment of COPD. Nowadays the only option for solving the problem will be the definition of the clinical phenotype of COPD, and the receipt of expanded data on its correlation with respiratory and other significant biomarkers. Materials and methods: We analyzed the correlations between FKN, CRP and TBA-active lipid peroxidation products in 373 patients with various COPD phenotypes and 60 healthy volunteers. Enzyme immunoassay was used to study the levels of inflammatory biomarkers. Results: We have identified a statistically significant increase in the levels of inflammatory biomarkers in patients with COPD compared with the control. The FKN level in the group of patients with COPD was 1.3 ng/ml, which was higher (p<0.001) than in the control (FKN level of 0.3 ng/ml, p<0.001). The CRP level in patients with COPD was 27.8 mg/L, whereas in control the CRP level was 1.2 mg/L (p<0.001). The TBA-active lipid peroxidation products level in patients with COPD was 14.5 mmol/L, which was higher when compared to the control (p<0.001). Discussion: The correlation analysis revealed very strong relationships between the levels of all the biomarkers studied. The highest values of the Kendall rank correlation coefficient (τ) were determined between the levels of all the inflammatory biomarkers in subgroups of patients with chronic bronchitis and mixed COPD phenotypes. Conclusion: Detection of the COPD phenotype will help actively monitor the therapy of COPD exacerbations. Graphical Abstract
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