The interplay between rheumatic diseases and pulmonary health.

Patients with rheumatic diseases (RDs) are prone to a number of comorbidities, particularly those affecting the respiratory system due to inflammatory and autoimmune mechanisms. Rheumatoid arthritis (RA), systemic sclerosis (SSc), and inflammatory idiopathic myopathies (IIMs) often present with progressive interstitial lung disease (ILD). The prevalence of ILD varies among patients with RDs, with 11% in RA, 47% in SSc, and 41% in IIMs. Some diagnostic markers, including KL-6, cytokines TNF-α and IL-6, and autoantibodies (anti-CCP), play a crucial role in assessing and predicting the course of pulmonary involvement in RDs. Lung fibrosis is a progressive disorder in SSc and RA, limiting the effiency of therapeutic interventions. Re-evaluating treatment approaches with disease-modifying anti-rheumatic drugs (DMARDs) is crucial for understanding their impact on the risk of lung affections. Despite initial concerns surrounding methotrexate, recent evidence points to its benefits in RA-associated interstitial lung disease (RA-ILD). Recognizing the intricate relationship between autoimmune RDs and lung affections is crucial for formulating effective treatment strategies. Emphasis is placed on collaborative efforts of rheumatologists and pulmonologists for early diagnosis, comprehensive care, and optimal patient outcomes in RA-ILD.

Influence of trimetazidine and levocarnitine on clinical course, structural and functional changes and myocardial fibrosis in patients with myocardial infarction.

OBJECTIVE: Introduction: Modern strategies of STEMI/NSTEMI management, that include revascularization by coronary stenting, bypass grafting, nowadays are used in 30-40% of urgent patients of such category. The prevalent part of patients is treated by administration of the optimal drug therapy. The aim of the research was to study the influence of trimetazidine and levocarnitine on the clinical course of STEMI/NSTEMI. PATIENTS AND METHODS: Materials and methods: 100 patients with STEMI/NSTEMI were included into the research. Depending on the therapy scheme, patients were divided into three groups and the control one. Determination of the key parameters was performed initially after hospitalization and at the day of patient discharge. RESULTS: Results: Promising results were shown while slowing the myocardial fibrosing. Limiting of the infarcted and `stunned` myocardium area resulted in ejection fraction increase, increase of the myocardial reserve, measured by echocardiographic indexes. CONCLUSION: Conclusions: Decreasing of myocardial fibrosing can be potentiated by the pharmacological postconditioning as well as limiting of the necrotic myocardium area and increase of viable myocardium area. Pharmacological postconditioning is effective and save, that can be proved by the absence of any serious complications.