Background/Aim. The main clinical phenomena in acute low back pain (LBP) with radiculopathy are pain and neurological disorders. Although some studies show that low level laser therapy (LLLT) has the ability to modulate inflammatory processes and relieve acute pain condition, the laser therapy dose protocol has not been yet completely established. The aim of this study was to investigate the effects of three different energy doses of LLLT in patients with acute LBP and radiculopathy. Methods. The study included 66 patients with acute LBP and radiculopathy who had been randomly divided into three groups (22 patients each) received three different doses of LLLT. The patients were treated 5 times weekly, for a total of 10 treatments, with the following parameters: wave length 904 nm, frequency 3,000 Hz, average diode power 25 mW; energy dose of 0.1 J per point in the first group, 1 J per point in the second and 4 J per point in the third group; daily treatment time and accumulated energy were 16 s and 0.4 J in the first group, 160 s and 4 J in the second group and 640 s and 16 J in the third group, respectively. The parameters of assessment before and after the therapy were: lumbar and leg pain measured by visual analogue scale (VAS), local and general functional changes (Schober test, manual muscle test, straight leg raise test and the modified North American Spine Society-Low Back Pain Outcome Instrument-NASS LBP). Results. Highly significant improvements (p < 0.01) were noted in all the groups after LLLT with respect to all the investigated parameters. The VAS scores were significantly lower in all the groups without a difference between the groups (p > 0,05). Functional improvements were better in the third group treated with the dose of 4 J per point than in other two groups (p < 0.05). Conclusions. Three different energy doses of LLLT were equally effective in alleviating lumbar and leg pain without side effects, but the dose of 4 J per point seemed to be more effective in improving the activities of daily living and lumbar mobility.

The aim of this study was to examine the incidence and significance of right heart failure (RHF) in the early and late phase of left ventricular assist device (LVAD) implantation with the identification of predictive factors for the development of RHF. This was a prospective observational analytical cohort study. The study included 92 patients who underwent LVAD implantation and for whom all necessary clinical data from the follow-up period were available, as well as unambiguous conclusions by the heart team regarding pathologies, adverse events, and complications. Of the total number of patients, 43.5% died. The median overall survival of patients after LVAD implantation was 22 months. In the entire study population, survival rates were 88.04% at one month, 80.43% at six months, 70.65% at one year, and 61.96% at two years. Preoperative RHF was present in 24 patients, 12 of whom died and 12 survived LVAD implantation. Only two survivors developed early RHF (ERHF) and two late RHF (LRHF). The most significant predictors of ERHF development are brain natriuretic peptide (BNP), pre-surgery RHF, FAC < 20%, prior renal insufficiency, and total duration of ICU stay (HR: 1.002, 0.901, 0.858, 23.554, and 1.005, respectively). RHF following LVAD implantation is an unwanted complication with a negative impact on treatment outcome. The increased risk of fatal outcome in patients with ERHF and LRHF after LVAD implantation results in a need to identify patients at risk of RHF, in order to administer the available preventive and therapeutic methods.

Background: The aim of this study was to evaluate the frequency of postoperative complications in patients who underwent coronary artery bypass grafting (CABG) and simultaneous carotid endarterectomy (CEA) and find predictors of postoperative complications. Methods: We retrospectively evaluated 86 patients after simultaneous CABG and CEA. Inclusion criteria were: patients with asymptomatic carotid stenosis with a reduction of the carotid lumen diameter of more than 70% detected with Doppler ultrasound and diagnosed with one, two, or three vessel coronary artery disease with coronary stenosis more than 75% and hemodynamic significant stenosis of the left main artery. Exclusion criteria were patients with urgent and previous cardiac surgery and patients with myocardial infarction and stroke in the past one month. We monitored preoperative (ejection fraction, coronarography status), operative (number of grafts, on-pump or off-pump technique) and postoperative (extubation, unit care and hospital stay, bleeding and reoperation) details and complications (myocardial infarction, neurological events, inotropic agents and transfusion requiry, infection, arrhythmic complication, renal failure, mortality). Results: Postoperative complications were observed in 18 (29.9%) patients. Two patients (2.3%) had postoperative stroke and one patient (1.2%) had transient ischemic attack (TIA). Previous stroke was a predictor for increased postoperative neurological events (P < .05). Intrahospital mortality was 8.1%. Conclusion: Simultaneous CEA and CABG were performed with low rates of stroke and TIA. Previous stroke was identified as a predictor for increased postoperative neurological complications.

Coronary artery disease is a leading cause of morbidity and mortality in modern medicine. In contrast, surgical myocardial revascularization via coronary artery bypass grafting (CABG) remains the gold standard of treatment for complex multivessel disease. The great saphenous vein remains the most frequently used conduit due to its availability and technical simplicity, but its long-term patency is significantly inferior to that of arterial grafts. The primary pathological process responsible for vein graft failure is intimal hyperplasia, which represents a complex response of the vascular wall to surgical trauma, vein arterialization, inflammation, and hemodynamic stress. This process is characterized by endothelial dysfunction, inflammatory cell activation, proliferation and migration of vascular smooth muscle cells, and extracellular matrix remodeling. Underpinning these alterations are numerous molecular pathways, including NF-κB, MAPK, PI3K/Akt, TGF-β, and mTOR signaling, as well as substantial contributions from oxidative stress, cytokines, growth factors, and microRNAs. Contemporary research indicates that the phenotypic transformation of vascular smooth muscle cells constitutes the central event in the development of intimal hyperplasia. Understanding the cellular and molecular mechanisms underlying this disease's onset enables the development of novel therapeutic strategies to preserve long-term graft patency. This review paper aims to provide a systematic overview of current knowledge regarding the molecular and cellular mechanisms of intimal hyperplasia development in vein grafts following CABG.

Coronary artery disease is a leading cause of morbidity and mortality in modern medicine. In contrast, surgical myocardial revascularization via coronary artery bypass grafting (CABG) remains the gold standard of treatment for complex multivessel disease. The great saphenous vein remains the most frequently used conduit due to its availability and technical simplicity, but its long-term patency is significantly inferior to that of arterial grafts. The primary pathological process responsible for vein graft failure is intimal hyperplasia, which represents a complex response of the vascular wall to surgical trauma, vein arterialization, inflammation, and hemodynamic stress. This process is characterized by endothelial dysfunction, inflammatory cell activation, proliferation and migration of vascular smooth muscle cells, and extracellular matrix remodeling. Underpinning these alterations are numerous molecular pathways, including NF-κB, MAPK, PI3K/Akt, TGF-β, and mTOR signaling, as well as substantial contributions from oxidative stress, cytokines, growth factors, and microRNAs. Contemporary research indicates that the phenotypic transformation of vascular smooth muscle cells constitutes the central event in the development of intimal hyperplasia. Understanding the cellular and molecular mechanisms underlying this disease’s onset enables the development of novel therapeutic strategies to preserve long-term graft patency. This review paper aims to provide a systematic overview of current knowledge regarding the molecular and cellular mechanisms of intimal hyperplasia development in vein grafts following CABG.

The coarctation of the aorta is a congenital anomaly characterized by a local narrowing of the aortic lumen localized near the ductus arteriosus. Typically diagnosed in child-hood, but it can remain until symptoms become evident. This aortic anomaly can also coexist with aortic valve stenosis. In our case report, we present a 46-year-old male with chest pain, dyspnea, and a significant blood pressure gradient between upper and lower extremities. Diagnostic examination included transthoracic echocardiography and computerised tomography. This diagnostic imaging showed narrowing of the aor-tic lumen with a residual lumen dimension of 3 mm and severe aortic stenosis. The pa-tient underwent a complex surgical procedure, replacment of the aortic valve and re-construction of the aorta. An extra-anatomic ascending to descending aortic bypass was constructed using a 20 mm Dacron graft, combined with mechanical aortic valve replacment. The operation was performed through median sternotomy with two arte-rial canula in the femoral artery and in the aorta, and one venous canula in the right atrium. Two canulae are placed for the safe performance of cardiopulmonary bypass. The patient was discharged at home without complication. This case highlights that a single surgical procedure may represent a definitive treatment of a complex problem with good short-term results.