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Conclusions. An unfavourable progression of SARS-CoV-2 infection can be expected in middle-aged, obese patients, and in those with elevated levels of inflammatory markers and LDH. Abnormally increased NLR and PLR values may also serve as potential indicators of disease severity; however, further evaluation in a larger patient sample is required to determine the predictive role of these rations in SARS-CoV-2 infection.

Objectives. The present study aims to describe the clinical and biological profile of heart failure patients from central Romania. Material and method. A single centre-based retrospective, observational, descriptive study involving heart failure patients admitted from January 2018 to March 2020 was conducted. Only patients who had echocardiographic data determined by the same examiner were included. Patients were classified according to LVEF at admission in three subgroups: preserved LVEF subgroup (HFpEF, LVEF ≥ 50%), moderate LVEF subgroup (HFmrEF, LVEF 40-49%), reduced LVEF subgroup (HFrEF, LVEF < 40%) and their clinical and biological profile was assessed. Comorbidities were recorded using the Charlson comorbidity index (CCI). Outcomes. A total of 175 patients (57.7% males) were included in our study, with a mean age of 65.3 ± 11.7 years. 44% of patients had more than one hospital admission during the studied timeframe. Mean calculated left ventricular ejection fraction was 47.1% ± 12.1%. According to LVEF 62.8% of patients were in HFpEF group, 20.5% in the HFrEF group and 16.5% in the HFmrEF group. Dyspnoea was the most common presenting symptom in 65.7% of patients, being accompanied by fatigue in majority of cases (63.4%). Charlson comorbidity index mean value for the study population was 4.6 ± 2.1, 4.6 ± 2 in the HFpEF group, 5.2 ± 1.9 in the HFmrEF group and 4.03 ± 2.2 in the HFrEF group. Arterial hypertension was the most frequent comorbid condition and risk factor at the same time, in both men and women. Conclusions. The clinical and biological profile of the heart failure patients is complex, diverse and further research is needed for improving therapeutic and follow-up management of these patients.

Atherosclerotic plaque ruptures with subsequent intraluminal thrombosis are the most prevalent causes of acute coronary syndromes, ischemic stroke, acute limb ischemia or cardiovascular death. Hyperlipidemia is no longer considered the primary cause of atherosclerotic disease, as recent data supports the involvement of other triggers such as age, excessive activation of sympathetic nervous system in arterial hypertension, and most importantly, inflammation. Arteriosclerosis is a consequence of interaction between similar mechanisms resulting in arterial stiffening. Furthermore, wall stiffening resulted from the arteriosclerotic process is a risk factor for atherosclerotic disease. This unstructured literature review aimed to present the underlying remodelling processes and mechanisms for atherosclerosis and arteriosclerosis highlighting the common aspects of this two entities and the continuous interrelation that eventually leads to cardiovascular events.

The primary cutaneous diffuse large B-cell lymphoma leg type (PCDLBCL-LT) is a rare form of cutaneous lymphoma with aggressive and unpredictable evolution. The patients are often aged and with comorbid conditions so that immunochemotherapy can be poorly tolerated. Despite its complexity, a differential diagnosis is possible in the primary care setting and it is of great importance in guiding further investigation and referral. We present the case of a 70-year-old man with reddish nodular lesions appeared on the anterior region of the right tibia. Anatomopathological subtype identified a PCDLBCL-LT, T2aN1M0 stage. The first line of R-CHOP regimen (rituximab – cyclophosphamide, doxorubicin, vincristine, prednisone) associating intrathecal prophylaxis with methotrexate was prescribed with a good response. An early relapse after first line chemotherapy was noticed. Salvage R-DHAP regimen (rituximab-dexamethasone, high dose cytarabine, cisplatin) with modest response and progression of the disease under chemotherapy was instituted. During targeted therapy, the patient experienced an acute myocardial infarction, heart failure, and acute kidney injury. Thus, comorbid conditions have dramatically reduced systemic therapeutic options. The multidisciplinary approach with the implication of general physician, hematologist, cardiologist and other specialists was necessary for the management of this case.

Introduction. Vascular calcification is an independent risk factor related to cardiovascular mortality in CKD patients. Advanced aortic arch calcification assessed by semi-quantitative estimation on posteroanterior chest X-ray is a strong independent predictor of cardiovascular events in CKD and non-CKD patients, beyond traditional risk factors. An association between aortic arch calcification and hypertension has been previously reported however, the presence of CKD has not recorded in most studies. The aim of our study was to identify risk factors related to aortic arch calcification in hypertensive CKD patients. Material and method. A retrospective observational study on 63 hypertensive patients with CKD stages G2 to G4, that had a posteroanterior chest X ray available was conducted. The study population was divided into 2 groups according to presence or absence of aortic arch calcification on chest X-rays. Chest X-ray identified 43 patients with aortic arch calcification. Laboratory data were recorded for every individual simultaneously with the following comorbidities: coronary artery disease, carotid stenosis, hypertensive cardiopathy, lower extremity arterial disease. Outcomes. Groups were homogenous regarding gender distribution, creatinine levels and diabetes mellitus prevalence. We found no a statistically significant difference regarding comorbidities between the two groups. Lactate dehydrogenase and alkaline phosphatase had a statistically significant association with aortic arch calcification (p = 0.043, p = 0.006 respectively). Conclusions. Increased alkaline phosphatase remains an important risk factor for aortic arch calcification even in patients with less advanced CKD. Lactate dehydrogenase is yet to be validated as a marker for aortic arch calcification in CKD patient, however, our study reports a statistically significant association between lactate dehydrogenase and aortic arch calcification in patients with CKD.