The possibility of SARS-CoV-2 transmission in a haemodialysis unit - report from a large in-hospital centre.

Data on the possibility of transmission of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) during the provision of chronic haemodialysis, which often entails many person-to-person contacts, are lacking. We report a follow-up of the in-centre contacts of three positive chronic haemodialysis patients. Under strict preventive measures, only one patient out of 21 patient-contacts and 29 personnel-contacts tested positive within 2 weeks after the last contact. This patient, case #3, most likely became infected during unprotected, organised group transportation to the dialysis centre.

Obesity dilemma in the global burden of cardiovascular diseases.

AIM: Obesity is a well-known risk factor in the cardiovascular disease continuum. However, its clinical effects are multimodal, perplexed and non-unanimously understood. Our aim was to assess the prevalence and effects of obesity on the cardiometabolic risk factors and systolic function of left ventricle ejection fraction (LVEF) in patients scheduled for cardiovascular rehabilitation. METHODS: A cohort of 302 consecutive patients recently treated for ischaemic or valvular heart disease was matched according to the existence of obesity, defined with body mass index (BMI ≥ 30 kg/m(2) ; n = 90 vs. 212), and the advanced grade of obesity (BMI ≥ 35 kg/m(2) ; n = 19 vs. 283). Nutritional risk screening was performed using the standardised NRS-2002 tool. RESULTS: The mean age of patients was 62.4 ± 11.2 (range 23-86) years; there were more men than women 244 (80.8%) : 58 (19.2%). Group of obese conveyed higher prevalence of ischaemic heart disease than non-obese (OR = 2.69; 95% CI: 1.01-7.20; p = 0.048); while the difference was insignificant for the advanced grade of obesity (n = 17; 89.5%) vs. controls (n = 233; 82.3%; p > 0.05). There was no significant difference in prevalence of other comorbidities (diabetes, glucose intolerance, hypercholesterolaemia, chronic renal and chronic obstructive pulmonary disease) between studied groups (p > 0.05). Utilisation of lipid-lowering drugs was of similar range between the studied groups (p > 0.05), respectively. LVEF (%) was 50.5 ± 8.2 vs. 50.7 ± 7.7 (p > 0.05) and 50.6 ± 7.8 vs. 49.6 ± 10.9 (p > 0.05; Rho = 0.001; p > 0.05), respectively. CONCLUSION: In studied set of patients, BMI positively correlated with left ventricle dimension and thickness. No significant connection of obesity was found with the prevalence of chronic comorbidities, increased nutritional risk, laboratory diagnostics or systolic function of left ventricle. Existence of obesity paradox in clinical practice was in part reaffirmed with our study.

Heart surgery stems increased nutritional risk, expressed during the course of stationary rehabilitation.

BACKGROUND: Cardiovascular diseases are a vast global health burden. Despite common prevalence, current knowledge and investigations concerning nutritional aspects are limited. Characteristics and dynamics of nutritional risk are not entirely known for most of the entities, disease stages or treatment-induced fluctuations. This study assessed the effects of heart surgery on unintentional weight loss and nutritional risk using the NRS-2002. METHODS: A noninterventional study that included patients scheduled for rehabilitation 1-6 months after heart surgery was performed. Evaluation included routine cardiovascular diagnostics and review of medical histories. Documented baseline weight was available for >85% of the patients. Nutritional risk screening was performed with the standardized NRS-2002 questionnaire. RESULTS: A total of 145 patients were involved, with a mean age of 65.3 ± 11.5 years in a range of 23-84 years. The male to female ratio was 121:24 (83.4%:16.6%), respectively. Coronary artery bypass graft surgery (CABG) was performed in 89 patients (61.4%), valvular surgery (VS) in 34 (23.4%) and combined operations (CABG + VS) in 22 (15.2%). Percentage weight loss history was 11.1 ± 3.4% in a range of 0-20.1%, while NRS-2002 was 4.77 ± 1.05 in a range of 1-6. Increased nutritional risk (NRS-2002 ≥3) was found in nearly all patients. Combined ischemic and valvular etiology displayed the highest values of NRS-2002 (5.0 ± 1.2). Patient age and creatinine showed significant correlations with NRS-2002 (Rho = 0.521, p < 0.001 and Rho = 0.335, p < 0.001, respectively). CONCLUSION: Increased nutritional risk was found to be frequently prevalent in patients scheduled for rehabilitation after heart surgery. Risk was found to be in relation with underlying coronary artery disease as well as with the age of patients and parameters of renal function. Routine application of nutritional risk screening appears to be a valuable clinical tool for detecting this relevant comorbidity, particularly since no connection was found with traditional anthropometrics.

Can we assess an acute myocardial infarction in patients with acute coronary syndrome according to diagnostic accuracy of heat shock proteins?

Heat shock proteins (HSPs) have changed very little with evolution, suggesting that they play important role(s) in cellular survival. Specifically, HSPs protect cells from induced cell death. Their expression is triggered by heat or other stress, such as ischemia. HSPs provide protection against protein denaturation, although they slightly differ with respect to group affiliation. Release of HSPs from necrotic and ischemic cardiomyocytes into the intercellular space and plasma may correlate with the intensity of the pro-inflammatory response observed during and immediately after myocardial infarction. We hypothesized that the plasma concentration of particularly inducible forms of HSPs from different groups (HSP 90, HSP 70, HSP 60 and/or HSP 20) can be used as early specific markers for diagnosing myocardial infarction in patients with acute coronary syndrome. Our hypothesis is supported by the following data: (I) HSP expression occurs very early after acute coronary events; (II) HSP concentrations increase rapidly in the peripheral blood; (III) HSP concentrations correlate with markers of myocardial necrosis and pro-inflammatory biochemical parameters. The magnitude of the increase in plasma HSP concentrations over initial concentrations during the period of highest sensitivity and specificity of the assay could be important for early detection of myocardial infarction and distinguishing it from unstable angina. We suggest that these parameters, along with close observation of patients with chest pain, will assist providers who must differentiate between acute myocardial damage and other organ diseases.

Harmful immune reactions during acute myocardial infarction.

Acute coronary syndrome, including myocardial infarction, can occur as a result of ischaemia-reperfusion injury caused by acute occlusion of the coronary vessel/s following the rupture of an atherosclerotic plaque. Superimposed thrombosis at the lesion obstructs blood supply to the myocardium causing myocardial necrosis and ischaemic inflammation. Although not fully described, researchers believe that this process is initiated by a dysfunctional endothelium that activates the nearby leukocytes in the blood stream, thus attracting them to the arterial wall and initiating a cascade of complex mechanisms that lead to myocardial infarction. Interestingly, this process is two sided as the leaking soluble factors from a damaged and/or necrotic myocardium enter the systemic circulation, activating the innate and adaptive cell-mediated immune responses, which include increasing cytotoxic mediators. We hypothesize that this unwanted side effect of increase in proinflammatory mediators can lead to harmful systemic immune reactions directed towards various dysfunctional endothelia. Additionally, a strong inflammatory response, caused by myocardial damage, can impair ventricular function, on top of baseline necrosis. To evaluate this hypothesis, we propose to use in vivo tests to measure endothelial dysfunction, as well as ventricular dysfunction by ultrasound methods, and their correlation with immunological and/or biochemical parameters. These tests will be useful in assessing the risk and therapeutic outcome in patients with acute coronary syndrome.

Granulysin Expression in Lymphocytes that Populate the Peripheral Blood and the Myocardium after an Acute Coronary Event.

We aimed to analyse granulysin (GNLY)-mediated cytotoxicity in the peripheral blood of patients with non-ST-segment elevation myocardial infarction (NSTEMI) treated with anti-ischaemic drug therapy. Thirty-nine NSTEMI patients with a median age of 70 years and 28 age-matched healthy subjects were enrolled in this study. On day 7 after MI, the number of GNLY(+) lymphocytes in the peripheral blood increased approximately six-fold of that in the healthy subjects, measured by flow cytometry. On day 14, the number of GNLY(+) cells significantly decreased in T, NKT, and both CD56(+dim) and CD56(+bright) NK subsets. GNLY(+) CD3(+) and GNLY(+) CD56(+) cells infiltrated central zone of myocardial infarction (MI). In persons who died in the first week after MI, GNLY(+) cells were found within accumulation of apoptotic leucocytes and reached the apoptotic cardiomyocytes in border MI zones probably due to the influence of interleukin-15 in peri-necrotic cardiomyocytes, as it is was shown by immunohistology. By day 28, the percentage of GNLY(+) lymphocytes in peripheral blood returned to the levels similar to that of the healthy subjects. Anti-GNLY mAb decreased apoptosis of K562 targets using peripheral blood NK cells from days 7 and 28 after MI, while in assays using cells from days 1 and 21, both anti-GNLY and anti-perforin mAbs were required to significantly decrease apoptosis. Using NK cells from day 14, K562 apoptosis was nearly absent. In conclusion, it seems that GNLY(+) lymphocytes, probably attracted by IL-15, not only participate partially in myocardial cell apoptosis, but also hasten resolution of cardiac leucocyte infiltration in patients with NSTEMI.

Perforin-mediated cytotoxicity in non-ST elevation myocardial infarction.

The aim of this investigation was to examine the role of perforin (P)-mediated cytotoxicity in the dynamics of tissue damage in patients with non-ST-segment elevation myocardial infarction (NSTEMI) treated with anti-ischaemic drugs. We enrolled 48 patients with NSTEMI in this study [age, 71.5 years; 61.5/76 (median, 25th/75th percentiles)]. The percentage of total peripheral blood P(+) lymphocytes was elevated owing to the increased frequency of P(+) cells within natural killer (NK) subsets, T and NKT cells in patients on day 1 after NSTEMI when compared with healthy controls. Positive correlations were found between cardiac troponin I plasma concentrations and the frequency of P(+) cells, P(+) T cells, P(+) NK cells and their CD56(+dim) and CD56(+bright) subsets during the first week after the NSTEMI. The expression of P in NK cells was accompanied by P-mediated cytotoxicity against K-562 targets at all days examined, except day 21, when an anti-perforin monoclonal antibody did not completely abolish the killing. The percentage of P(+) T cells, P(+) NKT cells and P(+) NK subsets was the highest on the day 1 after NSTEMI and decreased in the post-infarction period. CD56(+) lymphocytes were found in damaged myocardium, suggesting their tissue recruitment. In conclusion, patients with NSTEMI have a strong and prolonged P-mediated systemic inflammatory reaction, which may sustain autoaggressive reactions towards myocardial tissue during the development of myocardial infarction.