Predicting the survival of a patient with heart failure (HF) is a complex problem in clinical practice. Our previous study reported that extracellular HSP70 (HSPA1A) correlates with markers of heart function and disease severity in HF, but the predictive value of HSP70 is unclear. The goal of this study was to analyze extracellular HSP70 as predictive marker of mortality in HF. One hundred ninety-five patients with systolic heart failure were enrolled and followed up for 60 months. By the end of follow-up, 85 patients were alive (survivors) and 110 died (nonsurvivors). HSP70 (measured by ELISA in the serum) was elevated in nonsurvivors, compared with survivors (0.39 [0.27–0.59] vs. 0.30 [0.24–0.43] ng/ml, respectively, p = 0.0101). In Kaplan–Meier survival analysis higher HSP70 levels above median were associated with a significantly increased mortality. In multivariable survival models, we show that HSP70 level above the median is an age-, sex-, body mass index-, creatinine-, and NT-proBNP-independent predictor of 5-year mortality in HF. Extracellular HSP70 could prove useful for estimating survival in patients with HF.

Background: Proper basic life support (BLS) is key in improving the survival of out-of-hospital cardiac arrest. BLS skills deteriorate in three to 6 months after training. One method to improve skill retention may be using the “testing effect” to test skills at the end of a BLS course. The aim of our study was to investigate whether either testing or the timing of such testing after BLS training have any influence on skill retention. Methods: This was a post-test only, partial coverage, prospective quasi-experimental study designed to evaluate a BLS training course among 464 fifth year medical students at Semmelweis University in the first semester of 2013/2014. Groups were systematically but non-randomly assigned to either a control group that took no exam or one of two experimental groups that took an exam (N = 179, NoExam group; N = 165, EndExam group – exam at the end of the BLS training; N = 120, 3mExam group – exam 3 months after the BLS training). The ability to perform ten prescribed essential BLS steps was evaluated during a skill retention assessment 2 months after the course in the NoExam, 2 months after the course (and the exam) in the EndExam and 5 months after the course (2 months after the exam) in the 3mExam group to measure skill retention and the effect of our intervention. Scores were calculated for each BLS step, and also summed up as a total score. We used Kruskal-Wallis test to assess differences in skill retention. Results: Overall, NoExam and EndExam groups showed similar skill retention. The mean total score (and many of the sub-scores) of students was significantly higher in the 3mExam group compared to both the NoExam and the EndExam groups, and there was no difference in the total score (and many of the sub-scores) of the latter two groups. The 3mExam group had less variability in total scores (and many of the sub-scores) than the other two groups. Conclusion: Our study provides evidence that testing these skills 3 months after BLS training may be more effective than either testing immediately at the end of the course or no testing at all.

Predicting the prognosis of comatose, post-cardiac-arrest patients is a complex problem in clinical practice. There are several established methods to foretell neurological outcome; however, further prognostic markers are needed. HSP70 (HSPA1A), which increases rapidly in response to severe stress (among others after ischemic or hypoxic events), is a biomarker of cell damage in the ischemic brain and spinal cord. We hypothesized that HSP70 might be a reliable predictor of mortality in post-cardiac-arrest patients. The aim of this study was to analyze the role of extracellular HSP70 in the systemic inflammatory response over time, as well as the predictive value in cardiac arrest patients. Here, we show that the elevation of HSP70 levels in resuscitated patients and their persistence is an independent predictor of 30-day mortality after a cardiac arrest. Forty-six cardiac arrest patients were successfully cooled to 32–34 °C for 24 h, and followed up for 30 days. Twenty-four patients (52.2 %) were alive by the end of follow-up, and 22 patients (47.8 %) died. Forty-six patients with stable cardiovascular disease served as controls. Extracellular HSP70 (measured by ELISA in blood samples) was elevated in all resuscitated patients (1.31 [0.76–2.73] and 1.70 [1.20–2.37] ng/ml for survivors and non-survivors, respectively), compared with the controls (0.59 [0.44–0.83] ng/ml). HSP70 level decreased significantly in survivors, but persisted in non-survivors, and predicted 30-day mortality regardless of age, sex, complications, and the APACHE II score. Extracellular HSP70 could prove useful for estimating prognosis in comatose post-cardiac-arrest patients.

Cardiac arrest causes generalized ischaemia/hypoxia, and subsequent resuscitation inflicts reperfusion injury, the pathology of which is not fully understood. Moreover, predicting the prognosis of comatose, post‐cardiac arrest patients is a complex clinical challenge. We hypothesized that the extent of complement activation might be a reliable predictor of mortality in this population. Forty‐six comatose cardiac arrest patients were enrolled into our prospective cohort study, conducted in a tertiary care university clinic. All subjects were cooled to 32–34 °C body temperature for 24 h and then allowed to rewarm to normothermia. All patients underwent diagnostic coronary angiography. On admission, at 6 and 24 h, blood samples were taken from the arterial catheter. In these, complement products (C3a, C3, C4d, C4, SC5b9 and Bb) were measured by ELISA in blood samples. Patients were followed up for 30 days; 22 patients (47.8%) died by the end of this period. We observed that complement activation (determined as the C3a to C3 ratio) was higher in non‐survivors than in survivors at each time point. In the multivariate Cox regression analysis, the C3a/C3 ratio determined 24 h after the initiation of therapeutic hypothermia predicted 30‐day mortality regardless of age, sex and the APACHE II score. Complement activation occurs in post‐cardiac arrest patients, and its extent correlates with 30‐day survival. The C3a/C3 ratio might prove useful for estimating the prognosis of comatose post‐cardiac arrest patients.

Mitral annular calcification (MAC) is usually considered an incidental, benign, age-related finding without serious complications in patients evaluated for cardiovascular or pulmonary disease with imaging studies that may result in mitral regurgitation or stenosis when severe. Therefore, it is usually not considered a significant alteration. However, there is accumulating evidence that it is associated with a higher risk of cardiovascular events, such as atherosclerotic coronary artery disease, aortic artery disease, carotid artery disease, peripheral artery disease, stroke, atrial fibrillation, atrioventricular and/or intraventricular conduction disturbance, systemic embolization, infective endocarditis, heart failure and mortality. The presence of MAC also significantly influences the outcome of mitral valve transcatheter and surgical interventions. Several conditions may predispose to MAC. MAC is strongly related to cardiovascular risk factors, such as hypertension, diabetes, smoking and cardiovascular atherosclerosis, and inflammation may also play a role in the pathogenesis of MAC. Also, conditions that increase mitral valve stress, such as hypertension, aortic stenosis and hypertrophic cardiomyopathy, predispose to accelerated degenerative calcification of the mitral annulus area. Congenital disorders, e.g., Marfan syndrome and Hurler syndrome, are also associated with MAC, due to an intrinsic abnormality of the connective tissue composing the annulus.