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Serum lactate, a marker of tissue hypoxia, is an important prognostic factor in sepsis, trauma, and cardiogenic shock. Data on the direct correlation of serum lactate and in-hospital mortality in normotensive acute pulmonary thromboembolism (APE) patients, however, remains scarce. We analyzed normotensive APE patients admitted to our clinic from January 1, 2014, to December 31, 2021. Serum lactate was collected from arterial blood at admission. The study sample included 161 patients with an average age of 68.61 ± 11.54 years. 54.94% were female. In-hospital mortality was 19.88%. In ROC analysis, serum lactate was a predictor of in-hospital mortality with an AUC of 0.662 (95%CI 0.584 – 0.735, p = 0.005). The cut-off level identified by the Youden index-associated criterion was > 38 mg/dL (34.38% sensitivity, 94.57% specificity). In multivariable analysis for in-hospital mortality alongside the biomarkers proposed by the 2019 ESC guidelines for severity assessment, lactate > 38 mg/dL was an independent predictor of mortality (OR 10.92, 95%CI 3.04 – 39.29, p < 0.001). The prediction model including PESI score, right ventricular dysfunction, troponin I, and lactate > 38 mg/dL had the best predictive performance for in-hospital mortality (AUC 0.807, p < 0.001). Elevated serum lactate is an independent predictor of all-cause in-hospital mortality of normotensive APE patients, with the optimal cut-off > 38 mg/dL. Adding the lactate level for mortality prediction outperformed the 2019 ESC guidelines algorithm for severity assessment of normotensive APE patients. [ABSTRACT FROM AUTHOR]

Lately, easier and shorter tests have been used in the functional evaluation of cardiac patients. Among these, walking speed (WS) and Timed Up and Go (TUG) tests are associated with all-cause mortality, mainly cardiovascular and the rate of re-hospitalization, especially in the elderly population. We prospectively analyzed a group of 38 patients admitted to the Cardiology Clinic from Elias Hospital, Romania, with chronic coronary syndrome (CCS) (n=22) and STEMI (n=16). We assessed the patients immediately after admission and before discharge with G-WALK between the 1st and 30th of September 2019. Our study group had a mean age of 62.7±12.1 years. Patients with a low WS were older (69.90±12.84 vs. 59.90±10.32 years, p=0.02) and had a lower serum hemoglobin (12.38±1.20 vs. 13.72±2.07 g/dl, p=0.02). The WS significantly improved during hospitalization (p=0.03) after optimal treatment. The TUG test performed at the time of admission had a longer duration in patients with heart failure (14.05 vs. 10.80 sec, p=0.02) and was influenced by patients' age (r=0.567, p=0.02), serum creatinine (r=0.409, p=0.03) and dilation of right heart chambers (r=0.399, p=0.03). WS and TUG tests can be used in patients with CCS and STEMI, and are mainly influenced by age, thus having a greater value among the elderly. [ABSTRACT FROM AUTHOR]

Objective: We evaluated the effects of neuromuscular electrical stimulation (NMES) therapy on functional capacity and oxidative stress in patients hospitalized for acute heart failure (AHF). Design: We included 30 consecutive patients admitted for AHF with a left ventricular ejection fraction ≤ 50% who were randomized into two groups: NMES therapy added on conventional rehabilitation (CR) (n = 15, 67.2 ±13.35 years) and CR alone (n = 15, 63.26 ± 10.29 years). NMES therapy was performed at the level of the quadriceps muscle bilaterally, daily, for 60 minutes with a frequency of 10 Hz. Results: The mean duration of NMES therapy was 6.93 ± 2.54 days. Functional capacity assessed by the 6 minute walk test was significantly improved in the group with NMES therapy (p=0.036). The oxidized LDL value showed a decreasing trend compared to the admission value in the group with NMES therapy, but without statistical significance. Conclusion: This paper shows that for patients with AHF, NMES therapy used for a short term and initiated early during the hospitalization period improves exercise tolerance, suggesting the importance and possible necessity of including it as standard cardiac recovery therapy. NMES did not influence the plasmatic value of oxidized LDL. [ABSTRACT FROM AUTHOR]

Background and aims. Aortic sclerosis associates an increased risk of cardiovascular morbidity and mortality. Recent studies suggest that aortic sclerosis is able to produce ventricular remodeling through inflammatory, non-hemodynamic mechanisms. Our study aims to evaluate the correlation between ventricular remodeling and aortic sclerosis severity. Method. 68 patients with aortic sclerosis without other significant associated valvulopathies were examined clinically, biologically and echocardiographic. In 20 patients, we quantified the severity of aortic valve calcification using the backscatter ecographic technique, in parasternal long and short axis view. Backscatter values obtained at the valvular level were calibrated to the blood and pericardium backscatter values. Results. In the 68 patients group, transvalvular aortic velocity correlates with left ventricular mass (p =0.031), which in turn incline to augment with increasing calcification severity assessed by backscatter. Calcification severity assessed by backscatter corellates with transvalvular aortic velocity in parasternal long axis view (p =0.039 for blood calibrated backscatter, p =0.029 for pericardium calibrated backscatter), and tends to augment with increasing transvalvular aortic velocity in parasternal short axis view. Patients with normal ventricular geometry incline to have lower aortic transvalvular velocities and a lower degree of calcification (evaluated by backscatter) compared to patients with ventricular remodeling. Conclusions. Aortic sclerosis is not benign, and may lead, in time, to left ventricular remodeling. With the progression of valvular calcifications in aortic sclerosis patients, the prevalence of ventricular remodeling tends to increase. [ABSTRACT FROM AUTHOR]