Clinical, respiratory, haemodynamic, and metabolic determinants of lactate in heart failure

Background: Lactate is an end-product of anaerobic cell metabolism. Although it is believed to have prognostic significance in heart failure (HF), data on the pathomechanisms that lead to lactate accumulation are scarce. Aims: We aimed to determine the clinical, respiratory, biochemical, and haemodynamic correlates of lactate in HF. Methods: Patients diagnosed with HF hospitalised in a single cardiac centre, who underwent haemodynamic monitoring, were included in this retrospective analysis. Results: The population consisted of 93 patients (44 acute HF [AHF] and 49 chronic HF [CHF] cases). The mean age, left ventricular ejection fraction, and lactate level were 60 ± 13 years, 33% ± 17%, 1.4 ± 0.9 mmol/L, respectively. The mean cardiac index (CI), right atrial pressure (RAP) and pulmonary capillary wedge pressure (PCWP) were 2.2 ± 0.5 L/min/m2, 8.7 ± 6 mmHg, and 18 ± 6 mmHg, respectively. AHF patients had significantly higher RAP, heart rate (HR), and levels of N-terminal pro–B-type natriuretic peptide and creatinine, compared to the CHF group. Both HR and natriuretic peptide level were correlated with lactate. Among haemodynamic indices, lactate correlated with CI (r = –0.25, p = 0.01). We found no correlation between lactate and RAP (p > 0.05) or PCWP (p > 0.05). There was no relationship between lactate and peripheral blood gases. Lactate was strongly correlated with mixed venous oxygen saturation (svO2) (r = –0.61, p < 0.05). HR, svO2, and systemic vascular resistance (SVR) were found to be independent determinants of lactate. Conclusions: Lactate accumulation in HF is not a result of respiratory disturbances or hypoxaemia. Among haemodynamic indices, CI is correlated with lactate. The strongest determinants of lactate included svO2, SVR, and HR

Zastosowanie lewosimendanu u chorych z ostrą niewydolnością serca z objawami małego rzutu minutowego serca: opis serii przypadków

The report presents single centre experience in application of levosimendan in patients with acute heart failure with low cardiacoutput. All patients underwent haemodynamic measurement before and after administration of the drug. Levosimendanimproved haemodynamics and was useful in this subpopulation of patients

Elevated lactate in acute heart failure patients with intracellular iron deficiency as identifier of poor outcome

Background: We believe that there is a physiological link between intracellular iron status (assessed by soluble transferrin receptor [sTfR]) and efficiency of energy production/consumption (assessed by lactate, a product of anaerobic cell metabolism), which may further impact the outcome of patients with acute heart failure (AHF).  Aims: To examine if elevated levels of lactate ( > 2 mmol/L) accompanied by unmet cellular iron requirements (defined as sTfR > 1.59 mg/L) identify AHF patients with an unfavourable outcome.  Methods: The study is a single-centre, retrospective analysis of AHF patients in whom lactate and iron status were assessed on admission. The endpoint of the study was one-year mortality.  Results: The study population consisted of 89 patients at a mean age of 65 ± 13 years. Mean systolic blood pressure and creatinine level were 135 ± 36 mmHg and 1.3 ± 0.6 mg/dL, respectively, and median [25th–75th quartiles] lactate level on admission was 2.0 [1.6–2.6] mmol/L. In 17 (19%) patients, both lactate and sTfR were below the cut-off values (group 1). In 38 (43%) individuals one of the markers was elevated (group 2) and in the remaining 34 (38%) patients both markers were above the predefined cut-off values (group 3). There was no difference in clinical and laboratory characteristics between the groups. During one-year follow-up 23 (26%) patients died. Mortality risk in group 3 was higher compared to the rest of the population (hazard ratio 5.6, 95% confidence interval 2.2–14, p = 0.0003), even after adjustments for well-defined prognostic factors.  Conclusions: Patients with unmet iron cell requirements and hyperlactataemia on admission have significantly higher mortality risk compared to individuals without those pathologies.

Persistent hyperlactataemia is related to high rates of in-hospital adverse events and poor outcome in acute heart failure

Background: Although lactate is a well-established marker in intensive care, our understanding of its utility in acute heart  failure (AHF) is modest and based on studies with a single measurement of this marker.  Aims: We aimed to investigate whether persistent elevation of lactate during hospitalisation is related to a higher risk of ad- verse events.  Methods: We conducted a prospective study to assess AHF patients hospitalised in one cardiac centre. The diagnosis of persistent hyperlactataemia was based on two measurements of the marker (on admission and at 24 h of hospitalisation) and it was defined as lactate elevation (≥ 2 mmol/L) at both time points.  Results: The population consisted of 222 patients at a mean age of 70 ± 13 years. Mean ejection fraction and creatinine level on admission were 37% ± 16% and 1.36 ± 0.51 mg/dL, respectively. The percentage of patients with elevated lactates on admission, at 24 h of hospitalisation, and persistent hyperlactataemia were 47%, 35%, and 24%, respectively. The group with persistent hyperlactataemia did not differ in most clinical and laboratory variables from the rest of the population. Patients with persistent hyperlactataemia had higher rate of adverse events during hospitalisation: worsening of heart failure (22.6% vs. 6.5%, p < 0.05), inotrope use (22.6% vs. 5.3%, p < 0.05), and increase of N-terminal pro–B-type natriuretic peptide at 48 h of hospitalisation (30% vs. 18%, p < 0.05). Persistent hyperlactataemia was an independent predictor of one-year mortality (hazard ratio 2.5, 95% confidence interval 1.5–4.3, p < 0.001).  Conclusions: Persistent hyperlactataemia within the first 24 h of hospitalisation is a predictor of a worse outcome in AHF and is related to higher rates of in-hospital adverse events and one-year mortality.

Sodium-glucose co-transporter 2 inhibition in patients hospitalized for acute decompensated heart failure:rationale for and design of the EMPULSE trial

Aims Treatment with sodium-glucose co-transporter 2 (SGLT2) inhibitors improves outcomes in patients with chronic heart failure (HF) with reduced ejection fraction. There is limited experience with the in-hospital initiation of SGLT2 inhibitors in patients with acute HF (AHF) with or without diabetes. EMPULSE is designed to assess the clinical benefit and safety of the SGLT2 inhibitor empagliflozin compared with placebo in patients hospitalized with AHF. Methods EMPULSE is a randomized, double-blind, parallel-group, placebo-controlled multinational trial comparing the in-hospital initiation of empagliflozin (10 mg once daily) with placebo. Approximately 500 patients admitted for AHF with dyspnoea, signs of fluid overload, and elevated natriuretic peptides will be randomized 1:1 stratified to HF status (de-novo and decompensated chronic HF) to either empagliflozin or placebo at approximately 165 sites across North America, Europe and Asia. Patients will be enrolled regardless of ejection fraction and diabetes status and will be randomized during hospitalization and after stabilization (between 24 h and 5 days after admission), with treatment continued up to 90 days after initiation. The primary outcome is clinical benefit at 90 days, consisting of a composite of all-cause death, HF events, and >= 5 point change from baseline in Kansas City Cardiomyopathy Questionnaire total symptom score (KCCQ-TSS), assessed using a 'win-ratio' approach. Secondary outcomes include assessments of safety, change in KCCQ-TSS from baseline to 90 days and change in natriuretic peptides from baseline to 30 days. Conclusion The EMPULSE trial will evaluate the clinical benefit and safety of empagliflozin in patients hospitalized for AHF

Application of machine learning in predicting frailty syndrome in patients with heart failure

Prevention and diagnosis of frailty syndrome (FS) in patients with heart failure (HF) require innovative systems to help medical personnel tailor and optimize their treatment and care. Traditional methods of diagnosing FS in patients could be more satisfactory. Healthcare personnel in clinical settings use a combination of tests and self-reporting to diagnose patients and those at risk of frailty, which is time-consuming and costly. Modern medicine uses artificial intelligence (AI) to study the physical and psychosocial domains of frailty in cardiac patients with HF. This paper aims to present the potential of using the AI approach, emphasizing machine learning (ML) in predicting frailty in patients with HF. Our team reviewed the literature on ML applications for FS and reviewed frailty measurements applied to modern clinical practice. Our approach analysis resulted in recommendations of ML algorithms for predicting frailty in patients. We also present the exemplary application of ML for FS in patients with HF based on the Tilburg Frailty Indicator (TFI) questionnaire, taking into account psychosocial variables