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

Abstract

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. Aim: 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/m 2 , 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 (svO 2) (r =-0.61, p < 0.05). HR, svO 2 , 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 svO 2 , SVR, and HR.

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

“…In fact, our previous observations seem to confirm that assumption, as in HF patients; adrenergic drive (represented by heart rate), tissue hypoperfusion (expressed as systemic vascular resistance), and depressed lactate clearance (liver dysfunction) were strongly correlated with lactate [8,20]. There was no evidence to link lactate with hypoxia and hypoxaemia in our HF population [20]. Moreover, there are grounds to believe that lactate may facilitate modification of protein expression that leads to more efficient energy consumption [22].…”

“…Lactate itself may be a source of energy for some cells, thus it may have protective capabilities [22][23][24][25]. In fact, our previous observations seem to confirm that assumption, as in HF patients; adrenergic drive (represented by heart rate), tissue hypoperfusion (expressed as systemic vascular resistance), and depressed lactate clearance (liver dysfunction) were strongly correlated with lactate [8,20]. There was no evidence to link lactate with hypoxia and hypoxaemia in our HF population [20].…”

“…The aforementioned mechanism is definitely complex and much more sophisticated than just "simple" iron deficiency-driven anaemia or hypoxia because we found no differences in haemoglobin values and oxygen saturation across the three groups. Moreover, we have recently reported that lactate is not correlated with respiratory disturbances in the broad spectrum of HF patients [20]. We believe that the coexistence of these two factors is not accidental and may actually identify patients with functional intracellular iron insufficiency that leads to energy debt with its clinical consequences.…”

Controlled decongestion by Reprieve therapy in acute heart failure: results of the TARGET‐1 and TARGET‐2 studies

“…Mean blood pressure remained unchanged and there were no significant drops in systolic blood pressure in any patient. In those who underwent haemodynamic monitoring, we noticed a decrease in CVP (indicating effective decongestion) and a trend toward an increase in mixed venous oxygen saturation (as an indirect marker of preserved peripheral perfusion), accompanied by stable mean lactate level . Again, we interpret these findings as an additional piece of evidence that controlled fluid removal with the Reprieve System TM is safe and associated with stabilization of haemodynamic status.…”

Acute heart failure, iron deficiency, and hyperlactataemia: a high-risk combination

“…The metabolism of lactate is complex and not well known. Lactate increase was traditionally considered a consequence of tissue hypoxia caused by hypoperfusion [4], but this simple interpretation was progressively modified when it was demonstrated that hyperlactataemia in patients with acute HF was not related to blood pressure, arterial oxygen saturation, or cardiac output, even in the sickest population [5][6][7]. Instead, lactate accumulation is better explained by an imbalance between its production and clearance, which itself may be caused by several mechanisms, such as peripheral hypoperfusion due to low cardiac output, high central venous pressure or vasoconstriction, sympathetic activation, hypoxaemia, anaemia, and liver or renal dysfunction [8].…”