Due to the critical nature of acute HF (AHF), accurately gauging the risk for mortality may help determine treatment protocols and may improve outcomes, according to Yali Chao, MD, and colleagues. While N-terminal B-type natriuretic peptide precursor (NT-proBNP) is the typical prognostic indicator for patients with HF, its restricted sensitivity and specificity has led researchers to look to other markers to provide greater prognostic accuracy.


Predictive Value

For a study published in the International Journal of Clinical Practice, Dr. Chao and team examined the predictive value of arterial blood lactic acid concentration as a tool to promote quick and precise evaluation of patients with AHF; they did so based on the understanding that anaerobic glycolysis and lactic acid build up in patients with AHF due to the heart’s inability to provide satisfactory oxygenation and perfusion of tissues and organs resulting from infection, lessened cardiac function, coronary artery stenosis, and additional factors.

Prior studies have suggested the value of applying this correlation in a prognostic capacity; however, as the researchers wrote, “the association between the levels of lactic acid and nosocomial all-cause mortality in patients with AHF, especially in the critical care unit, has yet to be determined.”

To fill this knowledge gap, Dr. Chao and colleagues searched for and analyzed data from patients with AHF admitted to the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. They applied a multivariate logistic regression model, restricted cubic spline plot, and subgroup analysis to assess the association between lactic acid and in-hospital, all-cause mortality in this patient population. Receiver operating curve (ROC) analysis was also performed.

The 7,558 participants were divided into 6,792 survivors and 766 who died. Three models were developed to address different variables among them: Model 1 was not adjusted for any variables; Model 2 was adjusted for age, sex, and ethnicity; and Model 3 was adjusted for age, ethnicity, BMI, weight, systolic BP, history of atrial fibrillation, liver cirrhosis, acute myocardial infarction, chronic kidney disease, respiratory failure (RF), chronic obstructive pulmonary disease, ventricular fibrillation, diabetes mellitus, septicemia, anion gap, bicarbonate, blood urea nitrogen, calcium, serum creatinine, glucose, hematocrit, hemoglobin, platelet, red blood cells, C reactive protein, length of stay, albumin, white blood cells, NT-proBNP, cardiotonic drugs, nitroglycerin drugs, furosemide drugs, infection-fighting drugs, Simplified Acute Physiology Score (SAPS) II, and sequential organ failure assessment.


Fully Adjusted Model

When compared with the lowest quartiles, the ORs (95% CI) for in-hospital, all-cause mortality across the quartiles were 1.46 (1.07-2.00), 1.48 (1.09-2.00), and 2.36 (1.73-3.22) for lactic acid (Table). In-hospital, all-cause mortality gradually increased along with increased lactic acid levels (P for trend, <0.05). “A combination of lactic acid concentration and the [SAPS] II may improve the predictive value of in-hospital all-cause mortality in patients with AHF,” wrote Dr. Chao and team. “The correlation heatmap revealed that NT-proBNP was positively correlated with lactic acid (r=0.07) and positively correlated with in-hospital all-cause mortality (r=0.18). There was an inverse L-shaped curve relationship between NT-proBNP and in-hospital all-cause mortality, respectively. Mediation analysis suggested that a positive relationship between lactic acid and in-hospital all-cause death was mediated by NT-proBNP.”

The area under the ROC (AUC) constructed by the indicator variable indicated that lactic acid was able to predict in-hospital, all-cause mortality; the AUC was 0.616 (sensitivity, 52.22%; specificity, 63.35%). It should be noted that RF interacted with the association between arterial blood lactic acid and in-hospital, all-cause mortality (P for interaction, <0.05).

In further illustrating the significance of the correlation, Dr. Chao and colleagues wrote, “Once significant amounts of blood lactic acid and its metabolites are stored in the body, patients will gradually progress into severe metabolic acidosis, which will eventually result in PH decline, hyperkalemia, and a decrease in the ventricular fibrillation threshold, further increasing the incidence of sudden cardiac death.” The study team is hopeful that measuring lactic acid levels may improve the evaluation and treatment of patients with AHF.