Elevated serum lactate is a marker of organ damage related to impaired hemodynamics and indicates poor prognosis in acute heart failure

Zymliński, Robert; Biegus, Jan; Sokolski, Mateusz; Nawrocka, Sylwia; Siwołowski, Paweł; Szachniewicz, Joanna; Cotter, Gad; Jankowska, EA; Banasiak, W.; Ponikowski, Piotr

doi:10.1093/eurheartj/eht308.p1517

Cited by 3 publications

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“…8 Lactate is a normal product of anaerobic metabolism. 12 The blood lactate levels are elevated not only due to tissue hypoxia or anaerobic glycolysis, but also due to secondary activation of the stress response. Characteristics of lactate production best fit the notion of an adaptive survival response that grows in intensity as disease severity increases.…”

Section: Introductionmentioning

confidence: 99%

“…The neutrophil‐to‐lymphocyte ratio (NLR) is a rapid and simple parameter of systemic inflammation and stress, which expresses the severity of the disease in the critically ill patients . Lactate is a normal product of anaerobic metabolism . The blood lactate levels are elevated not only due to tissue hypoxia or anaerobic glycolysis, but also due to secondary activation of the stress response.…”

Section: Introductionmentioning

confidence: 99%

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Neutrophil‐lymphocyte ratio and plasma lactate predict 28‐day mortality in patients with sepsis

Liu

Zheng

Zhang³

et al. 2019

Clinical Laboratory Analysis

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ObjectiveThe predictive potential of the neutrophil‐to‐lymphocyte ratio (NLR) and plasma lactate was investigated in regard to the prognosis of patients with sepsis.MethodsSixty‐three nonsurgical and nontrauma adult patients with sepsis admitted to the intensive care unit (ICU) from September 2016 to October 2018 were consecutively included in the study. In addition, healthy subjects were assigned to a control group. Neutrophil and lymphocyte counts were evaluated via a complete blood count. Plasma lactate, procalcitonin (PCT), and C‐reactive protein (CRP) levels were measured. The main outcome was 28‐day mortality.ResultsNeutrophil‐to‐lymphocyte ratio and plasma lactate levels of the patients were significantly higher than those of control subjects: 19.44 (14.3‐34.53) vs 14.09 (8.17‐28.99), P = 0.049; and 3.7 (3‐6.6) vs 2.72 (2.13‐4.3) ng/mL, P = 0.008, respectively. There were no statistical differences in the concentrations of PCT and CRP between nonsurvivors and survivors: 6.1 (3.43‐33.59) vs 9.43 (4.24‐37.68) ng/mL, P = 0.44; and 108 (77.8‐153) vs 114.5 (71.43‐162) ng/mL, P = 0.672, respectively. With an optimal cutoff of 14.08, the sensitivity and specificity of NLR for prediction of 28‐day mortality were 78.3% and 50%, respectively. And the sensitivity and specificity of plasma lactate level to predict 28‐day mortality, at an optimal cutoff value of 2.99 mmol/L, were 82.6% and 55%, respectively.ConclusionsNeutrophil‐to‐lymphocyte ratio and plasma lactate were associated with poor outcomes in patients with sepsis and predicted mortality.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Neutrophil‐lymphocyte ratio and plasma lactate predict 28‐day mortality in patients with sepsis

Liu

Zheng

Zhang³

et al. 2019

Clinical Laboratory Analysis

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show abstract

“…However, in this case, lactate is released as a by-product of glucose consumption, a finding also observed in the CTRL constructs. [65][66][67] An initial decrease in metabolism and its subsequent improvement might suggest that allowing a longer recovery time would result in total functional recovery. Glucose, as well as other substrates are consumed by the hiPSC-CMs, mainly to provide energy for contraction.…”

Section: Paper Biomaterials Sciencementioning

confidence: 99%

Hypothermic and cryogenic preservation of cardiac tissue-engineered constructs

Janssen,

Chirico,

Ainsworth

et al. 2024

Biomater. Sci.

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“…Clinically, both heart failure secondary to alcoholic cardiomyopathy and alcohol-related acute liver failure were the final pathways reflecting the end-organ damage from alcohol abuse. Biochemically, lactate would build up in these two scenarios, with the former from switching metabolism from aerobic to anaerobic in the setting of low cardiac output induced hypoperfusion [ 7 ], the latter due to decreased lactate metabolism [ 8 ]. To compensate for the acidosis from the lactate generated by either pathway, the body will exhale CO 2 resulting in respiratory alkalosis [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

Detecting Concealing Heart Failure in a Young Alcohol-Related Liver Failure Patient Using the Most Basic Pathophysiological Principle

Lyu¹,

Miskovsky²

2022

Cureus

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Long-term alcohol abuse can cause alcohol-related liver injury (acute alcoholic hepatitis, acute liver failure, hepatic steatosis, fibrosis, or cirrhosis), as well as cardiac injury. Alcoholic cardiomyopathy is a severe consequence of chronic alcohol abuse. Incidence of alcoholic cardiomyopathy ranges from 1-2% of all heavy alcohol users. In the United States, excess alcohol consumption contributes to more than 10% of cases of heart failure. Here, we present a case of a 41-year-old male patient with severe alcohol abuse who presented with signs and symptoms of liver failure and was found to have severe left ventricular systolic dysfunction and dilated cardiomyopathy. More interestingly, the detection of heart failure in this patient was convoluted but also represented an amazing example of how the most basic pathophysiological principles help answer clinical questions in a perplexing scenario. The patient is a 41-year-old Caucasian male with severe alcohol abuse who presented with complaints of diffuse yellowish discoloration of skin, fatigue, and "feeling not like himself” for six weeks. A review of systems revealed mild exertional dyspnea and bilateral lower extremity swelling. Physical exam was remarkable for diffuse jaundice involving the whole body, tachycardia, and trace edema in the lower extremity bilaterally. Otherwise, lungs were clear to auscultation, normal heart sounds with regular heart rate and rhythm, no Jugular vein distention, and no carotid bruits were appreciated. Labs showed elevated total bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), ammonia, and lactate levels. Notably, venous blood gas (VBG) showed metabolic acidosis with compensating respiratory alkalosis with normal potential Hydrogen (pH). An electrocardiogram showed sinus tachycardia. Treatment was started for acute alcoholic liver failure, with intravenous fluids, intravenous prednisolone, and Clinical Institute Withdrawal Assessment for Alcohol (CIWA) protocol. The patient’s liver function markers went down stably. However, the patient’s mental status got worse and his lactate levels continued to rise. He was prescribed empirical antibiotics with a pan Computed tomography (CT) scan to look for any source of infection which revealed no meaningful positive findings. Surprisingly and interestingly, the venous blood gas pH started to trend up demonstrating alkalotic pH which contrasted the initial normal pH on admission. The metabolic acidosis was seemingly “over-compensated” by respiratory alkalosis. It was speculated that another underlying pathology existed to count for respiratory alkalosis. Chest X-ray (CXR) showed cardiomegaly but no pneumonia. An echocardiogram showed severe left ventricular systolic dysfunction with an Ejection Fraction of 20% and dilated left ventricle. The treatment direction was switched from treating liver failure to targeting heart failure with intravenous diuretics. The patient’s mental status improved remarkably after three days of diuresis and the patient wa...

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Elevated serum lactate is a marker of organ damage related to impaired hemodynamics and indicates poor prognosis in acute heart failure

Cited by 3 publications

References 0 publications

Neutrophil‐lymphocyte ratio and plasma lactate predict 28‐day mortality in patients with sepsis

Neutrophil‐lymphocyte ratio and plasma lactate predict 28‐day mortality in patients with sepsis

Hypothermic and cryogenic preservation of cardiac tissue-engineered constructs

Detecting Concealing Heart Failure in a Young Alcohol-Related Liver Failure Patient Using the Most Basic Pathophysiological Principle

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