Abstract
(1) Background: Sepsis is one of the most common critical care illnesses with increasing survivorship. The quality of life in sepsis survivors is adversely affected by several co-morbidities, including increased incidence of dementia, stroke, cardiac disease and at least temporary deterioration in cognitive dysfunction. One of the potential explanations for their progression is the persistence of lipid profile abnormalities induced during acute sepsis into recovery, resulting in acceleration of atherosclerosis. (2) Methods: This is a targeted review of the abnormalities in the long-term lipid profile abnormalities after sepsis; (3) Results: There is a well-established body of evidence demonstrating acute alteration in lipid profile (HDL-c ↓↓, LDL-C -c ↓↓). In contrast, a limited number of studies demonstrated depression of HDL-c levels with a concomitant increase in LDL-C -c in the wake of sepsis. VLDL-C -c and Lp(a) remained unaltered in few studies as well. Apolipoprotein A1 was altered in survivors suggesting abnormalities in lipoprotein metabolism concomitant to overall lipoprotein abnormalities. However, most of the studies were limited to a four-month follow-up and patient groups were relatively small. Only one study looked at the atherosclerosis progression in sepsis survivors using clinical correlates, demonstrating an acceleration of plaque formation in the aorta, and a large metanalysis suggested an increase in the risk of stroke or acute coronary event between 3% to 9% in sepsis survivors. (4) Conclusions: The limited evidence suggests an emergence and persistence of the proatherogenic lipid profile in sepsis survivors that potentially contributes, along with other factors, to the clinical sequel of atherosclerosis.
Highlights
Sepsis is one of the leading causes of mortality, affecting a vast stratum of society with increasing prevalence due to a multitude of factors [1,2]
monocyte 2 (M2) represents an atypical, activated monocyte that produces a significant amount of monocyte-colony stimulating factor (M-CSF) and free radicals, while not being able to mount an effective response to invading pathogens
The authors suggested that prolonged systemic endothelial and intimal inflammation was not related to accelerated atheroma. These findings suggested that lipid metabolism alterations, abnormalities on monocyte activation, or prolonged exposure to free radicals may be the underlying causes of accelerated atheroma formation in mice surviving sepsis
Summary
Sepsis is one of the leading causes of mortality, affecting a vast stratum of society with increasing prevalence due to a multitude of factors [1,2]. The healthcare stakeholders could choose to view their early intervention as having a significant long-term impact rather than focusing solely on short-term gains It has been known for some time that survivors of critical care illness suffer from post-sepsis syndrome, including anergy, hyperreactive airway, cognitive decline, sleep problems, mobility deterioration, and progressive organ dysfunction [5,29,30,31,32]. There are some gaps in the knowledge demonstrating how these dyslipidaemias may translate into long-term health maintenance This is a review of the current state of knowledge aimed at identifying potential abnormalities in lipoproteins and cholesterol as a potential culprit for the emergence of post-septic co-morbidities and long-term mortality due to atherosclerosis acceleration [21,22,23]. The review does not cover chronic inflammatory processes (chronic hepatitis, acquired immunodeficiency syndrome (AIDS), and others) as they represent different conditions and deserve dedicated reviews of their own
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