Association between sepsis survivorship and long-term cardiovascular outcomes in adults: a systematic review and meta-analysis

Kosyakovsky, Leah; Angriman, Federico; Katz, Emma; Adhikari, Neill K. J.; Godoy, Lucas C.; Marshall, John C.; Ferreyro, Bruno L.; Lee, Douglas S.; Rosenson, Robert S.; Sattar, Naveed; Verma, Subodh; Toma, Augustin; Englesakis, Marina; Burstein, Barry; Farkouh, Michael E.; Herridge, Margaret S.; Ko, Dennis T.; Scales, Damon C.; Detsky, Michael E.; Bibas, Lior; Lawler, Patrick R.

doi:10.1007/s00134-021-06479-y

Cited by 43 publications

(51 citation statements)

References 74 publications

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“…Only one study directly linked the abnormalities in lipid profile to the acceleration of atheroma, but these data were obtained from animals exquisitely prone to accelerated atherosclerosis. The large metanalysis of predominantly acute lipid profile changes in sepsis demonstrated increased atherosclerosis-related mortality [47].…”

Section: Discussionmentioning

confidence: 99%

“…All of these conditions are often seen in the aftermath of sepsis [10,29,30,32,33,46]. A large meta-analysis looking at the long-term complication of sepsis demonstrated that the risk of stroke, myocardial infarction, and congestive heart failure increased by 3% to 9% in sepsis survivors, but the data were of low certainty [47]. The pooled risk from 29 highly heterogeneous studies suggested, at a minimum, that acquired abnormalities in lipid profile post-sepsis may be one of the underlying mechanisms of attained and permanent post-sepsis allostasis balance.…”

Section: Introductionmentioning

confidence: 99%

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Persistence of Lipoproteins and Cholesterol Alterations after Sepsis: Implication for Atherosclerosis Progression

Laudański

2021

IJMS

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(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.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Persistence of Lipoproteins and Cholesterol Alterations after Sepsis: Implication for Atherosclerosis Progression

Laudański

2021

IJMS

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“…It has been demonstrated that each 1 mg/dl increase in HDL-c level conferred a 2–4% decrease in cardiovascular risk per year ( 31 , 32 , 39 ). Interestingly, in large meta-analysis, the cumulative incidence of myocardial infarct, stroke, and heart failure in sepsis survivors was reported between 3 and 9% over a 5-year period ( 26 ).…”

Section: Discussionmentioning

confidence: 99%

“…The time for return to optimal, or pre-insult, lipid profile in the aftermath of sepsis remains to be determined (20)(21)(22)(23)(24). Considering the pivotal role of lipid metabolism in homeostasis, their long-term abnormalities in sepsis survivors may explain excessive cardiac mortality and susceptibility to subsequent infections (2,4,13,25,26). Furthermore, abnormalities in the basic lipid profile composition may be compounded by sepsis-triggered lipoprotein modifications, serum level of lipoprotein a [Lp(a)] abnormalities, or apolipoprotein (Apo) B metabolism, contributing to atherosclerosis via different mechanisms than simple changes in composition of lipid profile components (16,(27)(28)(29)(30).…”

mentioning

confidence: 99%

Long-Term Abnormalities of Lipid Profile After a Single Episode of Sepsis

Felici¹,

Maret

et al. 2021

Front. Cardiovasc. Med.

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Background: Acute disturbances of the lipid profile are commonplace during acute sepsis episode. However, their long-term persistence has not to be investigated despite pivotal role of dyslipidemia in several comorbidities excessively noted in sepsis survivors (stroke, cardiomyopathy).Methods: A total of 9,861 individuals hospitalized for a singular episode of sepsis between 2009 and 2019 were identified from electronic medical records. Lab measurements of total cholesterol (Tchol), high-density lipoprotein (HDL-c), low-density lipoprotein (LDL-c), very low-density lipoprotein (VLDL), triglycerides (TG), lipoprotein(a) [Lp (a)], apolipoprotein B (ApoB), and C-reactive protein (CRP). The data were examined as baseline values before sepsis, during hospitalization, and <3 months, 3–6 months, 6–12 months, 1–2 years, and more than 2 years from initial sepsis.Results: Significant reductions in HDL-c (HDLbaseline = 44.06 vs. HDLsepsis = 28.2; U = −37.79, p < 0.0001, Cohen's d = 0.22) and LDL-c serum levels were observed during and up to three months post sepsis, with females much less affected. In contrast, male subjects had derangement in HDL present for up to two years after a singular septic episode. Total cholesterol levels were slightly yet significantly elevated for up to two years after sepsis. TG were elevated up to one year [TGbaseline = 128.26 vs. TGsepsis = 170.27, t(8255) = −21.33, p < 0.0001, Cohen's d = 0.49] and normalized. Lp(a) was elevated up to two years after initial episode [Lp(a)baseline = 24.6 ± 16.06; Lp(a)sepsis−2year = 8.25 ± 5.17; Lp(a)morethan2years = 61.4 ± 40.1; ANOVA F(2, 24) = 7.39; p = 0.0032]. Response to statin therapy was blunted in sepsis survivors for several years after sepsis resolution. Significant drop-out in prescription of statins and niacin after sepsis was observed. Serum high sensitivity C-reactive protein was elevated for up to five years after sepsis resolution (H [6;1685] = 502.2; p < 0.0001).Discussion: Lipid abnormalities persisted long after the initial septic insult suggesting potential role in accelerating atherosclerosis and other abnormalities. In addition, sepsis seems to blunt statin effectiveness. Additionally, a significant and unexplained drop in statin use was seen in post-septic period.Conclusions: Our study suggests that persistent derangements of lipid profile components for up to two years after sepsis may be associated with altered risk of atherosclerosis-related events among sepsis survivors.

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“…Critical illness may increase the risk of cardiovascular events after ICU and hospital discharge. Greater rates of atrial fibrillation, heart failure, and myocardial infarction Martín-Vicente et al Intensive Care Medicine Experimental (2021) 9:58 have been described after sepsis [112]. However, no clear organ-specific mechanisms have been identified to date [113].…”

Section: Emerging Pics Domainsmentioning

confidence: 99%

Molecular mechanisms of postintensive care syndrome

Martín-Vicente

López-Martínez

López-Alonso

et al. 2021

ICMx

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Effectiveness of intensive care must be evaluated not only by short-term survival after a critical illness, but also by the recovery to an adequate quality of life. The increased evidence of long-term functional disabilities in intensive care survivors led to the definition of post-intensive care syndrome (PICS) [1]. Early diagnosis and effective treatments for these newly recognized conditions are warranted. However, most of the initial efforts to limit long-term sequelae have not yielded satisfactory results [2]. The objective of this review is to identify the molecular mechanisms that lead to organ dysfunction after intensive care and to summarize them into several plausible unifying hypotheses. From these mechanisms, novel therapeutic targets with the potential to prevent PICS may arise [3], allowing for earlier interventions during acute organ failure aimed to improve the quality of life of intensive care unit (ICU) survivors. Cost-effective strategies based on growing pathogenetic evidence on PICS would hence allocate research efforts and funding to implement preventive treatments, to impede pathogenetic mechanisms triggered during ICU stay, rather than exclusively rehabilitate long-term sequelae when they are already established.

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Association between sepsis survivorship and long-term cardiovascular outcomes in adults: a systematic review and meta-analysis

Cited by 43 publications

References 74 publications

Persistence of Lipoproteins and Cholesterol Alterations after Sepsis: Implication for Atherosclerosis Progression

Persistence of Lipoproteins and Cholesterol Alterations after Sepsis: Implication for Atherosclerosis Progression

Long-Term Abnormalities of Lipid Profile After a Single Episode of Sepsis

Molecular mechanisms of postintensive care syndrome

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