Cardiac consequences of massive acetaminophen overdose

Mann, Jessica M.; Pierre-Louis, Marie; Kragel, Peter J.; Kragel, Amy H.; Roberts, William C.

doi:10.1016/0002-9149(89)90167-7

Cited by 14 publications

(7 citation statements)

References 2 publications

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“…Although indications about a connection between acute liver injury and myocardial damage had already been reported [133, 134], this was brought sharply into focus in a study by the US Acute Liver Failure Study Group which showed that elevation of serum troponin I (cTnI) levels is common (74% overall) in patients with ALF of various etiologies [135]. However, in both this and the previous studies, liver ischemia/reperfusion was absent as a mechanism of injury.…”

Section: Myocardial Injurymentioning

confidence: 99%

Global Consequences of Liver Ischemia/Reperfusion Injury

Nastos

Kalimeris

Papoutsidakis

et al. 2014

Oxidative Medicine and Cellular Longevity

249

225

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Liver ischemia/reperfusion injury has been extensively studied during the last decades and has been implicated in the pathophysiology of many clinical entities following hepatic surgery and transplantation. Apart from its pivotal role in the pathogenesis of the organ's post reperfusion injury, it has also been proposed as an underlying mechanism responsible for the dysfunction and injury of other organs as well. It seems that liver ischemia and reperfusion represent an event with “global” consequences that influence the function of many remote organs including the lung, kidney, intestine, pancreas, adrenals, and myocardium among others. The molecular and clinical manifestation of these remote organs injury may lead to the multiple organ dysfunction syndrome, frequently encountered in these patients. Remote organ injury seems to be in part the result of the oxidative burst and the inflammatory response following reperfusion. The present paper aims to review the existing literature regarding the proposed mechanisms of remote organ injury after liver ischemia and reperfusion.

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Section: Myocardial Injurymentioning

confidence: 99%

Global Consequences of Liver Ischemia/Reperfusion Injury

Nastos

Kalimeris

Papoutsidakis

et al. 2014

Oxidative Medicine and Cellular Longevity

249

225

View full text Add to dashboard Cite

show abstract

“…Although circulatory disturbances which accompany acute liver failure were reported early on [1], direct effects upon the myocardium have not been studied, except for sporadic references of paracetamol overdose cases accompanied by cardiac injury [2-4]. Recently, the US Acute Liver Failure Study Group [5] showed that elevations of serum troponin I (cTnI) levels are common (74% overall) in patients with ALF of various aetiologies.…”

Section: Introductionmentioning

confidence: 99%

Early myocardial injury is an integral component of experimental acute liver failure – a study in two porcine models

Papoutsidakis

Arkadopoulos²,

Smyrniotis³

et al. 2011

aoms

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IntroductionThere is accumulating clinical evidence that acute liver failure may be regularly associated with myocardial injury. To test this hypothesis in a standardized experimental setting, we used two porcine models of ALF.Material and methodsIn 14 domestic pigs ALF was induced by either a) surgical devascularization of the liver (DV group, n = 7), or b) partial (70-75%) hepatectomy and ischaemia/reperfusion of the liver remnant for 150 min (I/R group, n = 7). Four additional animals constituted the sham operation group. All animals were monitored for a 12-h period, at the end of which their hearts were harvested. Plasma troponin I (cTnI) and malondialdehyde (MDA) were measured before the operation (baseline) and at 6 h and 12 h postoperatively. The harvested hearts were histologically analysed, appointing a score from 0 (no injury) to 3 (maximum injury) to selected injury indicators.ResultsIn the sham group, all cTnI measurements and total myocardial injury score were zero in all animals. In both ALF groups, plasma cTnI levels increased by the 6th and remained elevated up to the 12th postoperative hour (p < 0.01 vs. sham animals). Total myocardial injury score and total histological score revealed some extent of myocardial injury. The rise of MDA levels suggests an underlying oxidative mechanism.ConclusionsOur study provides direct evidence of early myocardial injury in the setting of acute liver failure in pigs. The mechanism of injury remains to be elucidated.

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“…Nephrotoxicity may also accompany hepatotoxicity (Mazer & Perrone, ). Previous studies have reported that autopsy findings for fatal acetaminophen poisoning include subendocardial hemorrhage, necrosis, centrilobular liver necrosis and acute renal tubular necrosis (Mann et al, ; Price, Poklis, & Johnson, ).…”

Section: Discussionmentioning

confidence: 99%

“…Oxidative stress leads to the excessive production of ROS, which may cause the development and progression of maladaptive myocardial remodeling and congestive heart failure (CHF) (Griendling & FitzGerald, 2003;Sachidanandam, Fagan, & Ergul, 2005;Tsutsui, Kinugawa, & Matsushima, 2011). Few epidemiological studies have investigated the cardiac consequences of acetaminophen poisoning (Mann, Pierre-Louis, Kragel, Kragel, & Roberts, 1989) Therefore, we conducted a longitudinal cohort study to investigate the association between acetaminophen poisoning and CHF. (Chung et al, 2014;Chung, Lai, Lin, & Kao, 2015;Yen et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Increased risk of congestive heart failure in patients with acetaminophen poisoning: A nationwide cohort study

Chung

Lin

2018

J of Applied Toxicology

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Acetaminophen poisoning increases cytochrome P450 2E1 expression and reactive oxygen species production, which may lead to maladaptive myocardial remodeling and congestive heart failure (CHF). We conducted a nationwide cohort study to investigate the incidence and risk of CHF in patients with acetaminophen poisoning. We identified a cohort of adult patients with newly diagnosed acetaminophen poisoning in the inpatient claims of the Taiwan National Health Insurance Research Database for the 1998-2011 period. A comparison cohort was frequency matched at a 4:1 ratio for sex, age and index year. All patients were followed up until the occurrence of CHF, withdrawal from the National Health Insurance program, or December 31, 2011. Cox proportional hazards models were employed to calculate the risk of CHF in the acetaminophen poisoning cohort compared with the comparison cohort, and the hazard ratios with 95% confidence intervals are presented. A total of 3546 and 14 184 patients with and without acetaminophen poisoning were followed up for a total of 25 856 and 102 119 person-years, respectively. The overall incidence of CHF was higher in the acetaminophen poisoning cohort than in the comparison cohort (8.12 vs. 5.19 per 10 000 person-years). After adjustment for covariates, the acetaminophen poisoning cohort exhibited a 1.59-fold higher risk of CHF (adjusted hazard ratio = 1.59; 95% confidence interval = 1.43-1.75) than did the comparison cohort. Patients with acetaminophen poisoning exhibited a significantly higher risk of CHF compared with the comparison cohort. Clinicians should follow up heart function in patients with acetaminophen poisoning.

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Cardiac consequences of massive acetaminophen overdose

Cited by 14 publications

References 2 publications

Global Consequences of Liver Ischemia/Reperfusion Injury

Global Consequences of Liver Ischemia/Reperfusion Injury

Early myocardial injury is an integral component of experimental acute liver failure – a study in two porcine models

Increased risk of congestive heart failure in patients with acetaminophen poisoning: A nationwide cohort study

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