2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC.

Objective:To provide an update to the “Surviving Sepsis Campaign Guidelines for Management of Severe Sepsis and Septic Shock,” last published in 2008.Design:A consensus committee of 68 international experts representing 30 international organizations was convened. Nominal groups were assembled at ke

Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012.

ACE
: angiotensin-converting enzyme
ACS
: acute coronary syndrome
ADP
: adenosine diphosphate
AF
: atrial fibrillation
AMI
: acute myocardial infarction
AV
: atrioventricular
AIDA-4
: Abciximab Intracoronary vs. intravenously Drug Application
APACHE II
: Acute Physiology Aand Chronic

/pdf/esc-guidelines-for-the-management-of-acute-myocardial-vy5rt9aiqe.pdf

ESC Guidelines for the Management of Acute Myocardial Infarction in Patients Presenting With ST-Segment Elevation

ACC/AHA
: American College of Cardiology/American Heart Association
ACCF/AHA
: American College of Cardiology Foundation/American Heart Association
ACE
: angiotensin-converting enzyme
ACEI
: angiotensin-converting enzyme inhibitor
ACS
: acute coronary syndrome
AF
: atrial fibrillation

/pdf/2016-esc-guidelines-for-the-diagnosis-and-treatment-of-acute-z18hg30pp1.pdf

2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure

/pdf/2016-esc-guidelines-for-the-diagnosis-and-treatment-of-acute-53v7yllhiz.pdf

BACKGROUND Both dopamine and norepinephrine are recommended as first-line vasopressor agents in the treatment of shock. There is a continuing controversy about whether one agent is superior to the other. METHODS In this multicenter, randomized trial, we assigned patients with shock to receive either dopamine or norepinephrine as first-line vasopressor therapy to restore and maintain blood pressure. When blood pressure could not be maintained with a dose of 20 μg per kilogram of body weight per minute for dopamine or a dose of 0.19 μg per kilogram per minute for norepinephrine, open-label norepinephrine, epinephrine, or vasopressin could be added. The primary outcome was the rate of death at 28 days after randomization; secondary end points included the number of days without need for organ support and the occurrence of adverse events. RESULTS The trial included 1679 patients, of whom 858 were assigned to dopamine and 821 to norepinephrine. The baseline characteristics of the groups were similar. There was no significant between-group difference in the rate of death at 28 days (52.5% in the dopamine group and 48.5% in the norepinephrine group; odds ratio with dopamine, 1.17; 95% confidence interval, 0.97 to 1.42; P = 0.10). However, there were more arrhythmic events among the patients treated with dopamine than among those treated with norepinephrine (207 events [24.1%] vs. 102 events [12.4%], P<0.001). A subgroup analysis showed that dopamine, as compared with norepinephrine, was associated with an increased rate of death at 28 days among the 280 patients with cardiogenic shock but not among the 1044 patients with septic shock or the 263 with hypovolemic shock (P = 0.03 for cardiogenic shock, P = 0.19 for septic shock, and P = 0.84 for hypovolemic shock, in Kaplan–Meier analyses). CONCLUSIONS Although there was no significant difference in the rate of death between patients with shock who were treated with dopamine as the first-line vasopressor agent and those who were treated with norepinephrine, the use of dopamine was associated with a greater number of adverse events. (ClinicalTrials.gov number, NCT00314704.)

/pdf/comparison-of-dopamine-and-norepinephrine-in-the-treatment-p2kmp5vmof.pdf

Comparison of Dopamine and Norepinephrine in the Treatment of Shock

Background: The hepatopulmonary syndrome (HPS) is defined as the triad of liver disease, arterial deoxygenation, and pulmonary vascular dilatation. The reported prevalence of HPS in cirrhotic patients varies between 4% and 19%, and various threshold values defining arterial deoxygenation have been used and recommended previously. However, it is not known how the prevalence of HPS differs using different cut off values for arterial deoxygenation.

Methods: We studied 127 patients for the presence of HPS using transthoracic contrast echocardiography for detection of pulmonary vasodilation, pulmonary function tests, and blood gas analysis.

Results: Ninety eight patients were included in the study, of whom 33 (34%) had a positive contrast echocardiography. Using an increased alveolar-arterial difference for the partial pressure of oxygen (AaDO2) as an indication of hypoxaemia, the prevalence of HPS was considerably higher (>15 mm Hg, 32%; >20 mm Hg, 31%; and >age related threshold, 28%) than using reduced partial pressure of arterial oxygen (PaO2) as a threshold (<80 mm Hg, 19%; <70 mm Hg, 15%; and <age related threshold, 15%). For AaDO2 as the cut off, the positive predictive value for a diagnosis of HPS was low (34%, 37%, and 53%, respectively). In contrast, PaO2 as a cut off had considerably higher positive predictive values (44%, 93%, and 94%, respectively). Introducing PaO2 <65 mm Hg as the cut off, the positive predictive value increased to 100%. Dyspnoea was more often present in patients with “clinically significant” HPS (57%) compared with “subclinical HPS” (8%), and patients without HPS (6%). The Child-Pugh score correlated significantly with the severity of HPS. Two of five liver transplanted patients with “subclinical HPS” had embolic brain infarcts, possibly induced by venous emboli passing through dilated intrapulmonary vessels.

Conclusions: Defining arterial hypoxaemia in HPS by different, previously used, cut off values for arterial oxygenation leads to a wide variation in the prevalence of HPS in the same sample of cirrhotic patients.

https://gut.bmj.com/content/gutjnl/51/6/853.full.pdf

Hepatopulmonary syndrome: prevalence and predictive value of various cut offs for arterial oxygenation and their clinical consequences.

Wilson disease (WD) is an autosomal recessive inherited disorder of copper metabolism, resulting in pathological accumulation of copper in many organs and tissues. The hallmarks of the disease are the presence of liver disease, neurologic symptoms, and Kayser–Fleischer corneal rings. The leading neurologic symptoms in WD are dysathria, dyspraxia, ataxia, and Parkinsonian-like extrapyramidal signs. Changes in the basal ganglia in brain magnetic resonance imaging (MRI) are characteristic features of the disease. In presence of liver cirrhosis, some features may resemble hepatic encephalopathy. Symptoms and MRI abnormalities may be fully reversible on treatment with zinc or copper chelators. Improvement can be monitored by serial recording of brain-stem-evoked responses. The basic defect is an impaired traficking of copper in hepatocytes. ATP7B is the gene product of the WD gene located on chromosome 13 and resides in hepatocytes in the trans-Golgi network, transporting copper into the secretory pathway for incorporation into apoceruloplasmin and excretion into the bile. While about 40% of patients preset with neurologic symptoms, little is known about the role of copper and ATP7B in the central nervous system. In some brain areas, like in the pineal gland, ATP7B is expressed and functionally active. Increasing evidence supports an important role for metals in neurobiology. Two proteins related to neurodegeneration are copper-binding proteins (1) the amyloid precursor protein (APP), a protein related to Alzheimer's disease, and (2) the Prion protein, related to Creutzfeldt–Jakob disease. A major source of free-radical production in the brain derives from copper. To prevent metal-mediated oxidative stress, cells have evolved complex metal transport systems. APP is a major regulator of neuronal copper homeostasis and has a copper-binding domain (CuBD). The surface location of this site, structural homology of CuBD to copper chaperones, and the role of APP in neuronal copper homeostasis are consistent with the CuBD acting as a neuronal metallotransporter. There are several copper-containing enzymes in the brain, like dopamine beta hydroxylase or Cu/Zn superoxide dismutase (SOD1). Their function may be altered because of copper overload. WD appears to be associated with a dopaminergic deficit. Mutations in the SOD1gene cause familial amyotrophic lateral sclerosis. Survival of transgenic mice with a mutant SOD1 which fails to incorporate Cu(2+) in its active site was improved by copper depletion. Wilson disease (WD) is an autosomal recessive inherited disorder in which copper pathologically accumulates primarily within the liver and subsequently in the neurologic system and many other organs and tissues. Presence of liver disease, neurologic symptoms, and Kayser–Fleischer corneal rings are the hallmarks of the disease.

Wilson Disease

Purpose
Hypoxic hepatitis (HH) is a frequent cause of acute hepatocellular damage at the intensive care unit. Although mortality is reported to be high, risk factors for mortality in this population are unknown.

Hypoxic hepatitis: underlying conditions and risk factors for mortality in critically ill patients

To investigate the possible impact of obesity on morbidity and mortality in intensive care unit (ICU) patients included in the European observational sepsis occurrence in acutely ill patients (SOAP) study Planned substudy from the SOAP database One hundred and ninety-eight ICUs in 24 European countries All patients admitted to one of the participating ICUs Patients were classified, according to their body mass index (BMI), as underweight (<185 kg/m2), normal weight (185–249 kg/m2), overweight (25–299 kg/m2), obese (30–399 kg/m2), and very obese (≥40 kg/m2) The BMI was available in 2,878 (91%) of the 3,147 patients included in the SOAP study; 120 patients (42%) were underweight, 1,206 (419%) had a normal BMI, 1,047 (364%) were overweight, 424 (147%) were obese, and 81 (28%) were very obese Obese and very obese patients more frequently developed ICU-acquired infections than patients in lower BMI categories Very obese patients showed a trend towards longer ICU [median (IQ): 41 (18–121) vs 31 (17–72) days, P = 0056) and hospital lengths of stay [143 (84–274) vs 123 (51–244), days P = 0077] compared to those with a normal BMI However, there were no significant differences among the groups in ICU or hospital mortality rates In a multivariate Cox regression analysis, none of the BMI categories was associated with an increased risk of 60-day in-hospital death BMI did not have a significant impact on mortality in this mixed population of ICU patients

https://link.springer.com/content/pdf/10.1007%2Fs00134-008-1243-0.pdf

C Madl

Papers

Comparison of Dopamine and Norepinephrine in the Treatment of Shock

Hepatopulmonary syndrome: prevalence and predictive value of various cut offs for arterial oxygenation and their clinical consequences.

Wilson Disease

Hypoxic hepatitis: underlying conditions and risk factors for mortality in critically ill patients

Obesity is associated with increased morbidity but not mortality in critically ill patients