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Objective-To investigate whether ischaemic preconditioning could reduce myocardial injury, as manifest by troponin T release, in patients undergoing elective coronary artery bypass surgery. Design-Randomised controlled trial. Setting-Cardiothoracic unit of a tertiary care centre. Patients-Patients with three vessel coronary artery disease and stable angina admitted for first time elective coronary artery bypass surgery were invited to take part in the study; 33 patients were randomised into control or preconditioning groups. Intervention-Patients in the preconditioning group were exposed to two additional three minute periods of myocardial ischaemia at the beginning of the revascularisation operation, before the ischaemic period used for the first coronary artery bypass graft distal anastomosis. Main outcome measure-Serum troponin T concentration at 72 hours after cardiopulmonary bypass. Results-The troponin T assays were performed by blinded observers at a different hospital. All patients had undetectable serum troponin T (< 0a1 ugIl) before cardiopulmonary bypass, and troponin T was raised postoperatively in all patients. At 72 hours, serum troponin T was lower (P = 0.05) in the preconditioned group (median 0 3 ugIl) than in the control group (median 14 4ugl). Conclusions-The direct application of a preconditioning stimulus in clinical practice has been shown, for the first time, to protect patients against irreversible myocyte injury.

The effectiveness of levosimendan on veno-arterial extracorporeal membrane oxygenation management and outcome: a systematic review and meta-analysis,

Critical Care 2017, 21(Suppl 1):P349 Introduction Imbalance in cellular energetics has been suggested to be an important mechanism for organ failure in sepsis and septic shock. We hypothesized that such energy imbalance would either be caused by metabolic changes leading to decreased energy production or by increased energy consumption. Thus, we set out to investigate if mitochondrial dysfunction or decreased energy consumption alters cellular metabolism in muscle tissue in experimental sepsis. Methods We submitted anesthetized piglets to sepsis (n = 12) or placebo (n = 4) and monitored them for 3 hours. Plasma lactate and markers of organ failure were measured hourly, as was muscle metabolism by microdialysis. Energy consumption was intervened locally by infusing ouabain through one microdialysis catheter to block major energy expenditure of the cells, by inhibiting the major energy consuming enzyme, N+/K + -ATPase. Similarly, energy production was blocked infusing sodium cyanide (NaCN), in a different region, to block the cytochrome oxidase in muscle tissue mitochondria. Results All animals submitted to sepsis fulfilled sepsis criteria as defined in Sepsis-3, whereas no animals in the placebo group did. Muscle glucose decreased during sepsis independently of N+/K + -ATPase or cytochrome oxidase blockade. Muscle lactate did not increase during sepsis in naïve metabolism. However, during cytochrome oxidase blockade, there was an increase in muscle lactate that was further accentuated during sepsis. Muscle pyruvate did not decrease during sepsis in naïve metabolism. During cytochrome oxidase blockade, there was a decrease in muscle pyruvate, independently of sepsis. Lactate to pyruvate ratio increased during sepsis and was further accentuated during cytochrome oxidase blockade. Muscle glycerol increased during sepsis and decreased slightly without sepsis regardless of N+/K + -ATPase or cytochrome oxidase blocking. There were no significant changes in muscle glutamate or urea during sepsis in absence/presence of N+/K + -ATPase or cytochrome oxidase blockade. ConclusionsThese results indicate increased metabolism of energy substrates in muscle tissue in experimental sepsis. Our results do not indicate presence of energy depletion or mitochondrial dysfunction in muscle and should similar physiologic situation be present in other tissues, other mechanisms of organ failure must be considered. , and long-term follow up has shown increased fracture risk [2]. It is unclear if these changes are a consequence of acute critical illness, or reduced activity afterwards. Bone health assessment during critical illness is challenging, and direct bone strength measurement is not possible. We used a rodent sepsis model to test the hypothesis that critical illness causes early reduction in bone strength and changes in bone architecture. Methods 20 Sprague-Dawley rats (350 ± 15.8g) were anesthetised and randomised to receive cecal ligation and puncture (CLP) (50% cecum length, 18G needle single pass through anterior and posterior wa...

We sought to synthesize the available evidence regarding safety and efficacy of intermittent levosimendan (LEVO) infusions in ambulatory patients with end-stage heart failure (HF). Safety and efficacy of ambulatory intermittent LEVO infusion in patients with end-stage HF are yet not established. We systematically searched MEDLINE, EMBASE, SCOPUS, Web of Science, and Cochrane databases, from inception to January 30, 2021 for studies reporting outcome of adult ambulatory patients with end-stage HF treated with intermittent LEVO infusion. Fifteen studies (8 randomized and 7 observational) comprised 984 patients (LEVO [N = 727] and controls [N = 257]) met the inclusion criteria. LEVO was associated with improved New York Heart Association (NYHA) functional class (weighted mean difference [WMD] −1.04, 95%CI: −1.70 to −0.38, p < 0.001, 5 studies, I2 = 93%), improved left ventricular (LV) ejection fraction (WMD 4.0%, 95%CI: 2.8% to 5.3%, p < 0.001, 6 studies, I2 = 9%), and reduced BNP levels (WMD −549 pg/mL, 95%CI −866 to −233, p < 0001, 3 studies, I2 = 66%). All-cause death was not different (RR 0.65, 95%CI: 0.38 to 1.093, p = 0.10, 6 studies, I2 = 0), but cardiovascular death was lower on LEVO (RR 0.34, 95%CI: 0.13 to 0.87, p = 0.02, 3 studies, I2 = 0) compared to controls. Furthermore, health-related quality of life (HRQoL) was improved alongside with reduced LV size following LEVO infusions. Major adverse events were not different between LEVO and placebo. In conclusion, intermittent LEVO infusions in ambulatory patients with end-stage HF is associated with less frequent cardiovascular death alongside with improved NYHA class, quality of life, BNP levels, and LV function. However, the current evidence is limited by heterogeneous and relatively small studies.

BackgroundThe value of cardiac troponin as a risk assessment tool for cardiac disease in the setting of end-stage renal diseases (ESRD) is not equivalent to its value in those with normal renal function. This consideration had not been studied in settings of acute kidney injury (AKI). We aim to explore the diagnostic value of high sensitive troponin T (hsTnT) in the settings of cardiac surgery-induced AKI.MethodsSingle center observational retrospective study. Based on the AKI Network, patients divided into 2 groups, group I without AKI (259 patients) and group II with AKI (100 patients) where serial testing of hsTnT and creatine kinase (CK)-MB were followed in both groups. Patients with (ESRD) were excluded.ResultsThe mean age in our study was 55.1 ± 10.2 years. High association of AKI (27.8%) was found in our patients. Both groups were matched regarding the age, gender, body mass index, the association of diabetes or hypertension, and Euro score. AKI group had significantly higher mortality 5% vs group I 1.1% (p = 0.03). The hsTnt showed a significant sustained rise in the AKI group as compared to the non-AKI group, however CK-MB changes were significant initially but not sustained.The AKI group was more associated with heart failure 17.9% vs 4.9% (p = 0.001); and post-operative atrial fibrillation, 12.4% vs 2.9% (p = 0.005). Lengths of ventilation, stays in ICU and in hospital were significantly higher in the AKI group.ConclusionsUnlike the CK-MB profile, the hsTnT showed significant changes between both groups all over the course denoting possible delayed clearance in patients with AKI.

Objectives:Coronary artery anomalies are uncommon, but important cardiac malformations, representing the second commonest cause of death in young athletes.Methods:We utilized computerized tomographic angiography to screen and precisely delineate coronary artery anomalies in patients with minimal cardiac symptoms.Results:During 3.5-year period, we performed 2888 computerized tomographic angiographies. A total of 33 (1.1%; 95% confidence interval = 0.7–1.5) cases of coronary artery anomalies were identified (mean age = 44 ± 13.5 (15–70) years). In total, 23 patients (mean age = 43 years) had malignant coronary artery anomalies with an inter-arterial course of the aberrant vessel: of which 3 had left main coronary artery arising from right coronary sinus and 20 right coronary artery from left sinus; 19 patients were of Asian and 14 were of Arab origins. Of interest, 21 out of 33 patients had chest pain, 5 had palpitations, and 2 had breathlessness. There were no examples of sudden cardiac death. All patients received appropriate advice regarding physical exertion and medical management, and remained well for 2–5 years of follow-up. Of 33 patients, 4 had significant symptomatic coronary artery disease requiring intervention: 1 percutaneous coronary intervention and 3 coronary artery bypass graft surgery.Conclusion:There is a relatively high incidence of coronary artery anomalies with malignant course in Asians. The vast majority were managed conservatively.

Acadesine (AICA riboside, 5-amino-1-,fl-D-ribofuranosyl-imidazole-4-carboxamide) is the prototype of a new class of compounds termed adenosine regulating agents. Acadesine is a purine nucleoside analogue that enters the myocyte and is immediately phosphorylated to ZMP