Length of Stay, Mortality, Cost, and Perceptions of Care Associated With Transition From an Open to Closed Staffing Model in the Cardiac Intensive Care Unit.

Background: Organizational models in the intensive care unit (ICU) have classically been described as either closed or open, depending on the presence or absence of a dedicated ICU team. Although a closed model has been shown to improve patient outcomes in medical and surgical ICUs, the merits of various care models have not been previously explored in the cardiac ICU (CICU) setting.

Methods: From November 2012 to March 2014, data were prospectively collected on all admissions before and after transition from an open to closed CICU at our institution.

Delirium is a robust predictor of morbidity and mortality among critically ill patients treated in the cardiac intensive care unit.

Background: Delirium is common in the medical and surgical intensive care unit (ICU), and its association with morbidity and mortality is well described. Despite emerging data, which have highlighted a growing critical care burden in the contemporary cardiac ICU (CICU), much less is known about delirium in this specialized setting.

Methods And Results: Records for consecutive CICU patients aged ≥18 years who were admitted to our academic, tertiary care institution from December 2012 to March 2014 for a primary cardiovascular diagnosis were reviewed.

The role of heart failure pharmacotherapy after left ventricular assist device support.

Left ventricular assist devices (LVADs) are an increasingly common treatment for end-stage systolic heart failure. However, there are limited data on how to best treat patients pharmacologically after LVAD implantation, resulting in uncertainty about which heart failure medications provide the most benefit. Still, some evidence exists that certain medical therapies can prevent remodeling and improve right ventricular and, possibly, left ventricular function.

[Agonists of opioid receptors may aggravate ischemic and reperfusion damages of the heart].

Authors analyzed articles that opioids may aggravate ischemic and reperfusion damages of the heart but the opioid receptor antagonists may prevent these damages. Authors concluded the it is existed opioid receptor pool an activation of its decreases cardiac tolerance to an impact of ischemia-reperfusion.

[Protein kinases role in adaptive phenomenon of heart ischemic postconditioning development].

Authors submitted an analysis of papers given up an involvement of protein kinases in heart ischemic postconditioning. This analysis of literature source allowed to authors affirms that signaling system of postconditioning can involve kinases: PKC, PI3K, Akt, MEKl/2, ERK1/2, MTOR, p70s6K, GSK3b, PKG and also eNOS, NO, GC, motoKATP channel, ROS, MPT pore. At the same time it is unclear a real contributions of kinases mTOR, p70s6, AMPK and GSK3b in the mechanism of infarct limiting impact of postconditioning.

[Receptor and signalling mechanisms of antiarrhythmic effects of ischemic pre-conditioning].

It has been established that ischemic preconditioning (IP) exerts significant antiarrhythmic effects, as revealed in experiments both in vivo and in vitro. Consequently, processes arising within the myocardium play a key role in adaptive tolerance to ischemia/reperfusion. Preconditioning enhances cardiac electrical stability both in animals and humans.

[Signaling mechanism of cardioprotective effects of opioids].

It has been established that G(i/o)-proteins are an intermediate link that provides intracellular signaling between opioid receptors and protein kinases. Our investigations have shown that protein kinase C is involved in realization of the anti-necrotic and anti-apoptotic effects of opioids. PI3 and Akt kinases are involved in the cardioprotective effect of opioids.

[Trigger mechanism of adaptive phenomenon of ischemic heart postconditioning].

Analysis of published data indicates on trigger role of protons, adenosine, opioids, bradykinin, calcitonin gene-related peptide, nitric oxide, epoxyeicosatrienoic acid, reactive oxygen species, hydrogen sulfide in ischemic heart postconditioning. It is shown that B-type natriuretic peptide, transforming growth factor-beta1, cardiotrophin-1, urocortin, acetylcholine, insulin and carbon monoxide can mimic postconditioning phenomenon.

[Role of receptor transactivation in the cardioprotective effects of preconditioning and postconditioning].

Analysis of published data indicates that the activity of receptors for adenosine, opioids, bradykinin, calcitonin-gene related peptides (CGRP) and epidermal growth factor (EGF) play important role in triggering the cardioprotective effects of ischemic preconditioning. Cannabinoids mimic the infarct-sparing effects of preconditioning. Endogenous adenosine, opioids, bradykinin and CGRP have also been implicated in infarct-reduction with ischemic postconditioning.

Treatment of 25-OH vitamin D deficiency in older men with chronic kidney disease stages 3 and 4 is associated with reduction in cardiovascular events.

Observational studies in healthy people suggest an inverse relationship between serum 25-hydroxyvitamin D (25OHD) levels and cardiovascular (CV) mortality. Treating vitamin D deficiency in patients with moderate chronic kidney disease (CKD) may reduce CV events in this high-risk population. Study data were abstracted from Harry S.

Elevated serum parathyroid hormone is a cardiovascular risk factor in moderate chronic kidney disease.

Introduction: Over 8% of adults in the United States are estimated to have moderate (stages 3 and 4) chronic kidney disease (CKD), which is increasingly recognized as one of the independent predictors for cardiovascular (CV) disease and related mortality. Secondary hyperparathyroidism with elevated serum intact parathyroid hormone (iPTH) is associated with increased CV mortality in end-stage renal disease and this relationship is unclear in moderate CKD.

Methods: Medical records of 196 patients at Harry S.

Opioid peptide deltorphin II simulates the cardioprotective effect of ischemic preconditioning: role of δ₂-opioid receptors, protein kinase C, and K(ATP) channels.

The cardioprotective properties of a δ₂-opioid receptor agonist deltorphin II were studied in rats with coronary occlusion and reperfusion. Opioid receptor ligands and inhibitors (glybenclamide, chelerythrine, and 5-hydroxydecanoate) were injected intravenously before ischemia and reperfusion. A δ₂-opioid receptor agonist deltorphin II significantly decreased the infarction zone/risk zone index.

Tachycardia-induced cardiomyopathy: evaluation and therapeutic options.

Tachycardia-induced cardiomyopathy is caused by sustained rapid ventricular rates and is one of the well-known forms of reversible myocardial dysfunction. The diagnosis is usually made retrospectively after marked improvement in systolic function is noted following control of the heart rate. Physicians should be aware that patients with seemingly idiopathic systolic dysfunction may have tachycardia-induced cardiomyopathy and that controlling the heart rate may result in improvement or even complete restoration of systolic function.

[Significance of opioid receptors in regulation of cardiac tolerance in pathogenic impact of long-term ischemia-reperfusion in vivo].

The study aimed at investigation of the role of opioid receptor (OR) in regulation of cardiac tolerance to ischemia-reperfusion. Opioid receptor ligands and inhibitors were administered in vivo prior to coronary artery occlusion (45 min) and reperfusion (2 hrs). Occurring infraction size/area at risk (IS/AAR) ratio was determined.

Activation of kappa-opioid receptor as a method for prevention of ischemic and reperfusion arrhythmias: role of protein kinase C and K(ATP) channels.

Intravenous pretreatment with kappa-opioid receptor antagonist (-)-U-50,488 (1 mg/kg) improved heart resistance to the arrhythmogenic effect of coronary occlusion and reperfusion. Selective kappa1-opioid receptor antagonist norbinaltorphimine and nonselective blocker of peripheral opioid receptors methylnaloxone abolished this antiarrhythmic effect. Preliminary blockade of protein kinase C with chelerythrine or inhibition of ATP-dependent K+ channels (K(ATP) channels) with glybenclamide abolished the antiarrhythmic effect of kappa-opioid receptor activation.

[Role of kappa-opioid receptors in the regulation of cardiac resistance to arrhythmogenic effects of ischemia and reperfusion].

It was found that pretreatment of rats with selective agonist of kappa1-opioid receptors (OR) (-)--U--50.488 decreased the incidence of ischemic (10 min) and reperfusion (10 min) ventricular arrhythmias. The selective kappa2-OR agonist GR-89696 had no effect on the incidence of ventricular arrhythmias during a 10-min coronary artery occlusion and following reperfusion in anesthetized rats.

[Comparative study of the antiarrhythmic activity of mu- and delta-opioid receptor agonists during acute cardiac ischemia and reperfusion models in rats].

It has been established that pretreatment with the selective mu-opioid receptor (OR) agonist DALDA (0.1 mg/kg, i.v.

[The antiarrhythmic effect of (-)-U-50,488 in rats with acute ischemia and reperfusion of heart is mediated by kappa1-opioid receptor activation].

Pretreatment with a selective kappa1 opioid receptor (OR) agonist (-)-U-50,488 (1 mg/kg, i.v.) prevented the development of arrhythmias induced by occlusion (10 min) and reperfusion (10 min) in ketamine anesthetized rats, while the treatment with a less active enantiomer (+)-U-50,488 in the same dose produced no such effects.

[The effect of K(ATP)-channel activation on the electrical stability of myocardium in rats with postinfarction cardiosclerosis].

Opening of the ATP-dependent K-channels (K(ATP) channels) upon intravenous administration of the cardioselective activator BMS 180448 (3 mg/kg) decreased the ventricular fibrillation threshold (VFT) in rats with postinfarction cardiosclerosis (PIC). Preliminary injection of the selective K(ATP) channel blocker glibenclamide (0.3 mg/kg, i.

[Changes in cardiac resistance to arrhythmogenic effects during ATP-dependent K+ channel activation].

It has been found that pretreatment with ATP-dependent potassium channel (KATP-channel) opener, BMS 180448 (3 mg/kg, intravenously), increases cardiac resistance against arrhythmogenic action of coronary artery occlusion and reperfusion in anaesthetized rats. However, BMS 180448 induced a decrease in ventricular fibrillation threshold in rats postinfarction cardiac fibrosis. This effect was completely abolished by administration of the KATP-channel inhibitor, glibenclamide.

[Interactions of peripheral mu-opioid receptors and K(ATP)-channels in regulation of cardiac electrical stability in ischemia, reperfusion, and postinfarction cardiosclerosis].

It has been shown that mu-opioid receptor stimulation by intravenous administration of the selective mu receptor agonist DALDA in a dose of 0.1 mg/kg prevented ischemic and reperfusion arrhythmias in rats subjected to coronary artery occlusion (10 min) and reperfusion (10 min), and also increased the ventricular fibrillation threshold in rats with postinfarction cardiac fibrosis. These effects were abolished by pre-treatment with the selective mu receptor antagonist CTAP in a dose of 0.

[Stimulation of peripheral delta1-opioid receptors as a method of preventing ischemic and reperfusion arrhythmia: role of K(ATP)-channels].

Preliminary administration of the delta 1-opioid receptor (delta 1-OR) peptide agonist DPDPE (0.5 mg/kg, i.v.

[Participation of K(ATP)-channels in cardioprotective effect of mu-opioid receptor agonists in acute ischemia and reperfusion of the isolated heart].

Preliminary administration of the mu-opioid receptor (mu-OR) agonist DAMGO (0.1 mg/kg) 15 min before heart isolation led to attenuation of the postischemic systolic and diastolic contractility dysfunction in isolated perfused rat heart. In addition, the mu-OR decreased creatine kinase (CK) release from the heart during the postischemic period, which was indicative of an increase in the sarcolemma tolerance to reperfusion injury.

[Myocardial tolerance to arrhythmogenic exposure and pharmacological activation of K(ATP)-channels in rats].

The cardioselective KATP channel activator BMS 180448 (3 mg/kg) administered intravenously 15 min before the coronary artery occlusion (10 min) decreased the incidence of ischemic and reperfusion arrhythmias in rats. A similar antiarrhythmic effect was observed when BMS 180448 was infused 2 min before reperfusion. Pretreatment with BMS 180448 also prevented the occurrence of CsCl induced arrhythmias, but but did not affect the incidence of epinephrine induced arrhythmias.