Incorporation of the Transverse Thoracic Plane Block Into a Multimodal Early Extubation Protocol for Cardiac Surgical Patients.

Background: The aim for early extubation remains an important goal in cardiac surgical patients. Therefore, employment of a multimodal approach to pain management that includes a transverse thoracic plane block was retrospectively examined at a single-center tertiary care hospital on the effects of time to extubation, opioid consumption, and length of stay in patients undergoing cardiac surgery via median sternotomy.

Methods: Blocks were performed on all cardiac surgical patients except for those undergoing left ventricular assist device placement, thoracic transplant, emergent surgery, or redo sternotomy.

Perioperative Management for Rectal Migration of a Ventriculoperitoneal Shunt.

While ventriculoperitoneal shunt (VPS) is the most commonly performed surgical procedure for treating hydrocephalus, complications following shunt placement are associated with a high mortality rate. Preoperative medical optimization and surgery are the primary means of correcting shunt migration. We present the case of an 11-week-old patient who underwent emergent surgical intervention for transrectal VPS migration and associated infection.

Opiate-Free Tricuspid Valve Replacement: Case Report.

The utility of opioid pain medications for perioperative analgesia is well described. However, opioids have many dangerous side effects including respiratory depression, acute tolerance, hyperalgesia, and chronic opioid dependence. Multimodal approaches continue to be used in more invasive and complex surgical procedures for enhanced recovery and decreased postoperative complications from opioid administration.

Intima-media thickness at different arterial segments in pediatric type 1 diabetes patients and its relationship with advanced glycation end products.

Background: Patients with type 1 diabetes mellitus (T1DM) are at risk for premature atherosclerosis (AS), which has its origin in childhood. Carotid intima-media thickness (IMT) is an established surrogate marker for subclinical AS in adults. The first macroscopically detectable AS changes, however, begin in the abdominal aorta.

Clinical Case of the Month: A 49-Year-Old Man with Fever, Headache and Leg Weakness.

A 49-year-old man with an unremarkable past medical history presented to an outside hospital with a five-day history of fever, left leg weakness, myalgia and headache. The patient reported that the illness started as a fever and sore throat and he was originally diagnosed with streptococcal pharyngitis and prescribed antibiotics. The day after his initial diagnosis, his fever had progressed to include a headache, myalgia, a rash on his upper torso and right shoulder and sudden-onset left leg weakness with preserved sensation.

Inhibition of TNF in the brain reverses alterations in RAS components and attenuates angiotensin II-induced hypertension.

Dysfunction of brain renin-angiotensin system (RAS) components is implicated in the development of hypertension. We previously showed that angiotensin (Ang) II-induced hypertension is mediated by increased production of proinflammatory cytokines (PIC), including tumor necrosis factor (TNF), in brain cardiovascular regulatory centers such as the paraventricular nucleus (PVN). Presently, we tested the hypothesis that central TNF blockade prevents dysregulation of brain RAS components and attenuates Ang II-induced hypertension.

Angiotensin II-induced hypertension is modulated by nuclear factor-κBin the paraventricular nucleus.

Hypertension is considered a low-grade inflammatory condition, and understanding the role of transcription factors in guiding this response is pertinent. A prominent transcription factor that governs inflammatory responses and has become a focal point in hypertensive research is nuclear factor-κB (NFκB). Within the hypothalamic paraventricular nucleus (PVN), a known brain cardioregulatory center, NFκB becomes potentially even more important in ultimately coordinating the systemic hypertensive response.

ACE2 overexpression in the paraventricular nucleus attenuates angiotensin II-induced hypertension.

Aims: Angiotensin II (Ang II) has been shown to have both central and peripheral effects in mediating hypertension, for which the hypothalamic paraventricular nucleus (PVN) is an important brain cardio-regulatory centre. Angiotensin-converting enzyme 2 (ACE2) has been identified as a negative regulator of the pro-hypertensive actions of Ang II. Recent findings from our laboratory suggest that Ang II infusion decreases ACE2 expression in the PVN.

NF-κB in the paraventricular nucleus modulates neurotransmitters and contributes to sympathoexcitation in heart failure.

Findings from our laboratory indicate that proinflammatory cytokines and their transcription factor, nuclear factor-kappaB (NF-κB), are increased in the hypothalamic paraventricular nucleus (PVN) and contribute towards the progression of heart failure. In this study, we determined whether NF-κB activation within the PVN contributes to sympathoexcitation via interaction with neurotransmitters in the PVN during the pathogenesis of heart failure. Heart failure was induced in rats by left anterior descending coronary artery ligation.

Paraventricular nucleus corticotrophin releasing hormone contributes to sympathoexcitation via interaction with neurotransmitters in heart failure.

Recent studies indicate that systemic administration of tumor necrosis factor (TNF)-α induces increases in corticotrophin releasing hormone (CRH) and CRH type 1 receptors in the hypothalamic paraventricular nucleus (PVN). In this study, we explored the hypothesis that CRH in the PVN contributes to sympathoexcitation via interaction with neurotransmitters in heart failure (HF). Sprague-Dawley rats with HF or sham-operated controls (SHAM) were treated for 4 weeks with a continuous bilateral PVN infusion of the selective CRH-R1 antagonist NBI-27914 or vehicle.

Central TNF inhibition results in attenuated neurohumoral excitation in heart failure: a role for superoxide and nitric oxide.

This study examined the effect of central tumor necrosis factor-alpha (TNF) blockade on the imbalance between nitric oxide and superoxide production in the paraventricular nucleus (PVN) and ventrolateral medulla (VLM), key autonomic regulators, and their contribution to enhanced sympathetic drive in mice with congestive heart failure (CHF). We also used a TNF gene knockout (KO) mouse model to study the involvement of TNF in body fluid homeostasis and sympathoexcitation in CHF. After implantation of intracerebroventricular (ICV) cannulae, myocardial infarction (MI) was induced in wild-type (WT) and KO mice by coronary artery ligation.

TNF-α in hypothalamic paraventricular nucleus contributes to sympathoexcitation in heart failure by modulating AT1 receptor and neurotransmitters.

Proinflammatory cytokines, including tumor necrosis factor (TNF)-α, augment the progression of heart failure (HF) that is characterized by sympathoexcitation. In this study, we explored the role of TNF-α in hypothalamic paraventricular nucleus (PVN) in the exaggerated sympathetic activity observed in HF. Heart failure rats were made by ligating the left anterior descending coronary artery.

HDAC inhibition attenuates inflammatory, hypertrophic, and hypertensive responses in spontaneously hypertensive rats.

Reactive oxygen species and proinflammatory cytokines contribute to cardiovascular diseases. Inhibition of downstream transcription factors and gene modifiers of these components are key mediators of hypertensive response. Histone acetylases/deacetylases can modulate the gene expression of these hypertrophic and hypertensive components.