Extracorporeal Membrane Oxygenation for Protected Catheter Ablation in A Post-Cardiotomy Patient With Electrical Storm.

ABSTRACT: An electrical storm (ES) refers to multiple occurrences of ventricular arrhythmias within a short time. Catheter ablation is a treatment option for ES but can be challenging in unstable cardiovascular patients. We present the case of a 50-year-old patient with poor left ventricular function who experienced ES after emergency coronary artery bypass grafting (CABG). Despite maximal antiarrhythmic therapy, the patient had recurrent ventricular tachycardia and fibrillation (VT/VF), hindering catheter ablation. Elective venoarterial extracorporeal membrane oxygenation (ECMO) support was established, allowing a successful second catheter ablation attempt without complications. The patient was weaned off ECMO the following day and remained in normal sinus rhythm.

Incidence and outcome of anaphylaxis in cardiac surgical patients.

Introduction: Anaphylaxis is a rare but serious and potentially fatal complication of anesthesia. Little is known about the incidence and outcome of anaphylaxis in cardiac surgical patients, which we aimed to investigate. Methods: This was a 21-year retrospective study of cardiac surgical patients at Manchester Royal Infirmary, Manchester Foundation Trust, Manchester, UK. Results: A total of 19 cases of anaphylaxis were reported among 17,589 patients (0.108%) undergoing cardiac surgery. The majority (15/19) occurred before cardiopulmonary bypass (CPB), mostly during or within 30 min after the induction of anesthesia (10/19). Two occurred within 15 min of going onto CPB. Of these 17 cases, 11 were abandoned, and 6 proceeded. The severity of reactions in the patients who proceeded ranged from grade II to grade IV of the Ring and Messmer classification. Two cases occurred after the completion of surgery. All patients survived to 90 days. However, this did not appear to be related to CPB or protamine as most of the reactions occurred before CPB. Instead, the most common causative agents were gelofusine, antibiotics, muscle relaxants, and chlorhexidine. In 6 cases, surgery proceeded despite the anaphylaxis, in 11 cases the surgery was postponed, and in 2 cases the procedure had already been completed. Conclusion: As all patients survived, our results provide preliminary support for proceeding with surgery although we cannot speculate on the likely outcomes of patients who were postponed, had their surgery proceeded. Based on our data, the incidence of anaphylaxis in cardiac surgical patients may be 10-20 times higher than in the general surgical population.

Remodeling of the Purkinje Network in Congestive Heart Failure in the Rabbit.

BACKGROUND: Purkinje fibers (PFs) control timing of ventricular conduction and play a key role in arrhythmogenesis in heart failure (HF) patients. We investigated the effects of HF on PFs. METHODS: Echocardiography, electrocardiography, micro-computed tomography, quantitative polymerase chain reaction, immunohistochemistry, volume electron microscopy, and sharp microelectrode electrophysiology were used. RESULTS: Congestive HF was induced in rabbits by left ventricular volume- and pressure-overload producing left ventricular hypertrophy, diminished fractional shortening and ejection fraction, and increased left ventricular dimensions. HF baseline QRS and corrected QT interval were prolonged by 17% and 21% (mean±SEMs: 303±6 ms HF, 249±11 ms control; n=8/7; P=0.0002), suggesting PF dysfunction and impaired ventricular repolarization. Micro-computed tomography imaging showed increased free-running left PF network volume and length in HF. mRNA levels for 40 ion channels, Ca2+-handling proteins, connexins, and proinflammatory and fibrosis markers were assessed: 50% and 35% were dysregulated in left and right PFs respectively, whereas only 12.5% and 7.5% changed in left and right ventricular muscle. Funny channels, Ca2+-channels, and K+-channels were significantly reduced in left PFs. Microelectrode recordings from left PFs revealed more negative resting membrane potential, reduced action potential upstroke velocity, prolonged duration (action potential duration at 90% repolarization: 378±24 ms HF, 249±5 ms control; n=23/38; P<0.0001), and arrhythmic events in HF. Similar electrical remodeling was seen at the left PF-ventricular junction. In the failing left ventricle, upstroke velocity and amplitude were increased, but action potential duration at 90% repolarization was unaffected. CONCLUSIONS: Severe volume- followed by pressure-overload causes rapidly progressing HF with extensive remodeling of PFs. The PF network is central to both arrhythmogenesis and contractile dysfunction and the pathological remodeling may increase the risk of fatal arrhythmias in HF patients.

Structural and Functional Properties of Subsidiary Atrial Pacemakers in a Goat Model of Sinus Node Disease.

BACKGROUND: The sinoatrial/sinus node (SAN) is the primary pacemaker of the heart. In humans, SAN is surrounded by the paranodal area (PNA). Although the PNA function remains debated, it is thought to act as a subsidiary atrial pacemaker (SAP) tissue and become the dominant pacemaker in the setting of sinus node disease (SND). Large animal models of SND allow characterization of SAP, which might be a target for novel treatment strategies for SAN diseases. METHODS: A goat model of SND was developed (n = 10) by epicardially ablating the SAN and validated by mapping of emergent SAP locations through an ablation catheter and surface electrocardiogram (ECG). Structural characterization of the goat SAN and SAP was assessed by histology and immunofluorescence techniques. RESULTS: When the SAN was ablated, SAPs featured a shortened atrioventricular conduction, consistent with the location in proximity of atrioventricular junction. SAP recovery time showed significant prolongation compared to the SAN recovery time, followed by a decrease over a follow-up of 4 weeks. Like the SAN tissue, the SAP expressed the main isoform of pacemaker hyperpolarization-activated cyclic nucleotide-gated channel 4 (HCN4) and Na+/Ca2+ exchanger 1 (NCX1) and no high conductance connexin 43 (Cx43). Structural characterization of the right atrium (RA) revealed that the SAN was located at the earliest activation [i.e., at the junction of the superior vena cava (SVC) with the RA] and was surrounded by the paranodal-like tissue, extending down to the inferior vena cava (IVC). Emerged SAPs were localized close to the IVC and within the thick band of the atrial muscle known as the crista terminalis (CT). CONCLUSIONS: SAN ablation resulted in the generation of chronic SAP activity in 60% of treated animals. SAP displayed development over time and was located within the previously discovered PNA in humans, suggesting its role as dominant pacemaker in SND. Therefore, SAP in goat constitutes a promising stable target for electrophysiological modification to construct a fully functioning pacemaker.

CXCR5 Knockdown Attenuates Hippocampal Neurogenesis Deficits and Cognitive Impairment in a Mouse Model of Sepsis-associated Encephalopathy.

In this study, we investigated the potential role of C-X-C chemokine receptor type (CXCR) 5 in neurocognitive function in a mouse model of sepsis-associated encephalopathy (SAE). Adult male C57BL/6J mice received intracerebroventricular injections of small interfering RNAs (siRNAs) against CXCR5 or scrambled control siRNA. After 3 days, SAE was induced by cecal ligation and puncture (CLP, n = 16 per group). Memory and learning ability were tested using the Morris water maze (MWM) on days 5-9 after CLP. Hippocampal expression of CXCR5, interleukin (IL)-1ß and IL-6 were measured by western blot. Cell proliferation and the numbers of immature and mature neurons in the dentate gyrus were assessed by immunohistochemistry. CLP mice had deficits in memory and learning, as shown by increased latency in the MWM training sessions and decreased time spent in and crossing the target quadrant on day 9. CLP also increased the number of proliferating and immature neurons and decreased the number of mature neurons. This was accompanied by increased expression of CXCR5, IL-1ß and IL-6 in the hippocampus. CXCR5 knockdown attenuated the memory and learning deficits induced by CLP and partially reversed the effects of CLP on numbers of proliferating, immature and mature neurons, and on expression of IL-1ß and IL-6 in the hippocampus. These results suggest that CXCR5 knockdown can attenuate sepsis-induced deficits in hippocampal neurogenesis and cognitive function in mice with SAE.

Extracorporeal membrane oxygenation in adult congenital heart disease: a case series and literature review.

OBJECTIVE: Extracorporeal membrane oxygenation (ECMO) can be used as rescue intervention for cardiac and/or respiratory failure. High-risk adult patients with adult congenital heart disease (ACHD) may require pre- and post-operative ECMO support. DESIGN, SETTING AND PARTICIPANTS: Retrospective data collection within a five-year time period from 2011 to 2016, at a single-centre study at a tertiary university hospital and regional unit for ACHD. Patients with ACHD in cardiogenic shock or failure to be separated from cardio-pulmonary bypass (CPB) were included. INTERVENTION: Venoarterial (VA) ECMO. RESULTS: Three patients had Ebstein anomaly and one patient had a double-outlet right ventricle transposition type and severe atrioventricular valve insufficiency. Three male patients and one female patient were aged ranging from 19 to 52 years. All received VA ECMO, two each with central or peripheral cannulation. The mean duration of ECMO support was 7 days (range, 3-13 days) and bleeding complications were the main complications observed, with a range of 12 to 104 blood products used. One patient required renal replacement therapy for acute kidney injury and also had leg ischaemia. MAIN OUTCOME MEASURES: Two of four patients (50%) were successfully weaned off ECMO and survived to hospital discharge in this high-risk group of patients in severe heart failure. The patients are currently at 3 and 4 years follow-up, with improved mobility and exercise tolerance compared with pre-operatively. CONCLUSION: ECMO is a promising temporary rescue intervention for patients with ACHD and cardiogenic shock. The extracorporeal cardiac support is a useful bridge to recovery.

Dexmedetomidine protects against renal ischemia and reperfusion injury by inhibiting the JAK/STAT signaling activation.

BACKGROUND: The α2-adrenoreceptor agonist dexmedetomidine is known to provide renoprotection against ischemia and reperfusion (I/R) injury. However the underlying molecular mechanisms remain unclear. The purpose of this study was to investigate whether the Janus kinase and signal transducer and activator of transcription (JAK/STAT) signaling pathway plays a role in dexmedetomidine's renoprotection. METHODS: I/R model was induced by bilateral renal pedicle clamping for 45 min followed by 48 h of reperfusion in male Wistar rat. Sham laparotomy served as controls. Animals received dexmedetomidine (50 µg/kg, i.p.) in the absence or presence of atipamezole (250 µg/kg, i.p.), or vehicle (DMSO) in the absence or presence of selective JAK2 inhibitor tyrphostin AG490 (10 mg/kg, i.p.) before ischemia. Renal function, histology, apoptosis, expression of cleaved caspase 3 protein, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1) and phosphorylations of JAK2, STAT1 and STAT3 were assessed. RESULTS: The animals treated with either dexmedetomidine or AG490 exhibited an improved renal functional recovery, attenuated histological lesions and reduced number of apoptotic tubular epithelial cells. Either dexmedetomidine or AG490 inhibited the phosphorylations of JAK2 and its downstream molecule STAT1 and STAT3, accompanied by down-regulation the expression of cleaved caspase 3, ICAM-1 and MCP-1 proteins, and significantly ameliorated renal I/R injury. CONCLUSIONS: Dexmedetomidine protects kidney against I/R injury, at least in part, through its inhibitory effects on injury-induced activation of JAK/STAT signaling pathway. If our data can be extrapolated to clinical setting, then dexmedetomidine may therefore serve as a clinical strategy to treat/prevent perioperative renal I/R injury.

The reinforced laryngeal mask airway (RLMA) protects the airway in patients undergoing nasal surgery--an observational study of 200 patients.

PURPOSE: The laryngeal mask airway (LMA) is used in nasal surgery but there is some concern of tracheal or laryngeal contamination with blood and secretions. We have evaluated the ability of the LMA to prevent airway contamination until full emergence from anesthesia. METHODS: Two hundred adults, ASA I-III patients, undergoing nasal surgery under general anesthesia were included in a prospective observational study. A reinforced LMA, sizes 3-5, was used during surgery and removed with its cuff inflated, in recovery, when the patients awoke. The LMA was examined on its laryngeal aspect for contamination of blood and secretions and scored (0-3) independently by two observers according to soiling (score of 0 = no blood; score of 1 = staining on the cuff; score of 2 = staining on the inside of mask; score of 3 = blood in the tube). RESULTS: The contamination scores were [n (%)]: 0 =174 (87%); 1 = 22 (11%); 2 = 4 (2%); 3 = 0 (0%). CONCLUSION: Ninety-eight percent of patients had no or minimal contamination of the LMA. The 2% incidence of grade 2 LMA soiling is low and probably acceptable, since it did not result in symptoms of airway contamination. We suggest that the use of the LMA for nasal surgery may be appropriate.