Ventricular Tachycardia in Coronary Artery Disease

Ventricular arrhythmias are important contributors to morbidity and mortality in patients with coronary artery disease. Ventricular fibrillation accounts for the majority of deaths occurring in the acute phase of ischemia, whereas sustained, monomorphic ventricular tachycardia due to reentry generated in the scar tissue develops most often in the setting of healed myocardial infarction, especially in patients with lower left ventricular ejection fraction. Despite determinant advances in population education and myocardial infarction management, the ventricular tachycardia risk in the overall population with coronary artery disease continues to be a major problem in clinical practice. The initial evaluation of a patient presenting with ventricular tachycardia requires a 12-lead electrocardiogram, which can be helpful to confirm the diagnosis, suggest the presence of potential underlying heart disease, and identify the location of the ventricular tachycardia circuit. An invasive electrophysiologic study is usually crucial to determine the mechanism of the arrhythmia once induced and to provide guidance for ablation. The approach for ventricular tachycardia ablation depends on several factors, including inducibility, sustainability, and clinical tolerance of ventricular tachycardia. The paper also reviews other therapeutic options for patients with ventricular tachycardia associated with coronary artery disease, including antiarrhythmic drug therapy, surgical ablation, and current implantable cardioverter-defibrillator indications.     

Conversion to shockable rhythms during resuscitation and survival for out-of hospital cardiac arrest

Background

In out of hospital cardiac arrest (OHCA), the prognostic influence of conversion to shockable rhythms during resuscitation for initially non-shockable rhythms remains unknown. This study aimed to assess the relationship between initial and subsequent shockable rhythm and post-arrest survival and neurological outcomes after OHCA.

Therapeutic hypothermia: past, present, and future

Cardiac arrest causes devastating neurologic morbidity and mortality. The preservation of the brain function is the final goal of resuscitation. Therapeutic hypothermia (TH) has been considered as an effective method for reducing ischemic injury of the brain. The therapeutic use of hypothermia has been utilized for millennia, and over the last 50 years has been routinely employed in the operating room. TH gained recognition in the past 6 years as a neuroprotective agent in victims of cardiac arrest after two large, randomized, prospective clinical trials demonstrated its benefits in the postresuscitation setting. Extensive research has been done at the cellular and molecular levels and in animal models. There are a number of proposed applications of TH, including traumatic brain injury, acute encephalitis, stroke, neonatal hypoxemia, and near-drowning, among others. Several devices are being designed with the purpose of decreasing temperature at a fast and steady rate, and trying to avoid potential complications. This article reviews the historical development of TH, and its current indications, methods of induction, and potential future.     

Perceptions of Singaporean patients living with implantable cardioverter defibrillators: an exploratory qualitative study

Background

Despite the increasing use of implantable cardioverter defibrillators (ICDs) as a preventive approach for high-risk patients with arrhythmias, little is known about the perceptions of ICD recipients regarding these devices and their impact on quality of life.

Differences in Glucose Metabolism Among Women With Spinal Cord Injury May Not Be Fully Explained by Variations in Body Composition

ObjectiveTo investigate the differences in glucose metabolism among women with paraplegic, and tetraplegic spinal cord injury (SCI) in comparison to their able-bodied (AB) counterparts after adjusting for differences in body composition.DesignCross-sectional study. After an overnight fast, each participant consumed a 75-g glucose solution for oral glucose tolerance test (OGTT). Blood glucose, insulin, and C-peptide concentrations were analyzed before and 30, 60, 90, and 120 minutes after ingesting glucose solution. Insulin sensitivity index (ISI) was estimated using the Matsuda index. Percentage fat mass (%FM) and total body lean mass (TBLM) were estimated using data from dual-energy x-ray absorptiometry. Visceral fat (VF) was quantified using computed tomography. Outcome measures were compared among groups using analysis of covariance with %FM (or VF) and TBLM as covariates.SettingResearch university.ParticipantsWomen (N=42) with SCI (tetraplegia: n=8; paraplegia: n=14) and their race-, body mass index-, and age-matched AB counterparts (n=20).InterventionsNot applicable.ResultsAt fasting, there was no difference in glucose homeostasis (glucose, insulin, C-peptide concentrations) among 3 groups of women. In contrast, glucose, insulin, and C-peptide concentrations at minute 120 during OGTT were higher in women with tetraplegia versus women with paraplegia and AB women (P<.05, adjusted for TBLM and %FM). In addition, women with tetraplegia had lower ISI (P<.05, adjusted for TBLM and %FM) versus AB women. These differences remained after adjusting for VF and TBLM.ConclusionOur study confirms that impaired glucose metabolism among women with tetraplegia may not be fully explained by changes in their body composition. Future studies exploring additional factors involved in glucose metabolism are warranted.     

Neuropeptide VF-associated satiety involves mu and kappa but not delta subtypes of opioid receptors in chicks

Neuropeptide VF (NPVF) induces satiety through hypothalamic interactions; however, the central mechanism that mediates these effects is poorly understood. Therefore, this study was conducted to explore some possible opioid receptor associated mechanisms of NPVF-induced satiety using chicks as models. Co-injection of NPVF and a mu opioid receptor antagonist (beta-funaltrexamine, FNA) did not have an additive suppressive effect on food intake compared to NPVF and FNA when injected alone. Contrary, co-injection of NPVF and a delta opioid receptor antagonist (ICI-174,864, ICI) caused a greater reduction in food intake than when both were injected alone. Co-injection of NPVF and a kappa opioid receptor antagonist (nor-binaltorphimine, BNI) did not cause an additive suppressive effect on food intake than when the two were injected alone. A reversal of neuropeptide Y and β-endorphin induction of food intake occurred when NPVF was co-injected. These results support that NPVF-induced satiety is mediated through mu and kappa but not delta subtypes of opioid receptors, and their ligands including neuropeptide Y and β-endorphin. Thus, NPVF-associated anorexia may be mediated via modulation of the chick's innate opioid-associated orexigenic system.     

Transient attenuation of neuropathic manifestations in rats following lesion or reversible block of the lateral thalamic somatosensory nuclei

BACKGROUND AND AIMS: Nociceptive behavior in animal models for mononeuropathy has been shown to be altered by spinal tract lesions which suggest a possible supraspinal modulation. The thalamus constitutes a chief center for the processing of nociception. We have, therefore, investigated the effects of transient or permanent blocks of the lateral somatosensory thalamic nuclei (the ventrobasal complex) on the neuropathic manifestations in rats. METHODS: Different groups of rats (n = 5-6) were subjected to mononeuropathy, following the spared nerve injury model, known to produce sustained heat hyperalgesia and tactile and cold allodynia which peaked about 2 weeks after nerve injury. This was followed by stereotaxic placement of either electrolytic or chemical lesions or implantation of mini osmotic pump for slow release of lidocaine in the ventrobasal complex. RESULTS: Chronic electrolytic and chemical lesions or reversible block of the lateral somatosensory thalamus produced transient (1-2 weeks) attenuation of neuropathic manifestations along with a persistent decrease of the hot plate latency. The most pronounced effect was observed on heat hyperalgesia, and the least significant and short-lived effect was observed on cold allodynia. CONCLUSION: We conclude that the lateral somatosensory thalamic complex is involved in the processing of neuropathic manifestations but cannot be considered as an obligatory or exclusive relay center for the neuropathic syndromes.     

Electrocardiographic features in a patient with the coexistence of long QT syndrome and coronary vasospasm

A 20-year-old woman suffered from cardiopulmonary arrest due to ventricular fibrillation. The electrocardiogram after resuscitation showed prolonged QTc interval with bifid T wave. On the third hospital day, the QTc interval and the T-wave changes improved. However, the QTc interval was distinctively prolonged after administration of epinephrine, oral glucose load, and intracoronary acetylcholine (Ach) into the left coronary artery. Moreover, an injection of Ach into the right coronary artery provoked severe coronary spasm. This is a case of the coexistence of long QT syndrome (LQTS) and coronary vasospasm, which may give an important clinical implication for the treatment of LQTS.     

Short-term anorexigenic effects of central neuropeptide VF are associated with hypothalamic changes in chicks

The present study was designed to measure food and water intake, changes in hypothalamic chemistry, and other behaviour modifications after central injection of neuropeptide (NP) VF in broiler type chicks. In Experiment 1, chicks responded to central NPVF with a reduction in food intake for up to 90 min post injection. Water intake was unaffected. In Experiment 2, NPVF exerted a less potent and shorter duration of attenuated food intake than did the structurally related NPFF. In Experiment 3, 16.0 nmol NPVF reversed the prolactin-releasing peptide induced orexigenic effect. In Experiment 4, central NPVF treatment was associated with decreased c-Fos immunoreactivity in the lateral hypothalamus, whereas c-Fos immunoreactivity in the dorsomedial nucleus, infundibular nucleus (homologue to the mammalian arcuate nucleus) and ventromedial nucleus was increased. In Experiment 5, behaviours unrelated to ingestion including sit, stand, deep rest and locomotion were affected by central NPVF injection. Some of these behaviours are incompatible with ingestion and may contribute to hypothalamic associated perception of satiety after central NPVF. In conclusion, NVPF is a short-term regulator of appetite and its effects are associated with hypothalamic and behaviour changes in chicks.