Type-2 diabetes mellitus (T2DM) plays a central role in the development of cardiovascular disease (CVD). However, its relationship to epicardial adipose tissue (EAT) and pericardial adipose tissue (PAT) in particular is important in the pathophysiology of coronary artery disease. Owing to its close proximity to the heart and coronary vasculature, EAT exerts a direct metabolic impact by secreting proinflammatory adipokines and free fatty acids, which promote CVD locally. In this review, we have discussed the relationship between T2DM and cardiac fat deposits, particularly EAT and PAT, which together exert a big impact on the cardiovascular health.

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The use of statins was independently associated with a reduction in the risk of delirium in hospitalized patients. When considering types of statins used, this reduction was significant in patients using atorvastatin, pravastatin, and simvastatin. Randomized trials of various statin types in hospitalized patients prone to delirium should validate their use in protection from delirium.

Magnesium (Mg) is an important intracellular ion with cardiac metabolism and electrophysiologic properties. A large percentage of patients with arrhythmias have an intracellular Mg deficiency, which is out of line with serum Mg concentrations, and this may explain the rationale for Mg's benefits as an atrial antiarrhythmic agent. A current limitation of antiarrhythmic therapy is that the potential for cardiac risk offsets some of the benefits of therapy. Mg enhances the balance of benefits to harms by enhancing atrial antiarrhythmic efficacy and reducing antiarrhythmic proarrhythmia potential as well as providing direct antiarrhythmic efficacy when used as monotherapy in patients undergoing cardiothoracic surgery.

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Background Our previous studies showed that in ischemic and nonischemic heart failure (HF), the voltage-gated cardiac Na+ channel α subunit (SCN5A) mRNA is abnormally spliced to produce two truncated transcript variants (E28C and D) that activate the unfolded protein response (UPR). We tested whether SCN5A post-transcriptional regulation was abnormal in hypertrophic cardiomyopathy (HCM). Material and Methods Human heart tissue was obtained from HCM patients. The changes in relative abundances of SCN5A, its variants, splicing factors RBM25 and LUC7A, and PERK, a major effector of the UPR, were analyzed by real time RT-PCR and the expression changes were confirmed by Western Blot. Results We found reduced full-length transcript, increased SCN5A truncation variants and activation of UPR in HCM when compared to control hearts. In these patients, real time RT-PCR revealed that HCM patients had decreased SCN5A mRNA to 27.8 ± 4.07% of control (P<0.01) and an increased abundance of E28C and E28D (3.4 ± 0.3 and 2.8 ± 0.3-fold, respectively, P<0.05). PERK mRNA increased 8.2 ± 3.1 fold (P<0.01) in HCM patients. Western blot confirmed a significant increase of PERK. Conclusions These data suggested that the full-length SCN5A was reduced in patients with HCM. This reduction was accompanied by abnormal SCN5A pre-mRNA splicing and UPR activation. These changes may contribute to the arrhythmic risk in HCM.

Mild therapeutic hypothermia (MTH) is used to lower the core body temperature of cardiac arrest (CA) patients to 32°C from 34°C to provide improved survival and neurologic outcomes after resuscitation from in-hospital or out-of-hospital CA. Despite the improved benefits of MTH, there are potentially unforeseen complications associated during management. Although the adverse effects are transient, the clinician should be aware of the associated complications when managing the patient receiving MTH. We aim to provide the medical community comprehensive information related to the potential complications of survivors of CA receiving MTH, as it is imperative for the clinician to understand the physiologic changes that take place in the patient receiving MTH and how to prepare for them and manage them if they do occur. We hope to provide information of how to manage these potential complications through both a review of the current literature and a reflection of our own experience.

The pathogenesis of postural orthostatic tachycardia syndrome (POTS) is poorly understood. However, it has been suggested that altered immune activity or denervation of the autonomic system following illness may be an important trigger. Patients infected with Lyme disease have a small incidence of post-Lyme disease syndrome that share similar characteristics to POTS. We report a short series of two women who present with persistent symptoms of orthostatic intolerance consistent with POTS after treated Lyme disease.