Initial experience with magnetic resonance imaging-safe pacemakers: A review

Due of its superior soft tissue imaging capabilities, magnetic resonance imaging (MRI) has become the imaging modality of choice in many clinical situations, as illustrated by the tremendous growth in the number of MRIs performed over the past 2 decades. In parallel, the number of patients who require pacemakers or implantable cardiac defibrillators is increasing as indications for these devices broaden and the population ages. Taken together, these phenomena present an important clinical issue, as MR scans are generally contraindicated—except in urgent situations—in patients who have implanted cardiovascular devices. Potentially deleterious interactions between the magnetic fields and radio frequency (RF) energy produced by MR equipment and implantable devices have been identified, including inhibition of pacing, asynchronous/high-rate pacing, lead tip heating, and loss of capture. New devices that incorporate technologies to improve MR safety in patients with pacemakers have recently received approval in Europe and are under evaluation in the United States. Initial data from these devices suggest that these devices are safe in the MRI environment

2017 HRS/EHRA/ECAS/APHRS/SOLAECE expert consensus statement on catheter and surgical ablation of atrial fibrillation: executive summary.

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Obesity, inflammation and endothelial dysfunction

Cardiovascular disease is the leading cause of morbidity and mortality in obese individuals. Obesity dramatically increases the risk of development of metabolic and cardiovascular disease. This risk appears to originate from disruption in adipose tissue function leading to a chronic inflammatory state and to dysregulation of the endocrine and paracrine actions of adipocyte-derived factors. These, in turn, impair vascular homeostasis and lead to endothelial dysfunction. An altered endothelial cell phenotype and endothelial dysfunction are common among all obesity-related complications. A crucial aspect of endothelial dysfunction is reduced nitric oxide (NO) bioavailability. A systemic pro-inflammatory state in combination with hyperglycemia, insulin resistance, oxidative stress and activation of the renin angiotensin system are systemic disturbances in obese individuals that contribute independently and synergistically to decreasing NO bioavailability. On the other hand, pro-inflammatory cytokines are locally produced by perivascular fat and act through a paracrine mechanism to independently contribute to endothelial dysfunction and smooth muscle cell dysfunction and to the pathogenesis of vascular disease in obese individuals. The promising discovery that obesity-induced vascular dysfunction is, at least in part, reversible, with weight loss strategies and drugs that promote vascular health, has not been sufficiently proved to prevent the cardiovascular complication of obesity on a large scale. In this review we discuss the pathophysiological mechanisms underlying inflammation and vascular damage in obese patients