Research Spotlight

El-Chami, M. F., P. R. Roberts, A. Kypta, P. Omdahl, M. D. Bonner, R. C. Kowal and G. Z. Duray (2016). “How to implant a leadless pacemaker with a tine-based fixation.” J Cardiovasc Electrophysiol: 2016 Sep [Epub ahead of print].

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Two major studies have shown that leadless pacemakers are safe and effective for patients requiring right ventricular rate responsive pacing therapy. This positive result recently led to FDA approval of one of the available leadless pacing devices. While this new technology is promising, it requires a different skill set for safe implantation. In this article, we review in detail the different steps required for implantation of tine-based leadless pacemakers while providing tips and tricks to minimize complications.

Emmett, M. and A. Mehta (2016). “Patiromer-an oral calcium-loaded potassium binder: Kalirrhea with calciuresis.” Clin J Am Soc Nephrol: 2016 Sep [Epub ahead of print].

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Until recently, the major way to bind K in the gastrointestinal (GI) tract and thereby enhance excretion in the stool was the administration of sodium polystyrene sulfonate, which is a poorly effective and potentially dangerous medication (1,2). Recently, two new K-binding agents have been developed (patiromer and zirconium cyclosilicate), and one (patiromer) has been approved for use by the Food and Drug Administration (FDA). A safe, oral, nonabsorbable K-binding agent should mitigate the hyperkalemia risk of RAAS blockers and thereby be very beneficial to patients who have been unable to tolerate optimal doses of these agents on that basis. However, while the GI K-binding agents which are currently available or in the developmental pipeline are relatively selective for K, they also bind other ions and substances. Also, these agents all release other cations when K (or another cation) is bound; patiromer releases calcium whereas sodium polystyrene sulfonate and zirconium cyclosilicate each release sodium.

Emmett, M. (2016). “Stewart versus traditional approach to acid-base disorders.” Anesth Analg 123(4): 1063-1064.

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Undoubtedly, the Stewart methodology (and the “base excess” approach) can be used to diagnose metabolic acidbase disorders, but it has no advantage over the classic physiologic methodology advanced by Schwartz and Relman2 and Narins and Emmett.3 The “Stewart Approach” is a more complicated and less-intuitive framework for diagnosing and understanding acid-base physiology/pathophysiology. Dr Story describes an intubated cirrhotic patient (who had received generous intravenous saline expansion) with the following laboratory results: Na: 133; Cl: 110; lactate: 5 (all mmol/L); albumin: 22 g/L; arterial blood gas—pH 7.20; Pco2 40; HCO3 15. Potassium and venous HCO3 (or total CO2) were not reported.

Frieder, J. and C. Ryan (2016). “Psoriasis and cardiovascular disorders.” G Ital Dermatol Venereol: 2016 Sep [Epub ahead of print].

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Psoriasis is associated with an increased risk of cardiovascular disease and related comorbidities such as diabetes mellitus, metabolic syndrome, dyslipidemia, and obesity. The precise mechanistic links underlying the association between psoriasis and cardiovascular disease remain unknown, however, multiple pathologic mechanisms have been proposed. Shared inflammatory pathways between psoriasis and atherosclerosis are likely involved. Other possible mechanisms include endothelial dysfunction, cytokine dysregulation, platelet upregulation, and dyslipidemia. Additional studies are needed to more clearly define the association between psoriasis and cardiovascular disease. Current, but limited, data suggests that psoriasis treatments targeting inflammation may be able to reduce the cardiovascular risks in this patient population. As new therapies become available, long-term prospective studies will be required to determine their potential effects on cardiovascular risk. This review summarizes the current literature on proposed pathogenic links between psoriasis and cardiovascular disease, the epidemiology of psoriasis and associated cardiovascular and cardiometabolic diseases, and the impact of anti-psoriatic treatments on cardiovascular risk profile. In addition, we provide a brief discussion of risk factor management strategies in patients with psoriasis.