Magnetic field-induced interactions between phones containing magnets and cardiovascular implantable electronic devices: Flip it to be safe?

BACKGROUND: Recent case reports and small studies have reported activation of the magnet-sensitive switches in cardiovascular implantable electronic devices (CIEDs) by the new iPhone 12 series, initiating asynchronous pacing in pacemakers and suspension of antitachycardia therapies in implantable cardioverter-defibrillators (ICDs). OBJECTIVE: The purpose of this prospective single-center observational study was to quantify the risk of magnetic field interactions of the iPhone 12 with CIEDs. METHODS: A representative model of each CIED series from all manufacturers was tested ex vivo. Incidence and minimum distance necessary for magnet mode triggering were analyzed in 164 CIED patients with either the front or the back of the phone facing the device. The magnetic field of the iPhone 12 was analyzed using a 3-axis Hall probe. RESULTS: Ex vivo, magnetic interference occurred in 84.6% with the back compared to 46.2% with the front of the iPhone 12 facing the CIED. In vivo, activation of the magnet-sensitive switch occurred in 30 CIED patients (18.3%; 21 pacemaker, 9 ICD) when the iPhone 12 was placed in close proximity over the CIED pocket and the back of the phone was facing the skin. Multiple binary logistic regression analysis identified implantation depth (95% confidence interval 0.02-0.24) as an independent predictor of magnet-sensitive switch activation. CONCLUSION: Magnetic field interactions occur only in close proximity and with precise alignment of the iPhone 12 and CIEDs. It is important to advise CIED patients to not put the iPhone 12 directly on the skin above the CIED. Further recommendations are not necessary.

Loss of CASK Accelerates Heart Failure Development.

[Figure: see text].

Suppression of Tumourigenicity 2 in Heart Failure With Preserved Ejection Fraction.

Heart failure (HF), with steadily increasing incidence rates and mortality in an ageing population, represents a major challenge. Evidence suggests that more than half of all patients with a diagnosis of HF suffer from HF with preserved ejection fraction (HFpEF). Emerging novel biomarkers to improve and potentially guide the treatment of HFpEF are the subject of discussion. One of these biomarkers is suppression of tumourigenicity 2 (ST2), a member of the interleukin (IL)-1 receptor family, binding to IL-33. Its two main isoforms - soluble ST2 (sST2) and transmembrane ST2 (ST2L) - show opposite effects in cardiovascular diseases. While the ST2L/IL-33 interaction is considered as being cardioprotective, sST2 antagonises this beneficial effect by competing for binding to IL-33. Recent studies show that elevated levels of sST2 are associated with increased mortality in HF with reduced ejection fraction. Nevertheless, the significance of sST2 in HFpEF remains uncertain. This article aims to give an overview of the current evidence on sST2 in HFpEF with an emphasis on prognostic value, clinical association and interaction with HF treatment. The authors conclude that sST2 is a promising biomarker in HFpEF. However, further research is needed to fully understand underlying mechanisms and ultimately assess its full value.

Reconstitution of interleukin-17-producing T helper cells after allogeneic hematopoietic cell transplantation.

Interleukin 17A (IL-17)-producing CD4(+) T helper type 17 (Th17) cells have recently drawn attention as possible effector cells of acute graft-versus-host disease (GVHD) after allogeneic hematopoietic cell transplantation (HCT) in murine models. Their role after allogeneic HCT in humans is unknown. In this prospective study, Th17, Th1/17, and Th1 cells were quantified in the peripheral blood of 80 patients within the first 3 months after allogeneic HCT using intracellular cytokine staining and flow cytometry. Within the observation period, Th1, Th1/17, and Th17 cells did not reconstitute to levels of healthy control subjects. In contrast to Th1 cells, no further expansion of Th1/17 and Th17 cells was observed during the first month after HCT. Antithymocyte globulin during conditioning significantly reduced the frequency of Th1/17 and Th17 cells but not of Th1 cells. Acute GVHD was not associated with significant changes in the size of the Th1, Th1/17, or Th17 cell subsets. Cytomegalovirus reactivation triggered the expansion of all T helper subsets, and Th1 cells showed the strongest increase. In contrast, no significant changes were found in the T helper cell compartment of patients with bacterial infections compared with time-matched control subjects. In conclusion, quantitative reconstitution of Th1, Th1/17, and Th17 cells is impaired within the first 3 months after HCT, especially when antithymocyte globulin is administered during conditioning. Cytomegalovirus reactivation, but not acute GVHD or bacterial infection, triggered the absolute expansion of these T cell subsets.

Reconstitution of 6-sulfo LacNAc dendritic cells after allogeneic stem-cell transplantation.

BACKGROUND: Infections and acute graft-versus-host disease (GvHD) represent major complications of allogeneic stem-cell transplantation (SCT). Dendritic cells (DCs) display an extraordinary capacity to induce innate and adaptive immune responses. Therefore, they play a crucial role in the elimination of pathogens and in the pathogenesis of acute GvHD. 6-Sulfo LacNAc DCs (slanDCs) are a major subpopulation of human blood DCs with a high proinflammatory capacity. We investigated for the first time the reconstitution of slanDCs in the blood of patients after SCT and the modulation of their frequency by bacterial infection, cytomegalovirus (CMV) reactivation, and acute GvHD. METHODS: The frequency of slanDCs, CD1c myeloid DCs (mDCs), and plasmacytoid DCs (pDCs) in the peripheral blood was quantified by flow cytometry in 80 patients after SCT. To assess individual DC subsets, we used pregating of the HLADRLin subset and antibodies against slanDCs, blood DC antigen 1 (CD1c mDCs), and blood DC antigen 2 (pDCs). RESULTS: SlanDCs showed the slowest reconstitution in the first month after SCT compared with CD1c mDCs and pDCs. Interestingly, in the second and third months after SCT, their percentage steadily increased, and slanDCs were the most abundant DC subset. In addition, we observed a markedly reduced frequency of slanDCs in the blood of patients with bacterial infection, CMV reactivation, or severe acute GvHD. Furthermore, slanDCs showed the most prominent reduction after steroid treatment of acute GvHD. CONCLUSIONS: These results indicate that SCT-associated complications such as bacterial infection, CMV reactivation, and acute GvHD can significantly modulate the frequency of slanDCs.