Accuracy and Reliability of Commercial Wrist-Worn Pulse Oximeter During Normobaric Hypoxia Exposure Under Resting Conditions.

Purpose: The present study analyzed peripheral blood oxygen saturation (SpO2) and heart rate (HR) measurements taken on the Garmin fenix® 5X Plus watch, comparing them to measurements taken on a standard medical-grade pulse oximeter during normobaric hypoxia exposure under resting conditions. Methods: Thirteen women (mean ± SD: Age 20 ± 1 years, height 165 ± 5 cm, mass, 67 ± 9 kg) and ten men (mean ± SD: Age 21 ± 3 years, height 177 ± 6 cm, mass 78 ± 11 kg) sat inside a customized environmental chamber while the fraction of inspired oxygen (FIO2) was adjusted to simulate altitudes of 12,000; 10,000; 8,000; 6,000; and 900 ft. The novel commercial device (Garmin fenix®) and a medical-grade pulse oximeter (Nonin® 7500) were used to measure SpO2 and HR in triplicate at each simulated altitude. Bland-Altman analyses were used to assess differences between methods. Results: Bland-Altman analysis indicated 3.3% bias for SpO2 measurements taken on the Garmin fenix® at 12,000 ft of simulated altitude (limits of agreement: -1.9-8.6%). Mean differences in SpO2 measurements were smaller at the remaining simulated altitudes, where bias measurements ranged from 0.7% to 0.8%. The Garmin fenix® also underestimated heart rate, but those discrepancies were minimal (bias measurements at all simulated altitude exposures were < 1.0 bpm). Conclusions: With the exception of readings taken at 12,000 ft of simulated altitude, the Garmin fenix® exhibits minimal overestimation of SpO2 and minimal underestimation of HR during simulated altitude exposure. These data suggest the Garmin fenix® watch may be a viable method to monitor SpO2 and HR under most ambient environmental conditions.

Secular Trend in the Use and Implementation of Impella in High-Risk Percutaneous Coronary Intervention and Cardiogenic Shock: A Real-World Experience.

OBJECTIVES: Cardiogenic shock carries high mortality despite advancements in therapeutic interventions. Impella (Abiomed) is a mechanical circulatory support device that is being increasingly used in cardiogenic shock patients. Impella is also utilized in high-risk patients undergoing percutaneous coronary intervention (PCI). We review the trend of Impella use at a single tertiary-care center, retrospectively analyze the outcomes, and discuss the increasing use of this device in the United States. METHODS: This a retrospective, observational study of Impella use for two indications, cardiogenic shock and high-risk PCI, at a tertiary-care center. The primary endpoint was the yearly implant rate of Impella and the secondary endpoint was periprocedural complications and major adverse cardiovascular events at 30 days. RESULTS: Forty-four Impella devices were implanted between 2008 and June of 2017. The rate of Impella implantation has significantly increased since its introduction in our facility in 2008. The most common complication was acute renal dysfunction (23%) followed by vascular complications (20%). Mortality at 30 days was 75% in the cardiogenic shock group and 11% in the high-risk PCI group. CONCLUSION: The use of the Impella device as a mechanical circulatory support has increased since its introduction, although its acceptance rate remains low. Despite its theoretical hemodynamic advantage, the outcome in cardiogenic shock patients remains poor.

Heat acclimation increases inflammatory and apoptotic responses to subsequent LPS challenge in C2C12 myotubes.

This work investigated the ability of a 6-day heat acclimation protocol to impart heat acclimation-mediated cross-tolerance (HACT) in C2C12 myotubes, as indicated by changes in inflammatory and apoptotic responses to subsequent lipopolysaccharide (LPS) challenge. Myotubes were incubated at 40 °C for 2 h/day over 6 days (HA) or maintained for 6 days at 37 °C (C). Following 24 h recovery, myotubes from each group received either no stimulation or 500 ng/ml LPS for 2 h (HA + LPS and C + LPS, respectively). Cell lysates were collected and analyzed for protein markers of the heat shock response, inflammation, and apoptosis. As compared to C, HA exhibited an elevated heat shock response [HSP70 (+ 99%); HSP60 (+ 216%); HSP32 (+ 40%); all p < 0.01] and reduced inflammatory and apoptotic signaling [p-NF-ĸB:NF-ĸB (- 99%%); p-JNK (- 49%); all p < 0.01]. When compared to C + LPS, HA + LPS also exhibited an elevated heat shock response [HSP70 (+ 68%); HSP60 (+ 32%); HSP32 (+ 38%); all p < 0.01]. However, inflammatory and apoptotic responses in HA + LPS were increased [p-IKBa:IKBa (+ 432%); p-NF-ĸB:NF-ĸB (+ 283%); caspase-8p18 (+ 53%); p-JNK (+ 41%); all p < 0.05]. This unanticipated finding may be due to increased TLR4-mediated signaling capacity in HA + LPS, as indicated by upregulation of TLR4 [(+ 24%); MyD88 (+ 308%); p-NIK (+ 199%); and p-IKKα/b (+ 81%); all p < 0.05]. Data suggest HA reduces inflammatory and apoptotic signaling in skeletal muscle cells that are maintained under basal conditions. However, HACT is selective and does not apply to TLR4 signaling in the present model.

Heat acclimation increases mitochondrial respiration capacity of C2C12 myotubes and protects against LPS-mediated energy deficit.

This work investigated the effect of a 6-day heat acclimation (HA) protocol on myotube metabolic responses at baseline and in response to a subsequent lipopolysaccharide (LPS) challenge. C2C12 myotubes were incubated for 2 h/day at 40 °C for 6 days (HA) or maintained at 37 °C (C). Following 24-h recovery, myotubes were challenged with 500 ng/ml LPS for 2 h, then collected for analysis of protein markers of mitochondrial biogenesis and macronutrient storage. Functional significance of these changes was confirmed with mitochondrial respiration and glycolytic measurements on a Seahorse XF-96 analyzer. HA stimulated mitochondrial biogenesis and increased indicators of mitochondrial content [SIRT1 (+ 62%); PGC-1α (+ 57%); NRF-1 (+ 40%); TFAM (+ 141%); CS (+ 25%); CytC (+ 38%); all p < 0.05]. Altered lipid biosynthesis enzymes [p-ACCa:ACC (+ 59%; p = 0.04) and FAS (- 86%; p < 0.01)] suggest fatty acid generation may have been downregulated, whereas increased GLUT4 (+ 69%; p < 0.01) and LDH-B (+ 366%; p < 0.01) suggest aerobic glycolytic capacity may have been improved. Mitochondrial biogenesis signaling in HA myotubes was suppressed by 500 ng/ml LPS (PGC-1α, NRF-1, TFAM; all p > 0.05) but increased LDH-B (+ 30%; p = 0.02) and CPT-1 (+ 55%; p < 0.01) suggesting improved catabolic function. Basal respiration was increased in HA myotubes (+ 8%; p < 0.01) and HA myotubes maintained elevated basal respiration during LPS challenge (+ 8%; p < 0.01). LPS reduced peak respiration in C myotubes (- 6%; p < 0.01) but did not impair peak respiration in HA myotubes (p > 0.05). Oxidative reliance was elevated in HA over that in control (+ 25%; p < 0.01) and in HA + LPS over C + LPS (+ 30%; p < 0.01). In summary, HA stimulated mitochondrial biogenesis in C2C12 myotubes. HA myotubes exhibited (1) elevated basal/peak mitochondrial respiration capacities; (2) greater oxidative reliance; and (3) protection against LPS-mediated respiration impairment. Collectively, these data suggest HA may improve aerobic metabolism in skeletal muscle and protect against LPS-mediated energy deficit.