A novel noninvasive method for remote heart failure monitoring: the EuleriAn video Magnification apPLications In heart Failure studY (AMPLIFY).

Current remote monitoring devices for heart failure have been shown to reduce hospitalizations but are invasive and costly; accurate non-invasive options remain limited. The EuleriAn Video Magnification ApPLications In Heart Failure StudY (AMPLIFY) pilot aimed to evaluate the accuracy of a novel noninvasive method that uses Eulerian video magnification. Video recordings were performed on the neck veins of 50 patients who were scheduled for right heart catheterization at the Palo Alto VA Medical Center. The recorded jugular venous pulsations were then enhanced by applying Eulerian phase-based motion magnification. Assessment of jugular venous pressure was compared across three categories: (1) physicians who performed bedside exams, (2) physicians who reviewed both the amplified and unamplified videos, and (3) direct invasive measurement of right atrial pressure from right heart catheterization. Motion magnification reduced inaccuracy of the clinician assessment of central venous pressure compared to the gold standard of right heart catheterization (mean discrepancy of -0.80 cm H2O; 95% CI -2.189 to 0.612, p = 0.27) when compared to both unamplified video (-1.84 cm H2O; 95% CI -3.22 to -0.46, p = 0.0096) and the bedside exam (-2.90 cm H2O; 95% CI -4.33 to 1.40, p = 0.0002). Major categorical disagreements with right heart catheterization were significantly reduced with motion magnification (12%) when compared to unamplified video (25%) or the bedside exam (27%). This novel method of assessing jugular venous pressure improves the accuracy of the clinical exam and may enable accurate remote monitoring of heart failure patients with minimal patient risk.

Molecular Diagnostic Testing in Cardiac Transplantation.

PURPOSE OF REVIEW: Acute rejection is one of the most feared complications of cardiac transplantation. Developing non-invasive methods for detection and surveillance of acute rejection have long been a goal for post-transplant care. RECENT FINDINGS: Here, we will review molecular diagnostic tests that are currently in use or under development to diagnose acute cellular rejection after cardiac transplantation. Gene expression, microRNA, molecular microscope, and cell-free DNA assays offer non-invasive alternatives to the endomyocardial biopsy for acute rejection surveillance.

Impact of a Genetic Risk Score for Coronary Artery Disease on Reducing Cardiovascular Risk: A Pilot Randomized Controlled Study.

PURPOSE: We tested whether providing a genetic risk score (GRS) for coronary artery disease (CAD) would serve as a motivator to improve adherence to risk-reducing strategies. METHODS: We randomized 94 participants with at least moderate risk of CAD to receive standard-of-care with (N = 49) or without (N = 45) their GRS at a subsequent 3-month follow-up visit. Our primary outcome was change in low density lipoprotein cholesterol (LDL-C) between the 3- and 6-month follow-up visits (ΔLDL-C). Secondary outcomes included other CAD risk factors, weight loss, diet, physical activity, risk perceptions, and psychological outcomes. In pre-specified analyses, we examined whether there was a greater motivational effect in participants with a higher GRS. RESULTS: Sixty-five participants completed the protocol including 30 participants in the GRS arm. We found no change in the primary outcome between participants receiving their GRS and standard-of-care participants (ΔLDL-C: -13 vs. -9 mg/dl). Among participants with a higher GRS, we observed modest effects on weight loss and physical activity. All other secondary outcomes were not significantly different, including anxiety and worry. CONCLUSION: Adding GRS to standard-of-care did not change lipids, adherence, or psychological outcomes. Potential modest benefits in weight loss and physical activity for participants with high GRS need to be validated in larger trials.

Comparison of three ECG criteria for athlete pre-participation screening.

UNLABELLED: Controversy regarding adding the ECG to the evaluation of young athletes centers on the implications of false positives. Several guidelines have been published with recommendations for criteria to distinguish between ECG manifestations of training and markers of risk for cardiovascular (CV) sudden death. With an athlete dataset negative of any CV related abnormalities on follow-up, we applied three athlete screening criteria to identify the one with the lowest rate of abnormal variants. METHODS: High school, college, and professional athletes underwent 12L ECGs as part of routine physicals. All ECGs were recorded and processed using CardeaScreen (Seattle, WA). The European (2010), Stanford (2011), and Seattle criteria (2013) were applied. RESULTS: From March 2011 to February 2013 1417 ECGs were collected. Mean age was 20±4years (14-35years), 36% female, 38.5% non-white (307 high school, 836 college and 284 professional). Rate of abnormal variants differed by criteria, predominately due to variation in interval thresholds for QT interval and QRS duration. There was a four-fold difference in abnormal variants between European and Seattle criteria (26% v 6%). CONCLUSION: The Seattle criterion was the most conservative resulting in 78% fewer abnormal variants than the European criteria. Variation was most evident with thresholds for QT prolongation, short QT interval, and intraventricular conduction delay. Continued research is needed to further understand normal training related adaptations and to improve modern ECG screening criteria for athletes.

Resting ST amplitude: prognosis and normal values in an ambulatory clinical population.

BACKGROUND: There is limited data describing ST segment amplitude in apparently healthy, asymptomatic populations. We analyzed ST amplitude in the standard resting electrocardiogram (ECG) in a large, multiethnic, stable, clinical population. METHODS: We evaluated computerized ST amplitude measurements from the resting ECGs of 29,281 ambulatory outpatients collected between 1987 and 1999 at the Palo Alto, VA. With the PR interval as the isoelectric line, both elevation criteria (≥0.1 mV, ≥0.15 mV, and ≥0.2 mV) and depression criteria (≤-0.05 mV or ≤-0.1 mV), were applied. Cox-Hazard survival analysis techniques were used to demonstrate in which leads ST amplitude displacement was associated with cardiovascular (CV) death. To create a cohort without ECG patterns clearly associated with disease, we excluded ECGs with inverted T waves, wide QRS, or diagnostic Q waves and coded the remaining "normal" ECGs for ST elevation and depression to determine a normal range. RESULTS: The only ST amplitudes that were significantly and independently associated with time to CV death when adjusted for age, gender, and ethnicity were ST depression in all of the lateral leads (I, V4 -V6 ). When isolated to the inferior leads, (II and AVF), no ST amplitude criteria were associated with CV death. Among the "normal ECG" subgroup the precordial leads exhibited the greatest median ST amplitudes and the most significant differences between the leads, genders and ethnicities. CONCLUSIONS: Significant differences in ST amplitude were present in the precordial leads according to gender and ethnicity. This was particularly apparent when amplitude threshold were set for comparisons. Our findings provide the normal range for ST amplitude that when exceeded, should raise clinical concern.

HIF-1 regulates hypoxia- and insulin-induced expression of apelin in adipocytes.

Apelin, a novel peptide with significant cardioactive properties, is upregulated by insulin in adipocytes. However, the mechanism by which insulin promotes apelin production is unknown. Hypoxia-inducible factor-1 (HIF-1), a heterodimeric transcription factor involved in the angiogenic and metabolic responses to tissue hypoxia, has been shown to be activated by insulin in various settings. We therefore hypothesized that HIF-1 regulates insulin-mediated apelin expression in adipocytes. 3T3-L1 cells were differentiated into adipocytes in culture. For experiments, serum-starved 3T3-L1 cells were exposed to insulin and/or a 1% O(2) environment. Apelin expression was assessed using quantitative real-time PCR and ELISA. To directly assess the role of HIF-1 in apelin production, we differentiated mouse embryonic fibroblasts (MEFs) containing a targeted deletion of the HIF-1alpha gene into adipocytes and measured their response to insulin and hypoxia. Apelin expression in mature 3T3-L1 adipocytes was increased significantly by insulin and was attenuated by pharmacological inhibition of insulin signaling. Exposure of cells to either hypoxia or the chemical HIF activators cobalt chloride (CoCl(2)) and dimethyloxaloylglycine (DMOG) resulted in significant upregulation of apelin, consistent with a role for HIF in apelin induction. Moreover, hypoxia-, CoCl(2)-, DMOG-, and insulin-induced apelin expression were all attenuated in differentiated HIF-1alpha-deficient MEFs. In summary, in cultured 3T3-L1 adipocytes and differentiated MEFs, HIF-1 appears to be involved in hypoxia- and insulin-induced apelin expression.