Background Atrial fibrillation (AF) screening using mobile single-lead electrocardiogram (ECG) devices has demonstrated variable sensitivity and specificity. However, limited data exists on the use of such devices in low-resource countries. Objective The goal of the research was to evaluate the utility of the KardiaMobile device’s (AliveCor Inc) automated algorithm for AF screening in a semirural Ethiopian population. Methods Analysis was performed on 30-second single-lead ECG tracings obtained using the KardiaMobile device from 1500 TEFF-AF (The Heart of Ethiopia: Focus on Atrial Fibrillation) study participants. We evaluated the performance of the KardiaMobile automated algorithm against cardiologists’ interpretations of 30-second single-lead ECG for AF screening. Results A total of 1709 single-lead ECG tracings (including repeat tracing on 209 occasions) were analyzed from 1500 Ethiopians (63.53% [953/1500] male, mean age 35 [SD 13] years) who presented for AF screening. Initial successful rhythm decision (normal or possible AF) with one single-lead ECG tracing was lower with the KardiaMobile automated algorithm versus manual verification by cardiologists (1176/1500, 78.40%, vs 1455/1500, 97.00%; P<.001). Repeat single-lead ECG tracings in 209 individuals improved overall rhythm decision, but the KardiaMobile automated algorithm remained inferior (1301/1500, 86.73%, vs 1479/1500, 98.60%; P<.001). The key reasons underlying unsuccessful KardiaMobile automated rhythm determination include poor quality/noisy tracings (214/408, 52.45%), frequent ectopy (22/408, 5.39%), and tachycardia (>100 bpm; 167/408, 40.93%). The sensitivity and specificity of rhythm decision using KardiaMobile automated algorithm were 80.27% (1168/1455) and 82.22% (37/45), respectively. Conclusions The performance of the KardiaMobile automated algorithm was suboptimal when used for AF screening. However, the KardiaMobile single-lead ECG device remains an excellent AF screening tool with appropriate clinician input and repeat tracing. Trial Registration Australian New Zealand Clinical Trials Registry ACTRN12619001107112; https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=378057&isReview=true

BackgroundThe increased adverse cardiac events in women undergoing coronary artery bypass grafting are multifactorial and may include clinical, psychosocial, and biological factors. Potential contributing biological factors could include vascular hyperreactivity of the internal mammary artery (IMA) to endogenous vasoconstrictors in women, resulting in a predilection to myocardial ischemia. This study evaluated sex differences in serotonin and thromboxane A2 dependent vasoconstriction in human isolated IMA, with the mechanistic role of (1) the endothelium, (2) nitric oxide (NO), (3) prostaglandins, and (4) receptor activity investigated for any observed sex difference.Methods and ResultsViable isolated human IMA segments were obtained from 116 patients (44 women [mean age, 66.8±12.2 years] and 72 men [mean age, 66.6±10.4 years]) undergoing coronary artery bypass grafting. Cumulative concentration‐response curves for serotonin and thromboxane A2 mimetic, U46619, were determined and revealed an increased sensitivity to serotonin but not U46619 in women. This sex difference to serotonin was further assessed by the following: (1) endothelial denudation, (2) endothelial NO synthase inhibition and NO quantification using electron paramagnetic resonance, (3) cyclooxygenase inhibition and prostaglandin metabolite quantification using mass spectrometry, and (4) quantification of receptor activity status. The female hyperreactivity to serotonin was (1) abolished by endothelial denudation; (2) unaffected by NO synthase inhibition, with no difference in electron paramagnetic resonance–assessed NO levels; (3) abolished by cyclooxygenase inhibition (quantification of prostaglandins in IMA revealed a trend towards reduced 6‐keto prostaglandin F1α in female IMA; P=0.08); and (4) unrelated to receptor activity.ConclusionsThese data indicate that female IMAs are hyperreactive to serotonin but not U46619, with the former attributable to an endothelium‐dependent cyclooxygenase pathway.

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HR was also lower in SEM relative to UP (p=0.031), but similar between SEM and SUP. Peak SV was lower in SUP relative to SEM (p=0.003), with a trend toward a reduction in peak Q (p=0.071). Peak Q and SV in UP and SEM were similar. Conclusion: VO 2 max is significantly reduced in SEM and SUP cycling relative to UP, due, in part, to a blunted cardiac response which is exacerbated as you move closer to horizontal. Thus, posture must be accounted for when interpreting CPET results.

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