Spatial representation of sub-endocardial electrogram parameters during sub-endocardial pacing from the apex (left panels) and base of the left ventricle (right panels).

<p>Two dimensional space is based on spherical coordinates derived from needle locations, representing elevation (−1 =  apex to +1 =  base), and azimuth (−2 =  mid lateral to +2 =  anterior). Numbered contours represent parameters derived from unipolar contact electrograms represented in milliseconds (ms) for activation time (AT) and millivolts (mV) for V_-P and V_P-P corresponding to panels from top to bottom respectively. Solid arrows represent preferential path of activation. Dotted arrows represent the approximate electrophysiological gradient of V_-P and V_P-P away from the stimulus site.</p

Within subject analysis examining the effect of propagation distance (covariate), transmural recording depth (treatment), and pacing depth (treatment) on minimally filtered unipolar electrogram parameters measured.

<p>Probabilities for the interaction term Depth*Distance represents whether there was a significant effect of propagation distance on electrogram amplitude recorded at each intra-myocardial depth level. Probabilities for the interaction term Depth*Pacing Depth indicate whether pacing depth had a significant effect on electrogram amplitude recorded at different intra-myocardial depth levels. Mean ± SD where indicated.</p><p>Within subject analysis examining the effect of propagation distance (covariate), transmural recording depth (treatment), and pacing depth (treatment) on minimally filtered unipolar electrogram parameters measured.</p

Transmural comparison of activation time between the epicardial and endocardial layer (shown as difference ΔAT) at various distances from the stimulus site during endocardial and epicardial pacing.

<p>Comparisons shown are: A. Unipolar and B. Bipolar minimally filtered electrograms.</p

Left: Three dimensional electroanatomic map of the left ventricle (anterior projection) displaying activation time derived from non-contact electrograms during pacing from a needle (D) located at the left ventricular apex.

<p>The figure shows earliest activation (dark blue) at the apex with gradual spreading towards the base (red). Numbers on electroanatomic map (fineprint) represent randomised locations of multipole needles (shown rightmost), which were deployed via the epicardium. <b>Right: Panels A, B and C demonstrating transmural unipolar and bipolar contact electrograms recorded from multipole needles corresponding to sites A, B and C on the electroanatomic map.</b> Y-axis is represented in mV. Electrodes; E1–E4  =  endocardial-epicardial unipolar recording depth; E12–E34  =  endocardial-epicardial bipolar recording depth.</p

Plots showing effect of recording distance from stimulation source and recording depth on contact electrograms measured during multisite pacing of left ventricular myocardium.

<p>There was a significant inverse relationship between recording distance from stimulus location and unipolar electrogram amplitude that was not significant for bipolar electrograms. Values represent between-sheep mean ± S.E, where; <i>p</i>^↔ is the probability of effects relative to propagation distance; and <i>p</i>^↕ is probability of transmural effects. A. Unipolar V_-P; B. Unipolar V_P-P; C. Bipolar V_P-P; and D. Filtered bipolar V_P-P. See <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0110399#pone-0110399-g001" target="_blank">figure 1</a> for electrode locations.</p

Two representative stained histological sections using haematoxylin-eosin of normal myocardium from different sites in the Ovine left ventricle.

<p>Left: unprocessed image. Right: convolved images identifying transmural anisotropy vectors in two dimensions from multiple sites indicated (circles) within each section. Circles arranged from epicardium (top) to endocardium (bottom). Anisotropy vectors orientated vertically at epicardial layer with distinct transitioning to horizontal orientation at the mid myocardial layer followed by diagonal orientation at the endocardial layer.</p

Illustration of electrocardiographic recording method, signal processing, and measurement of electrograms.

<p><b>E1–E4</b>  =  endocardial – epicardial plunge needle electrodes. +/−  =  electrode terminals. <b>Diff</b>  =  differential of +/− terminals. <b>Triangle</b>  =  Analogue Amplifier. <b>GND</b>  =  Ground Terminal attached to rib-retractors. <b>ADC</b> =  Analogue to Digital Converter (1 kHz sampling). <b>Step Functions</b> (<b>f</b>): Band-Pass filtering in analogue domain (0.2–300 Hz) and High-Pass filtering in the digital domain (not performed or 30 Hz). <b>V_-P</b>  =  Maximum negative deflection amplitude of QRS complex. <b>V_P-P</b>  =  Maximum peak positive to peak negative deflection amplitude of QRS complex.</p

Within subject analysis of the effect of propagation distance (covariate), transmural recording depth (treatment), and pacing depth (treatment) on unfiltered and 30 Hz high-pass filtered bipolar electrogram parameters measured.

<p>See <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0110399#pone-0110399-t001" target="_blank">Table 1</a> for interpretation of ANOVA probabilities.</p><p>Within subject analysis of the effect of propagation distance (covariate), transmural recording depth (treatment), and pacing depth (treatment) on unfiltered and 30 Hz high-pass filtered bipolar electrogram parameters measured.</p

Prediction of Coronary Artery Disease Extent and Severity Using Pulse Wave Velocity

<div><p>Background</p><p>Pulse-wave velocity (PWV) measures aortic stiffness. It is an independent predictor of cardiovascular events and mortality, yet there is paucity in the literature on its association with the severity and extent of coronary artery disease (CAD).</p><p>Methods</p><p>To examine the utility of PWV in predicting CAD burden in men and women the PWV was determined in 344 patients (Men = 266, Women = 78) presenting for invasive coronary angiography for the assessment of suspected CAD. Pearson correlations and multivariate analysis were used to evaluate the relationship between these coronary scores, PWV and traditional cardiovascular risk factors.</p><p>Results</p><p>Compared to men, women with chest pain had lower mean Extent scores (19.2 vs. 35.6; p = 0.0001) and Gensini scores (23.6 vs. 41.9; p = 0.0001). PWV was similar between men and women (12.35 ± 3.74 vs. 12.43 ± 4.58; p = 0.88) and correlated with Extent score (r = 0.21, p = 0.0001) but not Gensini or vessel score (r = 0.03, p = 0.64 and r = 0.06, p = 0.26, respectively). PWV was associated with Extent score in men (B = 2.25 ± 0.78, p = 0.004 for men and B = 1.50 ± 0.88, p = 0.09 for women). It was not a predictor of Gensini score (B = -0.10, P = 0.90).</p><p>Conclusion</p><p>PWV correlates with the extent of CAD, as measured by the ‘Extent’ score in men more than women. However, it does not correlate with the severity of obstructive CAD in either gender.</p></div

The relationship of pulse-wave velocity (PWV) with Extent and Gensini score in men (A) and women (B) using a univariate linear regression analysis.

<p><i>Caption</i>: Solid line = regression line, dotted line = 95% confidence interval. The Δβ represents the change in value of the Extent or Gensini score with every 1 m/s increase in the PWV result. Significant dependent correlations have p < 0.05. PWV, pulse-wave velocity.</p