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Background: Studies have reported an inverse relationship between late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) signal intensity and left atrial (LA) endocardial voltage after LA ablation. However, there is controversy regarding the reproducibility of atrial LGE CMR and its ability to identify gaps in ablation lesions. Using systematic and objective techniques, this study examines the correlation between atrial CMR and endocardial voltage.Methods and Results: Twenty patients who had previous ablation for atrial fibrillation and represented with paroxysmal atrial fibrillation or atrial tachycardia underwent preablation LGE CMR. During the ablation procedure, high-density point-by-point Carto voltage maps were acquired. Three-dimensional CMR reconstructions were registered with the Carto anatomies to allow comparison of voltage and LGE signal intensity. Signal intensities around the left and right pulmonary vein antra and along the LA roof and mitral lines on the CMR-segmented LA shells were extracted to examine differences between electrically isolated and reconnected lesions. There were a total of 6767 data points across the 20 patients. Only 119 (1.8%) of the points were ≤ 0.05 mV. There was only a weak inverse correlation between either unipolar (r = -0.18) or bipolar (r = -0.17) voltage and LGE CMR signal intensities with low voltage occurring across a large range of signal intensities. Signal intensities were not statistically different for electrically isolated and reconnected lesions.Conclusions: This study demonstrates that there is only a weak point-by-point relationship between LGE CMR and endocardial voltage in patients undergoing repeat LA ablation. Using an objective method of assessing gaps in ablation lesions, LGE CMR is unable to reliably predict sites of electrical conduction. [ABSTRACT FROM AUTHOR]

Aortic pulse wave velocity (aPWV), a major prognostic indicator of cardiovascular events, may be augmented in hypertension as a result of the aorta being stretched by a higher distending blood pressure or by a structural change. We used a novel technique to modulate intrathoracic pressure and thus aortic transmural pressure (TMP) to examine the variation of intrathoracic aPWV with TMP in hypertensive (n=20; mean±SD age, 52.1±15.3 years; blood pressure, 159.6±21.2/92.0±15.9 mm Hg) and normotensive (n=20; age, 55.5±11.1 years; blood pressure, 124.5±11.9/72.6±9.1 mm Hg) subjects. aPWV was measured using dual Doppler probes to insonate the right brachiocephalic artery and aorta at the level of the diaphragm. Resting aPWV was greater in hypertensive compared with normotensive subjects (897±50 cm/s versus 784±43 cm/s; P<0.05). aPWV was equal in hypertensive and normotensive subjects when measured at a TMP of 96 mm Hg. However, dependence of aPWV on TMP in normotensive subjects was greater than that in hypertensive subjects (9.6±1.6 versus 3.8±0.7 cm/s per mm Hg increase in TMP, respectively, means±SEM; P<0.01). This experimental behavior was best explained by a theoretical model incorporating strain-induced recruitment of stiffer fibers in normotensive subjects and fully recruited stiffer fibers in hypertensive subjects. These results explain previous contradictory findings with respect to isobaric aPWV in hypertensive compared with normotensive subjects. They suggest that hypertension is associated with a profound change in aortic wall mechanical properties possibly because of destruction of elastin leading to less strain-induced stiffening and predisposition to aortic dissection. [ABSTRACT FROM AUTHOR]