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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]

The incidence of abdominal aortic aneurysms (AAAs) has increased during the last decades. However, there is still controversy about the management of medium-sized AAAs. Therefore, novel biomarkers, besides aneurysmal diameter, are needed to assess aortic wall integrity and risk of rupture. Elastin is the key protein for maintaining aortic wall tensile strength and stability. The progressive breakdown of structural proteins, in particular, medial elastin, is responsible for the inability of the aortic wall to withstand intraluminal hemodynamic forces. Here, we evaluate the usefulness of elastin-specific molecular MRI for the in vivo characterization of AAAs.To induce AAAs, ApoE-/- mice were infused with angiotensin-II. An elastin-specific magnetic resonance molecular imaging agent (ESMA) was administered after 1, 2, 3, and 4 weeks of angiotensin-II infusion to assess elastin composition of the aorta (n=8 per group). The high signal provided by ESMA allowed for imaging with high spatial resolution, resulting in an accurate assessment of ruptured elastic laminae and the compensatory expression of elastic fibers. In vivo contrast-to-noise ratios and R1-relaxation rates after ESMA administration were in good agreement with ex vivo histomorphometry (Elastica van Gieson stain) and gadolinium concentrations determined by inductively coupled plasma mass spectroscopy. Electron microscopy confirmed colocalization of ESMA with elastic fibers.Changes in elastin content could be readily delineated and quantified at different stages of AAAs by elastin-specific molecular magnetic resonance imaging. ESMA-MRI offers potential for the noninvasive detection of the aortic rupture site prior to dilation of the aorta and the subsequent in vivo monitoring of compensatory repair processes during the progression of AAAs. [ABSTRACT FROM AUTHOR]

Increased systemic inflammation has been linked to myocardial dysfunction and heart failure in patients with systemic lupus erythematosus (SLE). Accurate detection of early myocardial changes may be able to guide preventive intervention. We investigated whether multiparametric imaging by cardiovascular magnetic resonance can detect differences between controls and asymptomatic SLE patients.A total of 33 SLE predominantly female patients (mean age, 40±9 years) underwent cardiovascular magnetic resonance for routine assessment of myocardial perfusion, function, and late gadolinium enhancement. T1 mapping was performed in single short-axis slice before and after 15 minutes of gadolinium administration. Twenty-one subjects with a low pretest probability and normal cardiovascular magnetic resonance served as a control group. Both groups had similar left ventricular volumes and mass and normal global systolic function. SLE patients had significantly reduced longitudinal strain (controls versus SLE, -20±2% versus -17±3%; P<0.01) and showed intramyocardial and pericardial late gadolinium enhancement. SLE patients had significantly increased native myocardial T1 (1056±27 versus 1152±46 milliseconds; P<0.001) and extracellular volume fraction (26±5% versus 30±6%; P=0.007) and reduced postcontrast myocardial T1 (454±53 versus 411±62 milliseconds; P=0.01). T1-derived indices were associated with longitudinal strain (r=0.37-0.47) but not with the presence of late gadolinium enhancement. Native myocardial T1 values showed the greatest concordance with the presence of clinical diagnosis of SLE.In patients with SLE who are free of cardiac symptoms, there is evidence of subclinical perimyocardial impairment. We further demonstrate that T1 mapping may have potential to detect subclinical myocardial involvement in patients with SLE. [ABSTRACT FROM AUTHOR]

Background: Pulmonary vein reconnection after pulmonary vein isolation is common and is usually associated with recurrences of atrial fibrillation. We used cardiac magnetic resonance imaging after radiofrequency ablation to investigate the hypothesis that acute pulmonary vein isolation results from a combination of irreversible and reversible atrial injury.Methods and Results: Delayed enhancement (DE; representing areas of acute tissue injury/necrosis) and T2-weighted (representing tissue water content, including edema) cardiac magnetic resonance scans were performed before, immediately after (acute), and later than 3 months (late) after pulmonary vein isolation in 25 patients with paroxysmal atrial fibrillation undergoing wide-area circumferential ablation. Images were analyzed as pairs of pulmonary veins to quantify the percentage of circumferential antral encirclement composed of DE, T2, and combined DE+T2 signal. Fourteen of 25 patients were atrial fibrillation free at 11-month follow-up (interquartile range, 8-16 months). These patients had higher DE (71±6.0%) and lower T2 signal (72±7.8%) encirclement on the acute scans compared with recurrences (DE, 55±9.1%; T2, 85±6.3%; P<0.05). Patients maintaining sinus rhythm had a lesser decline in DE between acute and chronic scans compared with recurrences (71±6.0% and 60±5.8% versus 55±9.1% and 34±7.3%, respectively). The percentage of encirclement by a combination of DE+T2 was almost similar in both groups on the acute scans (atrial fibrillation free, 89±5.4%; recurrences, 92±4.8%) but different on the chronic scans (60±5.7% versus 34±7.3%).Conclusions: The higher T2 signal on acute scans and greater decline in DE on chronic imaging in patients with recurrences suggest that they have more reversible tissue injury, providing a potential mechanism for pulmonary vein reconnection, resulting in arrhythmia recurrence. [ABSTRACT FROM AUTHOR]

The article discusses a study which investigated the hypothesis that acute pulmonary vein isolation (PVI) results from a combination of irreversible and reversible atrial injury. The study used cardiac magnetic resonance imaging (CMRI) after radiofrequency ablation and involved 25 paroxysmal atrial fibrillation (AF) patients. The study found the higher T2 signal on acute scans. Greater decline in delayed enhancement (DE) on chronic imaging in patients with recurrences is also observed.

The article presents a study which evaluated the safety and efficacy of a magnetic resonance (MR)-safe and compatible passive guide wire in helping MR-guided cardiac interventions in a swine model. Catheter manipulations were monitored in this study. The study concludes that with the availability of the new MR-compatible and safe guide wire, certain percutaneous cardiac interventions will become feasible to perform under MR guidance in the future.