Prior reports have associated increased circulating levels of matrix metalloproteinase-9 (MMP-9), an endopeptidase active in the extracellular matrix, with the formation and rupture of aortic aneurysms, raising the possibility that MMP-9 may be a useful diagnostic or therapeutic target for aortic pathology. However, associations between MMP-9 and pathological abdominal aortic phenotypes in the general population have not been reported. In the Dallas Heart Study, a population-based sample of Dallas County residents (n = 2304), we measured MMP-9 and performed magnetic resonance imaging (MRI) of the abdominal aorta, measuring aortic compliance, plaque, wall thickness and luminal diameter. After adjustment for traditional cardiac risk factors and body size, higher MMP-9 quartiles were independently associated with higher aortic wall thickness and larger luminal diameter (p < 0.0001 for each), but not abdominal aortic plaque (p = 0.08), coronary artery calcium (p = 0.20) or the aortic luminal diameter/aortic wall thickness ratio (p = 0.37), supporting the hypothesis that therapies targeting MMP-9 may affect the abdominal aortic wall and modify aortic pathology.

As an isolated finding, an elevated preprocedure WBC should not delay the implantation of an indicated device.

The past 40 years have taught us much about the use of pulmonary artery catheters and their complications. Pulmonary artery rupture carries high morbidity and mortality, and therefore a high index of suspicion and timely management are key to the survival of patients who suffer from this rare complication. While surgical therapy has been considered the mainstay of treatment, endovascular therapy is feasible when surgery is not possible or desirable, as demonstrated in our patient. It is unknown which approach is optimal.

Our approach to the ablation of atrioventricular nodal reciprocating tachycardia (AVNRT), the most common supraventricular tachycardia, is as follows: We first attempt ablation in the right atrial posteroseptum anterior to the coronary sinus ostium with a 4-mm non-irrigated tip catheter. If ablation within the triangle of Koch is unsuccessful with radiofrequency (RF), we switch to cryoablation and target a more superior (mid septal) region. We also utilize cryoablation if RF ablation produces transient VA block (absence of retrograde conduction during junctional rhythm) or a fast junctional rhythm (<350 msec). If cryoablation were to fail, or is not available, we would then suggest ablation within the coronary sinus targeting the roof (2-4 cm from the os) using a 3.5-mm irrigated tip catheter. If tachycardia were still inducible despite these measures, we would then proceed with transseptal puncture (given our greater experience with this over a retrograde aortic approach) and perform RF ablation along the posteroseptal left atrium and inferoseptal mitral annulus utilizing an irrigated tip catheter. In our experience, cryoablation reliably results in elimination of the slow pathway. The only left atrial ablation for AVNRT at our institution in the past year was performed because a patent foramen ovale allowed for rapid left atrial access, facilitating left atrial ablation of the slow pathway.

ABSTRACT. Mapping and ablating premature ventricular complexes (PVCs) that originate near the great cardiac vein (GCV) and anterior interventricular vein (AIV) can pose several challenges related to the advancement and positioning of catheters within these veins, the delivery of effective lesions, and the risk of collateral injury to the left coronary arteries and left phrenic nerve. When ablation of these PVCs from inside the GCV/AIV is not possible, a systematic assessment of nearby vantage points, such as the left coronary cusp (LCC) and left ventricular (LV) endocardial breakout site, should be considered, in addition to the performance of a more invasive epicardial ablation procedure via a percutaneous pericardial puncture or thoracotomy. Several electrocardiographic, anatomic, and electrogram timing features have been shown to predict the likelihood of successful ablation from a non-epicardial site, such as the LCC or LV endocardium, but none of these spots is considered to be a perfect location. The case described here in this report is a demonstration of a safe and successful ablation of GCV PVCs from the LV endocardial breakout site using adequate power and lesion duration, even when the site was 17 mm away from the putative origin, and some previously described electrocardiographic and electrogram-based predictors of success suggested the outcome would not be positive.