Search

Women with heart disease are at high risk for pregnancy complications. Obesity is an emergent health risk for women, and in the non-cardiac pregnant population, it has been shown to adversely impact the health of mother and baby. Therefore, we sought to determine if obesity increased maternal

Background— The therapeutic potential of renal denervation (RDN) for arrhythmias has not been fully explored. Detailed mechanistic evaluation is in order. The objective of the present study was to determine the antiarrhythmic potential of RDN in a postinfarct animal model and to determine whether any benefits relate to RDN-induced reduction of sympathetic effectors on the myocardium. Methods and Results— Pigs implanted with single-chamber implantable cardioverter defibrillators to record ventricular arrhythmias (VAs) were subjected to percutaneous coronary occlusion to induce myocardial infarction. Two weeks later, a sham or real RDN treatment was performed bilaterally using the St Jude EnligHTN basket catheter. Parameters of ventricular remodeling and modulation of cardio–renal sympathetic axis were monitored for 3 weeks after myocardial infarction. Histological analysis of renal arteries yielded a mean neurofilament score of healthy nerves that was significantly lower in the real RDN group than in sham controls; damaged nerves were found only in the real RDN group. There was a 100% reduction in the rate of spontaneous VAs after real RDN and a 75% increase in the rate of spontaneous VAs after sham RDN ( P =0.03). In the infarcted myocardium, presence of sympathetic nerves and tissue abundance of neuropeptide-Y, an indicator of sympathetic nerve activities, were significantly lower in the RDN group. Peak and mean sinus tachycardia rates were significantly reduced after RDN. Conclusions— RDN in the infarcted pig model leads to reduction of postinfarction VAs and myocardial sympathetic effectors. This may form the basis for a potential therapeutic role of RDN in postinfarct VAs.

Introduction: Changes in cardiac repolarization parameters such as QT interval and QT dispersion have been implicated in cardiac arrhythmogenesis following acute myocardial infarction (AMI). These parameters are susceptible to sympathetic modulation. We therefore hypothesized that renal sympathetic denervation (RDN) may produce potential anti-arrhythmic actions through its effects on cardiac repolarization. Methods: Fifteen pigs randomized to AMI & RDN (6 pigs), AMI & sham RDN (6 pigs) and sham MI & sham RDN (3 pigs) underwent percutaneous occlusion of the mid to distal LAD to achieve AMI. 2 weeks after infarction, the St. Jude EnligHTN® basket catheter was used to perform RDN bilaterally. Cardiac repolarization parameters were measured at 3 time points over the course of the 3 week study: baseline (immediately before MI), midpoint (2 weeks post MI; at time of RDN) and end (1 week post RDN). ECG data were acquired from limb leads. Results: In a ten beat span, the range in the durations of the QT interval was seen to increase from 18+/-7ms to 19+/-11ms in the real AMI & sham RDN group while in the real AMI & real RDN group it decreased from 17+/-5ms to 14+/-5ms (p=0.11). The mean QT interval which increased by 25% in the real AMI & sham RDN group saw only an 11% increase in the real AMI & real RDN group (p=0.048). The standard deviation of the average QT intervals post AMI, which quantifies the reduction in global dispersion of repolarization, saw a 41% decrease with RDN compared to an 8% decrease with sham RDN. The temporal dispersion of repolarization was also diminished by RDN. The dispersion of T wave peak to T wave end durations which increased in the real AMI & sham RDN group (from 15+/-6ms to 22+/-10ms), was decreased in the real AMI & real RDN group (from 19+/-7ms to 16+/-6ms) (p=0.05). T wave alternans values displayed no significant response to RDN (p=0.977). Conclusions: Adverse changes in cardiac repolarization parameters were attenuated via renal denervation in this post infarct pig model. These effects may mitigate post infarct arrhythmogenesis but require further study to evaluate the influence of local, reflex and circulating mediators.

Renal denervation (RDN) was primarily developed to treat hypertension and is potentially a new method for treating arrhythmias. Because of the lack of a standardized protocol to measure renal sympathetic nerve activity, RDN is administered in a blind manner. This inability to assess efficacy at the time of treatment delivery may be a large contributor to the ambiguity of RDN outcomes reported in the hypertension literature. The advancement of RDN as a treatment of hypertension or arrhythmias will be hampered by the lack of delivery assessment, a deficiency that the cardiovascular electrophysiology community, with its expertise in recording and mapping, may have a role in addressing and overcoming. The development of endovascular recording of renal nerve action potentials may provide a useful accessory tool for RDN. Innovation in this area will be crucial as we as a community reconsider the therapeutic value of RDN.