Ablation using 3D maps adjusted for spatial displacement of premature ventricular complexes relative to sinus beats: Improving precision by correcting for the shift.

INTRODUCTION: Point-by-point 3-dimensional (3D) electroanatomic mapping (EAM) is used to guide catheter ablation of premature ventricular complexes (PVCs). Due to the differences in the spatial excursion of the cardiac chambers during cardiac cycles in PVCs vs sinus rhythm, the 3D location registration during PVCs is shifted relative to sinus rhythm. In this study, we describe our strategy to adjust for this displacement in real-time during PVC mapping. METHODS AND RESULTS: We report 21 patients who underwent catheter ablation of 23 unique PVCs using Carto 3. After mapping the earliest site for each PVC, we reregistered its 3D location to a sinus rhythm beat in real-time, and used this to guide ablation lesion delivery. The PVC earliest location was spatially displaced from the successful ablation lesion in sinus rhythm by average 6.7 (range 3.3-13.0) mm. Offline, we subsequently analyzed 25 unique chamber maps and 606 PVC points. For each point, we reregistered the 3D location to a preceding sinus beat. The PVC points were displaced from sinus rhythm location by average 4.4 (0.3-13.7) mm. The maximally displaced point for each chamber was 7.7 (4.7-13.7) mm. The general direction of shift during PVC was leftward and inferior relative to sinus rhythm. CONCLUSIONS: During electroanatomic mapping of PVCs using the Carto 3 system, points mapped during PVCs are spatially displaced relative to their location in sinus rhythm. Electrophysiologists should recognize this phenomenon and account for the shift to guide accurate delivery of ablation lesions.

Pacemaker Dependency after Cardiac Surgery: A Systematic Review of Current Evidence.

BACKGROUND: Severe postoperative conduction disturbances requiring permanent pacemaker implantation frequently occur following cardiac surgery. Little is known about the long-term pacing requirements and risk factors for pacemaker dependency in this population. METHODS: We performed a systematic review of the literature addressing rates and predictors of pacemaker dependency in patients requiring permanent pacemaker implantation after cardiac surgery. Using a comprehensive search of the Medline, Web of Science and EMBASE databases, studies were selected for review based on predetermined inclusion and exclusion criteria. RESULTS: A total of 8 studies addressing the endpoint of pacemaker-dependency were identified, while 3 studies were found that addressed the recovery of atrioventricular (AV) conduction endpoint. There were 10 unique studies with a total of 780 patients. Mean follow-up ranged from 6-72 months. Pacemaker dependency rates ranged from 32%-91% and recovery of AV conduction ranged from 16%-42%. There was significant heterogeneity with respect to the definition of pacemaker dependency. Several patient and procedure-specific variables were found to be independently associated with pacemaker dependency, but these were not consistent between studies. CONCLUSIONS: Pacemaker dependency following cardiac surgery occurs with variable frequency. While individual studies have identified various perioperative risk factors for pacemaker dependency and non-resolution of AV conduction disease, results have been inconsistent. Well-conducted studies using a uniform definition of pacemaker dependency might identify patients who will benefit most from early permanent pacemaker implantation after cardiac surgery.

Endothelial dysfunction in chronic inflammatory diseases.

Chronic inflammatory diseases are associated with accelerated atherosclerosis and increased risk of cardiovascular diseases (CVD). As the pathogenesis of atherosclerosis is increasingly recognized as an inflammatory process, similarities between atherosclerosis and systemic inflammatory diseases such as rheumatoid arthritis, inflammatory bowel diseases, lupus, psoriasis, spondyloarthritis and others have become a topic of interest. Endothelial dysfunction represents a key step in the initiation and maintenance of atherosclerosis and may serve as a marker for future risk of cardiovascular events. Patients with chronic inflammatory diseases manifest endothelial dysfunction, often early in the course of the disease. Therefore, mechanisms linking systemic inflammatory diseases and atherosclerosis may be best understood at the level of the endothelium. Multiple factors, including circulating inflammatory cytokines, TNF-α (tumor necrosis factor-α), reactive oxygen species, oxidized LDL (low density lipoprotein), autoantibodies and traditional risk factors directly and indirectly activate endothelial cells, leading to impaired vascular relaxation, increased leukocyte adhesion, increased endothelial permeability and generation of a pro-thrombotic state. Pharmacologic agents directed against TNF-α-mediated inflammation may decrease the risk of endothelial dysfunction and cardiovascular disease in these patients. Understanding the precise mechanisms driving endothelial dysfunction in patients with systemic inflammatory diseases may help elucidate the pathogenesis of atherosclerosis in the general population.

Acute carpal tunnel syndrome caused by diffuse giant cell tumor of tendon sheath: a case report.

A 46-year-old male developed spontaneous acute carpal tunnel syndrome of the right wrist without any antecedent trauma. Surgical exploration revealed hemorrhage secondary to diffuse giant cell tumor of tendon sheath as the underlying cause.

The prevalence of hereditary neuropathy with liability to pressure palsies in patients with multiple surgically treated entrapment neuropathies.

PURPOSE: Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal-dominant peripheral neuropathy that results from deletion of a 1.5-Megabase pair (Mb) segment of the short arm (p) of chromosome 17. Hereditary neuropathy with liability to pressure palsies increases susceptibility of peripheral nerves to pressure and trauma and can be associated with symptoms at multiple anatomic entrapment sites. Many patients present with multiple upper-extremity entrapment neuropathies and the etiology is uncertain. We hypothesized that some of these patients have an underlying hereditary neuropathy. The purpose of this study was to determine the prevalence of HNPP in patients with multiple surgically treated upper-extremity entrapment neuropathies. METHODS: The inclusion criterion for the study was history of more than 1 carpal tunnel release and/or ulnar nerve transposition. The exclusion criteria were history of diabetes or history of Charcot-Marie-Tooth neuropathy. Fifty-nine patients were in the study group. Two patients known to have the 17p11.2 deletion were used as controls. Genomic DNA was extracted from peripheral blood. Each sample was genotyped using polymerase chain reaction (PCR) amplification with short tandem repeat polymorphism markers within the 1.5-Mb region of 17p deleted in HNPP. Markers were scored as homozygous or heterozygous after resolution by polyacrylamide gel electrophoresis and silver staining. RESULTS: The 2 control patients were homozygous for 11 markers. None of the 59 study patients were homozygous for all markers tested in the deleted region. No study patient had the 17p deletion diagnostic for HNPP. Based on the sample size of 59 patients the 95% confidence interval for the prevalence of the 17p11.2 deletion in this population is 0% to 5%. CONCLUSIONS: We found no evidence for an association between HNPP and patients who have multiple surgical releases for upper-extremity entrapment neuropathies.

The effects of graded compression of the median nerve in the carpal canal on grip force.

The relationship between tactile hypoesthesia and precision grip force was examined using compression of the median nerve in healthy adults. Hypoesthesia was graded by varying the pressure that an external clamp exerted over the carpal canal. Electrical stimulation of the median nerve in the forearm evoked a compound sensory nerve action potential (SNAP) that we recorded from the digital nerves of the index finger. Clamp pressure was varied to achieve SNAPs that were 75%, 50%, and 25% of precompression amplitude (100%). Grip force and tactile sensibility (Semmes-Weinstein filaments, cotton wisps, sharp/dull) did not change in parallel with reductions of the SNAP. Subjects reported paresthesias at the thumb and index finger at 75% SNAP. Tactile pressure thresholds increased to the clinical range of 'diminished light touch', but subjects detected cotton wisps stroked along the finger. At 75% SNAP grip force did not change compared to 100% SNAP. Simple prehension can proceed efficiently despite these modest reductions in tactile signals. At 50% SNAP the digits remained sensate, but were reported to feel "thick, like cardboard". No subject could detect cotton wisps and tactile thresholds increased by one filament. Sharp/dull distinctions remained. Grip force increased by 55% compared to grip force at SNAPs of 100% and 75%. There were no changes in skin slipperiness, so the increased grip force represented elevated 'safety margin' (grip force exceeding that needed to prevent slip). At 25% SNAP subjects described the skin innervated by the median nerve as feeling "numb", but grip force increased little compared to 50% SNAP. Grip force continued to reflect changes in grip surface friction, and mechanical transients from setting the object on the table triggered coordinated reductions in grip force. We suspect that the loss of information from SA I and FA I, but not FA II, tactile afferents provoked the increased grip force.

Recurrent carpal tunnel syndrome.

Persistent or recurrent symptoms following carpal tunnel release surgery are an infrequent but challenging clinical problem. A thorough evaluation of these patients is mandatory and must confirm the accuracy of the original diagnosis and rule out the presence of concurrent conditions or disorders that may cause persistent symptoms that mimic carpal tunnel syndrome. If an alternative explanation of the patients' symptoms cannot be identified, and if conservative care is ineffective, then surgical treatment should be considered. Adequate exposure of the median nerve and carpal tunnel are mandatory. The general approach should include gentle mobilization of the nerve from adherent scar tissue and interposition of a biologic barrier between the nerve and surrounding tissues. No published data conclusively demonstrate that internal neurolysis provides superior results. Postoperative care should include early mobilization to encourage tendon and nerve gliding.

Practical Management of Carpal Tunnel Syndrome.

Carpal tunnel syndrome can result from occupational or recreational overuse. Cycling, rowing, and weight lifting are examples of sports that can provoke or exacerbate the syndrome. A detailed sensory examination, motor testing, and provocative tests such as Phalen's maneuver are essential. Nerve conduction studies may also be useful. Conservative treatment is usually attempted first. Modification of technique and equipment, together with use of a splint, often allows patients to continue their desired activities. In selected cases, carpal tunnel release is effective, but complication rates are high.