Spinal cord stimulation (SCS) is efficacious for pain due to injury of peripheral nerves, and therefore models of mononeuropathy appear to be particularly suitable for an experimental approach to the study of mechanisms underlying the clinical effect of this mode of treatment in chronic neuropathic pain. Virtually all previous experimental studies on SCS have utilized acute and nociceptive types of peripheral pain stimuli to explore the attenuating effects of SCS. In the present study we made use of the two models of supposedly painful neuropathy developed by Bennett and Xie (1988) and Seltzer et al. (1990) to explore the effect of SCS applied with stimulus parameters similar to those used in clinical practice. In rats subjected to ligatures of the sciatic nerve according to these two methods, SCS was applied via chronically implanted electrodes, or acutely via a laminectomy in the lower thoracic region. In awake, freely moving animals SCS produced a marked increase of the withdrawal thresholds to innocuous mechanical stimuli in the form of von Frey filaments. This threshold elevation lasted for up to 40 min after 10 min of SCS. In about one-half of the animals there was also a moderate, but short-lasting increase in the intact leg. The degree and duration of the withdrawal threshold elevation was clearly related to the intensity of SCS which was kept below the level of which a response in the thoracic or leg musculature was produced. In a second series of experiments the effect of SCS, applied acutely via a laminectomy, on the early component (latency: 8-12 msec) of the flexor reflex was studied. As a result of nerve ligation with either of the methods used, the thresholds for evoking the early as well as the late component in the nerve-ligated leg were significantly lower than in the intact one. SCS resulted in a marked and long-lasting increase of the threshold of the early component in the nerve-ligated leg. On the intact side only a slight and short-lasting increase was observed. The late, C fibre-mediated component was not influenced by SCS. The first component of the flexor reflex is conceivably mediated by A beta-fibre activation and it presumably corresponds to the withdrawal response induced by innocuous mechanical stimuli. The lack of effect of SCS on the late reflex component indicates that it selectively influences transmission of A-fibre activity. (ABSTRACT TRUNCATED AT 400 WORDS)

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Calcification of the aortic annulus is associated with a subsequent eccentric shape of the CoreValve prosthesis. This eccentric shape results in more PVL, with the localization of PVL related to the shape of stent frame eccentricity.

The current improved version of the automated adaptive algorithm is accurate for the assessment of left heart chamber volumes, albeit a small underestimation of left ventricular end-diastolic volume is seen, when compared with manual 3D echocardiography.

In spite of the routine usage of spinal cord stimulation (SCS) as treatment of chronic pain, there is an insufficient understanding of the mechanisms underlying its effect. The method was originally developed as a spin-off from experiments demonstrating the inhibitory control of nociceptive signals by the activation of large afferent fibers, and on the basis of these findings the gate-control theory was advanced. Later experiments showed that stimulation of the dorsal columns can inhibit the relay of nociceptive impulses to second-order neurons in the dorsal horn. It should be emphasized that all these experiments were performed with acute noxious stimuli; it is now universally recognized that SCS in patients is preferentially, or exclusively, effective for chronic neuropathic types of pain. For these and other reasons the mode of action of SCS in clinical pain cannot be inferred from these early animal experiments. In ongoing studies we have used animal models of mononeuropathy (rat) in which we have applied SCS acutely or chronically with stimulation parameters similar to those used in patients. In these animals the first component of the flexor reflex appears with a lower stimulus threshold in the nerve lesioned than in the intact, sham-operated leg. SCS was applied at the approximate level of Th-XII during 10–20 min and produced a marked augmentation of the stimulus threshold. This abnormally high threshold was not normalized until 30–60 min after the end of SCS. In awake animals SCS was applied via an implanted spinal electrode and the effect on behavior changes associated with mononeuropathy was studied. There are several behavioral and neurological features of animal models of mononeuropathy resembling those associated with pain due to peripheral nerve injury in patients. Therefore, this model is particularly suitable for studies aiming at the exploration of mechanisms involved in SCS as treatment of chronic pain.

Overall, haemodynamic performance was comparable between the Lotus and SAPIEN3 valves. Lotus valve required less oversizing and was associated with less PAR than SAPIEN3.

Spinal cord stimulation (SCS) has been increasingly used in the treatment of ischemia caused by obliterative diseases in the extremities and in the cardiac circulation. The most promising effects have been obtained when physicians suspect that a major vasospastic component underlies the ischemic symptoms (e.g., as in Raynaud's disease). Despite the clinical success of this treatment method, little is known about the mechanisms underlying the pain relief it produces and its anti-ischemic effects. Most earlier experimental studies have used normal animals or animals with cerebral vasospasm induced by injection of autologal blood into the cerebrospinal fluid space. In the present study, we applied SCS in a rat model via implanted electrodes to study the effect of preemptive stimulation on the ischemia caused by vasospasm in a neurovascular flap in the groin; the vasospasm was induced by mechanical pressure applied to the feeding artery. In rats treated with SCS, delivered with parameters similar to those used clinically, the percentage of flaps recovering normal microcirculation after the spasm was significantly higher than in the untreated control group (100 and 28%, respectively; P < 0.05), and the maximal blood flow after the ischemic episode was significantly higher in the SCS group than in the control group (127 and 51 arbitrary units, respectively; P < 0.05). The percentage of animals regaining the premanipulation circulation after the provocation of a second spasm was also greater in the SCS-treated group than in the control animals (50 and 14%, respectively; P < 0.05). Pilot studies showed that this protective effect was specific to SCS given before spasm induction, an observation corroborated by clinical experiences.(ABSTRACT TRUNCATED AT 250 WORDS)

Patients in coronary intervention trials may require more than 1 procedure to complete the intended revascularization strategy. However, these staged interventions are not consistently defined. Standardized definitions are needed to allow meaningful comparisons of this outcome among trials. This document provides guidance on relevant parameters involving staged procedures, including minimum data collection and consistent classification of coronary procedures initially identified as staged; the aim is to achieve consistency among clinical trialists, sponsors, health authorities, and regulators. Definitions were developed jointly among representatives of academic institutions and clinical research organizations based on clinical trial experience and published literature. Reasons for staged procedures were identified and include baseline kidney function, contrast load and radiation exposure, lesion complexity, and patient or operator fatigue. Moreover, nonclinical reasons include procedure scheduling and reimbursement. Management of staged procedures should be a standalone section in clinical trial protocols and clinical events committee charters. These documents should clearly define a time window for staged procedures that allows latitude for local policies, while respecting accepted clinical guidelines, and consistency with study objectives. Investigators should document in the case report form the intent to stage a procedure, the lesions to be treated, and the reasons for staging, preferably before randomization. Ideally, all reinterventions, or at least all procedures performed after the recommended time window, those in which data suggest an anticipated procedure due to a worsening condition and those where a revascularization is attempted in the target vessel, should be reviewed by an independent clinical events committee.