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Introduction: Advances in decision support have allowed for simulated medical decision making on a population. These models allow for simulation of policy implementation in disease management. Avoidance of high insulin therapy is frequently mentioned as a preferred strategy for the management of type 2 diabetes. Methods: Using the GlucosePATH decision support software, a sample of 368 patients drawn from the software’s database was clinically and economically optimized for scenarios matching the full therapeutic options, a scenario excluding sulfonylurea and glinides (NoSU), and a scenario excluding high dose insulin, sulfonylurea and glinides (LowInsulin). Results: Baseline patient data showed an A1c of 8.7% with mean monthly cost of $28 on standard commercial insurance, $84 on basic commercial insurance, and $354 on Medicare. Optimized with full options resulted in an estimated A1c 7.0% on standard, 7.2% on basic, and 7.5% on Medicare. Monthly cost was on $73 on standard, $168 on basic, and $371 on Medicare. Both the NoSU and LowInsulin scenarios did not show significant difference for basic or standard commercial insurance in terms of cost and A1c. In Medicare, A1c was unchanged for the NoSU model, but increased to 7.8% (+0.3%, p=0.01) in the LowInsulin model. Cost increased to $412 in NoSU model(+$41, p=0.004) and $445 in LowInsulin model (+$64, p=0.015). In the basic commercial and Medicare plan, TZD and insulin use increased. Use of incretin and SGLT2 agents did not demonstrate significant change. Discussion: Traditional commercial models allow for near ideal implementation of modern diabetes strategies in terms of patient cost, challenges develop when coinsurance or shared-risk models are implemented. It will be important to be able to measure benefit in longitudinal economic terms in addition to laboratory markers. Disclosure B. Eilerman: Advisory Panel; Self; Dexcom, Inc., Medtronic. Speaker's Bureau; Self; AbbVie Inc., AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Corcept Therapeutics, Janssen Pharmaceuticals, Inc., Lilly Diabetes, Novo Nordisk Inc. Stock/Shareholder; Self; PATH Decision Support Software LLC. L.J. Testa: Stock/Shareholder; Self; PATH Decision Support Software LLC. M. Canos: None.

Evaluation fellows from the George Washington University School of Public Health and Health Services conducted an evaluation of the Road to Recovery program of the Mid-Atlantic division of the American Cancer Society. The evaluation included qualitative analysis of program operation, mailed surveys, in-depth interviews with patients and drivers, and interviews with social workers from treatment centers. Results indicated that patients and drivers were satisfied with the program. Patients appreciated the ability of drivers to provide personalized, reliable service. The recruitment of sufficient drivers to meet transportation demand was a problem. High staff turnover and a lack of electronic tracking of standard information hindered program monitoring. A Mid-Atlantic Advisory Transportation Group reviewed the findings and made recommendations for service improvement. The Mid-Atlantic division evaluation contributed to an "evaluation synthesis" in which participants from the three divisions that had conducted Road to Recovery evaluations examined study data and made recommendations for reorganizing the national transportation program. A Transportation Program Design Team then held fact-finding meetings and adopted goals and objectives for a new national transportation program. The primary lesson learned was the far-reaching effects that a single program evaluation may have for various stakeholders and for an organization.

Background High-resolution intravascular ultrasound (IVUS) performed immediately after stent deployment often reveals dissection at the stent margin that may not be appreciated by angiography. However, the natural history of these edge dissections is unknown. These intimal disruptions at the stent margins have been previously reported to occur in 5% to 23% of stent implantations. The short-term prognosis of these lesions appears to be good; however, the longer-term effect on restenosis and/or vessel remodeling is not known. We therefore studied a cohort of patients with the use of IVUS immediately after stent implantation and at 6 months to assess the incidence and prognosis of coronary edge dissections. Methods and Results One hundred fifty patients undergoing Palmaz-Shatz stent implantation were imaged with IVUS with the use of a motorized pullback, and the incidence of edge dissections was determined and graded according to depth and circumferential extent. Arterial and lesional morphometric parameters were assessed by digital planimetry. Six-month IVUS images were aligned with the poststent IVUS to determine the natural history of these lesions. Sixteen (10.7%) of 150 had edge tears. All were angiographically silent. Most lesions (n = 9) were superficial intimal tears. Vessel, lumen, and plaque area were similar in the nondissection and dissection groups in both the proximal and distal reference segments. Plaque eccentricity was likewise similar in both groups. At 6 months, lesions (n = 12) healed without a change in plaque burden, undergoing a “tacking down” process. Vessel area (19.1 ± 6.4 vs 18.4 ± 7.1 mm2, P = not significant), lumen area (8.2 ± 4.1 vs 9.2 ± 4.0 mm2, P = not significant), and plaque area (10.0 ± 3.3 vs 9.8 ± 3.3 mm2, P = not significant) were unchanged when compared with the lesion site taken at stent deployment. Conclusions Edge dissections as detected by IVUS do not necessarily proscribe an adverse prognosis at 6 months. This finding may provide reassurance to interventionalists because these lesions are frequently seen by IVUS after stent deployment. Further studies are warranted to precisely define specific morphometric features of edge dissections that affect the long-term clinical outcome. (Am Heart J 2000;139:59-63.)

We used paired transcranial magnetic stimulation (TMS) to evaluate inhibitory mechanisms in eight patients with writer's cramp during rest and isometric wrist extension. Both stimuli were 110% of the motor threshold; the interstimulus intervals (ISIs) were 20 to 200 ms in increments of 10 ms. Surface EMG was recorded from wrist extensors. In the symptomatic hemisphere, there was no significant difference in the amplitude of the test (second) motor evoked-potential (MEP) between patients and age-matched controls at rest. However, with voluntary muscle activation, inhibition of the test MEP by the conditioning MEP was significantly less in writer's cramp patients than in controls (p = 0.02). The difference was most prominent at ISIs of 60 to 80 ms in which inhibition is maximum. In the asymptomatic hemisphere, there was no significant difference between patients and controls in both rest and active conditions. The silent period was shorter in patients than controls on the symptomatic side (p = 0.003) but not on the asymptomatic side. We conclude that the inhibitory effects induced by magnetic stimulation are reduced in patients with writer's cramp, but only on the symptomatic side during muscle activation. This may relate to the overflow of muscle activity that characterizes this condition.

We studied the effects of a loading dose of phenytoin on motor cortex excitability in five healthy volunteers. Phenytoin elevated motor thresholds to transcranial magnetic stimulation (TMS) in all subjects, but had no effects on motor-evoked potential amplitudes, silent period durations, and intracortical excitability tested by paired TMS during rest and voluntary muscle activation. These results are consistent with the hypothesis that blockade of voltage-gated sodium channels decreases membrane excitability and elevates the threshold to TMS, but will not reduce intracortical excitability.

Intimal hyperplasia within the body of the stent is the primary mechanism for in-stent restenosis; however, stent edge restenosis has been described after brachytherapy. Our current understanding about the magnitude of in vivo intimal hyperplasia and edge restenosis is limited to data obtained primarily from select, symptomatic patients requiring repeat angiography. The purpose of this study was to determine the extent and distribution of intimal hyperplasia both within the stent and along the stent edge in relatively nonselect, asymptomatic patients scheduled for 6-month intravascular ultrasound (IVUS) as part of a multicenter trial: Heparin Infusion Prior to Stenting. Planar IVUS measurements 1 mm apart were obtained throughout the stent and over a length of 10 mm proximal and distal to the stent at index and follow-up. Of the 179 patients enrolled, 140 returned for repeat angiography and IVUS at 6.4 ± 1.9 months and had IVUS images adequate for analysis. Patients had 1.2 ± 0.6 Palmaz-Schatz stents per vessel. There was a wide individual variation of intimal hyperplasia distribution within the stent and no mean predilection for any location. At 6 months, intimal hyperplasia occupied 29.3 ± 16.2% of the stent volume on average. Lumen loss within 2 mm of the stent edge was due primarily to intimal proliferation. Beyond 2 mm, negative remodeling contributed more to lumen loss. Gender, age, vessel location, index plaque burden, hypercholesterolemia, diabetes, and tobacco did not predict luminal narrowing at the stent edges, but diabetes, unstable angina at presentation, and lesion length were predictive of in-stent intimal hyperplasia. In a non-radiation stent population, 29% of the stent volume is filled with intimal hyperplasia at 6 months. Lumen loss at the stent edge is due primarily to intimal proliferation.

Women have worse outcomes after myocardial infarction and coronary revascularization. The explanations are likely multifactorial but may include smaller coronary artery size. Smaller luminal diameter has been confirmed angiographically; however, because of possible confounding effects of coronary remodeling, angiographically silent atherosclerosis, and body size, it is unclear if there is a true sex influence on arterial size.We performed intravascular ultrasound on left main (LM) and proximal left anterior descending (LAD) coronary artery segments that were free of significant atherosclerosis in 50 men and 25 women. Arterial and luminal areas were measured by planimetry and corrected for body surface area. We evaluated associations between sex and coronary dimensions with univariate and then multiple linear regression analyses.Mean uncorrected LM and LAD arterial areas were smaller in women than in men (21.53 vs 26.95 mm(2), P.001, and 14. 68 vs 19.94 mm(2), P =.002, respectively), as were mean LM and LAD luminal areas (15.94 vs 18.79 mm(2), P =.020, and 10.13 vs 12.71 mm(2), P =.036, respectively). In multivariate models accounting for body surface area and controlling for other factors, sex independently predicted corrected LM and LAD arterial area. In analyses that additionally controlled for plaque area, sex independently predicted corrected LAD luminal area.LM and LAD arteries are smaller in women, independent of body size. This suggests an intrinsic sex effect on coronary dimensions. Future studies should investigate underlying mechanisms because they may lead to novel therapeutic strategies and improved outcomes for women with coronary artery disease.

We have previously described post-exercise facilitation and post-exercise depression of motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS). To determine the presence of post-exercise facilitation after exercise of a contralateral muscle, MEPs were recorded from the resting right extensor carpi radialis (ECR) muscle while the left ECR muscle was activated, then immediately after brief left ECR activation, and, finally, immediately after brief right ECR activation. We repeated the experiment using the first dorsal interosseous (FDI) muscle. To determine the presence of post-exercise depression after exercise of a contralateral muscle, MEPs were recorded from the right ECR after prolonged exercise of the left ECR, followed by right ECR recording after its fatigue. The mean MEP amplitudes from the right ECR and the right FDI after brief activation were 187% and 266% of their pre-exercise values, respectively. There were no significant changes in MEPs recorded from the right ECR or FDI muscles during or immediately after brief activation of their left counterparts. The mean amplitude of MEPs recorded from the right ECR after it fatigued was approximately half the pre-exercise value, but there was no significant change in MEPs recorded from the right ECR after prolonged exercise of the left ECR. Therefore, neither post-exercise facilitation nor post-exercise depression occurred after contralateral homologous muscle exercise.