The perspective of the vascular surgery trainee on new ACGME regulations, fatigue, resident training, and patient safety.

OBJECTIVE: To assess the opinions of vascular surgery trainees on the new Accreditation Council for Graduate Medical Education (ACGME) guidelines. METHODS: A questionnaire was developed and electronically distributed to trainee members of the Society for Vascular Surgery. RESULTS: Of 238 eligible vascular trainees, 38 (16%) participated. Respondents were predominantly 30 to 35 years of age (47%), male (69%), in 2-year fellowship (73%), and at large academic centers (61%). Trainees report occasionally working while fatigued (63%). Fellows were more likely to report for duty while fatigued (P = .012) than integrated vascular residents. Respondents thought further work-hour restrictions would not improve patient care or training (P < .05) and may not lead to more sleep or improved quality of life. Respondents reported that duty hours should vary by specialty (81%) and allow flexibility in the last years of training (P < .05). CONCLUSIONS: Vascular surgery trainees are concerned about further duty-hour restrictions on patient care, education, and training and fatigue mitigation has to be balanced against the need to adequately train vascular surgeons.

FRNK overexpression limits the depth and frequency of vascular smooth muscle cell invasion in a three-dimensional fibrin matrix.

Pathological vascular smooth muscle cell (VSMC) behavior after vascular interventions such as angioplasty or bypass is initiated within the 3D environment of the vessel media. Here VSMCs proliferate, invade the surrounding matrix, migrate adluminally, and deposit substantial amounts of matrix, leading to myointimal hyperplasia and decreased blood flow to critical organs and tissue. Since focal adhesion kinase (FAK) mediates many of the VSMC responses to these pathologic events, it provides a reasonable pharmacologic target to limit this invasive VSMC behavior and to better understand the cellular pathophysiology of this disease. Here we quantified the effectiveness of disabling FAK in VSMCs with its dominant-negative inhibitor, FAK-related nonkinase (FRNK), in a clinically relevant 3D assay. We found that FRNK overexpression decreased VSMC invasion (both the length and frequency) in this matrix. These effects were demonstrated in the presence and absence of chemical mitotic inhibition, suggesting that FAK's effect on cellular matrix invasion, migration, and proliferation utilize separate and/or redundant signaling cascades. Mechanistically, FAK inhibition decreased its localization to focal adhesions which led to a significant decrease in FAK autophosphorylation and the phosphorylation of the serine/threonine kinase, AKT. Together these findings suggest that disruption of FAK signaling may provide a pharmaceutical tool that limits pathological VSMC cell behavior.

Cardiovascular gene delivery: The good road is awaiting.

Atherosclerotic cardiovascular disease is a leading cause of death worldwide. Despite recent improvements in medical, operative, and endovascular treatments, the number of interventions performed annually continues to increase. Unfortunately, the durability of these interventions is limited acutely by thrombotic complications and later by myointimal hyperplasia followed by progression of atherosclerotic disease over time. Despite improving medical management of patients with atherosclerotic disease, these complications appear to be persisting. Cardiovascular gene therapy has the potential to make significant clinical inroads to limit these complications. This article will review the technical aspects of cardiovascular gene therapy; its application for promoting a functional endothelium, smooth muscle cell growth inhibition, therapeutic angiogenesis, tissue engineered vascular conduits, and discuss the current status of various applicable clinical trials.

Are your arteries older than your age?

PURPOSE: To determine the effect of age and atherosclerotic risk factors on the carotid intima-media layer thickness and morphology characteristics. PATIENTS AND METHODS: Three groups of subjects were included in the study: Individuals with atherosclerotic risk factors including a family history of CHD, hypertension, hyperlipidemia, diabetes, and/or smoking (group A, n=180), age- and sex-matched healthy subjects without risk factors (group B, n=60) and a group of significantly younger volunteers (group C, n=25). The carotid artery was imaged longitudinally with B-mode ultrasound. Intima media thickness (IMT) was measured in the common (CCA) and internal carotid (ICA) arteries. Surface irregularity and continuity of the intima-media layer (IML) were assessed by high definition imaging. Echogenicity of the wall was quantified using Adobe Photoshop. The presence of calcium deposits was recorded. The double line wall pattern seen in young healthy people was used as a control to assess patterns and texture of the carotid IML. Fifteen subjects had their measurements repeated for intraobserver variability. RESULTS: IMT measurements were reproducible in both the CCA and ICA (coefficient of variation 6% and 9%). IMT increased linearly with age (adjusted R(2)=0.72, p<0.0001), which was also an independent risk factor for increased IMT. All the risk factors had a significant association with increased IMT. In the lowest (third) decade the wall/blood interface was smooth and the double line was visualized with an echolucent center. With increased age and number of risk factors present, the wall/blood interface became more irregular (p<0.01), the double line was distorted (p<0.01) and the IML was more echogenic (p<0.01). The increase in IMT and the changes in the echogenicity of the IML were more pronounced in the ICA. CONCLUSIONS: Age is an independent risk factor for increased IMT. Atherosclerotic risk factors are associated with the age-related changes seen in the IML. Such changes are also seen in younger asymptomatic volunteers with risk factors indicating that their arteries are older than their age.