Purpose Perivascular adipose tissue (PVAT) surrounds the arterial adventitia and plays an important role in vascular homeostasis. PVAT expands in obesity, and inflamed PVAT can locally promote endothelial dysfunction and atherosclerosis. Here, using adipose tissue transplantation, we tested the hypothesis that expansion of PVAT can also remotely exacerbate vascular disease. Methods Fifty milligrams of abdominal aortic PVAT was isolated from high-fat diet (HFD)-fed wild-type mice and transplanted onto the abdominal aorta of lean LDL receptor knockout mice. Subcutaneous and visceral adipose tissues were used as controls. After HFD feeding for 10 weeks, body weight, glucose/insulin sensitivity, and lipid levels were measured. Adipocytokine gene expression was assessed in the transplanted adipose tissues, and the thoracic aorta was harvested to quantify atherosclerotic lesions by Oil-Red O staining and to assess vasorelaxation by wire myography. Results PVAT transplantation did not influence body weight, fat composition, lipid levels, or glucose/insulin sensitivity. However, as compared with controls, transplantation of PVAT onto the abdominal aorta increased thoracic aortic atherosclerosis. Furthermore, PVAT transplantation onto the abdominal aorta inhibited endothelium-dependent relaxation in the thoracic aorta. MCP-1 and TNF-α expression was elevated, while adiponectin expression was reduced, in the transplanted PVAT tissue, suggesting augmented inflammation as a potential mechanism for the remote vascular effects of transplanted PVAT. Conclusions These data suggest that PVAT expansion and inflammation in obesity can remotely induce endothelial dysfunction and augment atherosclerosis. Identifying the underlying mechanisms may lead to novel approaches for risk assessment and treatment of obesity-related vascular disease.

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Objective The aim of the study was to study the feasibility, safety, and efficacy of transesophageal echocardiography–guided intraoperative left ventricular lead placement via a video-assisted thoracoscopic surgery approach in patients with failed conventional biventricular pacing. Methods Twelve patients who could not have the left ventricular lead placed conventionally underwent epicardial left ventricular lead placement by video-assisted thoracoscopic surgery. Eight patients had previous chest surgery (66%). Operative positioning was a modified far lateral supine exposure with 30-degree bed tilt, allowing for groin and sternal access. To determine the optimal left ventricular location for lead placement, the left ventricular surface was divided arbitrarily into nine segments. These segments were transpericardially paced using a handheld malleable pacing probe identifying the optimal site verified by transesophageal echocardiography. The pacing leads were screwed into position via a limited pericardiotomy. Results The video-assisted thoracoscopic surgery approach was successful in all patients. Biventricular pacing was achieved in all patients and all reported symptomatic benefit with reduction in New York Heart Association class from III to I–II ( P = 0.016). Baseline ejection fraction was 23 ± 3%; within 1-year follow-up, the ejection fraction increased to 32 ± 10% ( P = 0.05). The mean follow-up was 566 days. The median length of hospital stay was 7 days with chest tube removal between postoperative days 2 and 5. Conclusions In patients who are nonresponders to conventional biventricular pacing, intraoperative left ventricular lead placement using anatomical and functional characteristics via a video-assisted thoracoscopic surgery approach is effective in improving heart failure symptoms. This optimized left ventricular lead placement is feasible and safe. Previous chest surgery is no longer an exclusion criterion for a video-assisted thoracoscopic surgery approach.

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