A retrospective study of open thoracotomies versus thoracoscopic surgeries for persistent postthoracotomy pain.

OBJECTIVE: Persistent thoracotomy pain syndrome (PTPS) is a recognized complication and is considered to be less after video-assisted thoracoscopic surgery (VATS) compared with open thoracic surgery (OTS). The primary objective was to compare the incidence of PTPS at 6 months. Secondary objectives were to compare the incidence of neuropathic pain between VATS and OTS and to report perioperative factors associated with the development of PTPS. METHODS: This historical cohort study involved patient contact by a questionnaire regarding the presence of PTPS and its type. Patient, surgical, and analgesia factors were collected from health records, acute pain, and thoracic surgery databases. The data were analyzed using a multivariable logistic regression analysis, with results reported as adjusted odds ratio (OR) (95% confidence interval; P value). RESULTS: Of 308 patients, 130 returned their questionnaire, and 106 responses were analyzed. The incidence of PTPS was 35% and 54% with VATS and OTS respectively, with an adjusted OR, 0.33 (95% confidence interval, 0.13-0.86), P= .024. The percentage of neuropathic pain was 18% and 48%, with VATS and OTS respectively, with an adjusted OR, 0.18 (0.04-0.85), P= .031. The diagnosis of cancer and previous chronic pain history were observed to be significantly associated with PTPS. CONCLUSIONS: Our study indicates that PTPS is significantly more common and has a higher chance of being neuropathic with OTS. Despite being relatively less traumatic, VATS still carries a significant potential for PTPS. A diagnosis of cancer and history of previous pain are highly predictive of its development.

SR-BI in bone marrow derived cells protects mice from diet induced coronary artery atherosclerosis and myocardial infarction.

SR-BI deficient mice that are also hypomorphic for apolipoprotein E expression develop diet induced occlusive coronary artery atherosclerosis, myocardial infarction and early death. To test the role of SR-BI in bone marrow derived cells, we used bone marrow transplantation to generate SR-BI-null; apoE-hypomorphic mice in which SR-BI expression was restored solely in bone marrow derived cells. SR-BI-null; apoE-hypomorphic mice were transplanted with SR-BI(+/+)apoE-hypomorphic, or control, autologous SR-BI-null; apoE-hypomorphic bone marrow. Four weeks later, mice were fed a high-fat, high-cholesterol, cholate-containing diet to induce coronary artery atherosclerosis. Mice transplanted with autologous bone marrow developed extensive aortic atherosclerosis and severe occlusive coronary artery atherosclerosis after 4 weeks of feeding. This was accompanied by myocardial fibrosis and increased heart weights. In contrast, restoration of SR-BI expression in bone marrow derived-cells reduced diet induced aortic and coronary artery atherosclerosis, myocardial fibrosis and the increase in heart weights in SR-BI-null; apoE-hypomorphic mice. Restoration of SR-BI in bone marrow derived cells did not, however, affect steady state lipoprotein cholesterol levels, but did reduce plasma levels of IL-6. Monocytes from SR-BI-null mice exhibited a greater capacity to bind to VCAM-1 and ICAM-1 than those from SR-BI(+/+) mice. Furthermore, restoration of SR-BI expression in bone marrow derived cells attenuated monocyte recruitment into atherosclerotic plaques in mice fed high fat, high cholesterol cholate containing diet. These data demonstrate directly that SR-BI in bone marrow-derived cells protects against both aortic and CA atherosclerosis.