The effect of current and former tobacco use on outcomes after primary reverse total shoulder arthroplasty.

BACKGROUND: The purpose of this study was to determine the influence of current and former tobacco use on minimum 2-year clinical and radiographic outcomes after reverse total shoulder arthroplasty (RTSA). METHODS: Review of primary RTSA patient data identified 186 patients with at least 2 years of follow-up. Patients were classified as nonsmokers (76 patients), former smokers (89 patients), or current smokers (21 patients). Assessment included preoperative and postoperative visual analog scale pain scores, American Shoulder and Elbow Surgeons scores, strength, range of motion, complications, revisions, and narcotic use. Radiographs were analyzed for signs of loosening or mechanical failure. RESULTS: Overall mean age of the patients was 70 (48-87) years, and mean follow-up was 2.6 (2.0-5.7) years. Smokers (62.1 years) were significantly younger than nonsmokers (70.7 years) and former smokers (70.8 years; P = .00002). All patients had significant improvements in pain, American Shoulder and Elbow Surgeons score, strength, and forward flexion range of motion; however, smokers had higher visual analog scale pain scores (mean, 2.5) than nonsmokers (mean, 1.8) or former smokers (mean, 1.0; P = .014). Otherwise, no differences were found regarding any of the postoperative parameters (P > .05). CONCLUSIONS: Aside from increased patient-reported pain, current tobacco use does not appear to negatively affect outcomes after primary RTSA. The RTSA design obviates the need for a functioning rotator cuff, possibly mitigating tobacco's negative effects previously demonstrated in rotator cuff repair and anatomic total shoulder arthroplasty. Former users obtained outcomes similar to those of nonusers, suggesting that tobacco use is a modifiable risk factor to achieve optimal pain relief after RTSA.

Estrogen metabolism by cytochrome P450 1B1 modulates the hypertensive effect of angiotensin II in female mice.

To determine the role of cytochrome P450 (CYP) 1B1 in the sex difference in response to angiotensin II (Ang II)-induced hypertension, female Cyp1b1(+/+) and Cyp1b1(-/-) mice were infused with Ang II (700 ng/kg per minute) or vehicle with or without ovariectomy. In addition, mice were treated with the CYP1B1 inhibitor, 2,3',4,5'-tetramethoxystilbene (TMS; 300 µg/kg IP, every third day), and 17-ß estradiol metabolites, 2-hydroxyestradiol (2-OHE), 4-OHE, or 2-methoxyestradiol (1.5 mg/kg per day IP, for 2 weeks) and systolic blood pressure (SBP) measured. Ang II increased SBP more in Cyp1b1(-/-) than in Cyp1b1(+/+) mice (119±3-171±11 versus 120±4-149±4 mm Hg; P<0.05). Ang II caused cardiovascular remodeling and endothelial dysfunction and increased vascular reactivity and oxidative stress in Cyp1b1(-/-) but not in Cyp1b1(+/+)mice. The Ang II-induced increase in SBP was enhanced by ovariectomy and TMS in Cyp1b1(+/+) but not in Cyp1b1(-/-) mice. 2-OHE did not alter Ang II-induced increase in SBP in Cyp1b1(+/+) mice but minimized it in Cyp1b1(-/-) mice, whereas 4-OHE enhanced Ang II-induced increase in SBP in Cyp1b1(+/+) mice but did not alter the increased SBP in Cyp1b1(-/-) mice. 2-OHE-derived catechol-O-methyltransferase metabolite, 2-methoxyestradiol, inhibited Ang II-induced increase in SBP in Cyp1b1(-/-) mice. Ang II increased plasma levels of 2-methoxyestradiol in Cyp1b1(+/+) but not in Cyp1b1(-/-) mice and increased activity of cardiac extracellular signal-regulated kinase 1/2, p38 mitogen-activated kinase, c-Src, and Akt in Cyp1b1(-/-) but not in Cyp1b1(+/+) mice. These data suggest that CYP1B1 protects against Ang II-induced hypertension and associated cardiovascular changes in female mice, most likely mediated by 2-methoxyestradiol-inhibiting oxidative stress and the activity of these signaling molecules.