Discussion
In this cohort study, both smokers and non-smokers experienced improved outcomes after arthroscopic rotator cuff repair. Both groups achieved the minimal clinically important difference (MCID) at 2 years follow-up for ASES, WORC and VAS pain scores (12–17, 30 and 245, respectively).16–18 At baseline, smokers presented with worse comorbidities, pain and ASES scores. When controlling for comorbidities and demographics, smoking resulted in lower improvement in ASES but not WORC or VAS pain scores.
The impact of smoking on the pathogenesis of rotator cuff tears is not well-defined. The pathogenesis of rotator cuff tears is linked to a poor vascular region or ‘critical zone’ within the distal 15 mm of the tendon insertion.7 Cigarette smoke may further exacerbate this phenomenon by the vasoconstricting effect of nicotine and the decreased oxygen availability caused by carbon monoxide. Additionally, in a rat model, Ichinose et al delivered a constant concentration of nicotine via an implanted pump onto the supraspinatus tendon. Nicotine caused the supraspinatus tendon to become stiffer, which may biomechanically predispose the tendon to injury and tearing.19
Whether smoking is a risk factor for rotator cuff tears is controversial. Several authors have reported that smokers tend to present with larger rotator cuff tears at an earlier age than non-smokers,20–22 while others have found no association between smoking and rotator cuff tears.23 24 In our cohort, smokers presented on average 5 years younger with cuff tears that were 1.9 cm2 larger in area compared with non-smokers. However, neither difference reached statistical significance with our sample size.
In addition to pathogenesis, smoking may impair the healing potential of the rotator cuff. Lundgreen et al took biopsies of torn supraspinatus tendons at the time of surgery and demonstrated that torn tendons from smokers have greater degenerative changes and cellular apoptosis compared with non-smokers.25 Furthermore, Galatz et al used a rat model of rotator cuff repair to show that nicotine prolonged rotator cuff tendon-to-bone healing and reduced the mechanical properties of the repair site.26
Despite this basic science evidence, mixed results have been published on whether smoking has a negative impact on arthroscopic rotator cuff repairs.11 27–29 In our study, we noted a pronounced decrease in patient-reported outcomes after 1 year for smokers that was not present in non-smokers. Follow-up imaging was not available in the present study, so it is unclear if cuff tear integrity may have contributed to this decline in the smoking group.
Mallon et al first reported that smokers have worse UCLA scores at baseline and lower improvement in scores following open rotator cuff repair.10 Similarly, Balyk studied predominantly open rotator cuff repairs and found smoking was an independent predictor of lower ASES and WORC scores at 6 months.12 Meanwhile, Prassad observed no effect of smoking on Constant scores after open cuff repairs, but the study was likely underpowered with only 42 patients. For arthroscopic repairs, Nho reported that patients who were current or former smokers had no difference in healing rates or outcomes.28
Our study is one of the first reports of worse functional improvement as measured by ASES in active or recent smokers after arthroscopic rotator cuff repair. WORC scores also trended to a lower functional improvement in smokers in our study, but this did not reach statistical significance. Interestingly, smokers in our study had a non-significant trend towards a greater improvement in VAS pain, probably related to the fact that smokers presented with more baseline pain and the VAS pain measure may have had a floor effect.
A strength of our study is the rigorous data collection and follow-up of patients as part of our single institution cohort. We used an array of patient-reported outcome measures that were collected in a standardised fashion across 2 years, enabling us to compare smokers versus non-smokers at multiple time points. Additionally, a number of demographic factors, coexisting comorbidities, surgeon and tear size were controlled for by our study design.
An important limitation to recognise in our study is the low number of smokers in our study population. Only 14% of our study population were active or recent smokers. While this number is much lower than previous reports, our smoking prevalence is on par with the 2015 CDC estimate of 15.1% active smokers in the USA.30 A posthoc power analysis to detect MCID in ASES revealed that our sample size achieved a power of 0.7. The large effect sizes in our study allowed us to demonstrate statistical differences in ASES, but our study may have still been underpowered to report differences in presentation CTI and WORC scores. Additionally, although we collected quantity of smoking, the number of smokers in our study did not permit a subgroup analysis. Finally, this was a retrospective review of a prospective cohort, and imaging was not available to determine whether smoking impacted cuff repair healing rates in addition to outcomes. Instead, we used patient-reported outcomes to determine response to rotator cuff repair.