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8th Combined Meeting Of Orthopaedic Research Societies (CORS)



recent studies recognised metabolic abnormalities as additional factors in the development of rotator cuff (RC) tendinopathy. It has been hypothesised that the insertional area of this tendon is susceptible to degenerative changes due to intrinsic hypovascularization. The mechanisms underlying this process are not yet clear. In this study we attempted to confirm if larger lesions of the RC are related to impaired vasodilatatory response of the local circulation in conditions of “hemodynamic stress”.

Patients & Methods

it was assumed that impaired vasal reaction to “hemodynamic stress” was a systemic condition. This phenomenon should therefore be not limited to the critical area of the tendon tear. Given this assumption post-ischemic vasodilation of brachial artery was studied through an echo-doppler (US) evaluation. 50 patients (mean 61 ± 4, range 50–65) all scheduled for surgical rotator cuff repair following a tendon tear, were enrolled. Three preoperative measurements of the brachial artery diameter before and after application of an ischemic band were collected. The size of the lesions was later assessed at the time of surgery. A statistical analysis was carried on to investigate the correlation between US assessment of brachial artery diameter and the corresponding size of the RC lesions. UCLA and ASES scores were also measured to assess clinical and functional outcomes.


Patients were classified into 4 groups according to Cofield's classification of tear size; respectively, 4 patients had massive lesions, 32 large, 10 medium and 4 had finally small lesions. The extent of the RC lesion showed an inverse correlation with the diameter of brachial artery after an ischemic stimulus: an increase in size of the lesion corresponded to lower mean post-ischemic diameter of the vessel (p <0.0001). UCLA and ASES data showed no statistically significant differences between the subgroups (p > 0.534).


It is not clear why the insertional area of tendons composing the RC is hypovascularised. We hypothesised there is an imbalance between local vasodilator and vasoconstrictor factors. The prevalence of vasoconstrictor substances determines a reduced post-ischemic vasodilation. The data presented provide the basis for the future identification of vascular impairment that could underlie the beginning of tendon degeneration in patients that are not yet affected by injury. This would be beneficial for effective prevention of this type of injury. An imbalance between vasodilator and vasoconstrictor factors could be the basis for vascular distress of RC eventually evolving into tendon lesions when other risk factors are associated. More specific vascular pathophysiological studies are however needed to further understand this mechanism and its potential in prevention of rotar cuff lesion.