False Tendon‐Related Polymorphic Ventricular Tachycardia

A 39‐year‐old woman showed nonsustained polymorphic ventricular tachycardia (PVT) during light physical activity. Cardiac multidetector row computed tomography demonstrated false tendons, one of which proved to be the focus triggering premature ventricular contraction (PVC) in electrophysiological studies. The triggered PVC arose during the diastolic period, which might have caused tension in the false tendon. Radiofrequency catheter ablation targeting the triggered PVC by pace mapping was performed and proved partially effective against PVT. (PACE 2012;35:e341–e344)     

Ultrasound Evaluation of the Protector Role of the Pronator Quadratus Suture in Volar Plating

The main complication of volar locking plates for distal radius fractures is flexor tendon rupture. The flexor pollicis longus (FPL) is the most commonly ruptured. Repair of the pronator quadratus (PQ) is one of the ways to prevent tendon rupture. The main purpose of this series was to evaluate the role of PQ repair after volar plating to prevent flexor tendon rupture using ultrasound (US). This work was a mono‐operator prospective series of 20 consecutive patients with volar locking plates for distal radius fracture between September 2014 and May 2015. The PQ was repaired in all patients. A clinical, ultrasound, and perioperative evaluation of the flexor tendon was performed by this same surgeon. There was no flexor tendon rupture or tenosynovitis. There were no type A cases, which are characterized by contact between the plate and the FPL, and mostly type C cases, which are characterized by no contact between the plate and the FPL on US imaging. The suture of the PQ was sustainable over time when we removed the plate. Pronator quadratus repair is one of the ways to prevent flexor tendon rupture after volar plating. The outward‐running suture is an effective technique for repairing the PQ. Ultrasound may be helpful during follow‐up to detect asymptomatic flexor tendon irritation.     

Tenosynovial complications identify TTR cardiac amyloidosis among patients with hypertrophic cardiomyopathy phenotype

Recent evidence suggests that carpal tunnel syndrome (CTS) and brachial biceps tendon rupture (BBTR) represent red flags for ATTR cardiac amyloidosis (ATTR-CA). The prevalence of upper limb tenosynovial complications in conditions entering differential diagnosis with CA, such as HCM or Anderson–Fabry disease (AFD), and hence their predictive accuracy in this setting, still remains unresolved. Objective: To investigate the prevalence of CTS and BBTR in a consecutive cohort of ATTR-CA patients, compared with patients with HCM or AFD and with individuals without cardiac disease history. Participants: Consecutive patients with a diagnosis of ATTR-CA, HCM and AFD were evaluated. A control group of consecutive patients was recruited among subjects hospitalized for noncardiac reasons and no cardiac disease history. The presence of BBTR, CTS or prior surgery related to these conditions was ascertained. Results: 342 patients were prospectively enrolled, including 168 ATTR-CA (141 ATTRwt, 27 ATTRm), 81 with HCM/AFD (N = 72 and 9, respectively) and 93 controls. CTS was present in 75% ATTR-CA patients, compared with 13% and 10% of HCM/AFD and controls (P = 0.0001 for both comparisons). Bilateral CTS was present in 60% of ATTR-CA patients, while it was rare (2%) in the other groups. BBTR was present in 44% of ATTR-CA patients, 8% of controls and 1% in HCM/AFD. Conclusions: CTS and BBTR are fivefold more prevalent in ATTR-CA patients compared with cardiac patients with other hypertrophic phenotypes. Positive predictive accuracy for ATTR-CA is highest when involvement is bilateral. Upper limb assessment of patients with HCM phenotypes is a simple and effective way to raise suspicion of ATTR-CA.     

Anatomie et tendinopathie patellaire : un malentendu

The anatomical structure linking the patella and the tibia is called the “patellar ligament” in the international nomenclature. This term is well accepted yet can be a source of confusion for non-specialists. This is because the priority role of this structure is not to maintain joint stability, the primary role of the cruciate ligaments and the collateral ligaments, but rather to prolong the mechanical action of the quadriceps muscle onto the leg skeleton beyond the “patellar sesmoid”. Patellar tendon injuries are a common observation in sports medicine. The proximal third of the tendon below the patella is most generally involved. This highly frequent tendinopathy sometimes termed an “insertion” tendiopathy. Based on 100 consecutive magnetic resonance imaging studies and cadaveric dissection, we confirm that the insertion of the patellar tendon is situated on the anterior aspect of the patella and not the tip. We describe two anatomical variants of the healthy patellar tendon (type 1 and 2) that should not be confused with a site of tendinopathy. The anatomical limits between tendinous tissue and infrapatellar adipose body (the Hoffa adipose ligament), notably on the upper third is still debated and merits further work.     

终腱斜行游离延长治疗陈旧性锤状指畸形

正2013年10月~2015年9月,我们采用改良术式终腱斜行游离延长方法治疗14例陈旧性锤状指畸形患者,疗效满意,报道如下。1材料与方法1.1病例资料本组14例,男10例,女4例,年龄20~65岁。畸形手指:食指3例,中指5例,环指5例,小指1例。伤后至手术时间:7~12 d 11例,21 d以上3例。     

Ultrasound‐Guided Injection of the Temporalis Tendon: A Novel Technique

A novel technique, ultrasound‐guided injection of the temporalis tendon in adults, is described. Ultrasound‐guided injection of the temporalis tendon is based on visualization of the temporalis muscle, temporalis tendon, and coronoid process. A practical step‐by‐step guide to doing the procedure is given. This technique is effective and reproducible. Two patients successfully treated with this technique will be briefly discussed. The anatomic location and size of the temporalis tendon make it mandatory to use ultrasound to ensure precision.     

Proliferative Responses to Platelet-Derived Growth Factor in Young and Old Rat Patellar Tendon

Musculoskeletal soft tissue repair is often a slow process that may be complicated by aging, thus we investigated the mitogenic response of young and old rat patellar tendon (PT) explants to platelet-derived growth factor-AB (PDGF-AB). Bilateral PT explants from young (4 months) and old (29 or 36 months) rats of two strains (Fisher 344 and Fisher-Brown-Norway) were cultured for 72 h in platelet-poor horse serum in the presence or absence of 100 ng/ml recombinant human PDGF-AB. The explants were radiolabeled with [³H]-TdR for the final 24 h in culture. Tendon cellularity and DNA synthesis data were analyzed by multiple factor ANOVA (age, strain, and side), Mann-Whitney t-test (cellularity and DNA synthesis), and a sign test (proliferative response to PDGF). Tendon cellularity declined significantly with age in both strains (p < 0.05), while both young and old patellar tendon fibroblasts in both strains had a significant (>100%) increase in DNA synthesis with the addition of PDGF (p < 0.05). Although there was a trend to lower proliferative responses in older tendons, the differences were not significant. Autoradiographic analysis of labeling indices in F344 tendons showed a diminished responsiveness to PDGF (p < 0.04, ANOVA). Strain and side response on a per cell or tissue weight basis were not significant factors. Under appropriate experimental conditions, these two animal models of aging showed declines in responses to high levels of PDGF, suggesting that the PT reflects an age-dependent diminished capacity for wound repair.