Endovascular reconstruction of extracranial traumatic internal carotid artery dissections: a systematic review

Neurosurgical Review - Extracranial internal carotid artery dissection (ICAD) is a potential source of morbidity and mortality in trauma patients and requires high degree of suspicion for diagnosis...     

Useful animal models for the research of osteoarthritis

Osteoarthritis (OA) is a major cause of suffering for millions of people. Investigating the disease directly on humans may be challenging. The aim of the present study is to investigate the advantages and limitations of the animal models currently used in OA research. The animal models are divided into induced and spontaneous. Induced models are further subdivided into surgical and chemical models, according to the procedure used to induce OA. Surgical induction of OA is the most commonly used procedure, which alters the exerted strain on the joint and/or alter load bearing leading to instability of the joint and induction of OA. Chemical models are generated by intra-articular injection of modifying factors or by systemically administering noxious agents, such as quinolones. Spontaneous models include naturally occurring and genetic models. Naturally occurring OA is described in certain species, while genetic models are developed by gene manipulation. Overall, there is no single animal model that is ideal for studying degenerative OA. However, in the present review, an attempt is made to clarify the most appropriate use of each model.     

Percutaneous versus open repair of acute Achilles tendon ruptures

Background

Controversy exists regarding the optimal treatment for acute Achilles tendon ruptures. Conservative and surgical treatments have been reported with variable results and complications rates. The purpose of this study is to compare the postoperative clinical and functional results of percutaneous versus open repair of acute Achilles tendon ruptures.

Materials and methods

We present 34 patients with acute Achilles tendon ruptures treated with open and percutaneous surgical repair. There were 15 patients who had open surgical repair and 19 patients who had percutaneous repair. The mean follow-up was 22 months (range 10–24 months) for the open repair group and 20 months (range 9–24 months) for the percutaneous repair group; no patient was lost to follow-up. Postoperative rehabilitation was the same for both groups. Wound healing, complications, ankle range of motion, and patients’ return to work, activity level, weight-bearing, and subjective assessment of their treatment were recorded.

Results

No significant difference was observed with respect to any of the examined variables between the open and percutaneous repair groups. Tendon healing was observed in all patients of both groups by 7–9 weeks. The mean time of patients’ return to work was 7 weeks for the open repair group and 9 weeks for the percutaneous repair group. All patients were capable of full weight bearing by the 8th postoperative week time; the time to return to previous activities including non-contact sports was 5 months for both groups. All patients expressed satisfaction and graded their treatment as good. As expected, cosmetic appearance was significantly better in the percutaneous repair group. One patient who had open repair experienced skin incision pain and dysesthesia and graded his operation as fair. No patient experienced other complications such as re-rupture, infection, sural neuroma, or Achilles tendinitis within the period of this study.

Conclusions

The present study showed similarly successful clinical and functional results after both open and percutaneous repair of acute Achilles tendon ruptures are similar. Cosmetic appearance is superior in the group of patients who had a percutaneous treatment.     

Communication between left main stem trunk and proximal segment of left anterior descending coronary artery rescues left ventricular ejection fraction of a patient with three-vessel disease

The well-known congenital anomalies of the left main stem refer mainly to its anomalous origin from the pulmonary artery or the right aortic sinus. We present a patient with a large communication between the left main stem trunk and the proximal segment of the left anterior descending coronary artery which preserves the left ventricular systolic performance in the setting of significant three-vessel disease.     

Influence of aortic elastic properties on pulse pressure changes induced by rapid ventricular pacing

The mechanism of aortic pulse pressure decline induced by acute rapid ventricular pacing remains incompletely understood. It has been ascribed to changes in stroke volume or aortic compliance. This becomes more complicated by the dependence of aortic compliance on the level of the mean aortic pressure as well as the aortic wall properties. To test the role of such mechanical factors, aortic pressure-diameter hemodynamics, derived from simultaneous tip-micromanometer aortic pressure recordings and high-fidelity ultrasonic intravascular aortic diameter recordings, were measured in 15 normal subjects during and after abrupt cessation of rapid ventricular pacing (up to 160 bpm). Immediately after terminating the pacing, diastolic aortic pressure declined (–9%, from 87.4±1.2 to 79.5±1.7 mmHg,P<0.0001) while systolic aortic pressure increased (+19%, from 109.5±1.6 to 130.1±2.8 mmHg,P<0.0001). Thus, pulse pressure increased from 22.1±2.2 to 50.6±3.1 mmHg,P<0.0001. To quantify systolic and diastolic aortic pressure differences we compared the first postpaced beat (a) and the last paced beat (b). To estimate what the aortic pressure would have been for the paced beats had the aortic diameter differences due to the different heart rate not occurred we calculated the theoretical pressure of the paced beat P_b=E_b·D_a, where E_b was the instantaneous aortic elastance of the paced beat and D_a was the aortic diameter for the postpaced beat. The corrected pressure difference was then calculated by the following: P_cor=(D_a·E_b)–P_a. It was found that systolic P_cor was 25% of systolic P_raw and diastolic P_cor was 89% of diastolic P_raw. P_raw was the pressure difference between paced and spontaneous beat measured from the raw data. P_cor indicates the portion of P_raw that results from a change in aortic stiffness as a consequence of viscous behavior or aorto-ventricular coupling. These data indicate that the majority of diastolic pressure decline after pacing was terminated, may reflect a change in aortic stiffness while the majority of systolic pressure rise, and may be attributable to differences in hemodynamics alone.     

Challenges in the treatment of angiosarcoma: a single institution experience

Background

Angiosarcomas are rare tumors that carry poor prognosis. Because of insidious growth rate, the diagnosis is often difficult and delayed.

Methods

Between 1990 and 2011, 72 (41 female, 31 male) patients were treated at our institution. Pathologic confirmation was obtained and multiple prognostic factors were evaluated for survival.

Results

Forty-four cases were sporadic and 28 cases were secondary. In the sporadic group, 16 (36%) patients had increased sun exposure, while in the secondary group, the majority (n = 23, 82%) of patients had prior exposure to radiation. The latent period between radiation exposure and diagnosis was predictive of survival (P = .037). Presentation was delayed by more than 3 months in 41% of patients. The majority of men developed head and neck angiosarcomas (n = 15, 48.5%), while women developed breast angiosarcomas (n = 21, 51%). Median survival was prolonged in patients treated initially with surgery.

Conclusions

A delay in the diagnosis of angiosarcoma can affect survival. Clinical suspicion and prompt diagnosis are essential for successful multimodal therapy. Initial surgical resection with adjuvant chemotherapy provides survival advantage.     

The acute-phase protein PTX3 is an essential mediator of glial scar formation and resolution of brain edema after ischemic injury

Acute-phase proteins (APPs) are key effectors of the immune response and are routinely used as biomarkers in cerebrovascular diseases, but their role during brain inflammation remains largely unknown. Elevated circulating levels of the acute-phase protein pentraxin-3 (PTX3) are associated with worse outcome in stroke patients. Here we show that PTX3 is expressed in neurons and glia in response to cerebral ischemia, and that the proinflammatory cytokine interleukin-1 (IL-1) is a key driver of PTX3 expression in the brain after experimental stroke. Gene deletion of PTX3 had no significant effects on acute ischemic brain injury. In contrast, the absence of PTX3 strongly compromised blood–brain barrier integrity and resolution of brain edema during recovery after ischemic injury. Compromised resolution of brain edema in PTX3-deficient mice was associated with impaired glial scar formation and alterations in scar-associated extracellular matrix production. Our results suggest that PTX3 expression induced by proinflammatory signals after ischemic brain injury is a critical effector of edema resolution and glial scar formation. This highlights the potential role for inflammatory molecules in brain recovery after injury and identifies APPs, in particular PTX3, as important targets in ischemic stroke and possibly other brain inflammatory disorders.     

Prophylaxis of cancer-associated venous thromboembolism with low-molecular-weight heparin-tinzaparin: Real world evidence

Thromboprophylaxis, as a preventive measure for cancer-associated thrombosis (CAT), may be beneficial for patients with active cancer and high-risk for thrombosis. The present post hoc analysis include a total of 407 patients enrolled in the Greek Management of Thrombosis study, who received thromboprophylaxis with tinzaparin. The objectives of the present analysis were: i) To obtain sufficient evidence for the administration of prophylaxis in patients with active cancer, irrespective of Khorana risk assessment model score; ii) to identify the selection criteria for both dose and duration of tinzaparin; and iii) to evaluate the efficacy and safety of tinzaparin administered for CAT prophylaxis. The main tumor types for the patients included in the present study were as follows: Lung (25.1%), pancreatic (14.3%), breast (9.1%), stomach (8.4%), colorectal (7.9%) and ovarian (7.6%). Furthermore, metastatic disease was observed in 69.5% of the patients. High thrombotic burden agents (HTBAs) were administered to 66.3% of the patients, and 17.4% received erythropoietin. A total of 43.7% of the patients exhibited a Khorana score <2. The results of the present study demonstrated that both the presence of metastatic disease and the use of HTBAs seemed to influence oncologists'' decisions for the use of thromboprophylaxis in patients with active cancer, regardless of Khorana score. Tinzaparin, in dose expressed in the standard notation for heparins, i.e., anti-Xa factor international units (Anti-Xa IU), was administered at an intermediate dose (InterD; 8,000-12,000 Anti-Xa IU; once daily) to 52.4% of patients, while the remaining patients received a prophylactic dose (ProD; ≤4,500 Anti-Xa IU; once daily). The average duration of thromoprophylaxis was 5 months. Furthermore, a total of 14 (3.4%) thrombotic events and 6 (1.5%) minor bleeding events were recorded. A total of four thrombotic events were observed following an InterD treatment of tinzaparin, while 10 thrombotic events were observed following ProD treatment. The present study also demonstrated that an InterD of tinzaparin was administered more frequently to patients with a body mass index >30 kg/m², a history of smoking and a history of metastatic disease, along with administration of erythropoietin. InterD tinzaparin treatment was found to be potentially more efficacious and without safety concerns. The present study is a registered clinical trial (ClinicalTrials.gov code, {"type":"clinical-trial","attrs":{"text":"NCT03292107","term_id":"NCT03292107"}}NCT03292107; registration date, September 25, 2017).