Summary In this paper new evidence is presented for long‐distance trade in the western Atlantic in the Roman period, chiefly from Augustus to the second century AD, on the basis of documented shipwrecks and numerous amphora types. Well‐dated contexts from northern Portugal and Spain, as well as similar sites in northern France and Germany, suggest a thriving trade of amphora‐borne commodities during the Principate. The Atlantic route was initially developed during Augustus' campaigns against the Cantabri and Astures, and later consolidated with the exploitation of the mines in the north‐west of the Iberian Peninsula. Supplying the Roman armies in the German Limes gave a new impetus to this commercial route, complemented by the conquest of Britain.

Background COVID-19 is a new form of acute respiratory failure leading to multiorgan failure and ICU admission. Gathered evidence suggests that a 3-fold rise in D-dimer concentrations may be linked to poor prognosis and higher mortality. Purpose To describe D-dimer admission profile in severe ICU COVID19 patients and its predictive role in outcomes and mortality. Methods Single-center retrospective cohort study. All adult patients admitted to ICU with COVID19 were divided into 3 groups: (1) Lower-values group (D-dimer levels < 3-fold normal range value [NRV] [500ng/mL]), Intermediate-values group (D-dimer ≥3-fold and <10-fold NRV) and Higher-value group (≥10-fold NRV). Results 118 patients (mean age 63 years, 73% males) were included (N = 73 Lower-values group, N = 31 Intermediate-values group; N = 11 Higher-values group). Mortality was not different between groups (p = 0.51). Kaplan-Meier survival curves revealed no differences (p = 0.52) between groups, nor it was verified even when gender, age, ICU length of stay, and SOFA score were considered as covariables. Conclusions In severe COVID19 patients, the D-dimer profile does not retain a predictive value regarding patients’ survivability and should not be used as a surrogate of disease severity.

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DesCripTionAn 82-year-old man presented with hypoxaemic respiratory insufficiency due to left-sided pneumonia and lung atelectasis, with a large, long-standing (>7 days) ipsilateral pleural effusion ( figure 1A,B). Four hours after draining 1500 mL of transudative pleural fluid, the patient had worsening hypoxaemia and increasing supplemental oxygen necessity (fractional inspired oxygen 60% with high-flow face mask). The left lung had expanded, as noted by normal vesicular lung sounds, while diffuse crackles were exhibited on the right side. The chest radiograph (figure 1C) shows asymmetrical diffuse alveolar opacity in the right lung field, which in this setting relates to non-cardiogenic pulmonary oedema after contralateral pulmonary re-expansion. After 12 days of conservative treatment, the patient was well, his left lung was expanded and his right-sided oedema had completely resolved (figure 1D), with no need for supplemental oxygen.This case reports an acute non-cardiogenic pulmonary oedema due to contralateral pulmonary re-expansion after pleural effusion drainage, adding to the scarce literature of this rare yet clinically meaningful event. It is unique as oedema is noted asymmetrically and mostly evident contralateral to thoracentesis.The pathogenesis of this phenomenon is unknown and only five previous cases have had similar findings. In a previous report, overperfusion of the contralateral lung was thought to be the main mechanism for re-expansion pulmonary oedema (RPO). The patient had a hepatopulmonary syndrome and uneven pulmonary vasoconstriction of the ipsilateral lung, as a result of hypoxaemia related to an intrapulmonary shunt.1 In our case, whether overperfusion and/or contralateral lung underlying disease (eg, right lower lobe atelectasis, as noted by deviated trachea) must be present for contralateral RPO could be argued. On a cellular level, polymorphonuclear leucocytes have been implicated, yet inflammation was less severe contralaterally.2 Other investigations show a fundamental role of both leucocytes and platelets for contralateral RPO. 3 Similarly, the pathophysiology of ipsilateral oedema is not completely defined. An increase in microvascular permeability and ensuing lesion secondary to free radicals is often proposed as the main mechanism to ipsilateral re-expansion of the lung leading to ischaemic-reperfusion injury. Accordingly, one would expect the ipsilateral lung to be the most affected. In contrast, we here presented a rare case with the contralateral lung being the most distressed.In conclusion, RPO, an infrequent but life-threatening condition, occurs mostly in the affected collapsed lung. Given the potential mechanisms, the British Thoracic Society 2010 Guidelines recommend avoiding high intrapleural pressures during the procedures, draining no more than 1.5 L in the first hour. Younger patients, those with large pleural effusions or pneumothoraces and collapsed lung for >7 days, are at greater risk. Adequate supplemental oxygen and ventilation are paramount to success...

Vasovagal reflex is the most common cause of syncope. Pacemaker with rate drop response (RDR) or closed‐loop stimulation (CLS) anti‐syncope algorithms have been studied in recurrent vasovagal syncope (VVS), with conflicting results. We aim to investigate the role of pacemaker therapy and anti‐syncope pacing mode in cardioinhibitory recurrent VVS. MEDLINE, Cochrane Library and registered clinical trials were searched for single or double‐blind randomized controlled trials on pacing as a treatment for recurrent VVS. Five studies were eligible, overall enrolling 228 patients. After pooling data from all trials, pacemaker therapy showed a 63% reduction in syncope recurrence compared to control [Risk Ratio (RR): 0.37; 95% CI: 0.14‐0.98; I2 = 67%)]. Subgroup analyses suggested that the effect was greater in single‐blind studies (RR: 0.07; 95% CI: 0.01‐0.52, I2 = 0%). When comparing pacing algorithms, the results from RDR versus no pacing trials (n = 2) did not show a significant reduction in syncope recurrence (RR: 0.73; 95% CI: 0.25‐2.16, I2 60 = 75%). In contrast, the data from the CLS versus standard pacing trials (n = 3) evidenced a statistically meaningful reduction in syncopal burden (RR: 0.18; 95% CI: 0.07‐0.47, I2 = 0%). It is unclear whether pacemaker therapy reduces syncopal burden in cardioinhibitory recurrent VVS. However, our results suggest effectiveness of CLS pacing mode.