BackgroundIn patients with acute pulmonary embolism (PE), rapid and accurate risk assessment is paramount in selecting the appropriate treatment strategy. The prognostic value of right ventricular dysfunction (RVD) assessed by multidetector CT (MDCT) in normotensive patients with PE has lacked adequate validation. Methods The study defined MDCT-assessed RVD as a ratio of the RV to the left ventricle short axis diameter greater than 0.9. Outcomes assessed through 30 days after the diagnosis of PE included all-cause mortality and 'complicated course', which consisted of death from any cause, haemodynamic collapse or recurrent PE. Results MDCT detected RVD in 533 (63%) of the 848 enrolled patients. Those with RVD on MDCT more frequently had echocardiographic RVD (31%) than those without RVD on MDCT (9.2%) ( p<0.001). Patients with RVD on MDCT had significantly higher brain natriuretic peptide (269±447 vs 180±457 pg/ml, p<0.001) and troponin (0.10±0.43 vs 0.03±0.24 ng/ml, p=0.001) levels in comparison with those without RVD on MDCT. During follow-up, death occurred in 25 patients with and in 13 patients without RVD on MDCT (4.7% vs 4.3%; p=0.93). Those with and those without RVD on MDCT had a similar frequency of complicated course (3.9% vs 2.3%; p=0.30). Conclusions The PROgnosTic valuE of CT study showed a relationship between RVD assessed by MDCT and other markers of cardiac dysfunction around the time of PE diagnosis, but did not demonstrate an association between MDCT-RVD and prognosis.
Cranial nerve involvement in Charcot-Marie-Tooth disease (CMT) is rare, though there are a number of CMT syndromes in which vocal cord paralysis is a characteristic feature. CMT disease due to mutations in the ganglioside-induced differentiation-associated protein 1 gene (GDAP1) has been reported to be associated with vocal cord and diaphragmatic palsy. In order to address the prevalence of these complications in patients with GDAP1 mutations we evaluated vocal cord and respiratory function in nine patients from eight unrelated families with this disorder. Hoarseness of the voice and inability to speak loudly were reported by eight patients and one had associated symptoms of respiratory insufficiency. Patients were investigated by means of peripheral and phrenic nerve conduction studies, flexible laryngoscopy, pulmonary function studies and polysomnography. Nerve conduction velocities and pathological studies were compatible with axonal CMT (CMT2). Flexible laryngoscopy showed left vocal cord palsy in four cases, bilateral cord palsies in four cases and was normal in one case. Restrictive respiratory dysfunction was seen in the eight patients with vocal cord paresis who were all chair-bound. These eight had confirmed phrenic nerve dysfunction on neurophysiology evaluation. The patient with normal vocal cord and pulmonary function had a less severe clinical course.This study shows that CMT patients with GDAP1 mutations develop severe disability due to weakness of limb muscles and that laryngeal and respiratory muscle involvement occurs late in the disease process when significant proximal upper limb weakness has developed. The early and predominant involvement of the left vocal cord innervated by the longer left recurrent laryngeal nerve suggests a length dependent pattern of nerve degeneration. In GDAP1 neuropathy, respiratory function should be thoroughly investigated because life expectancy can be compromised due to respiratory failure.
A year long multicentre prospective study was carried out in the Valencia region of Spain, to determine the cause of community acquired pneumonia. The study was based on 510 of 833 patients with pneumonia. Of these, 462 were admitted to hospital, where 31 patients died. A cause was established in only 281 cases-208 of bacterial, 60 of viral, and 13 of mixed infection. The most common microorganisms were Streptococcus pneumoniae (14-5%), Legionella sp (14%), Influenza virus (8%), and Mycoplasma pneumoniae (4%). There was a higher incidence of Legionella sp than in other studies.
The effect of thoracentesis on pulmonary gas exchange was studied in 33 patients with unilateral pleural effusions of various causes. Arterial blood gases were measured before thoracentesis and at 20 minutes, two hours, and 24 hours after the procedure. In 13 patients alveolar arterial oxygen gradient (PA-ao), physiological dead space:tidal volume ratio (VD/VT), physiological shunt, and "sanatomical" shunt were also determined before and two hours after thoracentesis. The Pao, showed a significant increase at each time, reaching a maximum at 24 hours (mean (SD) increase f 1 (0.74) kPa; 8-17 (5.57) mm Hg). A concurrent significant decrease of PA-ao, was observed (mean (SD) 1-72 (0.77) kPa; 12-92 (5.78) mm Hg). This was accompanied by a small but significant decrease of "anatomical" shunt (2.4% (1-5%)) and a greater decrease of the physiological shunt (6.5% (4-3%)), while VD/VT did not change. The results are probably due to improved ventilation perfusion relationships with, in particular, an increase in the ventilation of parts of the lung previously poorly ventilated but well perfused.The effect of thoracentesis on arterial blood oxygenation is controversial; most studies report a decrease in arterial oxygen tension (Pao)'-' and this has been attributed to alteration of ventilation perfusion (VA/ Q) matching. Two of these studies, however, were limited to measuring the changes in Pao, and only Brown et a1' made measurements of the alveolararterial oxygen tension difference (PA-ao,) and of the "anatomical" shunt fraction. The changed VAIQ relationships have been attributed to interstitial oedema occurring when blood flow increases abruptly through previously compressed lung, and to negative pressure in the capillary bed produced by decompression.' 4In our experience, decrease of Pao, is not a frequent finding and improvement of the-Pao, is the rule. We have studied changes in the arterial-blood gases immediately after thoracentesis and two and 24 hours later. We have investigated the possible causes of observed changes by measuring the PA-ao, physiological shunt, "anatomical" shunt, and the physiological dead space to tidal volume ratio (VD/ VI).
for the PROTECT and the RIETE investigators. Prognostic significance of tricuspid annular displacement in normotensive patients with acute symptomatic pulmonary embolism. J Thromb Haemost 2014; 12: 1020-7.Summary. Background: Tricuspid annular plane systolic excursion (TAPSE) is an emerging prognostic indicator in patients with acute symptomatic pulmonary embolism (PE). Methods and Results: We prospectively examined 782 normotensive patients with PE who underwent echocardiography in a multicenter study. As compared with patients with a TAPSE of > 1.6 cm, those with a TAPSE of ≤ 1.6 cm had increased systolic pulmonary artery pressure (53.7 AE 16.7 mmHg vs. 40.0 AE 15.5 mmHg, P < 0.001), right ventricle (RV) end-diastolic diameter (3.5 AE 0.8 cm vs. 3.0 AE 0.6 cm, P < 0.001), and RV to left ventricle end-diastolic diameter ratio (1.0 AE 0.3 vs. 0.8 AE 0.2, P < 0.001), and a higher prevalence of RV free wall hypokinesis (68% vs. 11%, P < 0.001). Patients with a TAPSE of ≤ 1.6 cm at the time of PE diagnosis were significantly more likely to die from any cause (hazard ratio [HR] 2.3; 95% confidence interval [CI] 1.2-4.7; P = 0.02) and from PE (HR 4.4; 95% CI 1.3-15.3; P = 0.02) during follow-up. In an external validation cohort of 1326 patients with acute PE enrolled in the international multicenter Registro Informatizado de la Enfermedad TromboEmb olica, a TAPSE of ≤ 1.6 cm remained a significant predictor of all-cause mortality (HR 2.1; 95% CI 1.3-3.2; P = 0.001) and PE-specific mortality (HR 2.5; 95% CI 1.2-5.2; P = 0.01). Conclusions: In normotensive patients with PE, TAPSE reflects right ventricular function. For these patients, TAPSE is independently predictive of survival.
Significant differences in the clinical profile of venous thromboembolic-related outcomes were observed according to the site of cancer. These findings suggest the development of cancer-specific anticoagulant strategies as an area for further research.
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