https://journal.chestnet.org/article/S0012-3692(12)60129-9/pdf

Antithrombotic therapy for VTE disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines.

Background Inflammation may be important in the pathogenesis of atherothrombosis. We studied whether inflammation increases the risk of a first thrombotic event and whether treatment with aspirin decreases the risk. Methods We measured plasma C-reactive protein, a marker for systemic inflammation, in 543 apparently healthy men participating in the Physicians' Health Study in whom myocardial infarction, stroke, or venous thrombosis subsequently developed, and in 543 study participants who did not report vascular disease during a follow-up period exceeding eight years. Subjects were randomly assigned to receive aspirin or placebo at the beginning of the trial. Results Base-line plasma C-reactive protein concentrations were higher among men who went on to have myocardial infarction (1.51 vs. 1.13 mg per liter, P<0.001) or ischemic stroke (1.38 vs. 1.13 mg per liter, P = 0.02), but not venous thrombosis (1.26 vs. 1.13 mg per liter, P = 0.34), than among men without vascular events. The men in the quartile wit...

https://www.nejm.org/doi/pdf/10.1056/NEJM199704033361401

Inflammation, Aspirin, and the Risk of Cardiovascular Disease in Apparently Healthy Men

https://www.healthcare.uiowa.edu/familymedicine/fpinfo/Docs/Chest%20Rx%20VTE%20Feb%202016.pdf

Antithrombotic Therapy for VTE Disease: CHEST Guideline and Expert Panel Report

Non-thrombotic PE does not represent a distinct clinical syndrome. It may be due to a variety of embolic materials and result in a wide spectrum of clinical presentations, making the diagnosis difficult. With the exception of severe air and fat embolism, the haemodynamic consequences of non-thrombotic emboli are usually mild. Treatment is mostly supportive but may differ according to the type of embolic material and clinical severity.

/pdf/guidelines-on-the-diagnosis-and-management-of-acute-1usqw9xdub.pdf

Guidelines on the Diagnosis and Management of Acute Pulmonary Embolism: The Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC)

Background Heparin-induced thrombocytopenia, defined by the presence of heparin-dependent IgG antibodies, typically occurs five or more days after the start of heparin therapy and can be complicated by thrombotic events. The frequency of heparin-induced thrombocytopenia and of heparin-dependent IgG antibodies, as well as the relative risk of each in patients given low-molecular-weight heparin, is unknown. Methods We obtained daily platelet counts in 665 patients in a randomized, double-blind clinical trial comparing unfractionated heparin with low-molecular-weight heparin as prophylaxis after hip surgery. Heparin-induced thrombocytopenia was defined as a decrease in the platelet count below 150,000 per cubic millimeter that began five or more days after the start of heparin therapy, and a positive test for heparin-dependent IgG antibodies. We also tested a representative subgroup of 387 patients for heparin-dependent IgG antibodies regardless of their platelet counts. Results Heparin-induced thrombocytope...

https://www.nejm.org/doi/pdf/10.1056/NEJM199505183322003

Heparin-Induced Thrombocytopenia in Patients Treated with Low-Molecular-Weight Heparin or Unfractionated Heparin

Not all the risk factors for primary pulmonary hypertension (PPH) are known. Appetite suppressants, including fenfluramine derivatives, are strongly suspected aetiological agents. In a 5 year retrospective study fenfluramine use was evaluated among patients referred to a medical centre specialising in the management of PPH. Fifteen (20%) of 73 patients with PPH had used fenfluramine: all of them were women and in 10 (67%) there was a close temporal relation between fenfluramine use and the development of exertional dyspnoea. Initial right heart catheterisation in the 15 women showed severe resting pulmonary hypertension (mean (SD)) with pulmonary artery pressure (PAP) 57 (9) mm Hg, cardiac index 2.1 (0.5) l/min/m2, and pulmonary vascular resistance (PVR) 29 (10) U/m2. Short-term epoprostenol infusion produced a significant vasodilator response in 10 patients (mean fall in PVR 24 (15%) compared with control values). Three fenfluramine users with PPH showed spontaneous clinical and haemodynamic improvement 3, 6 and 12 months after drug withdrawal but there was no significant difference in overall survival (transplant recipients excluded) between fenfluramine users and controls. Histological examination of lung tissue from five women who had used fenfluramine and 22 controls, with PPH showed features typical of advanced plexogenic pulmonary arteriopathy in all. These results do not accord with earlier reports that PPH associated with fenfluramine is less severe and has a better outcome. Fenfluramine may be one aetiological agent that can precipitate or hasten the development of PPH. The results of a European case-control study should give new insights into risk factors for PPH and the cause and effect relation with fenfluramine.

https://heart.bmj.com/content/heartjnl/70/6/537.full.pdf

Primary pulmonary hypertension and fenfluramine use.

In a multicenter, randomized, double-blind study, we compared the effects of nebulized (5 mg x 2) and intravenous (0.5 mg) albuterol (salbutamol) over 1 h in 47 patients admitted to hospital with severe acute asthma defined as a peak expiratory flow (PEF) below 150 L/min and hypercapnia (Pa(CO2) > or = 40 mm Hg). Additional treatment included nasal oxygen and hydrocortisone succinate. The efficacy was assessed after 1 h. In the group treated by nebulization (NEB group, n = 22) 19 (86%) patients (95% confidence interval: 65 to 97%) had been treated successfully according to predefined criteria, versus 12 (48%) patients (95% confidence interval: 28 to 69%) in the intravenously treated group (i.v. group, n = 25), p = 0.006. The mean increase in PEF was greater in the NEB group than in the i.v. group (+107 +/- 94 L/min versus +42 +/- 66 L/min, p = 0.01) as well as the decrease in Pa(CO2) values (-10 +/- 5 mm Hg versus -2 +/- 12 mm Hg, p < 0.01). Beta agonist-induced hypokalemia was more pronounced in the i.v....

Nebulized versus intravenous albuterol in hypercapnic acute asthma. A multicenter, double-blind, randomized study.

In a multicenter, randomized, double-blind study, inhaled beclomethasone dipropionate (BDP) 1,500 µg/day was compared to placebo in 43 chronic asthmatic patients uncontrolled by inhaled salbutamol and oral theophylline. During the prestudy period, a test of maximal steroid reversibility with oral prednisolone 0.5 mg/kg/day for 14 days was performed. The therapeutic response was measured over an 8-wk period as the ability to maintain the clinical improvement and the optimal pulmonary function induced by prednisolone. During the study, severe asthma exacerbation occurred in one (5%) of the 21 patients who received BDP and in 15 (78%) of the 22 patients who received placebo (p < 0.001). In patients who received BDP, FEV1 and peak expiratory flow (PEF) remained above the optimal postprednisolone value, with a trend to improvement during the 8-wk study period. In patients who received placebo, FEV1 and PEF decreased and remained below the optimal value. We conclude that, in chronic asthma, inhaled BDP 1,500 µg...

High Doses of Inhaled Corticosteroids in Unstable Chronic Asthma: A Multicenter, Double-blind, Placebo-controlled Study

Diaphragm dysf~ction induced by upper abdominal surgery. Role of postoperative pain. G. Simonneau, A. Vivien, R. Sartene, F. Kunstlinger, K. Samii, Y. Noviant and P. Duroux (Service de Pneumologie, Hopital Antoine Beclere, 157, rue de la Porte de Trivaux, 92141-Clamart, France), Amer. Rev. resp. Dis., 128 (1983) 899-903. The effects of upper abdominal surgery on diaphragmatic function were studied in 5 patients. During quiet tidal breathing, diaphragmatic function was assessed by measuring the volume displacement of the abdomen within the tidal volume (V,,/V,) and the ratio of abdominal and transdiaphragmatic pressure changes (AP,,/AP,,). This function was also studied during forced inspiratory efforts by measuring maximal transdiaphragmatic pressure (Pdi ,,,) and diaphragmatic displacement (DD). V,,/V, and AP,,/AP,i decreased significantly on the first postoperative day. Diaphragmatic dysfunction also occurred during maximal inspiratory efforts as shown by the significant fall in PdimaX and DD on the first and third postoperative days. On the first postoperative day, opiate epidural analgesia did not modify V,/Vr, APatJAP,i, and Pdimax. These parameters spontaneously returned towards control values on the seventh postoperative day. The authors conclude that upper abdominal surgery induces a marked diaphragmatic dysfunction lasting about 1 week and that it is not suppressed by postoperative pain relief. The mechanism of this dysfunction remains to be determined. It may be the main cause of the postoperative pulmonary restrictive pattern.

Surgery Diaphragm dysfunction induced by upper abdominal surgery. Role of postoperativepain: Amer. Rev. resp. Dis., 128 (1983) 899–903

1. Svensson PJ, Dahlbàck B. Resistance to activated protein C as a basis for venous thrombosis. N Engl J Med 1994; 330:517-22. 2. Dahlbàck B, Hildebrand B. Inherited resistance to activated protein C is corrected by anticoagulant cofactor activity found to be a property of factor V. Proc Natl Acad Sci USA 1994; 91: 1396-400. 3. Griffin JH, Evatt B, Wideman C, Fernandez JA. Anticoagulant protein C pathway defective in majority of thrombophilie patients. Blood 1993; 82: 1989-93. 4. Koster T, Rosendaal FR, de Ronde H, Briet E, Vandenbroucke JP, Bertina RM. Venous thrombosis due to poor anticoagulant response to activated protein C: Leiden Thrombophilia Study. Lancet 1993; 342: 1503-6. 5. Cadroy Y, Sié P, Boneu B. Frequency of a defective response to activated protein C in patients with a history of venous thrombosis. Blood 1994;83:2008-9. 6. Lindblad B, Svensson PJ, Dahlbàck B. Arterial and venous thromboembo­ lism with fatal outcome and resistance to activated protein C. Lancet 1994; 343: 917. 7. Halbmayer WM, Haushofer A, Schon R, Fischer M. The prevalence of poor anticoagulant response to activated protein C among patients suffering from stroke or venous thrombosis and among healthy subjects. Blood Coag Fibrinol 1994; 5: 51-7. 8. Cushman M, Bhushan F, Bovill E, Tracy R. Plasma resistance to activated protein C in venous and arterial thrombosis. Thromb Haemostas 1994; 72: 643-51. 9. Bertina RM, Koeleman BP, Koster T, Rosendaal FR, Dirven RJ, De Ronde H, Van Der Velden PA, Reitsma PH. Mutation in blood coagulation factor V associated with resistance to activated protein C. Nature 1994; 369: 64-7. 10. Sun W, Evatt B, Griffin JH. Blood coagulation factor Va abnormality asso­ ciated with resistance to activated protein C in venous thrombophilia. Blood 1994; 83:3120-5. 11. Gandrille S, Goosens M, Aiach M. A scanning method to establish the molecular basis of protein C deficiency. Human Mutation 1994; 4: 20-30.

Continuous infusion of prostacyclin decreases plasma levels of t-PA and PAI-1 in primary pulmonary hypertension.

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