Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A suicide bomb blast in 2013 at a distant city of Pakistan killed 84 and wounded more than 150 people. Some patients were transferred to our tertiary care hospital because of extreme load on medical services there. This patient arrived at the Aga Khan Hospital, 2 days after the bomb blast injury and underwent an orthopedic procedure. Next day, he developed sudden tachypnea, desaturation, and circulatory collapse. After initial cardiopulmonary resuscitation, he was immediately transferred to surgical intensive care unit. Based on history, echocardiography findings and patient parameters, a clinical diagnosis of massive pulmonary embolism was made and immediate thrombolytic therapy with alteplase was started. The immediate improvement in hemodynamic status was evident following 2 hours of alteplase infusion. This case also highlights the aggressiveness of resuscitation, decision making in initiating thrombolytic therapy on clinical grounds, importance of deep venous thrombosis prophylaxis, and exhaustion of health resources due to blast related mass destruction.
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PMID:Bomb Blast and Its Consequences: Successful Intensive Care Management of Massive Pulmonary Embolsim. 2737 30

Age is an important cardiovascular risk factor. Among others, age is associated with an increased risk to develop thrombotic cardiovascular complications, both in the arterial (acute myocardial infarction, stroke) and the venous (deep vein thrombosis, pulmonary embolism) system, which cannot be explained by the age-associated increase in cardiovascular risk factors alone. A number of studies have demonstrated that the accumulation of senescent endothelial cells and specific phenotypic and functional alterations associated with endothelial cell senescence may play an important role during the development and progression of cardiovascular disease. Prevention of platelet aggregation and thrombosis as well as fibrinolysis are important functions of the endothelium lining the vasculature. Moreover, impaired proliferation and migration of local endothelial cells as well as exhaustion of endogenous endothelial repair mechanisms involving progenitor cells may also contribute to thrombosis and its complications with age by impairing re-endothelialisation. In this short review, we present and discuss important findings regarding the effects of the cardiovascular risk factor age on endothelial cell morphology and function including the senescence-associated secretory phenotype and altered expression of factors involved in thrombosis and fibrinolysis. We also summarize results from clinical and experimental studies in rodent and other models on the possible connection between endothelial senescence and thrombotic events. Furthermore, major mechanisms and pathways underlying endothelial cell senescence and models to study its pathomechanisms are presented. Finally, we briefly discuss potential targets and therapeutic options to prevent, postpone or treat endothelial senescence and thus the increased burden of thrombosis associated with age.
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PMID:Endothelial cell senescence and thrombosis: Ageing clots. 2766 26