الفهرس 
Arterial thrombosisOnly 14 pages are availabe for public view
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Abstract
VTE and arterial thrombosis historically have been considered as two different disease entities with separate pathologies; venous thrombi at most consist of red blood cells and fibrin while arterial thrombi at most consist of platelets. Moreover, the risk factors for VTE and arterial thrombosis are also distinctly different. Acute arterial thrombosis is usually due to atherosclerotic plaque rupture such that the risk factors for arterial thrombosis are essentially those for atherosclerosis (i.e., diabetes mellitus, hypertension, tobacco smoking and dyslipidemia, while the risk factors for VTE include increasing patient age and body mass index, major surgery, hospitalization for acute medical illness, trauma, fracture, active cancer with or without concurrent chemotherapy, central vein catheterization or transvenous pacemaker, previous superficial vein thrombosis, varicose veins, neurologic disease with leg paresis, urinary tract infection, an increased baseline plasma fibrin D-dimer and family history of VTE.
Acute coronary syndromes (ACS) are still associated with high mortality and morbidity and represent the most common cause of death in industrialized countries. The term acute myocardial infarction should be used when there is evidence of myocardial injury (defined as an elevation of cardiac troponin values with at least one value above the 99th percentile upper reference limit) with necrosis in a clinical setting consistent with myocardial ischemia need for immediate treatment strategies such as reperfusion therapy.
The diagnosis of myocardial ischemia is usually made on the basis of clinical history, electrocardiography and cardiac biochemical marker. Measurement of a biomarker of cardiomyocyte injury, preferably high-sensitivity and specificty cardiac troponin, is mandatory in all patients with suspected myocardial infarction Cardiac troponins are more sensitive and specific markers of cardiomyocyte injury than creatine kinase (CK), its creatine kinase myocardial band (CK-MB) and myoglobin.
When pulmonary embolism is clinically suspected on the basis of dyspnoea chest pain, pre-syncope or syncope, and/or haemoptysis, there are three groups of risk: high-risk patients, who are hemodynamically unstable with shock or hypotension; intermediate- to high-risk patients, who are normotensive with a Pulmonary Embolism Severity Index (PESI) ≥ III or a simplified (s)PESI ≥1 and in whom there is right ventricular failure or elevated of cardiac biomarkers; and low risk patients, who have a PESI of class I or II, or a sPESI of 0.
DVT can be ruled out in an outpatient who is judged clinically unlikely to have it and who has a negative D-dimer test, but D-dimer levels can increase in some pathologies like atrial fibrillation, acute coronary syndromes, stroke, acute upper gastrointestinal hemorrhage, infection, disseminated intravascular coagulation, and severe renal dysfunction, which are frequent in critically ill patients. Compression ultrasound is now the first choice to diagnose DVT with high sensitivity and specificity.
Since the introduction of multi-detector computed tomographic (MDCT) angiography with high spatial and temporal resolution and quality of arterial opacification, CTPA has become the standard method of choice for imaging the pulmonary vasculature in patients with suspected PE. Current international guideline recommends anticoagulant as thromboprophylaxis in thromboembolism. In general surgical patients and medically ill inpatients LMWH and UFH have similar efficacy and safety.
VKAs have been the ‛gold standard’ in oral anticoagulant for more than 50 years and warfarin, acenocoumarol, phenprocoumon, phenindione and flundione remain the predominant anticoagulant prescribed for PE. VKAs treatment must regular monitoring to avoid both thrombotic and bleeding complications and guarantee safety and efficacy.