The absence of the inferior vena cava is a rare congenital anomaly and represents a modest risk for deep-venous thrombosis. When associated with genetic polymorphism or other hypercoagulable states, the risk can increase several times. A case of young man with the inferior vena cava agenesia and deep-venous thrombosis of both legs triggered by the physical effort is reported. The view that the congenital inferior vena cava malformation represents a predisposition to deep-venous thrombosis in spite of well-developed collateral circulation is supported. In these circumstances, various external triggers (physical effort, hormonal contraception etc) may precipitate thrombosis. Because the patient had no other convincing and permanent risk factors for thrombosis, the lifelong anticoagulant therapy was not recommended.
Aim To determine the appropriate timing of cardiac troponin T (cTnT) measurement for the early triage of pulmonary embolism (PE) patients. MethodsIn this single-center prospective study, PE was confirmed in all patients using computed tomography. 104 consecutive patients were divided into three groups (high-risk, intermediate, and low-risk) based on their hemodynamic status and echocardiographic signs of right ventricular dysfunction. cTnT levels were measured on admission and then after 6, 24, 48, and 72 hours with threshold values greater than 0.1 ng/mL. ResultsIntermediate-risk PE patients had higher cTnT levels than low-risk patients already in the first measurement (P = 0.037). Elevated cTnT levels significantly correlated with disease severity after 6 hours (intermediate vs low risk patients, P = 0.016, all three groups, P = 0.009). ConclusionIn hemodynamically stable patients, increased cTnT level on admission differentiated intermediate from low-risk patients and could be used as an important element for the appropriate triage of patients. Timing of troponin T measurements in triage of pulmonary embolism patients CLINICAL SCIENCE Croat Med J. 2013;54:561-8 doi: 10.3325/cmj.2013.54.561 CLINICAL SCIENCE 562 Nikola Bulj1Croat Med J. 2013;54:561-8 www.cmj.hrPulmonary embolism (PE) still remains one of the most frequent causes of death among patients in emergency settings. Early identification of high-risk patients and optimal treatment administration is often difficult due to the clinical variability of the disease. Several risk-stratification tools have been recently proposed based on echocardiography, biomarkers (troponins and natriuretic peptides), and computed tomography (1). Right ventricular dysfunction (RVD) is a central hemodynamic event in PE patients, and represents an independent prognostic factor of adverse events. Multiple clinical studies have convincingly shown that RVD in hypotensive and normotensive PE patients directly affects early mortality (2). A meta-analysis by ten Wolde et al clearly indicates that RVD is associated with a two times higher risk of PE related mortality (3). According to the current European Society of Cardiology (ESC) guidelines, therapy should be tailored to the estimated risk of death due to acute pulmonary embolism (4). The guidelines divide PE patients into three groups: high-risk (PE related mortality risk >15%), intermediate (PE related mortality risk 3%-15%), and low-risk patients (PE related mortality risk <1%) based on the presence of right ventricular dysfunction (measured by echocardiography, computed tomography, and natriuretic peptides) or injury (troponins). Higher risk patients should be treated with thrombolytic therapy in an intensive care unit (ICU), while non-high-risk patients should be additionally stratified and treated either in an ICU (intermediate-risk) or clinical ward (low-risk patients).Laboratory evaluations of acute right ventricular injury in PE patients have been extensively performed over the past few years, with a special emph...
Approximately 30% of all acute inferior myocardial infarctions (AIMI) are accompanied by acute right ventricular infarction (ARVI) as a consequence of proximal right coronary artery (RCA) occlusion. Fifty per cent of all patients with ARVI manifest hypotension, jugular venous distension, and dyspnoea with clear lung fields, which is then considered as dominant acute RVI (ARVI). The in hospital mortality rate of patients with ARVI who are treated traditionally is very high. Thrombolytic therapy is relatively ineffective, while primary angioplasty is a more recent approach yet to be established as optimal treatment for patients with ARVI. Thirty-eight patients with dominant ARVI were admitted to our CCU over a period of 24 months. The patients were retrospectively divided into 3 groups according to treatment: Group I (n = 16): traditional treatment; Group II (n = 12): thrombolytic therapy (streptokinase); Group III (n = 10): angioplasty after urgent coronarography. We tested the difference in the number of deaths in all groups by the Fisher exact test. There was a significant difference in the number of deaths between Group I and Group III (P < 0.05). Mortality reduction was also noted between Group II and Group III, which, however, proved to be statistically insignificant.
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