Only the echocardiographic and epidemiologic parameters were predictors of left atrial thrombi and SEC intensity, while the studied biomarkers had no predictive power. Using clinical data and transthoracic echocardiography, we can change the therapeutic strategy in high-risk patients.
SummaryCoumarin-induced skin necrosis is believed to be due to a transient hypercoagulable state resulting from a more rapid decline of the protein C activity relative to that of coagulation factors (F) II, IX and X during initiation of oral anticoagulant therapy. We studied hemostatic system activation during early oral anticoagulant treatment with a technique that investigates coagulation activation in the microcirculation.We determined in 10 healthy volunteers the concentrations of prothrombin fragment F1+2 (f1.2) and thrombin-antithrombin complex (TAT) in blood emerging from an injury of the microvasculature (bleeding time incision) before and after initiation of both high-inten- sity and low-intensity coumarin therapy. In addition, f1.2, TAT, activated F VII (F Vila) and the activities of FII, F VII, F X and protein C were measured in venous blood.A rapid decline of F VII and protein C was observed in venous blood with activities at 24 h of 7 ± 1% and 43 ± 2%, respectively, during the high-intensity regimen. A 20 to 30% reduction of f1.2 and TAT was seen in venous blood at 72 h with no major difference between the high- and the low-intensity regimen. F Vila levels were substantially affected by anticoagulation with a >90% reduction at 48 h during the high-intensity regimen. Following high-intensity coumarin, a >50% decrease in the fl.2 and TAT levels was found in shed blood at 48 h suggesting substantial inhibition of thrombin generation during early oral anticoagulation. An increase in the f1.2 and TAT levels was seen neither in shed blood nor in venous blood.Our data do not support the concept of a transient imbalance between generation and inhibition of thrombin as the underlying pathomechanism of coumarin-induced skin nekrosis.
Background
Cardiac masses include various tumorous and non-tumorous lesions. Primary cardiac tumours are very rare and most commonly benign. Primary cardiac lymphomas (PCL) account for 1–2% of malignant primary cardiac tumours. Only 197 cases of PCL have been reported between 1949 and 2009.
Case summary
We report a case of a 73-year-old patient who presented with atrial flutter. The diagnosis was a tumorous cardiac mass in the right atrium with signs of infiltration of the tricuspid valve insertion and pericardium. There were no signs of extracardiac disease at initial presentation. The patient was deemed to be inoperable by cardiac surgeons. Rapid tumour progression caused AV-block type Mobitz 2 with concomitant obstruction of the tricuspid valve and axillary lymph node metastasising. Excision of the axillary lymph node revealed a diffuse large B-cell non–Hodgkin lymphoma. An epicardial right ventricle single lead pacemaker was sited, and chemotherapy was administered, resulting in complete remission.
Discussion
Cardiac masses are rare and challenging cases. Although current imaging procedures deliver extensive Information, histological examination is still required in many cases. We encountered a tumorous mass with deep infiltration. After the patient was deemed inoperable, later lymph node invasion allowed histological examination, revealing PCL. PCL are life-threatening tumours with rapid and aggressive growth. Treatment is based on chemotherapy consisting of anthracycline-containing regimens. This case report highlights the curative potential of chemotherapy, as we report a rapid regression of the tumour as well as the disappearance of arrhythmias and conduction disorders after treatment.
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