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Popliteal venous aneurysm (PVA) and antiphospholipid syndrome (APS) are under-recognised as potential causes of pulmonary embolism (PE). A 66-year-old woman presented with progressive shortness of breath. A contrast-enhanced CT revealed bilateral PE, a small renal infarction and bilateral PVAs. Direct oral anticoagulant (DOAC) therapy was initiated immediately for venous thrombosis. Given the positivity for serum antiphospholipid antibody (aPL) in an initial blood test, low-dose aspirin was included to prevent further arterial thrombosis. Her symptoms resolved and she was discharged 1 week later. Twelve weeks later, she was diagnosed with APS because of persistent aPL. Surgical resection of the right PVA was performed 1 year later from her hospitalisation. To the best of our knowledge, this is the first case of PE caused by the combination of bilateral PVAs and APS. This report emphasises the importance of careful screening to identify PE causes, and its optimal management.

This study aimed to evaluate the clinical implication of the brachial-ankle pulse wave velocity (baPWV) for endovascular treatment (EVT). Eighty-four patients who underwent EVT for aortoiliac and femoropopliteal artery were included. In these patients, 36 (43 %) had an ABI improvement above 0.9 a day after EVT. The baPWV in patients who received re-EVT afterwards was significantly higher than that of patients who did not. The area under the receiver operating characteristic curve for the baPWV for predicting re-EVT was 0.788. The optimal cut-off values of the baPWV for re-EVT, specificity, and sensitivity were 2220 cm/s, 93.1 %, and 57.1 %, respectively.

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The clinical results of thromboembolism (TE) in Patients with prosthetic valVe endocarditis (PVE) and anticoagulant therapy were studied. 22 PVE patients (ll males and females each from 4 to 59 years old, average 32.7) were selected from 1939 patients who had undergone valve replacement at this hospital from 1964 and 1985. The complication frequency of TE and its clinical results, anticoagulant therapy and coagulation tests were investigated. Diagnostic criterion was determined in either of the following two: l) those patients who experienced valve replacement, with at least gradual pyrogenic symptons and inflammation factors such as a large increase in white blood cells, the progress of ESR and positive CRP, also with the same bacterium found more than twice in blood culture, also with the same bacterium found more than twice in blood culture, or 2) those patients who experienced valve replacement, with bacterial verruca found at re-valve replacement or at pathological anatomy. PVE onset took 2 days to 6.5 years (average 407 days) to appear after valve replacement. 8 out of the 22 PVE patients (36.3%) showed complications at TE onset, and 5 out of the 8 patients repeated. Embolism was found in 6 cases of brain, 4 cases of kidney, 2 cases of lung, 2 cases of limbs and 1 case of spleen, and 8 patients all died. On the other hand, 5 complications (22.7%) at bleeding were found in 3 cases of brain, 1 case of duodenum and 1 case of site of replaced aortic valve, and 4 patients died. Anticoagulant therapy was given to 21 out of the 22 PVE patients, and thrombotest (TT) values at TE onset were all less than 30%. Warfarin was administered as anticoagulant. 2 patients were administered with aspirin, but one was given with 250mg aspirin per day together with warfarin, and the other with 330mg aspirin per day alone. TT values at the onset of bleeding were from 10 to 56%. Anticoagulant therapy had been performed to the PVE patients since PVE onset did not yet appear, but complications coagulability by TT values, and all the patients died. In addition to this, complications at bleeding were found many and most of patients died even when the TT values were not so low. Therefore, we believe that the anticoagulant therapy that had been performed after PVE onset still needs further studies.

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a relatively rare inherited arrhythmic disease that causes sudden cardiac death, and is caused by mutations in the cardiac ryanodine receptor (RyR2) or sarcoplasmic reticulum protein calsequestrin 2 gene (CASQ2). A 16-year-old man was diagnosed with CPVT and was implanted with a Subcutaneous-implantable Cardioverter Defibrillator (S-ICD), but defibrillation electrode detachment occurred early after placement. We suspected that a two-incision technique was the possible cause. We also report on changes in surface ECG in remote monitoring of the device. TAKE HOME MESSAGE  Although two-incision techniques are becoming the mainstream method of S-ICD implantation, we should consider that the three-incision technique may be advantageous in highly active patients. Remote monitoring may also be useful for early detection of S-ICD dislodgement.