SummaryExtrathoracic subclavian/axillar venipuncture is an accepted method for implanting pacemaker leads. Although several procedures have been reported, no standard method has been established yet. We evaluated the usefulness of a method in which only J-type guidewires are used. Between August 2011 and November 2012, 33 patients (20 men and 13 women; age, 77.5 ± 10.3 years) underwent permanent pacemaker lead insertion by extrathoracic subclavian venipuncture at our hospital. Thirty-two of the patients underwent primary implantation, whereas 1 patient required an additional lead because of lead fracture. The guidewires were inserted from the cubital vein to the subclavian vein. After the pacemaker pockets were created, we set the X-ray projection in the ipsilateral anterior oblique view. The distal edge of the guidewire was positioned on the ventral side of the first rib on fluoroscopy. The needle tip was positioned within the Ushaped distal tip of the J-type guidewire. The needle was held parallel to the X-ray angle and advanced towards the first rib until the tip entered the subclavian vein. The guidewire was inserted through the cubital vein in 31 patients, and through the femoral vein in 2 patients. Using this method, we successfully performed subclavian venipunctures in all 33 patients (total, 60 punctures) without any complications. Extrathoracic subclavian venipuncture using only a J-type guidewire is an easy, safe, and economical method for pacemaker lead implantation. (Int Heart J 2013; 54: 129-132)
SummaryWe describe the case of a 45-year-old Japanese man who developed acute pericarditis following an acute pulmonary thromboembolism. He had developed shortness of breath 7 days prior to hospitalization and was admitted with severe dyspnea. Echocardiography and laboratory results were compatible with acute pulmonary thromboembolism, which was confirmed by contrast-enhanced chest computed tomography. On the third hospital day, he experienced chest pain exacerbated by inspiration. On the fourth hospital day, his body temperature increased to 39°C and echocardiography revealed circumferential pericardial effusion. A diagnosis of acute pericarditis was made and the patient was treated with colchicine and aspirin. On the fifth hospital day, his symptoms largely subsided. Auscultation revealed pericardial friction rub. Electrocardiography demonstrated diffuse ST-segment elevations. Twenty-four days later, computed tomography revealed the disappearance of both the pericardial effusion and pulmonary arterial emboli. This case was thought to be one of acute pericarditis following acute pulmonary thromboembolism.(Int Heart J 2017; 58: 1028-1033) Key words: Post-cardiac injury syndrome, Dressler syndrome, Pericardial effusion, Friction rub A cute pericarditis can be caused by infection, myocardial infarction, malignancy, trauma, and autoimmune diseases. Acute pericarditis due to pericardial injury is termed post-cardiac injury syndrome. Post-cardiac injury syndrome was first described after myocardial infarction by Dressler.1) Pericarditis after the incision of the pericardium is termed post-pericardiotomy syndrome. The development of post-cardiac injury syndrome following pulmonary thromboembolism has been reported in the literature, although it is considered rare, 2) especially in Japan. We present a case of acute pericarditis following acute pulmonary thromboembolism. Case ReportThe patient was a 45-year-old Japanese man. He developed shortness of breath 7 days prior to the hospital admission. His symptoms worsened by the day of admission, and he was transported to the emergency department with severe dyspnea. His body temperature was 36.0 , his heart rate was 87 beats per minute, his blood pressure was 105/62 mmHg, his respiratory rate was 24 breaths per minute, and his pulse oximetry showed 98% oxygen saturation on 5 L/minute oxygen via a non-rebreather mask. The heart sounds were normal, and breath sounds were clear in both lung fields. The abdomen was flat and soft without tenderness. No edema was noted in the extremities.Electrocardiography revealed sinus tachycardia (rate 136/minute), with an S1Q3T3 pattern and T-wave inversion in the right precordial leads ( Figure 1A). Bedside echocardiography revealed a dilated right ventricle. The tricuspid regurgitation pressure gradient (TRPG) was 53 mmHg (Figure 2) and the diameter of the inferior vena cava was 24 mm.Blood test results were as follows: white blood cell (WBC) count, 6,800 /μL; red blood cell count, 444 10 6 / μL; hemoglobin, 14.3 g/dL; prothrombin time (i...
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