Background The prevalence of extracorporeal cardiopulmonary resuscitation (ECPR) in patients with out-of-hospital cardiac arrest (OHCA) has been increasing rapidly worldwide. However, guidelines or clinical studies do not provide sufficient data on ECPR practice. The aim of this study was to provide real-world data on ECPR for patients with OHCA, including details of complications. Methods We did a retrospective database analysis of observational multicenter cohort study in Japan. Adult patients with OHCA of presumed cardiac etiology who received ECPR between 2013 and 2018 were included. The primary outcome was favorable neurological outcome at hospital discharge, defined as a cerebral performance category of 1 or 2. Results A total of 1644 patients with OHCA were included in this study. The patient age was 18–93 years (median: 60 years). Shockable rhythm in the initial cardiac rhythm at the scene was 69.4%. The median estimated low flow time was 55 min (interquartile range: 45–66 min). Favorable neurological outcome at hospital discharge was observed in 14.1% of patients, and the rate of survival to hospital discharge was 27.2%. The proportions of favorable neurological outcome at hospital discharge in terms of shockable rhythm, pulseless electrical activity, and asystole were 16.7%, 9.2%, and 3.9%, respectively. Complications were observed during ECPR in 32.7% of patients, and the most common complication was bleeding, with the rates of cannulation site bleeding and other types of hemorrhage at 16.4% and 8.5%, respectively. Conclusions In this large cohort, data on the ECPR of 1644 patients with OHCA show that the proportion of favorable neurological outcomes at hospital discharge was 14.1%, survival rate at hospital discharge was 27.2%, and complications were observed during ECPR in 32.7%.

A 26-year-old man, previously in good health, was transferred to the emergency unit of our hospital on July 19, 1995; however, he was dead on arrival. He was an employee of a machine industry with no history of chest pain or palpitation, and at company checkups, no abnormalities were pointed out except for marked left hilar calcification on chest radiograph in June 1991 (Fig 1); moreover, when he was 1 year old, he suffered from an acute self-limited febrile illness with diffuse erythematous macular rash followed by membranous desquamation of the fingertips and notable conjunctival infection resembling Stevens-Johnson syndrome or mucocutaneous lymph node syndrome that occurred 2 years after the first description of Kawasaki disease. 1 About half an hour before admission, he had suddenly lost consciousness while playing catch during the noon break. Despite cardiopulmonary resuscitation, he died, and an autopsy was performed immediately.A small, fresh hematoma was seen on the epicardial surface close to the proximal left anterior descending coronary artery (Fig 2A). The true lumen was heavily calcified and stenotic, and the pseudolumen was coated internally with a smooth intimal membrane (Fig 2B). A postmortem angiogram (Fig 3) revealed that the saccular aneurysm communicated with the true lumen. The circumflex artery was also depicted, suggesting that there was no thrombotic occlusion of the left descending artery, and secondary strangulation of the true lumen due to the aneurysm rupture might have evoked an anteroseptal acute myocardial infarction (Fig 3).Histologically, diffuse intimal thickening was seen throughout the epicardial artery, and leukocyte infiltration into the adventitia and vasa vasorum was seen around the aneurysm, indicating persistent mild vasculitis of the artery (Fig 4). Rupture of a coronary aneurysm is more common in the acute ). B, When epicardium was removed, true lumen (arrow) was revealed to be heavily calcified and stenotic; saccular aneurysm was depicted posteriorly (arrowheads).

The febrile reaction that occurs on rein fusion of ascites was studied. Intravenous rein fusion of ascites was performed 213 times in 63 cases of ascites, which were refractory to treatment with various drugs including diuretics. In order to prevent fever on rein fusion of ascites, a screen filter and a depth filter were used; the results were more favorable with the screen filter. Fibrin was considered to be one of the substances removable by the screen filter. HPLCanalysis of the filtered and concentrated ascites, after passage through the screen filter, revealed a fraction corresponding to albumin. Intravenous injection of this fraction into rabbits caused fever. Although the screen filter cannot completely prevent fever on rein fusion of ascites, it appears useful to prevent fever in some patients.

We encountered a case of malignant hyperthermia caused by intravenous lidocaine which had been administered as treatment for a ventricular arrhythmia. The patient, a 72-year-old male, was admitted with chronic renal failure and aortic valvular stenosis. His chronic renal failure progressed, and congestive heart failure developed, and ventricular arrhythmias occurred frequently. For the treatment of these arrhythmias, lidocaine was injected and continuous infusion was started. Despite initial improvement in symptoms and laboratory data following hemofiltration, refractory ventricular tachycardia occurred. The patient was treated with large doses of lidocaine. His body temperature rose to a maximum of 41.7°C, and generalized muscular twitching was observed before he lost consciousness. Serum and urinary myoglobin levels became elevated. This abnormally high fever was relieved only by dantrolene sodium. After we made a diagnosis of malignant hyper thermia and stopped the lidocaine infusion, the high fever resolved quickly. It is important to note that malignant hyperthermia can be caused by lidocaine and amide-linked local anesthetics.

Although many theories exist on the subject, the mechanisms responsible for a reduction of hypertensive cardiac hypertrophy in response to antihypertensive therapy are still unclear. In order to investigate the relationship between regression of hypertensive cardiac hypertrophy and cardiac nervous function, we studied ten patients with untreated essential hypertension (six men and four women, 62+/-12 years old). Both echocardiography and iodine-123 metaiodobenzylguanidine (MIBG) myocardial imaging were performed before and after antihypertensive therapy. Left ventricular mass (LVM) was significantly reduced in conjunction with the reduction of blood pressure following treatment. MIBG myocardial images showed that the heart-to-mediastinum activity ratio (H/M) was significantly increased while the washout ratio was significantly decreased. Patients were divided into two groups according to the ratio of the LVM values before and after therapy (LVM ratio). Patients with an LVM ratio of less than 0.75 were classified as group A and those with values higher than 0.75 as group B. Neither the change in blood pressure nor the length of treatment was significantly different between these two groups. On the other hand, both the increase in H/M and the decrease in the washout ratio were significantly greater in group A than in group B. These results indicate that an improvement in cardiac sympathetic nervous function may be related to the regression of hypertensive cardiac hypertrophy. Increasing the subject base in these studies and a more precise analysis of the relevance of the data obtained from MIBG myocardial images are recommended to clarify how changes in cardiac sympathetic nervous function relate to the regression of hypertensive cardiac hypertrophy.