Toshio Fujita

Coronary artery spasm is a major cause of sudden cardiac arrest in survivors without underlying heart disease.

BackgroundThe role of coronary spasm in underlying disease-free patients who were resuscitated from sudden cardiac arrest remained uncertain. This study investigated the cause of cardiac arrest, and the etiologic and prognostic differences were compared between patients with underlying heart disease (group I) and those patients without underlying heart disease (group II). MethodsTwenty-five survivors of sudden cardiac arrest were classified into two groups according to the presence or absence of underlying heart disease. To investigate the cause of cardiac arrest, we performed ergonovine testing and electrophysiologic study. Fifteen of the patients had underlying heart disease, while 10 did not. ResultsElectrophysiologic abnormalities were found in 13 of the 15 patients in group I. In group II, spontaneous attack of coronary spasm occurred in four patients during the observation period, and coronary spasm was induced in three of the remaining six patients. Four patients in group I had a cardiac event during a mean follow-up period of 32 ±23 months, whereas no patients in group II had recurrence of sudden cardiac arrest at a median follow-up of 32 months (range, 10 to 72 months). ConclusionsElectrophysiologic study identified a potential cause in 13 of 15 patients with underlying heart disease. Coronary spasm was involved in the pathogenesis of sudden cardiac arrest in survivors without identifiable underlying heart disease.

Increase of scavenger receptor A‐positive monocytes in patients with acute coronary syndromes

To evaluate the utility of the scavenger receptor A (SRA) index (no. SRA+ monocytes observed in 10 high‐power fields of peripheral blood (PB) smear samples, normal upper limit <30) as the indication of disrupted, fissured, or eroded plaque, 225 patients with acute myocardial infarction (AMI), 79 with unstable angina (UA) and 91 with stable angina (SA) were examined. Thrombus was gathered from 95 of 205 sequential AMI patients (46.3%), and classified into platelets, mixed, and two kinds of residual mural thrombus (RMT). RMT was observed in 56 of 169 (33.1%) AMI patients with SRA index ≥30 at hospitalization. The SRA index of 82.4% of AMI, and 75.9% of UA, and 70.3% of SA patients was ≥30 at hospitalization. For 36 AMI patients who initially had an SRA index of <30 at hospitalization, it exceeded 30 within 2 days, and the SRA index rapidly increased in most AMI patients after hospitalization. SRA+ monocytes were considered to differentiate from SRA– monocytes in PB. An abnormally high SRA index is considered to be a useful indication of disrupted or fissured or eroded plaque.

Fulminant type 1 diabetes mellitus and fulminant viral myocarditis. A case report and literature review.

A 35-year-old Japanese woman was admitted with coma following flu-like symptoms. She was diagnosed with diabetic ketoacidosis and fulminant type 1 diabetes (FT1D) and received intravenous infusion of insulin and saline. The next day, the ketoacidosis disappeared, and she recovered consciousness. However, extensive ST-segment elevations in the electrocardiogram appeared with a positive troponin test, and the patient developed pulmonary edema on day 3. An echocardiogram showed globally reduced wall motion of the left ventricle and mild pericardial effusion. Despite medical therapy with intravenous furosemide, carperitide, and catecholamines, her cardiac function deteriorated rapidly, with the left ventricular ejection fraction decreasing to 26% within 7 hours, and progressed to cardiogenic shock that afternoon. The patient received mechanical circulatory support for 4 days with intra-aortic balloon pumping and percutaneous cardiopulmonary support, and recovered fully from circulatory failure. A paired serum antibody test showed a significantly elevated titer against parainfluenza-3 virus, indicating a diagnosis of fulminant viral myocarditis. She was discharged on multiple daily insulin injection therapy, and her subsequent clinical course has been uneventful. In summary, we present a case of concurrent FT1D and fulminant viral myocarditis. Parainfluenza-3 viral infection was confirmed serologically and was considered to be a cause of both the FT1D and fulminant myocarditis.

Bidirectional Shunt Trajectory in Ventricular Septal Defect With Eisenmenger’s Syndrome

Received March 19, 2018; revised manuscript received April 13, 2018; accepted April 18, 2018; released online May 25, 2018 Time for primary review: 23 days Department of Cardiovascular Biology and Medicine (H.K., T. Kashimura, N.K., Y.I., T.T., T. Okubo, M.H., T.Y., T. Ozawa, K.O., T.M.), Department of Advanced Cardiopulmonary Vascular Therapeutics (T. Kashimura, M.H.), Department of Radiology (Y.H., T. Kanazawa), Niigata University Graduate School of Medical and Dental Sciences, Niigata; Division of Cardiology, Nagaoka Red-Cross Hospital, Nagaoka (T.F.), Japan Mailing address: Takeshi Kashimura, MD, PhD, Department of Cardiovascular Biology and Medicine, Niigata University Graduate School of Medical and Dental Sciences, 1-754 Asahimachi, Niigata 951-8510, Japan. E-mail: kashi@med.niigata-u.ac.jp ISSN-1346-9843 All rights are reserved to the Japanese Circulation Society. For permissions, please e-mail: cj@j-circ.or.jp Bidirectional Shunt Trajectory in Ventricular Septal Defect With Eisenmenger’s Syndrome

A case of central diabetes insipidus associated with cardiac dysfunction

Central diabetes insipidus (CDI) results from a deficiency of arginine vasopressin (AVP) secretion. It is treated by replacement therapy with the synthetic AVP analogue desmopressin. To prevent heart failure in patients with CDI accompanied by cardiac dysfunction, controlling sodium and water intake is essential, using the minimum effective dose of desmopressin.

Scavenger receptor A index and coronary thrombus in patients with acute ST elevation myocardial infarction

To examine the relationship between the scavenger receptor A (SRA) index (the number of SRA+ cells observed in 10 high power fields of peripheral blood (PB) smear samples; normal upper limit <30) and coronary thrombus, 389 thrombi obtained from 393 patients with acute ST elevation myocardial infarction were examined. Thrombi were classified into platelets (PT), mixed (MT), fibrin‐rich (FT) and organizing thrombi (OT); 387, 269, 57 and 29 cases were detected, respectively. Patients were divided into group A (PT only, 89 cases), B (containing MT and PT but not FT, 243 cases), and C (containing FT, 57 cases). SRA+ cells had infiltrated into all FT cases and 147 of the 269 MT, but no PT. At hospitalization, the SRA index exceeded 30 in 276 patients. PT was observed in 274 cases, and MT and FT (residual mural thrombus; RMT) observed in 230. Infarct‐related coronary artery was thought to be totally and rapidly occluded by PT that had formed as a result of severe stenosis due to extrusion of plaque content or growth of RMT. An abnormal increase of SRA+ cells is considered to be a useful finding to detecting the presence of PT and, probably, RMT.