Yozo Teramachi

Increased plasma type B natriuretic peptide in the acute phase of Kawasaki disease

Background:  The aim of this study was to identify possible factors associated with type‐B natriuretic peptide (BNP) production in the acute phase of Kawasaki disease (KD).

Microembolic signals measured by transcranial Doppler during transcatheter closure of atrial septal defect using the Amplatzer septal occluder.

PURPOSE To determine the frequency and factors associated with increase in microembolic signals during transcatheter closure of atrial septal defect using the Amplatzer septal occluder. METHODS During the procedure in 16 patients, we measured microembolic signals using transcranial Doppler. Procedure time was divided into five periods: right cardiac catheterisation; left cardiac catheterisation; left cardiac angiocardiography; sizing and long sheath placement; device placement and release. We compared numbers of microembolic signals among the five periods and identified factors associated with them. RESULTS Mean size of septal occluder was 16 millimetres in diameter. Total number of microembolic signals was a median of 31.5, ranging from 3 to 113. Microembolic signals in three periods, left cardiac catheterisation; sizing, and long sheath placement; and device placement and release, were not significantly different from one another, but were significantly higher than those in the remaining two periods, right cardiac catheterisation and left cardiac angiocardiography (median was 9 in left cardiac catheterisation; 6 in sizing and long sheath placement; 6.5 in device placement and release, versus 0 in right cardiac catheterisation and 1 in left cardiac angiocardiography, p less than 0.05, respectively). Importantly, the time for device manipulation positively correlated with total number of microembolic signals (r equals 0.77, p less than 0.001), although fluoroscopic time, age, or size of septal occluder did not. CONCLUSIONS Transcatheter closure of atrial septal defect using the Amplatzer septal occluder produces microemboli, especially during device placement. To minimise the risk of systemic embolism, we must decrease the time for device manipulation.

Circulating Myeloid Dendritic Cells is Decreased in the Acute Phase of Kawasaki Disease

Background: Kawasaki disease is the most prevalent vasculitis of children in the developed countries that affects middle-sized arteries. Though T-cells are known to be activated with ample production of cytokines in acute phase of Kawasaki disease, there is a paucity of data concerning dendritic cells (DCs), the most potent antigen presenting cells that initiates T-cell activation. This study examined change in circulating DCs in acute phase of Kawasaki disease. Methods: Using multi-color flow cytometry, we determined circulating myeloid DC (mDC), Lin-HLA-DR+CD11c+ cell, and plasmacytoid DC (pDC), Lin-HLA-DR+CD123+ cell in 33 patients with acute phase of Kawasaki disease (aKD), 24 febrile controls (FC), and 13 healthy controls (HC). Blood chemistry data including cytokines were determined at the same time. Numbers of DCs were compared among 3 groups and before and after immunoglobulin treatment in aKD. Correlation between numbers of circulating DCs and blood chemistry data were determined. Results: Number of circulating mDC was significantly lower in aKD on admission than in FC and HC [median (lower, upper quartile)=7260 (2463, 11550) vs. 12210 (9500, 22050) and 18600 (11520, 23460) cells/ml, p < 0.001]. This number of circulating DCs significantly correlated with disease severity represented by serum albumin (mDC, r=0.56, p < 0.0001; pDC, r=0.39, p < 0.02, respectively), C reactive protein (mDC, r=-0.42, p < 0.005), and interleukin-6 (mDC, r=-0.55, p < 0.007). Immunoglobulin treatment quickly restored number of mDC [7260 (2463, 11550) vs. 15200 (10840, 30965) after IVIG and 18600 (12950, 25510) cells/ml at convalescence, p < 0.001] in aKD. Conclusions: This study indicates that number of circulating mDCs is decreased in acute Kawasaki disease, and may be involved in the pathophysiology.

Entrapment of the Left Coronary Artery Ostium by the Aortic Valve Leaflet, Promoting Myocardial Ischemia

![Figure][1] [![Graphic][3] ][3][![Graphic][4] ][4][![Graphic][5] ][5][![Graphic][6] ][6] A 13-year-old girl was referred to us after an episode of post-exercise ischemic heart event. Ascending aortography, left coronary angiography (Online Videos [1A][6]and [1B][7]),

Takotsubo cardiomyopathy in a senile female patient after transcatheter coil embolization of patent arterial duct

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