Yoshitaka Fujimoto

A medical link between local maternity hospitals and a tertiary center using telediagnosis with fetal cardiac ultrasound image transmission.

Information and communication technology has been widely applied to various fields, including clinical medicine. We report here a telediagnosis system using ultrasound image transmission. The effect of telediagnosis, using a medical link between local maternity hospitals and our children’s medical center, was verified. The number of fetal teledignoses for cardiac disease, and cases referred to a perinatal care center and emergent transportation of neonates with congenital heart disease from maternity hospitals, were calculated based on the hospital records. The percentage of patients found to have heart disease was compared between out-patient clinic and telediagnosis cases. Telediagnosis increased, allowing maternity hospital staff to obtain support easily from a specialist when making a diagnosis. Many severe cases were transferred to tertiary centers with the correct diagnosis; consequently, the number of emergent transportations of neonates with severe cardiac anomalies continued to below. Telediagnosis was also useful as an educational tool for maternity hospital staff, who improved their skills during conversations with a specialist. Unlike in the outpatient clinic, consultation by telediagnosis was requested even for cases of mild abnormalities, and the number of false-positives increased, while many cardiac anomalies were found in the early stage. Furthermore, telediagnosis was helpful for pregnant women requiring bed rest, and also had the advantage of allowing a doctor to be able to talk with parents. Establishing a fetal telediagnosis system is a useful strategy to improve neonatal care through a medical link between local maternity hospitals and a tertiary center.

Pulmonary hypertension due to left heart disease causes intrapulmonary venous arterialization in rats

Objective: A rat model of left atrial stenosis–associated pulmonary hypertension due to left heart diseases was prepared to elucidate its mechanism. Methods: Five‐week‐old Sprague–Dawley rats were randomly divided into 2 groups: left atrial stenosis and sham‐operated control. Echocardiography was performed 2, 4, 6, and 10 weeks after surgery, and cardiac catheterization and organ excision were subsequently performed at 10 weeks after surgery. Results: Left ventricular inflow velocity, measured by echocardiography, significantly increased in the left atrial stenosis group compared with that in the sham‐operated control group (2.2 m/s, interquartile range [IQR], 1.9‐2.2 and 1.1 m/s, IQR, 1.1‐1.2, P < .01), and the right ventricular pressure‐to‐left ventricular systolic pressure ratio significantly increased in the left atrial stenosis group compared with the sham‐operated control group (0.52, IQR, 0.54‐0.60 and 0.22, IQR, 0.15‐0.27, P < .01). The right ventricular weight divided by body weight was significantly greater in the left atrial stenosis group than in the sham‐operated control group (0.54 mg/g, IQR, 0.50‐0.59 and 0.39 mg/g, IQR, 0.38‐0.43, P < .01). Histologic examination revealed medial hypertrophy of the pulmonary vein was thickened by 1.6 times in the left atrial stenosis group compared with the sham‐operated control group. DNA microarray analysis and real‐time polymerase chain reaction revealed that transforming growth factor‐&bgr; mRNA was significantly elevated in the left atrial stenosis group. The protein levels of transforming growth factor‐&bgr; and endothelin‐1 were increased in the lung of the left atrial stenosis group by Western blot analyses. Conclusions: We successfully established a novel, feasible rat model of pulmonary hypertension due to left heart diseases by generating left atrial stenosis. Although pulmonary hypertension was moderate, the pulmonary hypertension due to left heart diseases model rats demonstrated characteristic intrapulmonary venous arterialization and should be used to further investigate the mechanism of pulmonary hypertension due to left heart diseases.

Accuracy of telediagnosis of fetal heart disease using ultrasound images transmitted via the Internet

We verified the feasibility of telediagnosis of fetal disease by (i) grading telediagnosis by a pediatric cardiologist into five confidence levels; and (ii) comparison of fetal telediagnosis with hands‐on fetal diagnosis or postnatal diagnosis. In 114 patients suspected of having heart disease (real time, n = 15; recorded image transmission, n = 99), 79 patients were in level 5 (excellent), 17 in level 4 (good), eight in level 3 (fair), 10 in level 2 (poor), and no patients in level 1 (bad). The average was 4.5, and in 96 patients (84% of all) telediagnosis was accurate (above 4), whereas in 18 patients it was inaccurate (level 2 or 3). In re‐examination of 25 patients, telediagnosis was confirmed in patients in level 4 and 5, whereas heart disease was missed in patients in levels 2 or 3. The correct diagnosis matched the high confidence level of a specialist based on recognizable transmitted images.

Impairment of Excitation-Contraction Coupling in Right Ventricular Hypertrophied Muscle with Fibrosis Induced by Pulmonary Artery Banding.

Interstitial myocardial fibrosis is one of the factors responsible for dysfunction of the heart. However, how interstitial fibrosis affects cardiac function and excitation-contraction coupling (E-C coupling) has not yet been clarified. We developed an animal model of right ventricular (RV) hypertrophy with fibrosis by pulmonary artery (PA) banding in rats. Two, four, and six weeks after the PA-banding operation, the tension and intracellular Ca2+ concentration of RV papillary muscles were simultaneously measured (n = 33). The PA-banding rats were clearly divided into two groups by the presence or absence of apparent interstitial fibrosis in the papillary muscles: F+ or F- group, respectively. The papillary muscle diameter and size of myocytes were almost identical between F+ and F-, although the RV free wall weight was heavier in F+ than in F-. F+ papillary muscles exhibited higher stiffness, lower active tension, and lower Ca2+ responsiveness compared with Sham and F- papillary muscles. In addition, we found that the time to peak Ca2+ had the highest correlation coefficient to percent of fibrosis among other parameters, such as RV weight and active tension of papillary muscles. The phosphorylation level of troponin I in F+ was significantly higher than that in Sham and F-, which supports the idea of lower Ca2+ responsiveness in F+. We also found that connexin 43 in F+ was sparse and disorganized in the intercalated disk area where interstitial fibrosis strongly developed. In the present study, the RV papillary muscles obtained from the PA-banding rats enabled us to directly investigate the relationship between fibrosis and cardiac dysfunction, the impairment of E-C coupling in particular. Our results suggest that interstitial fibrosis worsens cardiac function due to 1) the decrease in Ca2+ responsiveness and 2) the asynchronous activation of each cardiac myocyte in the fibrotic preparation due to sparse cell-to-cell communication.

Low cardiac output leads hepatic fibrosis in right heart failure model rats

Background Hepatic fibrosis progresses with right heart failure, and becomes cardiac cirrhosis in a severe case. Although its causal factor still remains unclear. Here we evaluated the progression of hepatic fibrosis using a pulmonary artery banding (PAB)-induced right heart failure model and investigated whether cardiac output (CO) is responsible for the progression of hepatic fibrosis. Methods and Results Five-week-old Sprague-Dawley rats divided into the PAB and sham-operated control groups. After 4 weeks from operation, we measured CO by echocardiography, and hepatic fibrosis ratio by pathological examination using a color analyzer. In the PAB group, CO was significantly lower by 48% than that in the control group (78.2±27.6 and 150.1±31.2 ml/min, P<0.01). Hepatic fibrosis ratio and serum hyaluronic acid, an index of hepatic fibrosis, were significantly increased in the PAB group than those in the control group (7.8±1.7 and 1.0±0.2%, P<0.01, 76.2±27.5 and 32.7±7.5 ng/ml, P<0.01). Notably, the degree of hepatic fibrosis significantly correlated a decrease in CO. Immunohistological analysis revealed that hepatic stellate cells were markedly activated in hypoxic areas, and HIF-1α positive hepatic cells were increased in the PAB group. Furthermore, by real-time PCR analyses, transcripts of profibrotic and fibrotic factors (TGF-β1, CTGF, procollargen I, procollargen III, MMP 2, MMP 9, TIMP 1, TIMP 2) were significantly increased in the PAB group. In addition, western blot analyses revealed that the protein level of HIF-1α was significantly increased in the PAB group than that in the control group (2.31±0.84 and 1.0±0.18 arbitrary units, P<0.05). Conclusions Our study demonstrated that low CO and tissue hypoxia were responsible for hepatic fibrosis in right failure heart model rats.

An Infant with Bilateral Isolated Pulmonary Vein Stenosis

An Infant with Bilateral Isolated Pulmonary Vein Stenosis Yoshitaka Fujimoto1, 2), Kiyoshi Ogawa1), Fumie Kawachi1, 2), Kenji Sugamoto1), Takashi Hishitani1), Kenji Hoshino1, 2), Kouichi Muramatsu3), Gen Shinohara3), Kouji Nomura3), Hiroyuki Ida2) 1)Division of Cardiology, Saitama Children’s Medical Center, Saitama, Japan 2)Department of Pediatrics, Jikei University School of Medicine, Tokyo, Japan 3)Division of Cardiovascular Surgery, Saitama Children’s Medical Center, Saitama, Japan