著者
Kenshi Hayashi Toyonobu Tsuda Akihiro Nomura Noboru Fujino Atsushi Nohara Kenji Sakata Tetsuo Konno Chiaki Nakanishi Hayato Tada Yoji Nagata Ryota Teramoto Yoshihiro Tanaka Masa-aki Kawashiri Masakazu Yamagishi on behalf of the Hokuriku-Plus AF Registry Investigators
出版者
The Japanese Circulation Society
雑誌
Circulation Journal (ISSN:13469843)
巻号頁・発行日
pp.CJ-17-1085, (Released:2018-03-01)
参考文献数
22
被引用文献数
30

Background:B-type natriuretic peptide (BNP) may be a predictor of stroke risk in patients with nonvalvular atrial fibrillation (NVAF); because heart failure is associated with the incidence of stroke in AF patients. However, limited data exist regarding the association between BNP at baseline and risks of thromboembolic events (TE) and death in NVAF patients.Methods and Results:We prospectively studied 1,013 NVAF patients (725 men, 72.8±9.7 years old) from the Hokuriku-plus AF Registry to determine the relationship between BNP at baseline and prognosis among Japanese NVAF patients. During the follow-up period (median, 751 days); 31 patients experienced TE and there were 81 cases of TE/all-cause death. For each endpoint we constructed receiver-operating characteristic curves that gave cutoff points of BNP for TE (170 pg/mL) and TE/all-cause death (147 pg/mL). Multivariate analysis with the Cox-proportional hazards model indicated that high BNP was significantly associated with risks of TE (hazard ratio [HR] 3.86; 95% confidence interval [CI] 1.83–8.67; P=0.0003) and TE/all-cause death (HR 2.27; 95% CI 1.45–3.56; P=0.0003). Based on the C-index and net reclassification improvement, the addition of BNP to CHA2DS2-VASc statistically improved the prediction of TE.Conclusions:In a real-world cohort of Japanese NVAF patients, high BNP was significantly associated with TE and death. Plasma BNP might be a useful biomarker for these adverse clinical events.
著者
Hayato Tada Masa-aki Kawashiri Taiji Yoshida Ryota Teramoto Atsushi Nohara Tetsuo Konno Akihiro Inazu Hiroshi Mabuchi Masakazu Yamagishi Kenshi Hayashi
出版者
日本循環器学会
雑誌
Circulation Journal (ISSN:13469843)
巻号頁・発行日
pp.CJ-15-0999, (Released:2015-12-02)
参考文献数
39
被引用文献数
7 62

Background:It has been shown that serum lipoprotein(a) [Lp(a)] is elevated in familial hypercholesterolemia (FH) with mutation(s) of the LDL receptor (LDLR) gene. However, few data exist regarding Lp(a) levels in FH with gain-of-function mutations of the PCSK9 gene.Methods and Results:We evaluated 42 mutation-determined heterozygous FH patients with aPCSK9gain-of-function mutation (FH-PCSK9, mean age 52, mean LDL-C 235 mg/dl), 198 mutation-determined heterozygous FH patients with aLDLRmutation (FH-LDLR, mean age 44, mean LDL-C 217 mg/dl), and 4,015 controls (CONTROL, mean age 56, mean LDL-C 109 mg/dl). We assessed their Lp(a), total cholesterol, triglycerides, HDL-C, LDL-C, use of statins, presence of hypertension, diabetes, chronic kidney disease, smoking, body mass index (BMI) and coronary artery disease (CAD). Multiple regression analysis showed that HDL-C, use of statins, presence of hypertension, smoking, BMI, and Lp(a) were independently associated with the presence of CAD. Under these conditions, the serum levels of Lp(a) in patients with FH were significantly higher than those of the CONTROL group regardless of their causative genes, among the groups propensity score-matched (median Lp(a) 12.6 mg/dl [IQR:9.4–33.9], 21.1 mg/dl [IQR:11.7–34.9], and 5.0 mg/dl [IQR:2.7–8.1] in the FH-LDLR, FH-PCSK9, and CONTROL groups, respectively, P=0.002 for FH-LDLR vs. CONTROL, P=0.002 for FH-PCSK9 vs. CONTROL).Conclusions:These data demonstrate that serum Lp(a) is elevated in patients with FH caused by PCSK9 gain-of-function mutations to the same level as that in FH caused by LDLR mutations.
著者
Kiyoo Mori Kazunori Yamada Tetsuo Konno Dai Inoue Yoshihide Uno Michio Watanabe Miho Okuda Kotaro Oe Mitsuhiro Kawano Masakazu Yamagishi
出版者
一般社団法人 日本内科学会
雑誌
Internal Medicine (ISSN:09182918)
巻号頁・発行日
vol.54, no.10, pp.1231-1235, 2015 (Released:2015-05-15)
参考文献数
17
被引用文献数
4 24

We herein report the case of a 65-year-old man with pericardial involvement associated with autoimmune pancreatitis. Chest CT imaging showed pericardial thickening. The patient responded to corticosteroid therapy, and the pericardial thickening resolved. Multiple organs are involved in immunoglobulin G4 (IgG4)-related disease (IgG4-RD); however, only a few cases of IgG4-related chronic constrictive pericarditis have been reported. To our knowledge, this is the first reported case of IgG4-RD with pericardial involvement at an early stage. This case indicates that recognizing pericardial complications in autoimmune pancreatitis is important and that CT imaging may be useful for obtaining the diagnosis and providing follow-up of pericardial lesions in cases of IgG4-RD.
著者
Tadatsugu Gamou Kenji Sakata Hayato Tada Tetsuo Konno Kenshi Hayashi Hidekazu Ino Masakazu Yamagishi Masa-aki Kawashiri on behalf of the MILLION Study Group
出版者
日本循環器学会
雑誌
Circulation Journal (ISSN:13469843)
巻号頁・発行日
vol.81, no.10, pp.1490-1495, 2017-09-25 (Released:2017-09-25)
参考文献数
31
被引用文献数
4

Background:The MILLION study, a prospective randomized multicenter study, revealed that lipid and blood pressure (BP)-lowering therapy resulted in regression of coronary plaque as determined by intravascular ultrasound (IVUS). In the present study we performed additional analysis to investigate the associated factors with regression of coronary plaque.Methods and Results:We investigated serial 3D IVUS images from 68 patients in the MILLION study. Standard IVUS parameters were assessed at both baseline and follow-up (18–24 months). Volumetric data were standardized by length as normalized volume. In patients with plaque regression (n=52), plaque volumenormalizedsignificantly decreased from 64.8 to 55.8 mm3(P<0.0001) and vessel volumenormalizedsignificantly decreased from 135.0 to 127.5 mm3(P=0.0008). There was no difference in lumen volumenormalizedfrom 70.1 to 71.8 mm3(P=0.27). There were no correlations between % changes in vessel volume and cholesterol or BP. On the other hand, negative correlations between % change in vessel volume and vessel volumenormalizedat baseline (r=−0.352, P=0.009) or plaque volumenormalizedat baseline (r=−0.336, P=0.01) were observed.Conclusions:The current data demonstrated that in patients with plaque regression treated by aggressive lipid and BP-lowering therapy, the plaque regression was derived from reverse vessel remodeling determined by vessel volume and plaque burden at baseline irrespective of decreases in lipids and BP.