著者

Teruhiko Imamura Koichiro Kinugawa Masaru Hatano Takeo Fujino Toshiro Inaba Hisataka Maki Osamu Kinoshita Kan Nawata Shunei Kyo Minoru Ono Issei Komuro

出版者

日本循環器学会

雑誌

Circulation Journal (ISSN:13469843)

巻号頁・発行日

vol.78, no.9, pp.2259-2267, 2014-08-25 (Released:2014-08-25)

参考文献数

28

被引用文献数

17 48

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Background:Depressed hemodynamics stimulates arginine vasopressin (AVP) release, but the relationship between plasma AVP levels (P-AVP) and cardiac parameters, especially in patients with stage D heart failure (HF) receiving guideline-directed medical therapy, has not examined.Methods and Results:Data including P-AVP were obtained from 162 in-hospital patients with stage D HF and from 80 patients receiving ventricular assist device (VAD, n=46) or heart transplantation (HTx, n=34) at 3 months after surgery. In the HF group, considerably high P-AVP (5.9±6.1 pg/ml) negatively correlated with serum sodium concentration (S-Na, 135.3±5.8 mEq/L, r=–0.548 [P<0.01]) and cardiac index (CI, 2.2±0.5 L·min–1·m–2, r=–0.458 [P<0.01]). After VAD/HTx treatment, improvement in the CI (2.7±0.5 L·min–1·m–2[P<0.01] vs. HF) was accompanied by normalization of serum sodium concentration (S-Na; 138.2±2.0 mEq/L [P<0.01] vs. HF) and suppressed release of AVP (1.7±3.4 pg/ml [P<0.01] vs. HF). P-AVP positively correlated with only S-Na (r=0.454 [P<0.01]), whereas no correlation was observed with CI after VAD/HTx treatment. P-AVP ≥5.3 pg/ml well predicted poor 2-year survival in HF group (60% [P<0.01] vs. 90%).Conclusions:Low cardiac output stimulates AVP release via a non-osmotic process that results in hyponatremia and poor prognosis in patients with stage D HF. After sufficient recovery of cardiac output by cardiac replacement therapy, AVP release is suppressed and is mainly regulated by serum osmolality. (Circ J 2014; 78: 2259–2267)

著者

Norifumi Takeda Hiroki Yagi Hironori Hara Takayuki Fujiwara Daishi Fujita Kan Nawata Ryo Inuzuka Yuki Taniguchi Mutsuo Harada Haruhiro Toko Hiroshi Akazawa Issei Komuro

出版者

一般社団法人 インターナショナル・ハート・ジャーナル刊行会

雑誌

International Heart Journal (ISSN:13492365)

巻号頁・発行日

pp.16-094, (Released:2016-05-13)

被引用文献数

1 50

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Marfan syndrome (MFS) is an autosomal dominant heritable disorder of connective tissue that affects the cardiovascular, skeletal, ocular, pulmonary, and nervous systems and is usually caused by mutations in the FBN1 gene, which encodes fibrillin-1. MFS is traditionally considered to result from the structural weakness of connective tissue. However, recent investigations on molecular mechanisms indicate that increased transforming growth factor-β (TGF-β) activity plays a crucial role in the pathogenesis of MFS and related disorders, such as Loeys–Dietz syndrome (LDS), which is caused by mutation in TGF-β signaling-related genes. In addition, recent studies show that angiotensin II type 1 receptor (AT1R) signaling enhances cardiovascular pathologies in MFS, and the angiotensin II receptor blocker losartan has the potential to inhibit aortic aneurysm formation. However, the relationship between TGF-β and AT1R signaling pathways remains poorly characterized. In this review, we discuss the recent studies on the molecular mechanisms underlying cardiovascular manifestations of MFS and LDS and the ensuing strategies for management.

著者

Masahide Komagamine Kan Nawata Shota Kita Kiyoshi Chiba Shingo Kuwata Yoshihiro Akashi Takeshi Miyairi

出版者

The Editorial Committee of Annals of Thoracic and Cardiovascular Surgery

雑誌

Annals of Thoracic and Cardiovascular Surgery (ISSN:13411098)

巻号頁・発行日

pp.cr.22-00002, (Released:2022-03-26)

参考文献数

8

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From April 2018 to February 2021, 150 patients underwent MitraClip implantation for severe functional mitral regurgitation (MR) at our hospital. Two of our patients, an 85-year-old man and an 84-year-old woman, developed a single leaflet device attachment in the acute phase after the implantation and had severe residual MR requiring surgical correction. The recurrent MR was first pointed out on day 5 and day 4, and the duration between MitraClip implantation and surgery was 13 and 55 days, respectively. Due to strong adhesions with the clips and severe valve damage after MitraClip implantation, both cases underwent mitral valve replacement with a good postoperative course. In patients with a high-risk baseline profile, surgical mitral valve replacement after failed MitraClip implantation should be considered at an optimal timing, and a detailed echocardiographic follow-up is required.