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ABSTRACT: The mitral early to late diastolic flow velocity ratio (E/A ratio) is age-dependent. It has been considered that its age dependency reflects the age-related lengthening of left ventricular (LV) relaxation; however, the change in E/A ratio is far larger than that expected from those in LV relaxation. We hypothesized that an age-related reduction of the parasympathetic activity increases left atrial (LA) contractility, and that this accounts for the age-related change in E/A ratio. (1) Exercise stress test was performed in 61 normal subjects (age range, 8-80 years, mean, 40 years) to assess heart rate (HR) recovery because slowed HR recovery indicates lowered parasympathetic activity. There were good interrelations among age, E/A ratio, and HR recovery. Among those aged ≤30 years, the age no longer correlated with E/A ratio or HR recovery, but there was a significant correlation between HR recovery and E/A ratio (r = 0.44, p < 0.05). (2) Pulsed Doppler and two-dimensional speckle tracking echocardiography (2DSTE) were performed before and after administration of parasympathetic blockade (atropine) in ten young healthy subjects. LA booster pump function was assessed with LA emptying index calculated by 2DSTE. LA emptying index was calculated from ([LA volume before the atrial contraction - minimal LA volume]/LA volume before the atrial contraction) × 100. Atropine increased mitral A velocity (p < 0.001) and LA emptying index (p < 0.05) along with a decrease in E/A ratio (p < 0.001). Parasympathetic withdrawal enhances LA contraction and increases mitral A velocity, which likely cause a reciprocal decrease in mitral E velocity and E/A ratio. Thus, parasympathetic deactivation with aging should be closely involved in the age-related change in mitral E/A ratio.
Heart and Vessels 05/2013; · 2.05 Impact Factor
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ABSTRACT: OBJECTIVE:: Iron accumulation is associated with the pathogenesis of chronic kidney disease (CKD). However, little is known about the effects of isolated iron restriction against CKD. We have recently reported that iron restriction prevents the development of renal damage in the well established 5/6 nephrectomy rat model of CKD. Herein, we investigated the therapeutic effects of iron restriction on preexisting hypertension and renal damage in a rat model of CKD. METHODS:: CKD was induced by 5/6 nephrectomy in Sprague-Dawley rats. After surgery, 5/6 nephrectomized rats were given an iron-restricted diet from 1 day to 16 weeks for prevention protocol or from 8 to 16 weeks for rescue protocol. Other CKD rats were given a normal diet. RESULTS:: At 16 weeks after surgery, CKD rats developed hypertension and renal damage. Early intervention with iron restriction prevented the development of hypertension and vascular remodeling. By contrast, late intervention with iron restriction did not remarkably ameliorate preexisting hypertension and vascular remodeling in CKD rats. On the contrary, late intervention with iron restriction prevented further progression of preexisting renal damage in CKD rats. Interestingly, iron restriction led to increased urinary sodium and decreased urinary potassium excretions in CKD rats. Moreover, iron restriction markedly attenuated renal expression of nuclear mineralocorticoid receptor and Rac1 activity in CKD rats. CONCLUSION:: Iron restriction prevented further deterioration of preexisting renal damage. The beneficial effects of iron restriction on renal damage seem to be associated with inhibition of renal mineralocorticoid receptor signaling.
Journal of hypertension 04/2013; · 4.02 Impact Factor
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International journal of cardiology 02/2013; · 7.08 Impact Factor
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Hisashi Sawada,
Yoshiro Naito,
Shinichi Hirotani,
Hirokuni Akahori,
Toshihiro Iwasaku,
Yoshitaka Okuhara,
Kojiro Miki, Akiyo Eguchi,
Masataka Mitsuno,
Yuji Miyamoto,
Mitsumasa Ohyanagi,
Takeshi Tsujino,
Tohru Masuyama
International journal of cardiology 01/2013; · 7.08 Impact Factor
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ABSTRACT: : Iron is associated with the pathogenesis of chronic kidney disease (CKD). Activation of mineralocorticoid receptor signaling is implicated in CKD; however, a link between iron and mineralocorticoid receptor signaling in CKD remains unknown. We have previously shown that long-term dietary iron restriction leads to increased sodium and decreased potassium excretions in the rat urine. Herein, we investigated the effect of iron restriction on renal damage and mineralocorticoid receptor signaling in a rat model of CKD.
: CKD was induced by 5/6 nephrectomy in Sprague-Dawley rats. CKD rats were divided into untreated and dietary iron-restricted groups.
: CKD rats exhibited proteinuria, glomerulosclerosis, tubulointerstitinal damage, and podocyte injury. In contrast, these changes were attenuated by 16 weeks of iron-restricted diet. Consistent with these findings, iron restriction suppressed increased gene expression of collagen type III, transforming growth factor-β, CD68, and tumor necrosis factor-α in the CKD kidney. Importantly, increased expression of nuclear mineralocorticoid receptor and SGK1, a key downstream effector of mineralocorticoid receptor signaling, in the CKD kidney was markedly attenuated by iron restriction. Of interest, expression of cellular iron transport proteins, transferrin receptor 1, and divalent metal transporter 1 was increased in the CKD renal tubules, along with increased iron accumulation, superoxide production, and urinary iron excretion. CKD rats also developed hypertension, although iron restriction suppressed the development of hypertension.
: Taken together, these data uncover a novel effect of iron restriction on renal damage and hypertension through the inhibition of renal mineralocorticoid receptor signaling.
Journal of hypertension 08/2012; 30(11):2192-201. · 4.02 Impact Factor
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Hisashi Sawada,
Yoshiro Naito,
Shinichi Hirotani,
Hirokuni Akahori,
Toshihiro Iwasaku, Akiyo Eguchi,
Yoshitaka Okuhara,
Aya Fujii,
Mitsumasa Ohyanagi,
Masataka Mitsuno,
Yuji Miyamoto,
Takeshi Tsujino,
Tohru Masuyama
International journal of cardiology 07/2011; 152(1):107-9. · 7.08 Impact Factor
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Kenichi Fujii,
Daizo Kawasaki,
Katsumi Oka,
Hirokuni Akahori,
Toshihiro Iwasaku,
Masashi Fukunaga, Akiyo Eguchi,
Hisashi Sawada,
Motomaru Masutani,
Masaaki Lee-Kawabata,
Takeshi Tsujino,
Mitsumasa Ohyanagi,
Tohru Masuyama
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ABSTRACT: This study evaluated the effect of pravastatin pre-treatment on post-procedural index of microcirculatory resistance (IMR) values that are introduced for assessing the status of the microcirculation independently of the epicardial area.
Pre-treatment with statins decreased the incidence of cardiac enzyme increase after percutaneous coronary intervention (PCI). However, 2 different etiologies, distal embolization of atheroma or ischemia caused by side-branch occlusion, cannot be differentiated by measuring cardiac enzyme levels.
Eighty patients with stable angina were randomly assigned to either pravastatin treatment (20 mg/day, n = 40) or no treatment (n = 40) 4 weeks before elective PCI. An intracoronary pressure/temperature sensor-tipped guidewire was used. Thermodilution curves were obtained during maximal hyperemia. The IMR was calculated from the ratio of the mean distal coronary pressure at maximal hyperemia to the inverse of mean hyperemic transit time. Creatine kinase-myocardial band and troponin I values were measured at baseline and at 8 and 24 h after PCI.
Post-PCI troponin I levels tended to be lower in patients with pravastatin treatment (median: 0.13 [interquartile range (IQR): 0.10 to 0.31] vs. 0.22 [IQR: 0.10 to 0.74] ng/ml, p = 0.1). However, patients with pravastatin treatment had significantly lower IMR than did patients without pravastatin treatment (median: 12.6 [IQR: 8.8 to 18.0] vs. 17.6 [IQR: 9.7 to 33.9], p = 0.007). Multivariate analysis revealed that the lack of pravastatin pre-treatment was the only independent predictor of post-PCI impaired IMR (p = 0.03).
Post-PCI measurement of the IMR confirmed that pre-treatment with pravastatin was associated with reduced microvascular dysfunction induced by PCI regardless of side branch occlusions. These data suggest that pre-treatment with statin is desired in patients undergoing elective PCI. (The Impact of Pravastatin Pretreatment on Periprocedural Microcirculatory Damage After Percutaneous Coronary Intervention; UMIN000002885).
05/2011; 4(5):513-20. · 1.07 Impact Factor
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Chikako Yoshida,
Shinji Nakao,
Akiko Goda,
Yoshiro Naito,
Mika Matsumoto,
Misato Otsuka,
Miho Shimoshikiryo, Akiyo Eguchi,
Masaaki Lee-Kawabata,
Takeshi Tsujino,
Tohru Masuyama
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ABSTRACT: We assessed the comparative value of measurements of tissue Doppler early diastolic mitral annular velocity (E'), left atrial diameter (LAD), and left atrial volume (LAV) in patients with possible heart failure (HF) but with normal left ventricular (LV) ejection fraction (EF) and mitral flow velocity pattern.
We determined LAV and LAD indexes in addition to the ratio of peak early diastolic mitral flow velocity (E) to E' (E/E' ratio) in 91 patients with all three of the followings: HF, LVEF of greater than 55%, and normal mitral E/A ratio between 0.8 and 1.5. Twenty healthy subjects were used as controls. E/E' ratio was abnormal (>1.5) in 38 of the 91 patients (sensitivity=44%). LAV index was 32 mL/m(2) or greater in 71 of the 91 patients (sensitivity=78%), while LAD index was 27 mm/m(2) or greater in 81 of 91 patients (sensitivity=89%). The area under the curve by receiver-operator curve analyses was 0.995 for LA volume index, 0.998 for LAD index, and 0.885 for E/E' ratio.
LAV and LAD indexes are more useful in detecting with HF and normal EF patients than E' related parameters.
European Heart Journal – Cardiovascular Imaging 10/2008; 10(2):278-81. · 2.32 Impact Factor
