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Articles by H Kawano
Total Records ( 2 ) for H Kawano
  H Yamabe , Y Tanaka , K Morihisa , T Uemura , K Enomoto , H Kawano and H. Ogawa
 

Background— Calcium channel–dependent tissue has been suggested to be involved in the circuit of verapamil-sensitive atrial tachycardia originating from the atrioventricular (AV) node vicinity (V-AT), but little information exists.

Methods and Results— To examine the tachycardia circuit of V-AT, a single extrastimulus was delivered during tachycardia to 10 sites of the intraatrial septum: the earliest atrial activation site; His bundle (HB) site; 3 arbitrarily divided sites on the AV junction extending from the HB site to the coronary sinus ostium (CSOS) (sites S, M, and I); the internal-CSOS, inferior-CSOS, superior-CSOS, posterior-CSOS, and posteroinferior-CSOS in 10 patients with V-AT. The longest coupling interval that reset V-AT and subsequent return cycle were measured. The longest coupling interval at earliest atrial activation site was significantly longer than the longest coupling interval at the HB site, site S, M, and I, internal-CSOS, inferior-CSOS, superior-CSOS, posterior-CSOS, and posteroinferior-CSOS, respectively (P<0.001 for HB site and P<0.0001 for the remaining 8 sites). The return cycle at earliest atrial activation site did not differ from the tachycardia cycle length, whereas those at the remaining 9 sites were significantly longer than tachycardia cycle length (P<0.001). Furthermore, a single extrastimulus delivered from sites inferior to the HB site advanced His potential without resetting V-AT in 7 patients in whom AV block was not observed during tachycardia.

Conclusions— Atrial tissue within the Koch’s triangle extending from the HB site to posteroinferior-CSOS is not involved in the tachycardia circuit. Verapamil-sensitive atrial tissue close to the AV node but not the AV nodal conducting system forms the tachycardia circuit of V-AT.

  M Iemitsu , H Murakami , K Sanada , K Yamamoto , H Kawano , Y Gando and M. Miyachi
 

The TT genotype of C677T polymorphism in 5,10-methylenetetrahydrofolate reductase (MTHFR) induces elevation of homocysteine level and leads to atherosclerosis and arterial stiffening. Furthermore, cardiorespiratory fitness level is also associated with arterial stiffness. In the present study, a cross-sectional investigation of 763 Japanese men and women (18–70 yr old) was performed to clarify the effects of cardiorespiratory fitness on the relationship between arterial stiffness and MTHFR C677T gene polymorphism. Arterial stiffness was assessed by carotid β-stiffness with ultrasonography and tonometry. The study subjects were divided into high-cardiorespiratory fitness (High-Fit) and low-cardiorespiratory fitness (Low-Fit) groups based on the median value of peak oxygen uptake in each sex and decade. The plasma homocysteine level was higher in the TT genotype of MTHFR C677T polymorphism compared with CC and CT genotype individuals. MTHFR C677T polymorphism showed no effect on carotid β-stiffness, but there was a significant interaction effect between fitness and MTHFR C677T polymorphism on carotid β-stiffness (P = 0.0017). In the Low-Fit subjects, carotid β-stiffness was significantly higher in individuals with the TT genotype than the CC and CT genotypes. However, there were no such differences in High-Fit subjects. In addition, β-stiffness and plasma homocysteine levels were positively correlated in Low-Fit subjects with the TT genotype (r = 0.71, P < 0.0001), but no such correlations were observed in High-Fit subjects. In CC and CT genotype individuals, there were also no such correlations in either fitness level. These results suggest that the higher cardiorespiratory fitness may attenuate central artery stiffening associated with MTHFR C677T polymorphism.

 
 
 
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