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Hidekazu Miyazaki

Publications and source records attributed to Hidekazu Miyazaki.

12 recordsLinked to original sources

Dual mechanisms underlying pulmonary vein tachycardias in a patient with paroxysmal atrial fibrillation.

We report a case of a 46-year-old man with paroxysmal atrial fibrillation who underwent pulmonary vein isolation. After a complete isolation of each pulmonary vein was performed, two different types of pulmonary vein tachycardia appeared: a regular tachycardia in the left inferior pulmonary vein with a supposed reentrant mechanism, and an irregular tachycardia in the right superior PV showing a nonreentrant character.

Atrial Fibrillation↗

Behavior of atrial ectopic beats before and after pulmonary vein isolation in patients with atrial fibrillation: a reduction in the number and arrhythmogenicity of ectopic firings.

BACKGROUND: No studies evaluating in a quantitative manner the effect of pulmonary vein (PV) isolation on the behavior of atrial premature beats have been reported. OBJECTIVES: The purpose of this study was to reveal the behavior of atrial premature beats before and after PV isolation in patients with paroxysmal atrial fibrillation (AF). METHODS: In 108 patients free from AF following PV isolation, both the number of atrial premature beats and their coupling intervals before and following PV isolation were evaluated with periodic 24-hour ambulatory monitoring. RESULTS: After a successful PV isolation procedure (group 1, n = 78), the number of atrial premature beats significantly decreased with two distinct time courses: an acute reduction on the following day and a subsequent gradual decrease throughout the whole observation period. The mean atrial premature beat coupling interval at baseline was 420 +/- 30 ms, which was significantly prolonged to 560 +/- 100 ms at 3 months after PV isolation (P <.01). Although patients with AF recurrence after PV isolation (group 2, n = 30) had transiently depressed atrial premature beats shortly after the procedure, they recovered to the former level 3 months after PV isolation. Repeat PV isolation targeting the reconnected PVs successfully suppressed these residual atrial premature beats both in their number and the coupling interval in a manner similar to those in group 1. CONCLUSION: Successful PV isolation reduced the number of atrial premature beats with both rapid and gradual time courses. The residual atrial premature beats appeared less arrhythmogenic, with longer coupling intervals than those at baseline. AF recurrences after PV isolation were associated with increased atrial premature beat number and shortened coupling interval, which were depressed by reisolation of reconnected PVs.

Atrial Fibrillation↗

Entrainment mapping for rapid distinction of left and right atrial tachycardias.

BACKGROUND: Distinguishing left from right atrial tachycardia is a critical step for guiding ablation. OBJECTIVES: The purpose of this study was to develop and validate a simple algorithm predicting the location of macroreentrant atrial tachycardia (AT) circuits from limited entrainment mapping in right atrium (RA) and coronary sinus (CS). METHODS: In 180 patients with organized reentrant AT, entrainment was performed at the high RA, proximal CS, and distal CS. The difference between the postpacing interval (PPI) and tachycardia cycle length (TCL) was calculated at each site. The location of the AT reentrant circuit was determined by mapping and ablation. An algorithm predicting AT regions was developed from 104 ATs in the first 90 patients (group I) and prospectively evaluated in a validation cohort of 106 ATs in the second 90 patients (group II). RESULTS: In group I, PPI-TCL difference <50 or >50 ms at the high RA distinguished RA from LA reentrant circuits. For RA tachycardias, PPI-TCL difference at the proximal CS distinguished common flutter from lateral RA circuits. For LA circuits, PPI-TCL difference at the proximal and distal CS distinguished perimitral reentry from reentry involving the right pulmonary veins and septum. In group II, an algorithm based on PPI-TCL difference >50 or <50 ms at the high RA, proximal CS, or distal CS had sensitivity of 94%, specificity of 88%, and predictive accuracy of 93% for predicting the successful ablation region. CONCLUSION: Limited entrainment from sites accessible from the RA can expeditiously suggest the AT location to guide more detailed mapping and potentially avoid unnecessary transseptal punctures in some patients.

Adult↗

Myocyte morphological characteristics differ between the phases of pulmonary hypertension-induced ventricular hypertrophy and failure.

Pulmonary hypertensive model rats were prepared by treating them with monochrotaline (MCT). Using these model rats, we examined myocyte remodeling in the right ventricle in response to increased right ventricular pressure. Male Sprague-Dawley rats were divided into 2 groups. Group M received MCT and group C received physiological saline. The 2 groups were examined at weeks 2, 5, and 7 after MCT or saline injection, respectively. At week 2, a significant difference in cell form was not observed in either group. At week 5, cell volume and myocyte cross-sectional area (CSA) of the right ventricle in group M were significantly greater than those in group C. At week 7, cell volume, CSA, and cell length of the right ventricle in group M were all significantly greater than those in group C. These results suggest that pulmonary hypertension causes hypertrophy, accompanying the enlargement of CSA in the right ventricle, and that cells lengthen in the phase of right ventricular failure. These results are similar to the changes observed in left ventricular myocytes due to overload pressure. Both right and left ventricular myocytes may share a common mechanism for myocyte remodeling as an adaptive and maladaptive response to increased ventricular pressure.

Animals↗

Chronobiological analysis by ambulatory blood pressure monitoring of the hyperbaric and hypobaric indexes for evaluation of the antihypertensive effect of long-acting nifedipine.

BACKGROUND: It has been suggested that chronobiology can provide new insights into the evaluation and treatment of cardiovascular disease. In the present study the hyperbaric index (hyperBI) and hypobaric index (hypoBI) were compared with the mean blood pressure (BP) over 24 h to evaluate the antihypertensive effect of long-acting nifedipine on essential hypertension. METHODS AND RESULTS: Fourteen patients were treated with nifedipine CR (20-40 mg/day) for 6 months. Ambulatory BP monitoring was performed before and after treatment. The hyperBI (mmHg . h/day) was calculated as the integrated BP area above the conventional upper limit (140/90 mmHg for the daytime and 120/80 mmHg at night), and the hypoBI was calculated as the integrated BP area below the conventional lower limit (110/60 mmHg for the daytime and 100/50 mmHg at night). At baseline, both the systolic and diastolic 24-h hyperBI values closely correlated with the 24-h mean BP (r=0.994 and 0.935, p<0.0001). Treatment with nifedipine significantly lowered both the 24-h mean systolic and diastolic BP (143+/-14/89 +/-12 to 124+/-16/80+/-8 mmHg, p<0.001/p=0.001), as well as the casual BP (167+/-11/101 +/-8 to 140+/-13/86+/-10 mmHg, p<0.001/p<0.01). Reduction of both the systolic and diastolic hyperBI values was statistically significant over the 24-h period (274+/-266 to 90+/-155, p=0.009; 145+/-187 to 41+/-63, p=0.024), as well as during the daytime (200+/-181 to 66+/-116, p=0.014; 105+/-120 to 24+/-38, p=0.017) and at night (systolic, 74+/-106 to 24+/-52, p=0.021). The 24-h mean BP was normalized, but a small excess BP load persisted despite treatment. There was no significant increase of systolic hypoBI during the 24-h period (1+/-2 to 25+/-30, p=0.065), the daytime (0+/-0 to 14+/-38, p=0.20), or at night (1+/-3 to 11+/-19, p=0,052). Similar findings were obtained for diastolic hypoBI. CONCLUSIONS: Nifedipine CR improved the 24-h hyperBI and mean BP without causing excessive hypotension. These 2 parameters have a close relationship when assessment is done by 24-h BP monitoring. The hyperBI and hypoBI may assist in providing adequate antihypertensive therapy for individual patients by detecting an excessive BP load or hypotension, respectively.

Blood Pressure↗

Focal source of atrial fibrillation arising from the ostium of the inferior vena cava.

A patient presented with paroxysmal atrial fibrillation (AF) caused by focal rapid discharges arising from the ostium of the inferior vena cava (IVC). Surface ECG showed typical features of AF and flutter when rapid activation at the IVC ostium was conducted to the right atrium in a 1-to-1 and 2-to-1 fashion, respectively. Discrete radiofrequency energy applications at the medial ostium of the IVC completely eliminated the atrial tachyarrhythmias.

Atrial Fibrillation↗

Atrial septal pacing to resynchronize atrial contraction and improve atrial transport function.

OBJECTIVES: Atrial septal pacing via a trans-septal breakthrough site within the right atrial septum can shorten global atrial activation time, resulting in significant reduction of recurrence of atrial fibrillation events. This study examined whether this pacing method will lead to resynchronization of atrial contraction and its benefit on hemodynamic function can be maintained for 24 months. METHODS: Thirty patients with atrial fibrillation and delayed atrial conduction were enrolled (17 males, 13 females, mean age 73 +/- 7 years). Trans-septal breakthrough site within the right atrial septum was identified through pacing from the dorsal left atrium. Continuous atrial septal pacing at the trans-septal breakthrough site was performed for 24 months. Time difference (TD) between right and left atrial contractions was measured during atrial septal pacing and sinus rhythm by pulse Doppler echocardiography of the trans-tricuspid (P-At) and mitral (P-Am) blood flows (TD = P-Am - P-At). RESULTS: The atrial lead was screwed near the fossa ovalis in 29 of 30 patients. Atrial septal pacing yielded significantly shorter P wave duration (101.9 +/- 10.4 vs 139.6 +/- 14.7 msec, p < 0.001), leading to significant reduction of TD in atrial contraction (-8.8 +/- 10.0 vs 29.8 +/- 13.6 msec, p < 0.001)as compared to sinus rhythm. Both shorter P wave duration and reduced TD during atrial septal pacing remained statistically significant during the follow-up period as compared to sinus rhythm. Both left atrial diameter and A to E ratio of filling waves at mitral valve were significantly decreased at 12 months and remained decreased at 24 months. CONCLUSIONS: Atrial septal pacing at the trans-septal breakthrough site can resynchronize atrial contraction and results in improved hemodynamic effects during 24 months of follow-up.

Aged↗

A focal source of atrial fibrillation in the superior vena cava: isolation and elimination by radiofrequency ablation with the guide of basket catheter mapping.

Although it has been reported that pulmonary veins sometimes act as a focal driver of atrial fibrillation (AF), little has been reported concerning the contribution of the superior vena cava (SVC) to the maintenance of AF. Here we report a patient with sustained AF due to focal discharges inside the SVC after pulmonary vein isolation procedure. Stepwise radiofrequency current applications with the guide of multielectrode basket catheter mapping first disconnected the arrhythmogenic SVC from the right atrium and then eliminated the tachycardia.

Atrial Fibrillation↗

Various routes of septal propagation in common atrial flutter.

INTRODUCTION: Although in the treatment of common atrial flutter, the isthmus between the tricuspid valve annulus and the eustachian ridge is often chosen as the site for conduction block by radiofrequency ablation, the precise path of the flutter circuit remains unknown. We therefore investigated the propagation of the atrial flutter wave front around the coronary sinus ostium and how its path is altered by application of radiofrequency current. METHODS AND RESULTS: To assess activation pattern, activation in the region surrounding the coronary sinus ostium was mapped using a deflectable decapolar catheter under basal conditions and while applying radiofrequency current to the septal isthmus, between the tricuspid valve annulus and the eustachian ridge. In five of eleven patients studied, the eustachian ridge side, below the coronary sinus ostium, was activated earlier, and the flutter wave exited from either the tricuspid valve annulus side or the eustachian ridge side, above the coronary sinus ostium. In four patients, a partial line of block created by applying radiofrequency current between the tricuspid valve annulus and the coronary sinus ostium or between the coronary sinus ostium and the eustachian ridge led to a shift in the direction of propagation of the flutter wave front from anterior to posterior or from posterior to anterior of the coronary sinus ostium, and prolongation of the cycle length. CONCLUSION: Application of radiofrequency current to the septal isthmus, between the tricuspid valve annulus and the eustachian ridge, can shift both the anterior and posterior propagation of flutter around the coronary sinus ostium.

Aged↗

Effect of low-dose isoproterenol infusion on left atrial appendage function soon after cardioversion of chronic atrial tachyarrhythmias.

BACKGROUND: Cardioversion of chronic atrial fibrillation or atrial flutter to sinus rhythm is often associated with transient atrial mechanical dysfunction, i.e. 'atrial stunning', which may increase the risk of subsequent thromboembolic events. We hypothesized that, because of its positive inotropic action, a low-dose isoproterenol infusion might improve postcardioversion atrial mechanical function. METHOD: Eighteen patients (15 male, three female; 12 atrial fibrillation, six atrial flutter; mean age 65+/-10 years) exhibiting atrial postcardioversion stunning were included in the study. Isoproterenol was infused for 10 min at a dose sufficient to increase the heart rate by about 10%. Using transesophageal echocardiography, both the left atrial appendage emptying/filling flow velocity and function (fractional area change) were examined at baseline, before isoproterenol (immediately after cardioversion) and after isoproterenol. RESULTS: With infusion of 0.005-0.008 microg/kg/min isoproterenol, heart rate increased by 11.1+/-2.9%, and left atrial appendage emptying velocity, which was diminished following cardioversion, increased significantly (P<0.001) (baseline, before and after isoproterenol: 41.1+/-18.0, 20.3+/-8.5 and 27.3+/-9.6 cm/s, respectively). No major complications were associated with isoproterenol infusion. CONCLUSIONS: Short-term infusion of low-dose isoproterenol improved atrial function after cardioversion of chronic atrial fibrillation and atrial flutter.

Aged↗

Perindopril reverses myocyte remodeling in the hypertensive heart.

Studies have shown that the renin-angiotensin system (RAS) plays an important role in cardiac remodeling induced by hypertension. However, the role of this system on myocyte remodeling remains unclear. In the present study, we have assessed the effect of perindopril, an angiotensin converting enzyme (ACE) inhibitor, in spontaneously hypertensive rats (SHRs) as a means to evaluate the role of RAS in myocyte remodeling. We also investigated the effect of beta blockade on myocyte remodeling. We used female SHRs at 12 weeks of age. They were divided into four experimental groups: a control group, group C; low dose perindopril group (0.3 mg/kg/day, p.o.), group PL; high dose perindopril group (3 mg/kg/day, p.o.), group PH; and bisoprolol group (60 mg/kg/day, p.o.), group B. We isolated myocytes from these rats after 4 weeks. LV myocyte volume and cross-sectional area decreased in groups PL and PH compared to group C. LV myocyte length decreased in group PH compared to group C. However, there was no morphological change in LV myocytes in group B compared to group C. In summary, ACE inhibitors reversed cardiac hypertrophy mainly by a reduction in LV myocyte volume; however, beta blockade did not reverse myocyte remodeling. These results suggest that RAS plays an important role in myocyte remodeling in the hypertensive heart.

Adrenergic beta-Antagonists↗