Biomedical subjects

W Shimizu

Publications and source records attributed to W Shimizu.

At least 55 records · Page 3Linked to original sources

PubMed1999

Accelerated reoxygenation of a murine fibrosarcoma after carbon-ion radiation.

PURPOSE: Reoxygenation of a murine tumour after irradiation with carbon ions was investigated and compared to that after gamma-rays. MATERIALS AND METHODS: NFSa fibrosarcoma cells were transplanted into the right hind legs of syngeneic C3H male mice. Conditioning irradiation with either 290 MeV/u carbon ions or 137-Cs gamma-rays was delivered to the tumours at 8 mm diameter. At given times after irradiation the leg tumours, either clamped or not, received test doses of photons. Differences in tumour growth delay between the clamped and non-clamped tumours were interpreted in terms of reoxygenation. A lung-colony assay was used to obtain cell-survival curves. RESULTS: The oxygen enhancement ratio in the NFSa tumour for 74 keV microm(-1) carbon ions was 1.6 while that for gamma-rays was 3.4. The NFSa tumours reoxygenated 4 days after 30 Gy of gamma-ray irradiation, but reoxygenated as early as 1 day after 16 Gy of carbon ions. Reoxygenation after gamma-rays shortened to 1 day when the tumours were initially clamped for the conditioning irradiation. CONCLUSIONS: The fraction of surviving oxic cells in the NFSa tumours is larger after irradiation with carbon ions than with gamma-rays, resulting in accelerated reoxygenation.

Animals↗

PubMed1999

Preliminary results of pelvic autonomic nerve-preserving surgery combined with intraoperative and postoperative radiation therapy for patients with low rectal cancer.

BACKGROUND: In Japan, lateral lymphadenectomy was widely performed for patients with stage II-III rectal tumors because it was thought to contribute to good local control, but the pelvic autonomic nerves were thus sacrificed. Although autonomic nerve-sparing surgery with lateral lymph node dissection has been tried from around 1987, the type of nerve sparing varied and the indications were not established. To examine the possibility of expanding the indications for total pelvic autonomic nerve preservation for patients with low rectal cancer, we conducted a pilot study. METHODS: Between 1993 and 1997, a total of 50 patients with low rectal cancer underwent pelvic autonomic nerve preservation with lateral lymphadenectomy of both sides and intraoperative radiation therapy followed by postoperative radiation therapy. RESULTS: The median follow-up period for surviving patients was 41 months. The 3-year local control rates for all patients, with stage I-II and stage III tumors were 88% (95% confidence interval, 78-97%), 97% (90-100%) and 73% (52-94%), respectively. The site of local recurrences was not near or within the preserved plexus. CONCLUSIONS: The preliminary results showed good local control rate for patients with stage I-II tumors. For patients with stage III tumors, the local control rate was unsatisfactory, but nerve sparing was not the cause of local recurrence. Further investigation of function-preserving surgery without decreasing curability is needed.

Adult↗

PubMed1999

The M cell: its contribution to the ECG and to normal and abnormal electrical function of the heart.

The discovery and characterization of the M cell, a unique cell type residing in the deep layers of the ventricular myocardium, has opened a new door in our understanding of the electrophysiology and pharmacology of the heart in both health and disease. The hallmark of the M cell is the ability of its action potential to prolong much more than that of other ventricular myocardial cells in response to a slowing of rate and/or in response to agents that act to prolong action potential duration. Our goal in this review is to provide a comprehensive characterization of the M cell, its contribution to transmural heterogeneity, and its role in the normal electrical function of the heart, in the inscription of the ECG (particularly the T wave), and in the development of QT dispersion, T wave alternans, long QT intervals, and cardiac arrhythmias, such as torsades de pointes. Our secondary goal is to address the controversy that has arisen relative to the functional importance of the M cell in the normal heart. The controversy derives largely from the failure of some investigators to demonstrate transmural heterogeneity of repolarization in the dog in vivo under control conditions and after administration of quinidine. The inability to demonstrate transmural heterogeneity under these conditions may be due to the use of bipolar recording techniques that, in our experience, seriously underestimate transmural dispersion of repolarization (TDR). The use of sodium pentobarbital and alpha-chloralose as anesthesia also is problematic, because these agents reduce or eliminate TDR by affecting a variety of ion channel currents. Finally, attempts to amplify transmural dispersion of repolarization with an agent such as quinidine must take into account that relatively high concentrations can result in effects opposite to those desired due to drug inhibition of multiple ion channels. These observations may explain the inability of earlier studies to detect the M cell.

Action Potentials↗

PubMed1999

Sodium pentobarbital reduces transmural dispersion of repolarization and prevents torsades de Pointes in models of acquired and congenital long QT syndrome.

INTRODUCTION: Sodium pentobarbital is widely used for anesthesia in experimental studies as well as in clinics, and it is known to prevent the development of torsades de pointes (TdP) in in vivo models of the long QT syndrome (LQTS). METHODS AND RESULTS: This study examines the effects of pentobarbital on transmural dispersion of repolarization (TDR) and induction of TdP in arterially perfused canine left ventricular wedge preparations in which transmembrane action potentials were simultaneously recorded from epicardial, M, and endocardial regions using floating glass microelectrodes together with a transmural ECG. d-Sotalol and ATX-II were used to mimic the LQT2 and LQT3 forms of congenital LQTS. Both d-sotalol (100 micromol/L, n = 6) and ATX-II (20 nmol/L, n = 6) preferentially prolonged the action potential duration (APD90) of the M cell, thus increasing in the QT interval and TDR, and leading to the development of spontaneous and stimulation-induced TdP. In the absence and presence of d-sotalol, pentobarbital (10, 20, and 50 microg/mL) prolonged the APD90 of epicardial and endocardial cells, and, to a lesser extent, that of the M cell, thus prolonging the QT interval but reducing TDR. In the ATX-II model, the effects of pentobarbital on the QT interval and APD90 were biphasic: 10 microg/mL pentobarbital further prolonged APD90 of epicardial and endocardial cells more than that of the M cell; 20 to 50 microg/mL pentobarbital abbreviated the APD90 of epicardial and endocardial cells less than that of the M cell, thus abbreviating the QT interval and markedly reducing TDR. Twenty to 50 microg/mL pentobarbital totally suppressed spontaneous as well as stimulation-induced TdP in both models CONCLUSION: Our data indicate that pentobarbital reduces TDR in control and under conditions of congenital and acquired LQTS, and suggest that this mechanism may contribute to the ability of the anesthetic to prevent the development of spontaneous as well as stimulation-induced TdP under conditions mimicking LQT2, LQT3, and acquired (drug-induced) forms of the LQTS. The data also serve to illustrate that there are circumstances under which QT prolongation may not be arrhythmogenic.

Action Potentials↗

PubMed1999

[Chemoradiation therapy for advanced esophageal cancers--report of 3 cases].

Three cases of prominent-type advanced esophageal cancer were treated with chemoradiation therapy using a 5-FU analog and low dose CDDP. All cases showed a complete response after the treatment. Only mild bone marrow suppression was found in one case. This protocol will be applied for patients with prominent-type advanced esophageal cancers, especially high risk patients.

Aged↗

PubMed1998

Diagnostic value of plasma levels of brain natriuretic peptide in arrhythmogenic right ventricular dysplasia.

BACKGROUND: Arrhythmogenic right ventricular dysplasia (ARVD) is characterized by local or diffuse wall motion abnormalities in the right ventricle (RV), associated with recurrent ventricular tachycardia (VT) of RV origin. Brain natriuretic peptide (BNP) was first isolated from a porcine brain extract. In humans, BNP is expressed predominantly in the ventricles of failing hearts, and its expression has been observed primarily in myocytes in the interstitial fibrous area in dilated cardiomyopathy. We hypothesized that BNP is increasingly secreted from the residual myocytes within the atrophic tissue in patients with ARVD. METHODS AND RESULTS: Plasma BNP levels were measured in 17 patients with ARVD, 12 patients with idiopathic RV outflow tract tachycardia (RVOT), and 120 control subjects. We performed cardiac catheterization, RV endomyocardial biopsy, electron- beam CT, and biventricular endomyocardial mapping in the ARVD patients. There was a significant increase in plasma BNP levels in the ARVD patients compared with the RVOT patients and control subjects (61.4+/-59.6 pg/mL versus 8.3+/-5. 5 pg/mL and 9.3+/-5.8 pg/mL; P<0.0001, respectively). The plasma BNP levels had no correlation with any of the hemodynamic data, but they had a significant correlation with the RV ejection fraction (r=-0. 588, P=0.025) and with the fractionated-area scores (r=0.705, P=0. 005). Light microscopic immunohistochemistry showed strong BNP immunoreactivity in residual myocytes with fibrofatty replacement. CONCLUSIONS: These results suggest that plasma BNP levels were not increased in RVOT patients but were increased in ARVD patients, and that the increased BNP levels indicate the severity of both the RV dysfunction and the arrhythmogenic substrate.

Adolescent↗

PubMed1998

Clinical and electrophysiologic features of idiopathic left ventricular aneurysm with sustained ventricular tachycardia.

We examined 10 patients with idiopathic left ventricular (LV) aneurysm with sustained ventricular tachycardia (VT) (Id-An group), and compared them with those in 16 age- and sex-matched patients who had postinfarction aneurysm and VT (MI-An group) to clarify detailed clinical and electrophysiologic characteristics of idiopathic LV aneurysm. The clinical and laboratory data and results of electrocardiography, electrophysiologic, and morphologic examinations in the two groups were compared. In the Id-An group, the LV aneurysms were located more often at the posterior and/or inferior wall, while in the MI-An group, they were more often located at the anterior and/or apical wall (P<0.001). The LV end-diastolic volume index was significantly smaller and the LV ejection fraction was significantly higher in the Id-An group (P<0.001). The size of the aneurysm and the area with abnormal electrograms in the Id-An group were significantly smaller than those in the MI-An group (P<0.005 and P<0.001, respectively). The inducibility of VT was high in both groups, and ventricular pacing during VT showed entrainment phenomenon in most of the patients. Thus, in both groups, the abnormal electrograms were closely associated with the wall motion abnormality, and reentry was suggested as the mechanism of VT. In the Id-An group, since the lesions were anatomically and electrophysiologically confined to the posterior and/or inferior wall, the global LV function was more well preserved compared with the MI-An group.

Cardiac Catheterization↗

PubMed1998

Cellular basis for the ECG features of the LQT1 form of the long-QT syndrome: effects of beta-adrenergic agonists and antagonists and sodium channel blockers on transmural dispersion of repolarization and torsade de pointes.

BACKGROUND: This study examines the cellular basis for the phenotypic appearance of broad-based T waves, increased transmural dispersion of repolarization (TDR), and torsade de pointes (TdP) induced by beta-adrenergic agonists under conditions mimicking the LQT1 form of the congenital long-QT syndrome. METHODS AND RESULTS: A transmural ECG and transmembrane action potentials from epicardial, M, and endocardial cells were recorded simultaneously from an arterially perfused wedge of canine left ventricle. Chromanol 293B, a specific IKs blocker, dose-dependently (1 to 100 micromol/L) prolonged the QT interval and action potential duration (APD90) of the 3 cell types but did not widen the T wave, increase TDR, or induce TdP. Isoproterenol 10 to 100 nmol/L in the continued presence of chromanol 293B 30 micromol/L abbreviated the APD90 of epicardial and endocardial cells but not that of the M cell, resulting in widening of the T wave and a dramatic accentuation of TDR. Spontaneous as well as programmed electrical stimulation (PES)-induced TdP was observed only after exposure to the IKs blocker and isoproterenol. Therapeutic concentrations of propranolol (0.5 to 1 micromol/L) prevented the actions of isoproterenol to increase TDR and to induce TdP. Mexiletine 2 to 20 micromol/L abbreviated the APD90 of M cells more than that of epicardial and endocardial cells, thus diminishing TDR and the effect of isoproterenol to induce TdP. CONCLUSIONS: This experimental model of LQT1 indicates that a deficiency of IKs alone does not induce TdP but that the addition of beta-adrenergic influence predisposes the myocardium to the development of TdP by increasing transmural dispersion of repolarization, most likely as a result of a large augmentation of residual IKs in epicardial and endocardial cells but not in M cells, in which IKs is intrinsically weak. Our data provide a mechanistic understanding of the cellular basis for the therapeutic actions of beta-adrenergic blockers in LQT1 and suggest that sodium channel block with class IB antiarrhythmic agents may be effective in suppressing TdP in LQT1, as they are in LQT2 and LQT3, as well as in acquired (drug-induced) forms of the long-QT syndrome.

Adrenergic beta-Agonists↗

PubMed1998

Characteristics and distribution of M cells in arterially perfused canine left ventricular wedge preparations.

BACKGROUND: Much of the characterization of the M cell to date has been accomplished using isolated tissues and cells. This study uses an arterially perfused wedge preparation to examine the characteristics and distribution of M cells within the anterior wall of the canine left ventricle under more physiological conditions. METHODS AND RESULTS: Floating microelectrodes were used to record transmembrane action potentials simultaneously from epicardial, M region, and endocardial or subendocardial Purkinje sites in isolated arterially perfused canine left ventricular wedge preparations. A transmural ECG was recorded concurrently. M cells with the longest action potentials were found in the deep subendocardium in wedge preparations isolated from the anterior wall of the left ventricle. Fairly smooth transitions in action potential duration (APD) were observed except in the region between epicardium and deep subepicardium. Tissue resistivity increased 2.8-fold in this region and much more modestly in the deep subendocardium. Dispersion of APD90 across the left ventricular wall averaged 51+/-19 and 64+/-25 ms at basic cycle lengths of 1000 and 2000 ms, respectively, whereas transmural dispersion of repolarization time was smaller (34+/-18 and 45+/-25 ms), owing to the endocardial to epicardial activation sequence. CONCLUSIONS: We conclude that the qualitative differences between the 3 ventricular cell types previously described in isolated tissues and cells are maintained in intact canine left ventricular wall preparations in which the myocardial cells are electrically well coupled. As anticipated, differences in APD are quantitatively smaller because of electrotonic interactions among the 3 cell types. Our data indicate that transmural dispersion of repolarization is the result of intrinsic differences in APD of cells spanning the ventricular wall as well as a heterogeneous distribution of tissue resistivity across the wall.

Action Potentials↗

PubMed1998

Localization of optimal ablation site of idiopathic ventricular tachycardia from right and left ventricular outflow tract by body surface ECG.

BACKGROUND: Idiopathic ventricular tachycardia (VT) is known to arise from the right ventricular (RV) and left ventricular outflow tracts (LVOT). However, reliable noninvasive methods to localize the optimum ablation site for VT have not been reported. METHODS AND RESULTS: Body surface maps (BSM) and 12-lead ECGs were investigated in 35 VTs from the RVOT and 5 VTs from the LVOT in which the origin was confirmed during the ablation procedure. The RVOT was classified into 8 subdivisions with the use of a 3-dimensional anatomic relation: anterior (A) posterior (P), right (R) left (L), and superior (S) inferior (I). On the BSM, the following 3 indexes differentiated each location of the origin, with a diagnostic accuracy of 88% (A-P), 92% (R-L), and 77% (S-I): (1) the location of the minimum at the early-to-mid QRS (right, A; left, P), (2) the isopotential distribution in the left shoulder area after 30 ms of QRS (positive, R; negative, L), and (3) the downward moving time of the minimum at the early-to-mid QRS (>/=50 ms, S; <50 ms, I). On the 12-lead ECG, (1) the QRS duration (>140 ms, A; </=140 ms, P) and the R-wave pattern in leads II and III (RR' or Rr', A, R, P), (2) the QS wave amplitude in aVR and aVL (aVR>/=aVL, R; aVR /=1 in lead V3 was an index suggesting the LVOT origin. CONCLUSIONS: The origin or the optimum ablation site of idiopathic VT from RVOT and LVOT can be localized with the use of indexes obtained with a BSM or 12-lead ECG.

Adolescent↗

PubMed1998

Improvement of repolarization abnormalities by a K+ channel opener in the LQT1 form of congenital long-QT syndrome.

BACKGROUND: This study used monophasic action potential (MAP) to examine the effect of nicorandil, a K+ channel opener, on repolarization abnormalities induced by epinephrine in the LQT1 form of congenital long-QT syndrome in which the KvLQT1 mutation underlies the defect in the channel responsible for the slowly activating component of the delayed rectifier potassium current. METHODS AND RESULTS: MAPs were recorded simultaneously from two or three sites on the right ventricular and left ventricular endocardium in 6 patients with a congenital form of LQT1 syndrome with KvLQT1 defect (17 sites) and 8 control patients (24 sites). In LQT1 patients, epinephrine infusion prolonged the QT interval and 90% MAP duration (MAPD90) and increased the dispersion of MAPD90. Epinephrine also induced early after depolarizations (EADs) as well as ventricular premature complexes (VPCs) in 2 of the 6 patients. Nicorandil during epinephrine infusion abbreviated the QT interval and MAPD90, decreased the dispersion of MAPD90, and abolished the EADs as well as the VPCs in 1 patient. Addition of propranolol completely reversed the effect of epinephrine in prolonging the QT interval and MAPD90 and increasing the dispersion and eliminated the EADs and VPCs in another patient. In control patients, the effect of epinephrine and that of additional nicorandil and propranolol on repolarization parameters were much less than in the LQT1 patients. CONCLUSIONS: Our results suggest that nicorandil, a K+ channel opener, improves repolarization abnormalities in the LQT1 form of congenital long-QT syndrome with KvLQT1 defect.

Adolescent↗

PubMed1998

New mutations in the KVLQT1 potassium channel that cause long-QT syndrome.

BACKGROUND: Long-QT syndrome (LQTS) is an inherited cardiac arrhythmia that causes sudden death in young, otherwise healthy people. Four genes for LQTS have been mapped to chromosome 11p15.5 (LQT1), 7q35-36 (LQT2), 3p21-24 (LQT3), and 4q25-27 (LQT4). Genes responsible for LQT1, LQT2, and LQT3 have been identified as cardiac potassium channel genes (KVLQT1, HERG) and the cardiac sodium channel gene (SCN5A). METHODS AND RESULTS: After studying 115 families with LQTS, we used single-strand conformation polymorphism (SSCP) and DNA sequence analysis to identify mutations in the cardiac potassium channel gene, KVLQT1. Affected members of seven LQTS families were found to have new, previously unidentified mutations, including two identical missense mutations, four identical splicing mutations, and one 3-bp deletion. An identical splicing mutation was identified in affected members of four unrelated families (one Italian, one Irish, and two American), leading to an alternatively spliced form of KVLQT1. The 3-bp deletion arose de novo and occurs at an exon-intron boundary. This results in a single base deletion in the KVLQT1 cDNA sequence and alters splicing, leading to the truncation of KVLQT1 protein. CONCLUSIONS: We have identified LQTS-causing mutations of KVLQT1 in seven families. Five KVLQT1 mutations cause the truncation of KVLQT1 protein. These data further confirm that KVLQT1 mutations cause LQTS. The location and character of these mutations expand the types of mutation, confirm a mutational hot spot, and suggest that they act through a loss-of-function mechanism or a dominant-negative mechanism.

Case-Control Studies↗

PubMed1998

Cellular basis for QT dispersion.

The cellular basis for the dispersion of the QT interval recorded at the body surface is incompletely understood. Contributing to QT dispersion are heterogeneities of repolarization time in the three-dimensional structure of the ventricular myocardium, which are secondary to regional differences in action potential duration (APD) and activation time. While differences in APD occur along the apicobasal and anteroposterior axes in both epicardium and endocardium of many species, transitions are usually gradual. Recent studies have also demonstrated important APD gradients along the transmural axis. Because transmural heterogeneities in repolarization time are more abrupt than those recorded along the surfaces of the heart, they may represent a more onerous substrate for the development of arrhythmias, and their quantitation may provide a valuable tool for evaluation of arrhythmia risk. Our data, derived from the arterially perfused canine left ventricular wedge preparation, suggest that transmural gradients of voltage during repolarization contribute importantly to the inscription of the T wave. The start of the T wave is caused by a more rapid decline of the plateau, or phase 2 of the epicardial action potential, creating a voltage gradient across the wall. The gradient increases as the epicardial action potential continues to repolarize, reaching a maximum with full repolarization of epicardium; this juncture marks the peak of the T wave. The next region to repolarize is endocardium, giving rise to the initial descending limb of the upright T wave. The last region to repolarize is the M region, contributing to the final segment of the T wave. Full repolarization of the M region marks the end of the T wave. The time interval between the peak and the end of the T wave therefore represents the transmural dispersion of repolarization. Conditions known to augment QTc dispersion, including acquired long QT syndrome (class IA or III antiarrhythmics) lead to augmentation of transmural dispersion of repolarization in the wedge, due to a preferential effect of the drugs to prolong the M cell action potential. Antiarrhythmic agents known to diminish QTc dispersion, such as amiodarone, also diminish transmural dispersion of repolarization in the wedge by causing a preferential prolongation of APD in epicardium and endocardium. While exaggerated transmural heterogeneity clearly can provide the substrate for reentry, a precipitating event in the form of a premature beat that penetrates the vulnerable window is usually required to initiate the reentrant arrhythmia. In long QT syndrome, the trigger is thought to be an early afterdepolarization (EAD)-induced triggered beat. The likelihood of developing EADs and triggered activity is increased when repolarizing forces are diminished, making for a slower and more gradual repolarization of phases 2 and 3 of the action potential, which translates into broad, low amplitude and sometimes bifurcated T waves in the electrocardiogram. Our findings suggest that regional differences in the duration of the M cell action potential may be the basis for QT dispersion measured at the body surface under normal and long QT conditions. The data indicate that the interval delimited by the peak and the end of the T wave represents an accurate measure of regional dispersion of repolarization across the ventricular wall and as such may be a valuable index for assessment of arrhythmic risk. The presence of low amplitude, broad and/or bifurcated T waves, particularly under conditions of long QT syndrome, is indicative of diminished repolarizing forces and may represent an independent variable of arrhythmic risk, forecasting the development of EAD-induced triggered beats that can precipitate torsade de pointes. Although the QT interval, QT dispersion, the T wave peak-to-end interval, and the width and amplitude of the T wave often change in parallel, they contain different information and should not be expected to be e

Animals↗

PubMed1998

Mouse skin reactions following fractionated irradiation with carbon ions.

PURPOSE: Skin reactions in the mouse leg following various daily doses given with 290 MeV/u carbon ions were investigated. MATERIALS AND METHODS: Seven different LET (linear energy transfer) values ranging from 14 to 100keV/microm were selected. The fractionation schedules were 1-, 2-, 4- and 8-daily fractions. The isoeffect doses to produce moist desquamation on the dose-response curves were calculated with 95% confidence limits. RESULTS: The isoeffect doses for carbon ions of 14 and 20 keV/microm increased with an increase in the number of fractions up to 4 fractions, but became constant when the number of fractions further increased to 8 fractions. This leveling off in isoeffect dose was more prominent for 40 keV/microm. Recovered dose per fraction was largest for 2 fractions of the 14keV/microm carbon beam. The isoeffect doses for 50, 60, 80 and 100keV/microm consistently increased with an increase in the number of fractions and did not show saturation up to 8 fractions. RBE (relative biological effectiveness) increased linearly with LET for all fractionation schedules. CONCLUSIONS: These results suggest that daily fractionation with carbon ions could spare radiation damage in patients, and that changes the fractionation schedule affect clinical outcome.

Animals↗

PubMed1998

Successful treatment by radiation and hormone therapy of isolated local recurrence of breast cancer 24 years after mastectomy accompanied by immune thrombocytopenia: a case report.

We report a case of isolated local recurrence of breast cancer, which was accompanied by idiopathic thrombocytopenic purpura (ITP) and benign monoclonal gammopathy that presented 24 years after the patient underwent mastectomy. A 72-year-old female patient with a chest wall tumor was referred to our hospital in November 1994. Twenty-four years previously she had surgically treated breast cancer, of which the pathology was scirrhous carcinoma. Needle biopsy of the tumor revealed tubular carcinoma, which is compatible with local recurrence of breast cancer. She had no evidence of regional lymph node involvement or distant metastasis. Hematological and serological examination revealed a low platelet count accompanied by M-proteinemia (IgG, kappa-type) and a mild increase in platelet-associated IgG. She was initially treated with extensive-field chest wall radiation (60 Gy), followed by systemic administration of tamoxifen. Complete local control of isolated local recurrence (LR) was achieved after radiation therapy (RT) and the patient has been progression-free for more than 2 years. Platelet count recovered gradually to a normal level after achievement of complete remission induced by radiation and tamoxifen. This may be the first case suggestive of a paraneoplastic syndrome of immune thrombocytopenia accompanied by local recurrence of breast cancer.

Adenocarcinoma↗

PubMed1998

Radiofrequency catheter ablation of concealed atrioventricular accessory pathways using a "simultaneous pacing method".

The retrograde atrial potential at a successful ablation site is usually obscured by the wide and large ventricular potential during atrioventricular reentrant tachycardia or ventricular pacing, which makes it difficult to determine the appropriate ablation site for a concealed accessory pathway. A pacing maneuver named the "simultaneous pacing method" is proposed herein to differentiate the retrograde atrial potential from the ventricular potential for a successful ablation of the concealed accessory pathway. Catheter ablation was performed in 12 patients with a single left free-wall concealed accessory pathway. The atrial insertion site was determined by the simultaneous pacing method in six patients (group I) and by ventricular pacing in six patients (group II). In the simultaneous pacing method, electrograms recorded during ventricular pacing in the earliest retrograde atrial activation site are a fusion of the ventricular potential and the following retrograde atrial potential. When atrial and ventricular pacings are performed simultaneously (simultaneous pacing), the end portion of the electrograms recorded at the same site is solely the ventricular component, because atrial is activated earlier. The atrial potential can be confirmed during ventricular pacing in comparison with the electrograms during the "simultaneous pacing." Radiofrequency catheter ablation was successful in eliminating conduction through the accessory pathway in all 12 patients. The radiofrequency applications in group I were significantly fewer than those in group II (1.7 +/- 1.0 in group I, 5.3 +/- 3.2 in group II, P < 0.05). The total procedure time in group I was significantly shorter than in group II (57.8 +/- 15.7 vs 106.7 +/- 41.6 mins in group II, respectively, P < 0.05). The fluoroscopy time in group I was significantly shorter than in group II (54.0 +/- 7.9 vs 81.3 +/- 26.3 mins, respectively, P < 0.05). We were able to determine the atrial insertion site of accessory pathways by the simultaneous pacing method. The simultaneous pacing method was useful in eliminating concealed left free-wall accessory pathways.

Adult↗

PubMed1998

Mid-diastolic potential is related to the reentrant circuit in a patient with verapamil-sensitive idiopathic left ventricular tachycardia.

We report a case of verapamil-sensitive idiopathic ventricular tachycardia in which a mid-diastolic potential (MDP) 45 msec preceding the Purkinje potential (P potential) was recorded. Pacing during the tachycardia caused concealed entrainment, and the stimulus-QRS interval was equal to the P potential-QRS interval. The interval between the last pacing stimulus and the next P potential (postpacing interval) was longer than the ventricular tachycardia cycle length, but the MDP was orthodromically activated. These findings suggest that the MDP was on the reentrant circuit and the P potential was not on the reentrant circuit, but a bystander.

Adult↗

PubMed1998

Increased dispersion of repolarization time determined by monophasic action potentials in two patients with familial idiopathic ventricular fibrillation.

INTRODUCTION: The role of increased dispersion of repolarization in the genesis of torsades de pointes in patients with long QT syndrome has been clarified, but its role in the genesis of idiopathic ventricular fibrillation (VF) is not yet known. To investigate the pathogenesis of VF, we recorded monophasic action potentials (MAPs) from two siblings (48- and 36-year-old males) with familial idiopathic VF. METHODS AND RESULTS: The elder brother (patient 1) showed a late r' wave in lead V1 and ST segment elevation in leads V1 through V3. The younger brother (patient 2) had late r' waves and ST segment elevation in leads II, III, and aVF, and the configurations were very similar to those of patient 1. MAPs were recorded from several sites in the right ventricular (RV) and left ventricular (LV) endocardium during constant right atrial pacing. The repolarization time (RT) was defined as the sum of the activation time (AT) and action potential duration (APD) at 90% repolarization. In patient 1, marked prolongation of the AT (140 msec) and the RT (380 msec) was recorded in the RV septum of the outflow tract, and the RT dispersion was markedly increased (125 msec). In contrast, patient 2 showed prolongation of the AT (80 msec) and RT (310 msec), and fractionated electrograms in the RV floor of the inflow tract. The RT dispersion was also increased (80 msec). VF and nonsustained polymorphic ventricular tachycardia were induced by double premature stimulation in patients 1 and 2, respectively. Chronic amiodarone therapy decreased the RT dispersion and suppressed the induction of ventricular tachyarrhythmias in patient 2, although late r' waves and slight ST segment elevation were unmasked in leads V1 and V2. CONCLUSION: Our data suggest that the increased dispersion of the RT, which was due mainly to a localized conduction delay in the RV, created an arrhythmogenic substrate in the two patients with familial idiopathic VF.

Action Potentials↗