Biomedical subjects
Publications and source records attributed to A Kasai.
An 8-mm catheter does not appear superior to 4-mm tip electrode for atrial flutter ablation. The potential advantage of allowing higher energy delivery on a larger surface is compensated by the lack of consistent contact with the endocardial surface.
UNLABELLED: The purpose of this study was to examine the electrophysiological determinants of the elimination of recurrent atrioventricular nodal reentrant tachycardia (AVNRT) despite the persistence of dual AV nodal pathway physiology or single echo beats after ablation procedures. The study included 26 patients with common AVNRT who had undergone successful ablation treatment and no long-term recurrence of AVNRT. The slow pathway potential was targeted, and the endpoint of ablation was one echo during atrial extrastimulus testing (ET) with isoproterenol. Persistent dual pathways physiology or single echoes were present in 12 patients (group I) and absent in 16 (group II) after ablation. The number of anterograde AV nodal pathways and maximum AH interval (Max AH) during ET were measured before and after ablation, and ventriculoatrial conduction during ventricular pacing was examined. RESULTS: (1) multiple AV nodal pathways were more frequently observed in group I than in group II (50.0% vs 7%, P < 0.05); (2) Max AH decreased significantly after ablation in both groups (309 +/- 157 vs 171 +/- 53 ms in group II; P < 0.01, and 409 +/- 65 vs 274 +/- 86 ms in group I; P < 0.001); and (3) retrograde dual pathway conduction was more common in group I than in group II. These data suggest the presence of nonuniform conductive properties of the AV node in group I and that ablation targeting the slow pathway potential prevents recurrences of AVNRT by eliminating the pathway with the longest conduction time.
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A 21-year-old woman had paroxysmal wide QRS tachycardia with a left bundle branch block configuration and a retrograde conducted P wave just behind the QRS complex. An electrophysiological study revealed antidromic atrioventricular tachycardia involving an atrioventricular connection with decremental conduction as the anterograde limb and normal atrioventricular node as the retrograde limb. During constant pacing from the high right atrium (HRA) at the cycle length (CL) of 600 ms, the QRS configurations were not identical to those during the wide QRS tachycardia or constant pacing at the CL of less than 500 ms. The process by which this arborized atrioventricular accessory pathway with the Mahaim fibers physiology was interrupted by radiofrequency catheter ablation is described. Radiofrequency energy was delivered to the site recording a Mahaim potential at the tricuspid annulus during constant pacing from the HRA at the CL of 429 ms. The stimulus-QRS interval gradually shortened as it reached the power plateau without changing the preexcited QRS configuration. Shortening of the conduction time over the Mahiam pathway might have resulted in changing of the propagation from a slow to fast conduction zone or acceleration in response to thermal effect in a node-like structure on the atrial insertion site.
We reported a 36-year-old woman with metastatic liposarcoma originating in the retroperitoneum, which responded well to adjuvant chemotherapy. The primary tumor was removed by surgery. Two months later, the patient developed metastasis to the brain, and to the lung four months later. Metastatic liposarcomas to the brain generally are extremely rare. The patient was treated with combination chemotherapy using cyclophosphamide, vincristine, adriamycin, and dacarbazine (CYVADIC). After she was examined, the former two drugs were alternated with vindesine and ifosfamide, and another regimen with cisplatin and etoposide was given after a three-week interval. As a result, both of the metastases totally disappeared. No recurrent lesion has been noted for two years. Although the role of chemotherapy for liposarcoma has not been well defined and little data support its use in an adjuvant setting, this combination chemotherapy seemed to be effective for advanced liposarcoma.
The purpose of this study was to compare the electrophysiological characteristics of posterior and anterior atrioventricular junctional reentrant tachycardia (AVJRT) during radiofrequency (RF) catheter ablation of a slow pathway. Twenty-four patients with common AVJRT, including 4 posterior (P) and 20 anterior AVJRT (A) were studied. We analyzed the retrograde atrial activation sequence of junctional rhythm and the presence of transient HA block during slow pathway ablation. When HA block developed, the AH interval before ablation and immediately after the end of energy delivery was measured. Successful ablation sites were divided into three groups; high (H), middle (M), and low (L) from the His bundle to the floor of the coronary sinus orifice. The results were: (1) the number of successful ablation sites were H 0, M 1, L 3 in P and H 1, M 8, L 11 in A; (2) the HA interval during AVJRT in P was longer than that in A (109 +/- 48 ms vs 43 +/- 6 ms, P < 0.01); (3) the retrograde atrial activation sequence during junctional rhythm was strictly concordant with that during AVJRT in both groups, but HA block developed during slow pathway ablation more often in P than in A (100% vs 30%, P < 0.01); and (4) The AH interval did not lengthen after HA block developed in P. These data suggest that another pathway does exist from the AV node to the atrium in addition to anterograde fast pathway and slow pathway, and that this pathway is used as the retrograde limb of P.
UNLABELLED: Radiofrequency (RF) catheter ablation of supraventricular tachycardias (SVT) has been shown to result in local parasympathetic denervation. The purpose of this study was to estimate the correlation between RF cumulative energy and parasympathetic denervation at three different ablation sites. METHODS: 45 patients who underwent RF ablation of 36 AV reentrant tachycardias and 9 AV nodal reentrant tachycardias were studied. Twenty patients had left free-wall accessory pathways (group L), 8 patients right free-wall accessory pathways (group R), and 17 patients septal accessory pathways (n = 8) or slow pathways (n = 9) (group S). Time and frequency domain analysis of heart rate variability on 24-hour ambulatory ECG recordings was performed before and after RF ablation. pNN50 and the high frequency (0.15 to 0.40 Hz, HF) component were measured to examine the effects on parasympathetic nerve activity. The values of delta pNN50 and delta HF were expressed as the percent change of pNN50 and HF that occurred after versus before RF ablation. RESULTS: Both pNN50 and HF significantly decreased after RF ablation in all three groups. In group S, there was a significant correlation between RF cumulative energy and delta pNN50 (r = 0.66, P < 0.01) or delta HF (r = 0.58, P < 0.05). In contrast, there was no correlation between RF cumulative energy and delta pNN50 or delta HF in either group L or group R. CONCLUSION: These data suggest that RF ablation produces parasympathetic denervation at all three sites along the mitral or tricuspid annulus and that parasympathetic fibers may be located predominantly in the septal area.
MR diffusion-weighted imaging was performed to investigate changes in water diffusion in patients with cerebral infarction, and diffusion-weighted images (DWI) were compared with T2-weighted images (T2WI). Acute and subacute infarcts were seen as areas of high intensity on DWI and showed lower apparent diffusion coefficients (ADCs), while chronic infarcts showed a relative increase in ADCs. The relative ADC increased progressively over time, becoming renormalized at 3 to 4 weeks, and was elevated in the chronic state. On DWI, infarcts as small as 5 to 6 mm in diameter and lesions adjacent to the ventricular or subarachnoid space could be readily identified. DWI was useful for distinguishing acute lesions from chronic lesions in patients with multiple cerebral infarction, and provided valuable pathophysiologic information on the course of ischemic stroke evolution.
BACKGROUND: We investigated whether exercise-induced coronary spasms are influenced by the different exercise modes. METHODS: We compared ischaemic ECG responses in 67 patients with vasospastic angina who underwent both treadmill and bicycle ergometer exercise and also coronary angiography. RESULTS: ECG ST-segment elevation was provoked more frequently during treadmill exercise than it was during bicycle exercise (19 versus 9%, P < 0.05). Of 45 patients without significant coronary stenosis (coronary artery luminal diameter narrowing < 75%), 19 patients manifested ST-segment depression during treadmill exercise, whereas only seven patients did during bicycle exercise (42 versus 16%, P < 0.01). All patients with ST-segment elevation or depression during bicycle ergometer exercise also had ST-segment changes during treadmill exercise. Although higher systemic blood pressure levels and lower heart rates were found during bicycle exercise compared with during treadmill exercise the pressure-rate products at peak exercise did not differ between the two exercise tests. CONCLUSIONS: It seems that treadmill and bicycle exercise are different stressors in patients with vasospastic angina, and that coronary spasms are provoked more frequently during treadmill exercise than they are during bicycle exercise. The cause of this difference is not known, but it may be related in part to the difference in systemic haemodynamic or neurohumoral response.
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The acute effects of nifedipine (20 mg) on left ventricular diastolic function were investigated in 16 patients with chronic coronary artery disease by measuring left ventricular pressure with a manometer-tipped catheter and by measuring volume with cineangiography. Heart rates were maintained by right atrial pacing. Left ventricular peak systolic pressure (-15%; p less than 0.01 vs control) decreased significantly. With afterload reduction, left ventricular ejection fraction (+11%; p less than 0.01) increased. There was no significant change in left ventricular end-diastolic pressure. The diastolic peak filling rate of left ventricular volume significantly increased (+36%; p less than 0.05), whereas the time from end-systole to the peak filling rate remained unchanged. Administration of nifedipine did not improve left ventricular relaxation as assessed by the isovolumic pressure decay. There was also no significant change in the left ventricular diastolic pressure-volume relationship. We conclude that nifedipine improves left ventricular systolic function with afterload reduction but has little or no effect on left ventricular diastolic properties in patients with chronic coronary artery disease.
To investigate left ventricular (LV) diastolic function in patients with apical hypertrophic cardiomyopathy (AHCM), we analyzed the LV cineangiograms (RAO 30 degrees) and pressures (tip manometer) in 11 patients with AHCM who had giant negative T waves on their electrocardiograms and "ace of spades" configurations on the LV angiograms. Ten patients with non-obstructive HCM (HNCM) and 10 normal subjects served as controls. LV volumes and instantaneous rates of LV volume changes were derived from frame-by-frame analyses of their LV angiograms. LV isovolumic relaxation was assessed according to the time constant (T) of LV pressure decay. LV diastolic distensibility was evaluated by plotting diastolic pressure-volume curves. There was no significant change in the LV systolic functions among these 3 groups. Compared with normals, LV end-diastolic pressure was equally elevated in AHCM and HNCM. The T of isovolumic pressure decay was significantly prolonged in AHCM and HNCM. LV early diastolic filling was maintained at the normal level in AHCM as assessed by the peak filling rate (PFR) during the rapid filling period and the time from end-systole to PFR. The LV diastolic pressure-volume relation shifted upwards in both AHCM and HNCM. In conclusion, impaired LV isovolumic relaxation and decreased diastolic distensibility, which are associated with HNCM, may also be present in AHCM.
A case was presented in which a rare T wave alternans occurred in association with congenital long QT syndrome. A 71-year-old woman, who had experienced several syncopal attacks per year for the previous forty years, was admitted for further evaluation of the syncope. She had a family history of sudden death (sister) and QT prolongation (son). Electrocardiogram showed a corrected QT interval of 0.68 seconds. Treadmill exercise-tolerance test revealed both T wave alternans immediately after exercise and torsades de pointes 150 seconds after exercise. The syncope was induced by the mental excitation. A prolonged corrected QT interval reduced from 0.70 seconds to 0.58 seconds by the correction of her serum potassium and magnesium. The effect of propranolol, verapamil, phenytoin or mexiletine on T wave alternans and ventricular arrhythmia was evaluated by the treadmill exercise-tolerance test. The treatment with propranolol was most effective.
Two strikingly similar patients with arrhythmogenic right ventricular dysplasia which severely impaired not only the right ventricle but also the left ventricle are described in association with familial occurrence of sudden death. A 49-year-old man experienced syncope which was due to ventricular tachycardia. Electrocardiography revealed a first degree atrioventricular block, incomplete right bundle-branch block, T wave inversions in leads II, III, a VF and V1 to V5, and multiformal ventricular extrasystoles. Echocardiography and ventricular cineangiography showed not only the right ventricular dilatation with an aneurysm in the right ventricular apex, inflow and outflow tracts, but also mild dilatation of the left ventricle with left ventricular apical and posterior aneurysms. Radionuclide angiography also disclosed dysfunction of both ventricles, especially during exercise. His family history revealed that 3 members of his family died of sudden deaths. A 56-year-old woman experienced syncope secondary to ventricular tachycardia, with left bundle-branch block. Electrocardiography showed complete right bundle-branch block, left axis deviation, and T wave inversions in leads V1 to V4. Echocardiography and ventricular cineangiography revealed not only marked right ventricular dilatation with the "triangle of dysplasia", but also a left ventricular aneurysm in the apex and posterior portion. Her elder brother died of a sudden death, and electrocardiograms of 2 members of her family showed ventricular extrasystoles and T wave inversions. These 2 cases may well be termed "familial bi-ventricular dysplasia".
Two cases of eosinophilia-associated acute peri-myocarditis which coursed favorably are reported. Case 1 was a 47-year-old man whose ECG revealed QS, ST-T change, bundle branch block, and arrhythmias. Case 2 was a 30-year-old man whose ECG showed ST segment depression. The chest radiographs of both patients revealed enlarged hearts. Left ventriculography showed abnormal regional wall motion. Their endomyocardial biopsies revealed eosinophilic infiltration of the myocardium, but few eosinophils were degranulated. In Case 1, the development of eosinophilia preceded perimyocarditis and the eosinophilia continued even after the symptoms of peri-myocarditis were improved. In conclusion, it seems that eosinophilia did not have specific relation to the initial manifestation of the disease but that it occurred as a secondary reaction to peri-myocarditis of unknown etiology in these cases.
We analyzed left ventricular (LV) pulsus alternans in 49 patients with hypertrophic cardiomyopathy during cardiac catheterization. LV pulsus alternans was noted in 6 of 17 patients with hypertrophic obstructive cardiomyopathy, 5 of whom already showed intraventricular pressure gradient at rest. No patient with hypertrophic non-obstructive cardiomyopathy had LV pulsus alternans. Pulsus alternans was neither observed in the right ventricle nor in the pulmonary artery. There was little, if any, pulsus alternans in a low pressure LV chamber (subaortic portion) and peripheral artery during LV pulsus alternans in a high pressure chamber. LV end-diastolic pressure also remained unchanged during LV pulsus alternans, except in one case. It is suggested that LV pulsus alternans in hypertrophic obstructive cardiomyopathy may imply LV dysfunction associated with increased afterload.
To assess the difference between cardiovascular responses to treadmill exercise (TM) and those to bicycle ergometer exercise (EM) in provoking coronary spasm, we compared the ST segment shifts (elevation or depression) during TM and EM in 67 patients with vasospastic angina. Coronary artery spasm was demonstrated on angiography. Both TM and EM were performed on the same day during a medication-free period. For both tests, multistage, symptom-limited exercise protocols were used; EM in the morning and TM in the afternoon. The results obtained were as follows: 1. Rate-pressure products at peak exercise during TM and EM were similar. Systolic blood pressure levels at peak exercise were higher during EM than during TM (p < 0.01). The patients' heart rates at peak exercise were higher during TM than during EM (p < 0.01). Diastolic blood pressure levels at peak exercise were higher during EM than during TM (p < 0.05). 2. Exercise-induced ST elevation occurred more frequently with TM than with EM (19% vs 9%, p < 0.05). 3. Exercise-induced ST depression was provided in 27 patients during TM and in 13 during EM (40% vs 19%, p < 0.01). Among 45 patients without significant lesions, ST depression occurred in 19 during TM, but in only 7 during EM (42% vs 16%, p < 0.01). In conclusion, coronary spasm seemed to occur more frequently with TM than with EM. The mechanism causing such difference remains to be elucidated, however, we speculate that the difference between TM and EM as to enhanced autonomous nervous system activity and coronary perfusion exercise may be related to the difference in the incidence of coronary spasm.