Ipsilateral spontaneous pneumothorax after rapid development of large thin-walled cavities in two patients who had undergone radiation therapy for lung cancer.
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Biomedical subjects
Publications and source records attributed to K Ebe.
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PURPOSE: To evaluate the differences in the radiosensitizing effects of intravenous (i.v.) injection, intraarterial (i.a.) injection, and intratumoral (i.t.) injections of the hypoxic cell radiosensitizer RK28 ([1-(4'-hydroxy-2'-butenoxy)methyl-2-nitroimidazole], a 2-nitroimidazole with an acyclic sugar analogue substituted at the N-1 position of the imidazole ring) using an animal experimental system. METHODS AND MATERIALS: Rabbit VX2 tumors, which were implanted in the muscle of left hind legs and grown to 3 cm in diameter, were treated with RK28 (80 mg/kg x b.wt.) before 15 Gy of local x-ray irradiation. The auricular vein and the left saphenous artery were used for systemic injection and regional injection, respectively. For i.t. injection, a 21-gauge needle with three lateral holes was positioned in the central area of the tumor. Tumor regression was precisely evaluated by computed tomograpy (CT), and survival time was also studied. Using high-performance liquid chromatography (HPLC), pharmacokinetic studies for RK28 and its seven major metabolites were performed in tumor and serum at 0, 10, 20, 30, and 60 min after drug injection was completed. RESULTS: Radiosensitizing effects of RK28 were considered present after i.a. injection (p < 0.05) and i.t. injection (p < 0.05) after analyzing tumor volumes on day 21 after treatment. Increased survival was not observed in any group with RK28 injection compared with survival in the group treated by x-ray irradiation alone. Pharmacokinetic studies showed the average concentration of RK28 in the tumor during x-ray irradiation was 1.3 times higher after i.a. injection and 3.5 times higher after i.t. injection than that after i.v. injection. The time modifying factor50 (TMF50: ratio of time for tumor to decrease by 50%, radiation alone vs. radiation plus drug) was calculated to be 1.5 after i.v. injection, 1.7 after i.a. injection, and 2.3 after i.t. injection. The values of TMF50 correlated to the average concentrations of RK28 in the tumor. As to metabolites of RK28, beta-glucuronated compound and cysteine conjugate were highly detected. The concentrations of cysteine conjugate were higher in the tumor than in serum via i.v. injection. CONCLUSIONS: Radiosensitizing effects of RK28 were observed on the rabbit VX-2 tumor system after i.a. or i.t. injection. Pharmacokinetic studies proved that radiosensitizing effects depended on the concentration in the tumor, though the administration routes were different. Combined forms with nonprotein thiols were detected. However, survival benefits were not obtained by RK28. For clinical applications of RK28, i.a. or i.t. injection could facilitate better local control of cancer.
Primary brain tumors in two dogs were surgically removed followed by postoperative radiation therapy. The two tumors were confirmed histologically to be astrocytoma and meningioma, respectively. After the surgery, the neurological status of each dog improved dramatically and a total dose of 40 Gy was delivered to the surgical site to treat residual tumor tissue. Although the dog with astrocytoma died 6 months after surgery due to unknown causes, the dog with meningioma has lived for over 24 months with a degree of neurological disorder less severe than that before treatment. These results suggested the effectiveness of this type of therapy on brain tumor in dogs and therapeutic modality should be positively planned to treat canine brain tumors.
One hundred and forty-two consecutive patients with sustained monomorphic ventricular tachycardia (VT) were investigated. Only 26.1% of VTs were associated with ischemic heart disease (IHD). The induction rate of sustained VT upon electrophysiologic study (EPS) was 82.9% in patients with IHD and 65.3% in non-IHD. Of 76 inducible sustained VTs, pharmacologic therapy was finally selected in 35 cases, ablative therapy in 25 and surgical therapy in 12. Long-term prognosis was compared between groups divided according to type of ventricular arrhythmia induced at final EPS after antiarrhythmic therapy as follows: Group A: complete suppression of VT, Group B: clinical or non-clinical nonsustained VT, Group C: clinical sustained VT. The event rate in IHD was 6.3% in Group A, 44.4% in Group B and 100% in Group C. In non-IHD, the event rate was 24.0%, 25.0% and 75.0% (Groups A, B and C, respectively). Complete suppression of VT showed a good prognosis in IHD, however, a slightly higher recurrence rate was observed in non-IHD. In ablative therapy, some recurrences and sudden deaths were observed in spite of complete suppression of both VTs in both the IHD and non-IHD groups. Review of the efficacy of antiarrhythmic procedures is recommended during the follow-up period.
A 59-year-old man was admitted for evaluation of mild exertional angina in the morning. During graded treadmill exercise stress testing, the patient had reproducibly intermittent chest pains associated with ST-segment elevations in leads II, III and aVF. A baseline coronary angiogram showed a coronary narrowing of 90% in the middle segment of the right coronary artery. The coronary narrowing was immediately resolved by an intracoronary injection of nitroglycerin. This was a very rare case of variant angina with intermittent ST-segment elevations and chest pains which were reproducibly demonstrated during exercise and the recovery phase of treadmill testing.
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A case report of the sudden death of a 64-year-old man, three months after successful percutaneous transluminal coronary angioplasty (PTCA). He was admitted because of non-Q-wave acute myocardial infarction. Coronary angiography showed 90% stenosis in the anterior descending artery (No. 6). PTCA was successful, but the proximal portion of anterior descending artery was dissected because the balloon slipped from the dilated site during inflation. Acute coronary occlusion was not observed. However, he died suddenly shortly after he complained of severe chest pain three months after PTCA. Histologically, the site of the dissecting artery showed that the intima and media of the arterial wall was disrupted and the lumen was severely stenotic with cellular proliferation. This dissection of the coronary artery is also important because rapid and severe stenosis was induced by the artery's being badly injured.
A case is reported of a 56-year-old man with primary coronary dissection presenting as sudden death due to aortic rupture and cardiac tamponade. He was admitted because of loss of consciousness and chest pain. ECG showed complete atrioventricular block and myocardial infarction. Coronary angiography demonstrated coronary dissection and total obstruction of right coronary artery (RCA). Intracoronary injection of urokinase was not effective for recanalization of RCA. He died suddenly two days later. At autopsy, the proximal site of the ascending aorta was dissected locally and had ruptured into a pericardial space. RCA was torn off. The perivascular area around the torn coronary artery communicated with the dissecting space of the ascending aorta. Histologically, no degeneration or infiltration of inflammatory cells was observed in the media of the aorta and the right coronary artery. Histological change was observed only at the media of the torn site of the coronary artery. The thickness of the media was about half of that at the other site of the coronary artery. This is the third case reported in world medical literature of primary coronary dissection presenting as cardiac tamponade.
Polyurethane pacemaker leads are widely used nowadays. However, only a few studies have been done to investigate the fixation mechanism of polyurethane leads. To elucidate how pacemaker leads are fixed at the early phase after implantation, polyurethane-insulated tined ventricular leads were implanted in seven mongrel dogs. One to 4 months later, tips of the leads were anchored among the trabeculae and the distal part of the leads were encapsulated by whitish fibrous tissue. It was found that not organized thrombi, but cell reaction with various stages of inflammatory cells was responsible for forming the fibrous tissue. We attempted to remove the lead by delivering radiofrequency wave through the lead. However, no lead could be removed.
We developed a new simplified intraarterial infusion and angiographic method for rabbit VX-2 hind limb tumors. A 24 gauge cannula was placed in the saphenous artery of the tumor-bearing leg (not supplying the tumor) and used for intraarterial drug infusion or angiography. This method has several advantages as follows: 1) easy and time-saving in manipulation (about 15 minutes per a rabbit); 2) selective drug infusion into the tumor-supplying artery without fluoroscopy; 3) sequential follow-up angiographies available for weeks.
Experimental and clinical studies were done on intracavitary and interstitial hyperthermia with a 2 mm diameter applicator with a 7 cm tip (Aloka, Co., Ltd.). Microwave energy at 2450 MHz was used to heat tumors. An outer cannula of 16G Medicut was implanted in the tumor. When a rabbit VX-2 tumor was heated, the temperature reached over 40 degrees C at 15 watts. We applied the same method to two patients, one with recurrent oropharyngeal tumor and the other with recurrent pelvic tumor. This applicator looks promising.
Using transient entrainment, the effect of the paced cycle length on the conduction through the reentrant circuit was assessed in recurrent sustained ventricular tachycardia (VT). Fourteen patients were included in the present study and their VTs were paced at multiple cycle lengths while the criteria of entrainment were confirmed at each paced cycle length. Then, the effect of the paced cycle length upon the conduction time, which was evaluated by the measurement of the time interval from stimulus to the entrained electrogram, was analyzed. In the overdrive pacings of VT, 3 response patterns in conduction time were observed: an increasing pattern (n = 8), a flat pattern (n = 5) and a decreasing pattern (n = 1) while the local conduction time outside the reentrant circuit remained unchanged at comparable paced cycle lengths. A decremental property is the likely mechanism responsible for the paced cycle length-dependent prolongation. As for the flat pattern, the existence of a fully excitable gap may be responsible. A paced cycle length related change in the reentrant circuit may account for the decreasing pattern. By using transient entrainment, the electrophysiological characteristics of the reentrant circuit can be evaluated and the information so gathered may be valuable in analyzing the action of antiarrhythmic drugs on the slow pathway.
A case of sustained ventricular tachycardia (VT) with two possible exits from one re-entrant circuit is described in this paper. The patient was a 27-year-old female who had undergone corrective surgery for tetralogy of Fallot at the age of 8, and developed VT of distinctly different QRS configurations. The exit of one VT was at the right ventricular (RV) outflow tract and the other at the RV apex as determined by endocardial and pace-mapping. Continuous and split activities were observed at the RV outflow tract during both types of VT. One VT was entrained by rapid pacings, and the causal mechanism was thought to be re-entry and common re-entrant circuit was established for two QRS configurations of VTs. A discrepancy was observed between the site of the earliest activation and the site of the pace-mapping which resulted in QRS configuration of VT of the RV apex origin. The findings in this paper should be considered when contemplating aggressive therapy such as electrical ablation.
To investigate the mechanism of induction of ventricular tachycardia (VT) in patients with hypertrophic cardiomyopathy (HCM), we reviewed and analyzed the local ventricular electrograms (LVE) at the pacing sites in 15 patients with HCM and 52 control subjects. Each patient had a clinical history of nonsustained VT or syncope. The results were as follows: 1. Rapid and polymorphic VT was induced in six of the 15 patients with HCM and in 10 of the 52 control subjects. 2. The duration of the LVE at the pacing site was progressively prolonged as the number of extrastimuli were increased or the premature intervals were shortened. Compared with the controls, patients with HCM had longer durations of the LVE by basic drive, single extrastimulus, and by double extrastimuli: 113 +/- 31 vs 95 +/- 16 ms (p less than 0.005), 156 +/- 35 vs 109 +/- 17 ms (p less than 0.001), and 220 +/- 88 vs 133 +/- 25 ms (p less than 0.001), respectively. 3. In the HCM group, the maximum duration of the LVE by double ventricular extrastimuli was significantly longer in patients with inducible VT compared with those with non-inducible VT: 287 +/- 95 vs 183 +/- 56 ms (p less than 0.05). 4. Induction of VT in the HCM group was accompanied by the critical prolongation of the LVE at the pacing site. In two of the six patients with HCM, the LVE at the pacing site spanned the entire cardiac cycle at the time of the initiation of VT.(ABSTRACT TRUNCATED AT 250 WORDS)
We examined the effect of endothelin on the canine coronary artery (N = 20). The left circumflex coronary artery was cannulated and perfused with arterial blood at constant pressure. Coronary blood flow was monitored by an electromagnetic flowmeter. Intracoronary endothelin provoked a vasoconstriction that was dose-dependent. At a dose of 500 pmol, coronary blood flow was reduced remarkably (91.0 +/- 5.4%, n = 4), and endothelin subsequently produced a fall in systemic blood pressure and ST elevation in the electrocardiogram. At a dose of 100 pmol (n = 9), coronary flow decreased from 16.4 +/- 1.5 ml/min to 12.5 +/- 1.5 ml/min (p less than 0.001) and coronary vascular resistance increased from 6.3 +/- 0.8 mm Hg/ml/min to 9.9 +/- 1.9 mm Hg/ml/min (p less than 0.005). A cumulative dose-response curve to endothelin was obtained and the curves were shifted to the right after both verapamil and nifedipine administration. Therefore endothelin has a potent vasoconstrictor action that is attenuated by the calcium-channel blocker.
In the past 4 years, 34 asymptomatic patients with the Wolff-Parkinson-White (WPW) pattern underwent electrophysiologic study. The effective refractory period (ERP) of antegrade conduction over the accessory pathway was 288 +/- 29 msec. In three asymptomatic patients (9%), the antegrade ERP of the accessory pathway was shorter than 250 msec. The antegrade ERP of the accessory pathway became shorter than 250 msec in an additional 12 of 22 (55%) patients after isoproterenol administration. Nineteen (56%) of the asymptomatic patients showed the absence of retrograde conduction over the accessory pathway even after isoproterenol administration. The rate of induction of orthodromic reciprocating tachycardia in the asymptomatic WPW patients was 15% (5/34), which was significantly lower than that in the symptomatic patients. These data suggest that in the asymptomatic patients, the absence of retrograde conduction over the accessory pathway is the reason they remained asymptomatic, free of reciprocating tachycardia. However, even in the asymptomatic patients, some had the accessory pathway in which antegrade ERP was shorter than 250 msec. They may result in rapid ventricular conduction over the accessory pathway when atrial fibrillation develops.
Recently, we examined 2 cases of hypertrophic cardiomyopathy (HCM) presenting with sustained ventricular tachycardia (VT). One case was a 62 year old male with midventricular hypertrophy and monomorphic sustained VT. After admission, the efficacies of procainamide, disopyramide, aprindin, flecainide, mexiletine and verapamil were evaluated by means of continuous electrocardiographic monitoring. Verapamil prevented the recurrence of sustained VT and markedly reduced the frequency and number of runs of nonsustained VT. In the electrophysiologic study, rapid VT was induced by double extrastimuli at the right ventricular apex. Intravenous verapamil at a dose of 10 mg prevented the induction of VT. The patient was discharged on verapamil and remains asymptomatic after 3 months of follow up. The other case was a 34 year old female who was a survivor of cardiac arrest. Monomorphic VT was observed on emergency admission and was converted to sinus rhythm by direct current cardioversion after resuscitation. In the electrophysiologic study, rapid VT was induced by double extrastimuli at the right ventricular outflow tract. Verapamil at a dose of 10 mg prevented the induction of VT. These 2 cases of HCM are rare in that they presented with sustained VT. It is also of interest that verapamil, which has been used conventionally in HCM, prevented VT.
A 27-year-old woman had a history of palpitation at the age of nine. Ventricular tachycardia (VT) was detected four years ago and treatment with procainamide was started. Physical examination disclosed nothing abnormal other than an apical mid-systolic click. Electrocardiogram and chest radiograph were normal, and echocardiogram disclosed borderline mitral valve prolapse (MVP). VT was not provoked by exercise, and Holter monitorings of electrocardiogram were always within a normal limit. Angiography was normal. Electrophysiological study disclosed VT by left ventricular stimulation and the earliest activation was at the apex, VT was abolished by early stimulation from the right ventricular apex. The association of a mid-systolic click and VT was interesting in this case. When the patient had a systolic click at the outpatient clinic, VT frequently occurred within a month (six of seven times), while VT did not occur without an audible systolic click (three of four times). Although it is uncertain whether VT of this patient has any relationship to MVP or to the click, these problems remain to be solved in the future.