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T Eliasson

Publications and source records attributed to T Eliasson.

At least 37 records · Page 2Linked to original sources

Pressure-flow studies before and after transurethral microwave thermotherapy of benign prostatic hyperplasia using low- and high-energy protocols.

OBJECTIVE: To compare pressure-flow results before and 3 months after transurethral microwave thermotherapy (TUMT) for benign prostatic hyperplasia (BPH), performed with lower and higher energy protocols. PATIENTS AND METHODS: Twenty-four patients were treated using a high-energy protocol performed with a heatshock strategy, i.e. a rapid increase in intraprostatic temperatures to a maximum of 55-67 degrees C. A helical antenna was used which produced maximum heating at the base of the prostate. A further 25 patients were treated using a lower energy protocol with a slow increase in intraprostatic temperatures to a maximum of 45-53 degrees C. A first-generation filament antenna was used with the maximum heat produced at the prostatic apex. All treatments were performed as single-session outpatient procedures of 60-70 min duration. RESULTS: There was a significantly greater improvement in pressure-flow variables, i.e. maximum urinary flow rate, detrusor pressure at maximum flow and minimal urethral opening pressure, in those treated with higher energy TUMT than in those receiving the lower energy protocol. The Madsen and quality-of-life scores, and maximum urinary flow rate on uroflowmetry, were also significantly better in the higher energy group. CONCLUSION: Higher energy TUMT performed using a heat-shock strategy provides a better pressure-flow outcome than lower energy thermotherapy. Compared with previously published results, the outcome after higher energy TUMT is at least similar to other treatment alternatives for BPH.

Humans↗

Importance of thermal dose and antenna location in transurethral microwave thermotherapy for benign prostatic hyperplasia.

The importance of thermal dose and the location of the heat maximum for the outcome of transurethral microwave thermotherapy for benign prostatic hyperplasia was studied. It was originally designed as a two-arm randomized study of 196 patients comparing high and low effect with the heat maximum at the apex of the prostate. The inclusion criteria were: prostate volume 25 to 70 cc, Madsen score > or = 8, Qmax < or = 15 mL/sec, residual urine volume < 350 mL, and no median-lobe enlargement. Using the same inclusion criteria, another group of 31 patients was compared in which the location of the heat maximum was at the base of the prostate. Treatment was performed as an outpatient single session procedure for 70 minutes with the Prostcare (Bruker Medical, France). Improvement was found after 6 months in all three groups regarding Qmax and Madsen, bother, and quality of life scores. The improvement of Madsen score from baseline was more pronounced in the high-effect base group than in the other two groups. Responders were defined as patients showing improvement in Madsen score who were satisfied with treatment outcome and in no need of complementary treatment at 6 months' follow-up. Significantly more responders were found, and the increment of serum prostate specific antigen and side effects were more pronounced, in the high-effect base group than in the other two groups. Treatment outcome seems to be both dose related and dependent on the location of the heat maximum. However, the improvement in outcome is associated with increased morbidity.

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Effects of spinal cord stimulation on coronary blood flow velocity.

BACKGROUND: Spinal cord stimulation (SCS) has been used in the treatment of severe angina pectoris since the 1980s. Several studies have shown both an antianginal and an anti-ischaemic effect. There are several theories about the mechanism behind the anti-ischaemic effect of SCS, including the possibility that it is dependent on an increase in coronary flow velocity. OBJECTIVE: To determine if there were effects of SCS on coronary flow velocity during cardiac stress. METHOD: Eight patients with severe anginal pain secondary to coronary artery disease who had been implanted with an SCS device were included in the study. In addition, four patients with syndrome X were examined. If possible, a Doppler guidewire was placed in the vessel corresponding to the ischaemic area revealed on a prior myocardial scintigram. A temporary pacemaker electrode was placed in the right atrium. Atrial pacing started at 80 beats/min and increased by 10 beats/min every 2 min until the patient experienced moderate angina; the pacing frequency was then maintained at the same level. After 2 min of pacing at this frequency, SCS treatment commenced; after a further 5 min, pacing was stopped. Throughout the procedure, coronary flow velocity, assessed as average peak velocity (APV), was monitored continually. RESULTS: APV increased during pacing in all the patients with coronary artery disease (mean increase 53%; P < 0.02). There were no significant changes in APV during maximum pacing frequency when stimulation was introduced. CONCLUSIONS: The results of this study do not support the theory that the anti-ischaemic effect of SCS is dependent on an increase in coronary flow velocity.

Angina Pectoris↗

Myocardial turnover of endogenous opioids and calcitonin-gene-related peptide in the human heart and the effects of spinal cord stimulation on pacing-induced angina pectoris.

Earlier studies have shown that spinal cord stimulation (SCS) has antianginal and anti-ischemic effects in severe coronary artery disease. In the present study, 14 patients were subjected to right-sided atrial catheterization and atrial pacing. The patients were paced to angina during a control session and during spinal cord stimulation. Myocardial extraction of beta-endorphin (BE) during control pacing (8 +/- 22%) changed to release at the maximum pacing rate during treatment (-21 +/- 47%, a negative value representing release). Furthermore, the results indicate local myocardial turnover of leuenkephalin, BE and calcitonin-gene-related peptide. In addition, it is implied that SCS may induce myocardial release of BE which could explain the beneficial effects in myocardial ischemia.

Aged↗

Effects of pacing-induced myocardial stress and spinal cord stimulation on whole body and cardiac norepinephrine spillover.

AIMS: Spinal cord stimulation has been used in the treatment of intractable angina pectoris since the beginning of the 1980s. This study was designed to investigate whether the documented anti-ischaemic effects of spinal cord stimulation are mediated through a decrease in sympathetic activity. METHODS AND RESULTS: Ten patients with a spinal cord stimulator implanted as anti-anginal treatment were included in the study. Atrial pacing until the patient experienced moderate angina was performed and after 50 min rest the procedure was repeated during spinal cord stimulation. Total body and cardiac norepinephrine spillover was calculated and the former was found to have increased during pacing (47%, P = 0.02). When spinal cord stimulation was applied, total body norepinephrine spillover decreased at a comparable pacing rate (18%, P = 0.02). Cardiac norepinephrine spillover was not affected during the procedure. CONCLUSION: The results of this study indicate that the anti-ischaemic effect of spinal cord stimulation is not due to reduced cardiac sympathetic activity. However, spinal cord stimulation decreases overall sympathetic activity which may benefit the heart, possibly by reducing oxygen demand.

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Thermal injury during TUMT.

A 71-year-old man was treated with transurethral microwave thermotherapy because of symptoms of benign prostatic hyperplasia. The treatment session was performed without any abnormal complaints from the patient. Two hours post-treatment the patient felt pain in his penile shaft and noticed a wound. A thorough investigation revealed that the only possible explanation for the injury was a dislocation of the catheter.

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The heat is on--but how? A comparison of TUMT devices.

OBJECTIVE: To compare the heat characteristics of the microwave antennae, the absorbed energy in the target volume and the cooling capacity of the catheters of three common devices for transurethral microwave thermotherapy (TUMT), i.e. the Prostcare, Prostatron and ProstaLund. MATERIALS AND METHODS: The microwave emission from the respective catheters or antennae was measured in a tissue-equivalent 'phantom' prostate. From these measurements the distribution of absorbed energy from the respective catheters and antennae was calculated from the characteristics of the phantom, the absorbed energy and the temperature difference before and after heating. The cooling capacity of the different catheters were measured by submerging each catheter in a thermally isolated water bath at a known temperature and determining the cooling of the water bath caused by the catheter. RESULTS: The design of the microwave antenna influenced the heating profile significantly. The energy absorbed by the prostate model varied among the devices, but was between 13 and 21% of the stated applied energy. The cooling capacity also varied, being least in the Prostcare and greatest in the ProstaLund catheters. CONCLUSIONS: Users of TUMT should be aware of possible back-heating along the catheter, as this limits the microwave power that can be used safely. Furthermore, the 'treatment energy', which is commonly used as an indicator to describe the intensity of TUMT treatments, is ambiguous and not stringent, in that the microwave energy absorbed in the prostate is only a small fraction of this value.

Catheter Ablation↗

Spinal cord stimulation in severe angina pectoris.

Since 1985, 225 patients suffering from severe pectoris due to New York Heart Association classes III-IV have been treated with spinal cord stimulation (SCS). All patients have been considered not suitable for open heart surgery by technical reasons. The long-term follow-up has shown a very good positive response to stimulation with pain relief, less intake of medication and increased quality of life. Several invasive studies with catheters in the coronary sinus and peripheral arteries have shown a significant improvement with stimulation regarding heart muscle lactate metabolism, blood flow in the coronary sinus and oxygen demand. Recordings with the so-called Holter technique have demonstrated that SCS does not create arrhythmias, and pacing studies that SCS does not mask ischemia at extreme workload. In conclusion, apart from the positive effect on the quality of life, SCS in angina pectoris has demonstrated antianginal and anti-ischemic effects. The clinical results and the physiological and hemodynamic measurements will be presented in detail.

Angina Pectoris↗

Spinal cord stimulation in cardiovascular disease.

Spinal cord stimulation in ischemic pain conditions has proved to be an effective method of treatment for many patients. The indications are ischemic pain in the extremities from peripheral vascular disease and angina pectoris. The long-term results show that the response rate for ischemic pain is 70% to 90%, while the corresponding results for neuropathic pain average approximately 50% to 70%, which actually makes ischemic pain a very good indication for SCS. SCS system implantation is a safe and quick operation performed under local anesthesia and well tolerated by the patient. A total implant of the lead and the pulse-generator in one stage seldom takes more than 1 hour. High sterility and prophylactic antibiotics are prerequisites to avoid postoperative problems. In atherosclerosis, SCS should be regarded as a method supplementary to vascular surgery, to be used for symptom recurrence after treatment or when there are technical obstacles to reconstructive surgery. SCS has proven to be extremely effective for the relief of ischemic rest pain, which constitutes the most severe problem for these patients. Today it is estimated that more than 7000 implants for PVD have been done in Europe. In a prospective randomized study, Jivegård et al have shown that SCS is a limb-saving treatment. For angina pectoris, SCS by now has become a routine supplementary method to conventional medical and surgical treatment. The technique is clinically effective, and several studies have shown decreased myocardial ischemia and decreased anginal pain during treatment. It is probable that the use of SCS in refractory angina will increase considerably in the 1990s.

Cardiovascular Diseases↗

[Spinal cord stimulation in severe angina pectoris. Reduced ischemia and increased quality of life].

Promising clinical results have been obtained with spinal cord stimulation which in recent years has been used for treating the subgroup of patients with angina pectoris that has proved intractable to conventional medical and surgical treatment strategies. According to recent reports, the anti-angina effect of spinal cord stimulation is associated with a reduction in myocardial ischaemia due to decreased myocardial oxygen consumption. Candidates for the treatment require careful screening. It is important to ensure that the patient is capable of full co-operation, and that the chest pain is due to true reversible myocardial ischaemia. Results in the 206 patients given implants to date have been encouraging, with reductions both in the frequency of angina attacks and in the consumption of short-acting nitroglycerin.

Angina Pectoris↗

Safety aspects of spinal cord stimulation in severe angina pectoris.

BACKGROUND: Spinal cord stimulation has been used over the past decade for the treatment of patients suffering from intractable angina pectoris, despite having received optimal medical therapy, and who are unsuitable for further surgical intervention. The clinical results are promising and several studies have shown that the antianginal effect of the treatment is associated with a reduction in myocardial ischemia. It has been suggested, however, that spinal cord stimulation may only attenuate the transmission of pain from the heart, without influencing myocardial ischemia. This is a major safety concern when applying this treatment strategy. METHODS: The aim of this study was to assess the potentially unfavourable aspects of spinal cord stimulation in patients with severe coronary artery disease and angina pectoris by means of repeated long-term ECG recordings. Nineteen patients who had been accepted for implantation of spinal cord stimulators for the treatment of severe angina pectoris were included. RESULTS: No increases were noted in the frequency of ischemic episodes, the total ischemic burden, or the number of arrhythmic episodes during treatment. CONCLUSION: The results of this study do not indicate any unfavourable effects of spinal cord stimulation in severe angina pectoris in terms of an increase in the frequency or severity of myocardial ischemia during treatment with spinal cord stimulation.

Aged↗

Effects of spinal cord stimulation in angina pectoris induced by pacing and possible mechanisms of action.

OBJECTIVE: To investigate the effects of spinal cord stimulation on myocardial ischaemia, coronary blood flow, and myocardial oxygen consumption in angina pectoris induced by atrial pacing. DESIGN: The heart was paced to angina during a control phase and treatment with spinal cord stimulation. Blood samples were drawn from a peripheral artery and the coronary sinus. SETTING: Multidisciplinary pain centre, department of medicine, Ostra Hospital, and Wallenberg Research Laboratory, Sahlgrenska Hospital, Gothenburg, Sweden. SUBJECTS: Twenty patients with intractable angina pectoris, all with a spinal cord stimulator implanted before the study. RESULTS: Spinal cord stimulation increased patients' tolerance to pacing (p < 0.001). At the pacing rate comparable to that producing angina during the control recording, myocardial lactate production during control session turned into extraction (p = 0.003) and, on the electrocardiogram, ST segment depression decreased, time to ST depression increased, and time to recovery from ST depression decreased (p = 0.01; p < 0.05, and p < 0.05, respectively). Spinal cord stimulation also reduced coronary sinus blood flow (p = 0.01) and myocardial oxygen consumption (p = 0.02). At the maximum pacing rate during treatment, all patients experienced anginal pain. Myocardial lactate extraction reverted to production (p < 0.01) and the magnitude and duration of ST segment depression increased to the same values as during control pacing, indicating that myocardial ischaemia during treatment with spinal cord stimulation gives rise to anginal pain. CONCLUSIONS: Spinal cord stimulation has an anti-anginal and anti-ischaemic effect in severe coronary artery disease. These effects seem to be secondary to a decrease in myocardial oxygen consumption. Furthermore, myocardial ischemia during treatment gives rise to anginal pain. Thus, spinal cord stimulation does not deprive the patient of a warning signal.

Aged↗

Assessment of the influence of spinal cord stimulation on left ventricular function in patients with severe angina pectoris: an echocardiographic study.

Patients with severe, widespread coronary atherosclerosis and patients who have undergone several coronary artery bypass operations are often poor candidates for coronary bypass surgery (CABG). Spinal cord stimulation (SCS) has been shown to have an anti-anginal effect that is probably associated with an anti-ischaemic effect. In the present investigation, 15 patients with severe angina (mean age 64 years, range 49-71) were studied. All patients had a history of intractable angina pectoris despite optimal medical treatment and previous coronary bypass operation. The patients had multi-vessel disease and graft occlusion or graft stenosis on postoperative coronary angiograms. Left ventricular function was assessed echocardiographically at rest and during provocation with adenosine infusion in a control session without treatment and during treatment with SCS. The recovery time was at least 3 h. The decrease in the ejection fraction during adenosine infusion was more pronounced in the control situation (44 to 37%; P < 0.05) than during SCS (48 to 44%; ns), and the time to echocardiographic signs of dysfunction and to anginal pain during adenosine infusion was significantly prolonged during SCS (P < 0.001). In addition, the recovery time for these parameters was shorter during SCS (P < 0.001). It is concluded that the deterioration in left ventricular function during adenosine provocation was less pronounced with SCS than without. This possible anti-ischaemic effect is in agreement with results from earlier studies.

Adenosine↗

Spinal cord stimulation in angina pectoris with normal coronary arteriograms.

BACKGROUND: Patients with angina pectoris with normal coronary arteriograms, also known as Syndrome X (typical exercise-induced angina pectoris, positive exercise testing, and normal coronary arteriograms), are often difficult to treat with conventional forms of medical therapy. Spinal cord stimulation has been used in recent years for the treatment of severe angina pectoris refractory to conventional medical and surgical therapy in coronary artery disease. The aim of this study was to investigate the effects of spinal cord stimulation on angina pectoris with normal coronary arteriograms. METHODS: Twelve patients underwent five bicycle exercise tests, three tests without (control), and two tests with spinal cord stimulation treatment. RESULTS: The exercise tolerance of the patients increased (108 +/- 22 W versus 96 +/- 21 W; P < 0.001), the magnitude of ST-segment depression at comparable work load decreased (1.0 +/- 0.6 mm versus 1.5 +/- 0.9 mm; P < 0.01), time to angina increased (5.4 +/- 2.2 min versus 2.7 +/- 1.9 min; P < 0.01), and time to the appearance of ST-segment depression increased (3.5 +/- 1.9 min versus 2.4 +/- 1.6 min; P < 0.01). The rate-pressure product at maximum work load during treatment increased, compared with the maximum work load during the control session (28,038 +/- 6124 mmHg x bpm versus 25,222 +/- 4519 mmHg x bpm; P < 0.05) and the comparable work load during treatment (28,038 +/- th 6124 mmHg x bpm versus 24,795 +/- 5022 mmHg x bpm; P < 0.01). CONCLUSIONS: Spinal cord stimulation has beneficial effects in angina pectoris with normal coronary arteriograms in terms of relief of symptoms of angina pectoris and improvement of exercise tolerance. These effects may be associated with a reduction in myocardial ischemia.

Aged↗

Effect of spinal cord stimulation on regional myocardial perfusion assessed by positron emission tomography.

Spinal cord stimulation (SCS) can relieve symptoms in patients with severe angina pectoris refractory to conventional medical or surgical therapy. This symptomatic improvement may result from decreased myocardial ischemia. To test this hypothesis, positron emission tomography (PET) and potassium-38 as a flow tracer were used in 8 patients for the quantitative evaluation of regional myocardial perfusion at rest and after exercise, before and during SCS. Potassium uptake was evaluated as myocardial clearance (flow times net extraction) in ml/min/100 g. Tomographic segments were categorized as nonaffected and affected on the basis of the absence or presence of arterial stenosis on coronary angiography and on the basis of thallium scintigraphic data. In nonaffected segments, before SCS, regional myocardial clearance significantly increased from rest (28 +/- 4) to exercise (47 +/- 13 clearance units; p less than 0.004). A similar increase occurred after SCS. In affected segments, before SCS, regional myocardial clearance barely increased (p = 0.065) from rest (26 +/- 6) to exercise (33 less than or equal to 12). In comparison, after SCS, the resting regional myocardial clearance was slightly elevated (29 +/- 8) reflecting an increased double product, but did not increase (p = 0.192) with exercise (34 +/- 12). However, the magnitude and duration of ST-segment depression decreased during treatment with SCS. Anginal pain occurred in all patients during control exercise, but was attenuated in all but one with SCS. These results indicate that SCS improves exercise-induced angina and electrocardiographic signs of ischemia but this influence does not appear to be mediated by changes in regional myocardial perfusion.

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