Microbial communities in feed, bedding material, and bulk milk - experiences from a feeding trial.

There is an increasing interest in the microbiota of the dairy value chain, from field to fork. Studies to understand the effects of environmental, feed and management factors on the raw milk microbiota have been performed to elucidate the origin of the bacteria and find ways to control the presence or absence of specific bacteria. In this study, we explored the microbiota in feedstuff, bedding material and milk on a Swedish dairy farm to investigate the effects of feeding different silages on the bacterial compositions throughout the dairy value chain. Three ensiling treatments were evaluated: without additive, with acid treatment, and with inoculation of starter culture. The silage treatments were fed as partial mixed rations to 67 dairy cows for 3 weeks each, with one treatment fed twice to evaluate if a potential change in milk microbiota could be repeated. The highest average total bacteria counts were found in the used bedding material (9.6 log10 cfu/g), while milk showed the lowest (3.5 log10 cfu/g). Principal coordinate analysis of the weighted UniFrac distance matrix showed clear separation between 3 clusters of materials: 1) herbage, 2) silage and partial mixed ration, and 3) used bedding material and milk. Surprisingly, the expected effect of the ensiling treatments on silage microbiota was not clear. Transfer of major bacteria from the silages and resulting partial mixed rations to the used bedding material was observed, but rarely to milk. The milk microbiota showed most resemblance to that of the used bedding material. Lactobacillus was a major genus in both feed and milk, but investigations at amplicon sequence variant level showed that in most cases the sequences differed between materials. However, low total bacteria count in the milk in combination with a high diversity suggests that results may be biased due to environmental contamination of the milk samples. Considering that the study was performed on a research farm, strict hygienic measures during the feeding experiment may have contributed to the low transfer of bacteria from feed to milk.

Esophageal dysfunction in syndrome X.

Syndrome X is defined as anginal chest pain accompanied by objective signs of ischemia on exercise testing or myocardial scintigraphy, but with angiographically "normal" coronary arteries. The etiology of this enticing syndrome is still not known. Besides myocardial ischemia, esophageal dysfunction and visceral hypersensitivity may play a role in the development of pain. The purpose of this study was to study esophageal function and visceral sensitivity in patients with syndrome X. Twenty consecutive patients with the diagnosis of syndrome X were investigated with esophageal manometry and a 24-hour pH recording. Visceral esophageal sensitivity was explored by balloon distention of the distal esophagus, as well as by instillation of acid. Twelve patients (67% of the 18 evaluated) had some abnormality on 24-hour pH monitoring; 2 had abnormal global acid exposure time (pH <4) and 7 had symptoms coincidental with episodes of pH <4. Seven patients (35%) had esophageal dysmotility including 5 with the "nutcracker" esophagus. Esophageal hypersensitivity to acid (n = 9) or distention (n = 13) was seen in 14 of the 20 patients. Eleven patients received acid suppressive therapy that resulted in amelioration of chest pain in 8 (73%). Thus, results suggest that esophageal hypersensitivity rather than gross functional abnormality is an important factor for the development of chest pain in patients with syndrome X, and that acid in the context of a hypersensitive esophagus is the main culprit. Acid suppression may ameliorate pain in a substantial proportion of patients.

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.

Clinical outcome of patients treated with spinal cord stimulation for therapeutically refractory angina pectoris. The Working Group on Neurocardiology.

OBJECTIVE: To determine morbidity and mortality characteristics in patients treated with electrical neuromodulation for refractory angina pectoris. DESIGN: A retrospective multicentre study of patients treated with spinal cord stimulation between 1987 and 1997; 21 centres were contacted and 14 responded. SETTING: Specialist centres worldwide. PATIENTS: Questionnaires were returned on 517 patients, of whom 71% were male. One was lost to follow up. Mean (SD) age was 63.9 (10.1) years. Duration of angina pectoris was 8.1 (6.3) years. RESULTS: Before spinal cord stimulation, 66% of the patients had experienced myocardial infarction, 68% had three vessel disease, and in 24% the left ventricular ejection fraction (LVEF) was /= 71 years were independent predictors of mortality. During spinal cord stimulation, New York Heart Association functional class improved from 3.5 to 2.1 (p < 0.01); 25 of the deceased patients (24%) and 32 survivors (8%) experienced myocardial infarction; hospital admissions were significantly (p < 0.001) more common in the deceased group (66% v 37%). CONCLUSIONS: The clinical outcome of patients with intractable angina is not adversely affected by the chronic use of neurostimulation.

Transcutaneous electrical nerve stimulation in unstable angina pectoris.

BACKGROUND: Silent ischemia is a strong predictor of unfavorable outcome in unstable angina pectoris. Dynamic continuous vector cardiography provides online detection of ischemic episodes. Transcutaneous electrical nerve stimulation (TENS) has been reported to have antianginal effects in patients with severe coronary artery disease and this is associated with a reduction in myocardial ischemia. The aim of the present study was to investigate the applicability of TENS in patients with unstable angina in the coronary care unit and the effects on vector cardiographic and biochemical markers of ischemia. METHODS: Thirty patients (14 in the TENS group and 16 in a placebo group) were included in a single-blind, placebo-controlled study after being admitted to the coronary care unit. Continuous vector cardiography, leakage of cardiac enzymes and consumption of analgesics were recorded for 24 h. RESULTS: TENS was well tolerated and did not interfere with standard treatment, although vectorcardiographic recording during actual stimulation was disturbed. There was a reduction in the number of silent ischemic ST change vector magnitude episodes (P = 0.02) and their duration (P = 0.01) in the TENS-treated group, and a nonsignificant reduction in the total number of ST change vector magnitude (painful plus silent) episodes (P = 0.09) and their duration (P = 0.05) and in leakage of cardiac enzymes (P = 0.12). There were no detectable differences in terms of episodes of pain leading to stimulation or consumption of analgesics. CONCLUSIONS: TENS seems to be a safe additional treatment in unstable angina pectoris and may reduce the number of ischemic events, by mechanisms apparently unrelated to the reduction of pain.

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.

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.

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.

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.

Clinical results of microwave thermotherapy for benign prostatic hyperplasia.

Transurethral microwave thermotherapy is a truly office procedure without the need for anesthesia for the treatment of lower urinary tract symptoms caused by benign prostatic hyperplasia. Several devices have been developed. Continuous refinement of the procedure led to higher energy protocols and high-intensity dose protocols applying the heat-shock strategy. We report on the clinical results of these protocols. Symptom scores improve around 60%, whereas maximum urinary flow rate improve from an average 9 to 10 mL/sec at baseline to 14 to 15 mL/sec during follow-up. No significant differences have been shown between the outcomes with the different devices. Long-term data show satisfactory results after 4 years. Initial clinical results with the heat-shock strategy show results comparable to those of higher-energy protocols with decreased morbidity. Treatment morbidity of higher energy protocols is moderate and consists mainly of the need for catheterization and a higher percentage of retrograde ejaculation. To improve treatment efficacy, patient selection appears to be most important. Prostate size, bladder outlet obstruction, age, and prostate composition are of predictive value for treatment outcome. Further development of the treatment protocols and refinement of the urethral applicators might enhance outcome.

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.

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.

[Treatment guidelines for refractory angina pectoris now available. Therapeutic methods varying between behavior therapy and heart transplantation]. / Nu finns riktlinjer för behandling av refraktär angina pectoris. Terapimetoderna har varierat från beteendeterapi till hjärttransplantation.

Refractory angina pectoris is defined as severe angina despite optimal medical and surgical/invasive treatment (CABG, PTCA). The epidemiology of this condition is unknown. The estimated yearly incidence is 2,000 patients in Sweden and 30,000-50,000 patients in Europe. The patient group is growing as a result of improved therapy. A number of additional treatment modalities have been developed during the last decades. The article summarises the scientifically and clinical basis of these treatments and gives recommendations concerning their use.

[Spinal cord stimulation in severe angina pectoris. Reduced ischemia and increased quality of life]. / Ryggmärgsstimulering vid svår angina pectoris. Minskad ischemi och ökad livskvalitet.

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.

[Spinal cord stimulation in angina pectoris--what is the current situation?]. / Ryggmärgsstimulering vid angina--var står vi idag?

Spinal cord stimulation has been used to treat intractable angina pectoris since 1985 with good results. Several studies have shown the treatment to yield both anti-anginal and antiischaemic effects. The mechanisms underlying these effects have been investigated in a number of studies, but remain unclear. In a recent randomised prospective study, where spinal cord stimulation was compared to coronary artery bypass surgery, both treatments yielded adequate relief of symptoms, and there was no subgroup difference in this respect. The article consists in a review of current trends in this field.