[Magnetic resonance imaging of the disk cartilage of the temporomandibular joint].
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Biomedical subjects
Publications and source records attributed to P Held.
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This article discusses therapy with beta blockade and thrombolytic agents in acute myocardial infarction. In large and well-controlled studies both treatment strategies have been shown to increase survival. Both therapies have also been demonstrated to be safe in acute myocardial infarction. Historically, the 2 different treatment strategies have been tested during different time periods, resulting in few studies with the main objective to study the combined effects of the 2 agents. From the data that are presently available, however, there is a clear suggestion of additive beneficial effect and the 2 treatments given in combination are well tolerated.
A 32-year-old woman with migraine for several years again had a migraine attack with headache, nausea, vomiting and eye-muscle disorder, 14 days after an uncomplicated delivery. Within 24 hours a left-dominant hemiparesis developed, followed 12 hours later by tonic-clonic seizure and deep unconsciousness (Glasgow score: 3); the patient could not be aroused. Cranial computed tomography revealed extensive infarction of the brainstem and cerebellum. Angiography demonstrated occlusion of the basilar artery but not other abnormalities of other vessels. There was no evidence for vascular anomalies and the clotting tests were normal. Transoesophageal echocardiography demonstrated an atrial septal aneurysm. But any interatrial shunt (e.g. through a patent foramen ovale) was excluded by colour Doppler sonography, making it highly unlikely that a paradoxical embolus was the cause of the infarction. The brainstem infarction resulting from the basilar artery occlusion did not respond to treatment and the patient died 10 days after the initial seizure.
At least 44 randomized trials of beta blockade in acute myocardial infarction have been reported. All of these trials excluded patients with moderate-to-severe clinical signs of acute left ventricular dysfunction (LVD). Several of the larger trials did include high-risk patients with a history of compensated heart failure or with symptoms and signs suggesting mild LVD. Data from these trials indicate that beta-blocker treatment was well tolerated by patients with LVD, both in the acute phase of myocardial infarction and during long-term follow-up treatment. Further, data for LVD patients indicate that mortality in the beta-blocker group was reduced by 20-30% when compared with the placebo group. A similar mortality reduction was obtained for the entire patient population in the trials. Because of the high mortality among patients with mild LVD, the absolute gain in numbers of lives saved per 100 patients treated with beta blockers is even larger than that in patients without LVD. Data from two long-term trials indicate marked (47% and 43%) reductions in the likelihood of sudden death among LVD patients treated with beta blockers. These results suggest that all patients with LVD who can tolerate beta blockade may benefit from treatment with these agents.
Plasma levels of atrial natriuretic peptide (ANP), angiotensin II, aldosterone, and catecholamines were followed for 1 month and then for 4 to 6 months in 55 patients with acute myocardial infarction. Plasma hormones were highest within the first 24 hours after the onset of infarction but normalized during the first few days in patients without heart failure. In patients with symptoms of heart failure, angiotensin II and norepinephrine remained elevated for 1 month and ANP remained elevated for 4 to 6 months. During head-up tilt, angiotensin II and norepinephrine increased most in patients with overt heart failure. Among patients with a first myocardial infarction, a positive correlation was found between infarct size and ANP, angiotensin II, and norepinephrine on day 5 to 7 and between infarct size and angiotensin II during head-up tilt at 1 month, and between infarct size and ANP at 1 month. A similar relationship was found when only patients without heart failure were studied. It is concluded that sustained neurohormonal activation after myocardial infarction mainly occurs in patients with clinical heart failure but is related to the magnitude of myocardial damage, even in patients without heart failure. Measurement of neurohormones during head-up tilt may be an additive assessment for the detection of neurohormonal activation.
A total of 488 patients with neoplasms (in 474 cases with malignant tumours) of the oropharynx, floor of the mouth and oral cavity, were examined with MRI and CT. MRI proved superior to CT, on account of its coronal and sagittal slice orientation enabling not only a better demonstration of findings, but also improved tumour detection and staging. The diagnostic value of MRI was further enhanced with additional fast and ultrafast MR sequences rather than spin echo sequences alone, as previously practised.
Plasma neurohormones were sequentially analysed in 98 patients with acute myocardial infarction randomized to treatment with enalapril or placebo for 4-6 months. Plasma angiotensin converting enzyme activity was rapidly suppressed by enalapril, but unaffected by placebo (P = 0.0001). No significant differences were found in the plasma levels of angiotensin II, aldosterone, atrial natriuretic peptide, noradrenaline, adrenaline or dopamine between the two treatment groups. Among patients with infarct size above median, plasma angiotensin II increased during head-up tilt at one month in the placebo group, but not in the enalapril group. Left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) were evaluated by echocardiography in 28 patients (placebo 15, enalapril 13) and changes in left ventricular volumes between baseline and 4-6 months were calculated. Only in the placebo group was a positive correlation found between plasma levels of noradrenaline at day 5-7 and the subsequent increase in LVEDV (r = 0.78, P = 0.005) and LVESV (r = 0.75, P = 0.008). The same trend was found for angiotensin II, adrenaline and dopamine levels at days 5-7 and the subsequent increase in left ventricular volumes. In the placebo group a negative correlation was found between plasma aldosterone at days 5-7 and the subsequent increase in left ventricular ejection fraction (r = -0.77, P = 0.006) during the study period. Although circulating neurohormones were not significantly influenced by enalapril treatment, it is concluded that enalapril may influence the relationship found between sustained neurohormonal activation and left ventricular remodelling after acute myocardial infarction.
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BACKGROUND: Long-term administration of angiotensin-converting--enzyme (ACE) inhibitors has been shown to improve survival in patients with symptomatic left ventricular failure and to attenuate left ventricular dilatation in patients with myocardial infarction. We studied whether mortality could be reduced during the 6 months after an acute myocardial infarction with use of the ACE inhibitor enalapril. METHODS: At 103 Scandinavian centers patients with acute myocardial infarctions and blood pressure above 100/60 mm Hg were randomly assigned to treatment with either enalapril or placebo, in addition to conventional therapy. Therapy was initiated with an intravenous infusion of enalapril (enalaprilat) within 24 hours after the onset of chest pain, followed by administration of oral enalapril. RESULTS: Of the 6090 patients enrolled, 3046 were assigned to placebo and 3044 to enalapril. The life-table mortality rates in the two groups at one and six months were not significantly different (6.3 and 10.2 percent in the placebo group vs. 7.2 and 11.0 percent in the enalapril group, P = 0.26). The relative risk of death in the enalapril group was 1.10 (95 percent confidence interval, 0.93 to 1.29). Death due to progressive heart failure occurred in 104 patients (3.4 percent) in the placebo group and 132 (4.3 percent) in the enalapril group (P = 0.06). Therapy had to be changed because of worsening heart failure in 30 percent of the placebo group and 27 percent of the enalapril group (P less than 0.006). Early hypotension (systolic pressure less than 90 mm Hg or diastolic pressure less than 50 mm Hg) occurred in 12 percent of the enalapril group and 3 percent of the placebo group (P less than 0.001). CONCLUSIONS: Enalapril therapy started within 24 hours of the onset of acute myocardial infarction does not improve survival during the 180 days after infarction.
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Despite major advances in the prevention and treatment of cardiovascular diseases, the incidence and prevalence of congestive heart failure (CHF) have been increasing in recent years. As the average age of the population increases, the prevalence of CHF is expected to continue to increase. The number of deaths in which CHF was considered the underlying or contributing cause increased from 51,000 in 1955 to 274,000 by 1988 in the United States. Even accounting for population growth and an increase in the number of elderly, this represents a 2-fold increase. Additionally, CHF was responsible for about 643,000 hospitalizations in 1988. Digitalis is one of the drugs most commonly prescribed for CHF and has been used for greater than 200 years. In 1990, digoxin was one of the most commonly prescribed drugs in the United States, accounting for greater than 21 million prescriptions. There has been little decline in the drug's use over the last 5 years, indicating that newer treatments for CHF have not replaced the widespread use of digitalis. Despite these findings, considerable controversy surrounds the appropriateness of its role and value in treating CHF patients who are in sinus rhythm. A number of recent, uncontrolled studies have arrived at apparently contradictory conclusions concerning the effects of digitalis on mortality in postmyocardial infarction and heart failure patients. A large, double-blind, randomized, controlled clinical trial to evaluate the effects of digitalis on mortality, morbidity and quality of life is being sponsored by the National Heart, Lung, and Blood Institute in conjunction with the Department of Veterans Affairs Cooperative Studies Program.(ABSTRACT TRUNCATED AT 250 WORDS)
Recent work in yeast shows that eukaryotic origins of DNA replication are multipartite regulatory elements resembling promoters of transcription. As for the regulation of transcription, accessory transcription factors appear to function in concert with basic origin recognition factors to regulate initiation of DNA synthesis at specific subsets of origins. The participation of transcription factors in the regulation of DNA replication may facilitate temporal control of transcription and replication during the cell cycle, as well as providing a mechanism for integrating origin selection with the cellular transcriptional program.
Vascular smooth muscle cells exhibit a unique pattern of growth in culture. They have the capacity for multilayer growth and form large macroscopic nodules. We find that nodulation is inhibited in the presence of phorbol esters and that there is a concomitant decrease in the production of a 38 kd secreted protein associated with nodulation in porcine smooth muscle. Examination of the organization of actin filaments within the cells using a rhodamine phalloidin stain indicates that there is a rearrangement of actin filaments in response to phorbol esters. This rearrangement increases the number of attachment sites to the culture surface and may contribute to the inhibition of nodulation in smooth muscle cells by phorbol esters.
Magnetic resonance imaging (MRI) is now an established technique which is becoming increasingly important in the diagnosis, treatment planning and follow-up of ENT tumours. It offers numerous advantages over other diagnostic procedures, especially computed tomography (CT). The soft tissue contrast enabled by MRI is superior to that obtained with CT scanning. MRI also enables multiplane imaging, which facilitates evaluation of the complex anatomy of the head. Apart from spin echo sequences, the most commonly employed technique, gradient echo sequences are becoming ever more important. This technique is flow-sensitive, reduces the investigation time and permits 3D imaging.
Using a combination of T1 weighted snapshot-flash sequences and intravenous contrast bolus it was possible to demonstrate intraluminal signal differences in a period of seconds. 5 confirmed aortic lesions were studied; 2 old aortic dissections (with differentiation between the true and false lumen), 1 acute aortic dissection and a partially thrombosed thoracic aortic aneurysm were demonstrated. The advantage of this technique lies in its simplicity and reproducibility. Difficulties in interpreting the intraluminal phases arising from spin echo and flash techniques are made easier by interpreting the available signals from this method.
1. Seven randomized controlled trials of intravenous nitroglycerin in a total of about 850 patients have been reported. Overall, there were 51 deaths (12.5%) in the nitroglycerin group and 87 (20%) in the control group. This indicates a 48% reduction in the odds of death (P less than 0.001, 95% confidence limits (25% to 64%)). 2. There are five randomized trials of oral nitrates after acute myocardial infarction. In these trials, 11.8% of the patients in the nitrate group compared with 13.3% in the control group died. This indicates a nonsignificant 12% reduction in the odds of death but the 95% confidence interval overlaps widely with the i.v. trials. If all trials of i.v. or oral nitrates are considered the reduction in the odds of death is 32% (P less than 0.01). 3. Nitrates have a beneficial effect on haemodynamics in heart failure but the data on mortality effects are sparse. In combination with hydralazine, however, long-term mortality was reduced in the V-HEFT trial of chronic heart failure.