[42-year-old patient with fever and weight loss of unknown origin].
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Biomedical subjects
Publications and source records attributed to H U Lehmann.
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Of 68 patients successfully resuscitated within a period of 18 months 52 (38 men and 14 women; mean age 63 [32-90] years) were interviewed about their experience shortly after discharge. 37 reported to have been aware of the life-threatening nature of the acute episode; recurrent depressions were noted by 20; a positive change in attitude towards their life had resulted in 24 patients; 49 praised their doctors and nurses; 40 were appreciative of the medical technology used. All but one of the 52 patients would again choose to be resuscitated. After 12 months 38 patients were again interviewed (31 men and 7 women); 16 had died in the meantime. 21 of the 38 felt physically stronger than before, 25 were more cheerful and 34 were living more intensely. 36 of the 38 patients thought the interviews had been helpful and they would have liked more intensive psychiatric care even during their hospital stay.
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The haemodynamic effects of nifedipine, verapamil and diltiazem were measured and compared in an open randomized parallel investigation on 44 patients with coronary heart disease and compensated myocardial function. Each set of parameters was measured during a control phase and serially after a single dose (nifedipine in retard form, 20 mg; verapamil, 160 mg; diltiazem, 120 mg) over a period of 180 minutes at rest and after a standardized exercise. All three drugs produced a significant fall in systemic arterial pressure of 10-14% and of left-ventricular stroke work of 10-20% from the initial level. The main differences between the three drugs concerned heart rate and stroke volume. Nifedipine produced a significant rise in heart rate, while it fell by 8-10% below the control value after verapamil and diltiazem. On the other hand, verapamil caused a significant fall in stroke-volume index, while after nifedipine and diltiazem it remained unchanged. These results suggest differential therapeutic use of the various calcium antagonists.
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The influence of therapeutic digitalisation on ST depression due to myocardial ischemia was investigated in 11 patients, average age 53.6 years, with coronary heart disease, compared with the effectiveness of nitroglycerine. Therapeutic digitalis led to an average increase of ischaemic ST depression from -0.53 to -0.73 mV. The mean pulmonary arterial and pulmonary capillary pressure decreased slightly, the frequency of pectanginous attacks increased. Independent of the digitalis effect nitroglycerine had an opposing action on these parameters. In decompensated patients with coronary heart disease (n = 4) both digitalis and nitroglycerine produced a shift of the left ventricular function curve as an expression of improved cardiac action. This could not be observed in patients with compensated ventricular function (n = 7). In sufficient ventricular function digitalis led to a further increase of myocardial ischaemic ST depression. In ventricular insufficiency no uniform behaviour was apparent. ST depression induced by digitalis could be reversibly influenced by nitroglycerine.
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60 patients with chronic atrial fibrillation and flutter were randomly allotted to two groups and treated alternately with two different therapy regimes. 30 patients (group I) received lidoflazine in increasing dosage up to 480 mg/24 h and in cases where there was no conversion to sinus rhythm propafenon in a maximal daily dosage of 1800 mg orally. The duration of treatment was limited to 4 days for each substance. 30 patients (group II) were treated in the reverse order, i.e. propafenon and in cases of ineffectiveness with lidoflazine. Atrial fibrillation could be overcome in 21 patients in group I and in 23 patients in group II. The combined success rate in both groups was 73%. The conversion rates for the individual substances were 41% for propafenon (17 out of 41 patients) and 59% for lidoflazine (27 out of 46 patients). The difference was not statistically significant. Successive use of both substances leads to an increased conversion rate. Dangers arising from therapy are a conduction inhibitory action and depression of sinus node function as far as propafenol is concerned and the risk of ventricular ectopy and tachyarrhythmia in lidoflazine.
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22 pateints with a fixed, sometimes therapy-resistant (N = 18) hypertension were treated with a new antihypertensive agent, the pyridopyridazine derivative BQ 22-708 and hemodynamically investigated. 14 hypertensives received single oral doses of between 5 and 15 mg, 8 other patients also received additional treatment with a beta-receptor blocker (0.8 mg pindolol i.v.) or calcium antagonist (10 mg verapamil i.v.). In hypertension which is only poorly controllable or resistant, therapy with BQ 22-708 combined with beta-receptor offers a genuine alternative medication.
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It can be noted, a consequently discovered and treated hypertension is one of the most important achievements of modern medicine within the last 20 years. The earlier treatment begins, the better it success of treatment in avoiding complications on the basis of arterio sclerosis and expectation of life. For elderly hypertensives it is particularly important, what is good in younger decades too - but in higher age the acute threat of life by hypertension is much more pronounced.
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The influence of the calciumantagonistic agent Gallopamile (D 600) on cardiac conduction and sinus node function was studied by using His bundle recordings and atrial stimulation in 13 patients with normal sinus rhythm. Intravenous administration of a single dose of 4 mg produced a significant increase in the atrioventricular conduction time by 30 %. On atrial stimulation second degree a-v block occurred at lower stimulation rates in all patients after Gallopamile. The impulse propagation in atrial tissue and within the His-Purkinje system was not affected, even in patients with diseased conduction system. There was an impairment in sinus node automaticity, the sinus node recovery time was increased by 58 % of the control value.
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