[Echocardiography in the diagnosis of pulmonary embolism].
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Diagnosis, Differential↗
Biomedical subjects
T Hofmann
Publications and source records attributed to T Hofmann.
Domain flexibility in aspartic proteinases.
Comparison of the three-dimensional structures of native endothiapepsin (EC 3.4.23.6) and 15 endothiapepsin oligopeptide inhibitor complexes defined at high resolution by X-ray crystallography shows that endothiapepsin exists in two forms differing in the relative orientation of a domain comprising residues 190-302. There are relatively few interactions between the two parts of the enzyme; consequently, they can move as separate rigid bodies. A translational, librational, and screw analysis of the thermal parameters of endothiapepsin also supports a model in which the two parts can move relative to each other. In the comparison of different aspartic proteinases, the rms values are reduced by up to 47% when the two parts of the structure are superposed independently. This justifies description of the differences, including those between pepsinogen and pepsin (EC 3.4.34.1), as a rigid movement of one part relative to another although considerable distortions within the domains also occur. The consequence of the rigid body movement is a change in the shape of the active site cleft that is largest around the S3 pocket. This is associated with a different position and conformation of the inhibitors that are bound to the two endothiapepsin forms. The relevance of these observations to a model of the hydrolysis by aspartic proteinases is briefly discussed.
Aspartic Acid Endopeptidases↗
The probable conformation of substrates recognized by dipeptidyl-peptidase IV and some aspects of the catalytic mechanism derived from theoretical investigations.
By theoretical conformational investigations of substrates and nonsubstrates of the enzyme dipeptidyl-peptidase IV (DP IV) as well as dipeptide-esters using the ECEPP83 method we determined the structure of peptides recognized and cleaved by the enzyme. From a comparison of all possible structures for the substrates with conformations not possible in nonsubstrates we concluded that a single conformation explains substrate specificities of DP IV. This conformation is characterized by the following dihedral angles: psi 1 = 85 degrees, omega 1 = 180 degrees, phi 2 = -75 degrees, psi 2 = 80 degrees, and omega 2 = 180 degrees. The conclusions were supported by comparisons of molecular electrostatic potentials calculated with the molecular graphics program HAMOG.
Amino Acid Sequence↗
Diagnostic value of transesophageal echocardiography in atrial septal aneurysm.
Transthoracic and transesophageal echocardiography was performed in 40 consecutive adult patients with an atrial septal aneurysm. In 11 (27%) of 40 patients transthoracic echocardiography failed to demonstrate the lesion and the diagnosis was established by the transesophageal approach only. Interatrial shunting, assessed by echocardiographic contrast study and/or color flow mapping, was detected in 13 (54%) of 24 patients on transthoracic imaging and in 29 (76%) of 38 patients during transesophageal echocardiography. Identification of multiple fenestrations (n = 9) and thrombi within the aneurysm (n = 2) could be achieved only by transesophageal ultrasound. A cerebrovascular event of suspected embolic origin occurred in 20 (50%) of 40 patients; 11 (55%) of the 20 patients had repeated cerebral events. Except for mitral valve prolapse in 2 patients and spontaneous left atrial contrast phenomenon in 1 patient no other potential cardiac source of embolism could be identified by transesophageal echocardiography. A marked thickening of the aneurysm was present in 14 (70%) of 20 patients with a cerebrovascular event versus only 4 (20%) of 20 patients without a cerebrovascular event (p less than 0.01). The mechanism of embolization may be both primary thrombus formation within the aneurysm and paradoxical embolization through an interatrial communication as suggested by the findings on transesophageal ultrasound in 2 patients. Although the patients of this study represent a highly selected group it may be concluded that atrial septal aneurysm is a cardiac abnormality with embolic potential. Transesophageal echocardiography has to be regarded the imaging method of choice for evaluation of this lesion.
Adult↗
[Step-plasty for therapy of chronic subcutaneous ruptures of extensor tendons of finger end joints].
A new method for secondary operative treatment of subcutaneous ruptures of the extensor tendons in the DIP-joint region is described. A step-cut incision is performed in the area of the regenerative tissue and the adjacent original tendon. The sutures in the longitudinal incision line compensate the tension and give better anchoring. First results show a tendency to an improved relationship between pre- and postoperative extension lag compared to other methods. Also, the method is an improvement from the aesthetical point of view and in operative practicability.
Adult↗
[Sudden cardiac death: can individual risk be predicted?].
Only 30-40% of all victims of sudden cardiac death could so far be classified as risk patients during their lifetime. Risk factors for sudden death have little predictive value in an asymptomatic population: for example, the typical risk profile for the presence of coronary heart disease and changes in the surface-ECG at rest and especially in the surface-ECG under stress. Usually, the victims of sudden cardiac death among top performance athletes have been suffering from a heart disease of which they knew nothing beforehand: below 40 years of age, mostly from hypertrophic cardiomyopathy; beyond 40, predominantly from coronary heart disease. Among the heart diseases, sudden cardiac death is the cause of death most often in hypertrophic cardiomyopathy, in dilatative cardiomyopathy and in certain types of coronary heart disease. Notwithstanding the employment of fully update cardiological diagnostics the risk patients cannot be identified with reliable precision among those suffering from these diseases. It is only clinically manifest persistent ventricular tachycardia or successful reanimation in case of ventricular fibrillation that will definitely pinpoint the patient as being at risk of sudden cardiac death also in the future.
Cardiomyopathy, Dilated↗
Mechanism and pathway of penicillopepsin-catalyzed transpeptidation and evidence for noncovalent trapping of amino acid and peptide intermediates.
Penicillopepsin acting on Nph-Ala2-amide (where Nph = p-nitrophenylalanyl) catalyzes a transpeptidation reaction which leads to the formation of Nph2-Ala2-amide, which arises from condensation of the substrate with enzyme-bound Nph, as the first product released from the enzyme. This is followed by a stage during which Nph3 and Ala2-amide are the major products. A small amount of Nph4 is also formed during this time. Nph and Nph2, formed during the reactions, are tightly, but probably not covalently, bound to the enzyme. They appear as free products only as a result of the cleavage of Nph3 and Nph4 and after most of the substrate Nph-Ala2-amide has been used up. They act as acceptors for the substrate and for Nph2-Ala2-amide. Nph3-Ala2-amide, formed by condensation of Nph-Ala2-amide or of Nph2-Ala2-amide with enzyme-bound Nph2 or Nph, respectively, is also released but is cleaved rapidly to give Nph3 and Ala2-amide. Incorporation of 18O from [18O]water into the carbonyl oxygens of the products is extensive and shows that release of the intermediates is slower than peptide bond cleavage and peptide bond formation. Hence the rate-limiting step in these reactions is product release. No 18O is incorporated into the initial substrate. We propose that Nph and Nph2 as intermediates are held in the active site by hydrogen bonds and by two strong electrostatic interactions.
Amino Acids↗
Studies on the mechanism of action of penicillopepsin.
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Amino Acid Sequence↗
In vivo regulation of surfactant proteins by glucocorticoids.
Surfactant proteins have key roles in regulating surfactant secretion, in recycling, and in the assembly of the surfactant monolayer but little is known about their regulation in vivo. Surfactant proteins SP-A, SP-B, and SP-C have been shown to be upregulated by glucocorticoids in vitro, but the role of glucocorticoids in the physiologic regulation of surfactant protein synthesis remains unknown. We have studied the effects of exogenously administered glucocorticoids on the regulation of steady-state surfactant protein mRNA accumulation. We have also studied the effects of adrenalectomy on the accumulation of the surfactant protein mRNAs. Surfactant protein genes appear to have quantitatively different responses to exogenously administered glucocorticoids, with SP-C mRNA increasing at the lowest dose, SP-A and SP-B mRNA increasing in response to similar glucocorticoids doses but with SP-B yielding the highest maximum response. Adrenalectomy, however, does not alter surfactant protein mRNA levels. These observations support a minor role for glucocorticoids in maintaining the steady-state accumulation of surfactant protein mRNA. Adrenalectomy decreases total pulmonary SP-A when compared to sham-operated animals in the absence of changes in its mRNA. Therefore, glucocorticoids may have translational or post-translational effects that regulate total pulmonary SP-A accumulation, but the effects appear to be minor. These findings support a potential role for the adrenal in the pulmonary response to stress and demonstrate for the first time differential accumulation of the surfactant protein mRNAs to glucocorticoids in vivo.
Adrenalectomy↗
Can we predict sudden cardiac death?
Up to now only 30 to 40% of patients who die suddenly can be identified as likely candidates before the event. Risk factors in these asymptomatic subjects include a familial history of coronary artery disease, high blood cholesterol levels, hypertension, smoking and, more importantly, an abnormal ECG at rest or during exercise. The predictive value of these abnormalities is too low to justify more detailed clinical investigations in most of these asymptomatic subjects. Exceptions might be the group of patients with multiple risk factors and competitive sportsmen. Sudden cardiac death is a well known complication in patients with hypertrophic and dilated cardiomyopathy. Risk factors in hypertrophic cardiomyopathy include a familial history of this disease, syncope and increasing age. Furthermore, in the adult, the presence of nonsustained episodes of ventricular tachycardia during Holter monitoring seems to indicate an increased risk of sudden cardiac death. In idiopathic dilated cardiomyopathy, the presence of frequent episodes of ventricular pairs and/or episodes of ventricular tachycardia during Holter monitoring, together with a reduced left ventricular ejection fraction, characterises the patient at risk of sudden cardiac death. In patients with coronary artery disease, the patient at risk of sudden cardiac death can be identified by investigating the following: coronary anatomy; global and regional left ventricular function; the presence of ischaemia during rest and/or exercise; the presence of late potentials, by means of the signal-averaged ECG; the presence of spontaneous ventricular arrhythmias (especially sustained and nonsustained ventricular tachycardia); and the results of electrophysiological testing. On the basis of these investigations, 3 subgroups can be distinguished: patients at low risk, medium risk, and high risk of sudden cardiac death.
Death, Sudden↗
[The determination of left ventricular flow rates using single-probe radiocardiography in the steady-state distribution phase].
A new procedure of extracting data from measurements by single-probe radionuclide ventriculography is presented which reduces the phase differences during summation of single-beat actions and permits the use of a greater number of single actions for summation. Sum curves so determined are better suited for measurements of ejection fractions, compliance and ventricular blood flow rates.
Angina, Unstable↗
[Role of cephalometry in orthodontic treatment planning. A study with case report with various considerations of the Quick Ceph Image programs].
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Adolescent↗
[Arrhythmia and anti-arrhythmia therapy as prognostic risks].
The incidence of sudden death is estimated to be 0.25%/year in the industrialized world. 30 to 40% of patients are known to be at major risk before they succumb sudden death. Etiology is usually coronary heart disease (75%), dilated and hypertensive cardiomyopathy as well as valvular disease. 75% of patients dying suddenly die from ventricular fibrillation. The most common mechanism of sudden cardiac death in heart failure is sustained ventricular tachycardia deteriorating into ventricular fibrillation, the initiating factors being single ventricular beats, ventricular pairs or nonsustained ventricular tachycardia (trigger mechanism). At least 50% of patients dying during Holter monitoring have been on antiarrhythmic treatment during the time of sudden death and this percentage is increased to 70% in patients dying from torsade de pointes ventricular tachycardia. The question that has arisen is whether suppression of such arrhythmias by antiarrhythmic agents will reduce the incidence of sudden cardiac death. Unfortunately, the patient group at highest risk - low ventricular ejection fraction and high incidence of nonsustained ventricular tachycardia episodes during 24 hour-monitoring and thus, the group most in need of arrhythmia suppression - has the lowest responder rate as well as the highest incidence of serious toxicity. Until the suppression of those arrhythmias by antiarrhythmic agents is demonstrated to improve prognosis in this patient group, routine use of antiarrhythmic agents cannot be recommended in this patient population.
Anti-Arrhythmia Agents↗
[Progress in clinical cardiology. Echocardiography].
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Blood Flow Velocity↗
Rate-determining steps in penicillopepsin-catalysed reactions.
The hydrolysis of Ac-(Ala)2-Lys-Nph-(Ala)2-amide (II) by penicillopepsin is characterized by a solvent isotope effect of 2.11, whereas the hydrolysis of Ac-Lys-Nph-amide (I) shows no solvent isotope effect. The dependence of the isotope effect on the concentration of D2O in H2O for substrate II is not linear and suggests that two or more protons are involved in its rate-determining step. We propose that for substrate I the rate-determining step is the distortion of the scissile bond towards a tetrahedral configuration, and for substrate II a conformational change induced by the occupation of the S3 pocket in the enzyme.
Amino Acid Sequence↗
Echocardiographic evaluation of patients with clinically suspected arterial emboli.
153 patients (mean age 42 years, range 16-60) who had arterial embolic events were examined prospectively by transthoracic and transoesophageal echocardiography. Patients older than 60 years and those with evidence of extracranial carotid artery occlusive disease were excluded. 84 patients had a cerebral ischaemic event, 50 patients had embolic events in an abdominal organ or limb, and 19 patients had acute retinal ischaemia. The transthoracic echocardiographic examination was normal in 92 patients (60%), whereas only 65 patients (42%) had normal findings after both transthoracic and transoesophageal examination (p less than 0.005). Intracardiac masses, including valvular vegetations, were found in 39 patients (25%), including 27% of patients with cerebral embolism and 32% of these with peripheral embolism, but in none of the patients with retinal ischaemia (p less than 0.001). 47 patients (31%) had valvular disease, 10 (7%) had wall motion abnormalities, 23 (15%) had abnormalities of the interatrial septum, and 9 patients (6%) had diseases of the thoracic aorta. Cardiovascular abnormalities were frequently found by echocardiography in patients with arterial emboli. The transesophageal technique significantly increased the chance of detecting such abnormalities, especially intracardiac masses.
Adolescent↗
A ligand-induced, temperature-dependent conformational Change in penicillopepsin. Evidence from nonlinear Arrhenius plots and from circular dichroism studies.
The effect of temperature on the rate constants of hydrolysis of various substrates by penicillopepsin is dependent on the length of the substrate. For the series Ac-(Ala)m-Lys-Nph-(Ala)n-amide (where Ac- is acetyl- and Nph- is p-nitrophenylalanyl-), where m and n = 0-2, substrates lacking both P'2 and P3 residues give linear Arrhenius plots with an energy of activation of about 55 kJ.mol-1. The Arrhenius plots of substrates in which an alanine residue occupies P'2 show a sharp break at an average transition temperature of 10.5 degrees C. The activation energies are approximately 90 kJ.mol-1 below and approximately 54 kJ.mol-1 above the transition temperature, respectively. For substrates in which P3 is occupied, the average transition temperature is 14.2 degrees C. In this case, the activation energies are 66 kJ.mol-1 below and from 26 to 39 kJ.mol-1 above the transition point. The most probable explanation of these phenomena is that substrate interaction at subsites S3 and/or S'2 of the enzyme induces a temperature-dependent conformational change. Physical evidence for this comes from the observation that the temperature dependence of a CD absorption band at 242 nm of a penicillopepsin-pepstatin complex shows a sharp break that corresponds to those observed in the Arrhenius plots of substrates with alanine at P'2 and P3, whereas the same CD band in the free enzyme is linearly dependent on temperature.
Amino Acid Sequence↗
Repeat determination of left ventricular wall thickness from mass and volume during one cardiac cycle for the calculation of left ventricular wall stress parameters.
Left ventricular end-diastolic wall stress, end-systolic wall stress, and systolic stress-time integral are important parameters to characterize left ventricular load and function. To obtain these parameters, left ventricular pressure, volume, and wall thickness data must be determined at short time intervals throughout one cardiac cycle. However, the measurement of wall thickness at short intervals (i.e., 20 ms) throughout a cardiac cycle is tedious. Furthermore, measurements of wall thickness are less accurate at end-systole compared with end-diastole. For these reasons we developed a computer program for calculating wall thickness at short intervals (20 ms) throughout the cardiac cycle from one single determination of left ventricular wall mass and repetitive measurements of left ventricular (LV) volume.
Computer Simulation↗