Preoperative markers of postoperative persistent severe left ventricular dysfunction.
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Aortic Valve Insufficiency↗
Biomedical subjects
W Rudolph
Publications and source records attributed to W Rudolph.
[Doppler echocardiography determination of the orifice area in aortic valve stenosis using a continuity equation].
The continuity equation, derived from the study of fluid mechanics, may serve as the basis for calculation of orifice area of stenosed cardiac valves. As applied to aortic stenosis, the continuity equation states that the flow across the narrowed valve is equal to the flow in the left ventricular (LV) outflow tract such that A1 X v1 = A2 X v2, where A1 = LV outflow tract area, v1 = prestenotic velocity, A2 = stenotic orifice area and v2 = poststenotic velocity. Accordingly, at each point in time during pulsatile flow, the respective valve orifice area can be calculated. Hence, from the sum of all areas throughout the ejection time, the mean valve orifice area can be constructed as integral of A2/ET = A1 X integral of (v1/v2)/ET, assuming A1 to be constant, where integral of denotes the integral over the ejection time ET. To assess the usefulness of this method with respect to its clinical relevance, in 36 patients with aortic stenosis, the Doppler echocardiographically-determined orifice areas were compared with those calculated by the Gorlin formula based on invasively-obtained data. LV outflow tract area A1 was measured by echocardiography from a parasternal long-axis view. Prestenotic velocity v1 was recorded in the LV outflow tract by pulsed Doppler from an apical transducer position, whereby care was taken in positioning the sample volume not too close to the stenotic valve to avoid the prestenotic area of increased velocity. Continuous-wave Doppler was used, usually from an apical or right parasternal transducer position, to record the stenotic jet velocity v2.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[Doppler echocardiography determination of the pressure gradient and valve orifice area in mitral valve stenosis].
Pressure gradient and orifice area of stenosed mitral valves can be determined with Doppler echocardiography using the modified Bernoulli equation and the pressure half-time method, respectively (Figures 1 and 2). There was a close linear correlation between Doppler-echocardiographically determined pressure gradients and valve orifice areas with those obtained by invasive methods. In this study, in 85 patients with mitral stenosis of various severity, the valve orifice areas, as derived by the two methods respectively, correlated well (y = 0.89x + 0.15) with a correlation coefficient r = 0.96 and standard error of the estimate SEE = 0.12 cm2 (Figure 3). The correlation was not influenced by the prevailing cardiac rhythm, ventricular function, left ventricular mass or coexistent mitral or aortic regurgitation (Table 1). Accordingly, the Doppler echocardiographic method also appears applicable in the presence of concomitant mitral and aortic regurgitation which precludes an exact determination of valve orifice area with invasive methods. The Doppler echocardiographic method is currently so well validated that it can be regarded as a reliable noninvasive procedure for determination of the severity of mitral stenosis.
Blood Flow Velocity↗
[Doppler echocardiography determination of the severity of tricuspid valve stenosis].
To evaluate the diagnostic usefulness of Doppler echocardiography for assessment of tricuspid stenosis, data of eleven patients were compared with hemodynamic results. Using the pressure half-time method, stenotic tricuspid orifice area was calculated as the quotient of 220 divided by the pressure half-time. The pressure gradient across the stenotic valve was determined according to the modified Bernoulli equation using four times the square of the maximal velocity of the stenotic jet. A close correlation was found between the Doppler echocardiographically and invasively determined orifice areas (r = 0.97, SEE = 0.23 cm2). There was also a good linear relationship between the pressure gradients derived from both methods (r = 0.89, SEE = 1 mmHg). Thus, the assessment of tricuspid stenosis can be achieved reliably by noninvasive means with the aid of Doppler echocardiography.
Adult↗
[Noninvasive determination of the orifice area of aortic valve prostheses using Doppler echocardiography].
In aortic valve stenosis, Doppler echocardiography enables reliable estimation of the orifice area with the use of the continuity equation. This study was carried out to determine the usefulness of the method in evaluation of prosthetic aortic valve area. Accordingly, 32 patients with normally-functioning mechanical Björk-Shiley prostheses underwent Doppler investigations two to three weeks after aortic valve replacement. Pre(v1)- and post(v2)-prosthetic velocities were recorded by pulsed and continuous-wave Doppler, respectively, and the prosthetic annulus used as cross-sectional area of flow (A1). For calculation of prosthetic orifice area (A2), the continuity equation at peak flow (v1,p) was employed where A2 = A1 X v1,p/v2 (at the point in time of v1,p). Mean pressure gradients across the prostheses were determined with the use of the modified Bernoulli equation. In addition, the ratio of acceleration to ejection time (AT/ET) was derived from the velocity profile of v2. Consistent with increasing prosthetic sizes (A 23 to A 29), there were increases in the calculated orifice areas A2 (A 23: 1.46 +/- 0.26, A 25: 1.71 +/- 0.24, A 27: 2.12 +/- 0.26, A 29: 2.53 +/- 0.35 cm2). Albeit with a substantial overlap between the various sizes, mean values for the respective sizes differed statistically significant and were comparably within the range established by in-vitro measurements. Pressure gradients across the prostheses were also different for the various sizes and were within the range reported from hemodynamic studies. In contrast, the AT/ET-ratio showed no significant difference between different prosthetic sizes.(ABSTRACT TRUNCATED AT 250 WORDS)
Aortic Valve↗
Effectiveness of molsidomine in the long-term treatment of exertional angina pectoris and chronic congestive heart failure.
Molsidomine, similar to nitrates, improves myocardial blood flow in hypoperfused, poststenotic myocardial regions, reduces left ventricular pressure and volumes, and leads to improvement in impaired regional wall motion. In patients with chronic, stable anginal pectoris who underwent long-term treatment with 2 mg of molsidomine three times daily there were reductions in ST segment depression of 45% and 9% at 1 and 3 hours after administration, respectively, and slight but statistically significant reductions in the rates of anginal attacks and nitrate consumption of 16% and 18%. Administration of 3 mg three times daily did not render more significant effects. Doubling the frequency of administration--that is, 2 mg six times daily--led to reductions in the rates of anginal attacks and nitrate consumption of 38% and 36%, respectively, and 4 mg led to a more marked reduction in ST segment depression of 57%. With administration of 8 mg of sustained-release molsidomine, a prolonged antiischemic effect was documented with reductions in ST segment depression of 74% at 1 hour and 31% at 8 hours after medication. In patients with congestive heart failure, 1 hour after administration of 4 mg of molsidomine there were significant reductions in systolic and diastolic pulmonary artery pressures of 25% and 30%, respectively. After 7 days of continuous treatment with 4 mg of molsidomine four times daily, comparable reductions in pulmonary artery pressure were observed. Thus molsidomine, in adequate dosages, elicits an unequivocal anti-ischemic and antianginal effect as well as a salutary reduction in left ventricular filling pressure.
Angina Pectoris↗
Inhalation of U aerosols from UO2 fuel element fabrication.
Publication No. 30 of the International Commission on Radiological Protection (ICRP) assigns the uranium oxides UO2 and U3O8 to transportability class Y, i.e. the half-life of these compounds in the lungs is about 500 days. This assignment seemed not to be in accordance with our experience resulting from incorporation surveillance during UO2 fuel element fabrication. Persons who worked in atmospheres containing UO2 aerosols with activity concentrations significantly above the derived air concentrations (DAC) for class Y U showed much lower activity in the lungs than would be expected according to the ICRP. To understand this discrepancy, aerosol concentrations and aerosol particle-size distributions at work places with the possibility of UO2 incorporation, the activity of urine and feces and the lung activity of persons working at these places were measured in an investigation program. The results are only consistent with the ICRP lung model if one uses a measured biological half-life in the lungs of 109 days and a measured AMAD of 8.2 micron instead of the ICRP standard assumptions of 500 days and 1.0 micron, respectively. ICRP Publication No. 30 recommends application of specific parameters for health physics instead of standard model values. For the special conditions in our UO2 fuel fabrication plant we therefore derive limits of air concentrations, lung activities and fecal and urinary activity concentrations by applying our measured particle-size and lung-retention parameters to the ICRP model. Our special derived limits in comparison to class Y limits for U after ICRP Publication No. 30 for a 1-micron AMAD and 500-day half-life (in brackets) are: (a) annual limit of intake: 6 X 10(4) Bq/y (1 X 10(3) Bq/y); (b) derived air concentration: 20 Bq/m3 (0.6 Bq/m3); (c) derived lung activity: 1.6 X 10(3) Bq; (d) derived fecal activity: 14 Bq/day; and (e) derived urine activity: 8.9 Bq/day. The committed dose equivalents calculated from our measured data and from our modified derived limits proved consistent for the different incorporation control methods (determination of air concentration, lung, fecal or urinary activity). The authors recommend that in accordance with ICRP Publication No. 30, the national rules and regulations on activity incorporation provide the possibility to derive special limits from specific work-place parameters such as particle-size distributions and biological half-lives, thus supplementing the ICRP standard assumptions of 1 micron AMAD and biological half-lives of 0.5 days for class D, 50 days for class W and 500 days for class Y compounds.
Adult↗
[Therapy of ventricular arrhythmias with propafenone].
In 16 patients with angiographically-documented coronary artery disease and repetitive ventricular responses the effects of oral propafenon 300 mg t.i.d. on the continuous 24-hour ECG were analyzed in a study carried out according to a double-blind, randomized, crossover, placebo-controlled protocol. Comparisons were made for the number of couplets (Lown IVa) and ventricular tachycardias (Lown IVb) as well as the overall incidence of ventricular premature beats during the two last days of a five-day placebo phase and on the second and third day of treatment with propafenon. In 15 further patients with electrocardiographically-documented sustained ventricular tachycardias, the effect of intravenous propafenon (1.5 mg/kg in three minutes) was also investigated. Repeat electrophysiologic studies were performed in eight of the 15 patients after two to 13 days of continuous treatment with oral propafenon 300 mg t.i.d. The stimulation protocol incorporated delivery of a maximum of four extra stimuli during sinus rhythm and during apical right ventricular stimulation at each of four basic intervals (600, 500, 400 and 330 ms) as well as burst stimulation with intervals between 300 and 250 ms. Stimulation was terminated after induction of sustained ventricular tachycardia. In patients in whom ventricular tachycardia could be induced prior to medication with one or two stimuli, after propafenon no more than two extra stimuli were applied. As compared with placebo, propafenon led to a more than 90% reduction in couplets in 56% of the patients and in 64% of the patients there was a complete suppression of ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[Quantitative coronary angiography before and after PTCA. Rate of restenosis, analysis of modifying factors].
In 95 consecutive patients in whom 101 coronary artery stenoses were successfully dilated, angiography was performed before, immediately after and at an average of 6.6 months after the procedures with computer-derived stenosis measurements (based on three-dimensional vessel reconstruction). The results were referenced to an analysis of factors possibly exerting an influence on post-PTCA outcome. In 56 of the 101 dilated stenoses (minimal area prior to PTCA 0.83 +/- 0.57 mm2, after PTCA 4.09 +/- 1.7 mm2), the findings remained essentially unchanged throughout the six-month follow-up. 17 of the 56 dilated stenoses showed a further increase in minimal area as compared with the findings seen immediately after PTCA. A reduction of the minimal area of more than 1 mm2 from that achieved immediately after PTCA, associated with narrowing of the vascular lumen greater than 70% was found in 33 of the 101 stenoses (minimal area before PTCA 0.82 +/- 0.59 mm2, immediately after PTCA 3.92 +/- 1.55 mm2, six months post-PTCA 1.39 +/- 1.27 mm2). In twelve of the 101 stenoses, restenosis amounting to more than 1 mm2 was also observed but without critical compromise of the vascular lumen (minimal area before PTCA 0.81 +/- 0.39 mm2, immediately after PTCA 5.54 +/- 1.28, six months post-PTCA 3.22 +/- 1.43 mm2, corresponding to a mean luminal narrowing of 45 +/- 24%).(ABSTRACT TRUNCATED AT 250 WORDS)
Angina Pectoris↗
[Antihypertensive and anti-ischemic effect of nitrendipine. Double-blind, randomized, crossover and placebo controlled acute study].
Nitrendipine is a newly-developed calcium channel blocker derived from the dehydropyridine series which, according to experimental studies, affects marked dilation of the peripheral and coronary vessels. As compared with the parent compound nifedipine, nitrendipine exhibits a clearly more prolonged elimination half-time. This study was designed to evaluate the antihypertensive efficacy, in particular, with respect to the duration of action as well as the anti-ischemic effectiveness with a protocol encompassing as many factors as possible. In 13 patients with angiographically-documented coronary artery disease and elevated blood pressure at rest and/or during exercise, on two days separated by a three-day washout period, we investigated the effects of 20 mg nitrendipine, as compared with placebo, in a double-blind, randomized, crossover study. The systolic and diastolic arterial blood pressure as well as the heart rate were recorded prior to, at two, five, eight and twelve hours after medication and the blood pressure only at 24 hours. Blood pressure and heart rate were assessed during active standing at two hours, passive tilt at 2 1/2 hours and, together with analysis of the ST segments, before and during semisupine bicycle ergometry performed at three hours after tablet administration.(ABSTRACT TRUNCATED AT 250 WORDS)
Angina Pectoris↗
[High-dose transdermal nitroglycerin therapy: loss of effect within 24 hours?].
Within a relatively short period of time, nitroglycerin patches have come into widespread use for treatment of coronary artery disease in the absence of sufficient clinical data in support of their efficacy. Presently, there is still considerable controversy regarding the extent and duration of action as well as the dosage requirements. Accordingly, a study was carried out in six patients with angiographically-documented coronary artery disease, stable exercise-induced angina pectoris and reproducible ST-segment depression to analyze the effects of nitroglycerin patches, formulated to deliver 5 mg, 10 mg, 20 mg as well as 30 mg per 24 hours, respectively, on the extent of ST-segment depression. In a further study, the extent and duration of antianginal and anti-ischemic effects of nitroglycerin patches delivering 30 mg/24 hours were investigated in ten patients according to a randomized, double-blind, crossover placebo-controlled protocol. In seven of these patients, testing was again performed at 2.5 hours after repeated application (second application at 24 hours) (Figure 1). Nitroglycerin patches delivering 5 mg, 10 mg, 20 mg as well as 30 mg/24 hours, respectively, led to significant reductions in ST-segment depression at 2.5 hours of 59% (range 25 to 100%; p less than 0.025), 63% (0 to 100%, p less than 0.01), 77% (50 to 100%, p less than 0.001) as well as 82% (50 to 100%, p less than 0.005) as compared with control values (Figure 2).(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Topical↗
[Long-term therapy of stress angina pectoris by a single daily administration of 120 mg isosorbide dinitrate in retard form. Comparison of monotherapy and combination therapy with atenolol and nifedipine].
This study was undertaken to determine whether an effective antianginal treatment without tolerance development can be carried out with intermittent nitrate administration on a regimen with a single daily dose of 120 mg isosorbide dinitrate (ISDN) in sustained-release form (SR), as well as whether the concomitant administration of 100 mg atenolol or 100 mg atenolol and 20 mg nifedipine renders an additive antiischemic effect. In two independently performed investigations, the duration of action of a single dose of 120 mg ISDN SR was assessed after its initial administration in addition to the anti-ischemic effect during long-term treatment, each according to a randomized, double-blind, crossover, placebo-controlled protocol in a total of 15 patients with angiographically-documented coronary artery disease, stable angina pectoris and reproducible ST-segment depression during exercise. The test phases of four weeks each were separated by one week placebo phases. After completion of the study, for a further eight weeks, 120 mg ISDN SR was given together with 100 mg atenolol in the morning. Exercise testing was carried out after four weeks of treatment in a control period before and at two hours after administration of 120 mg ISDN SR with 100 mg atenolol as well as after another four weeks in a control period before and after concomitant administration of 120 mg ISDN SR, 100 mg atenolol and 20 mg nifedipine in sustained release form.(ABSTRACT TRUNCATED AT 250 WORDS)
Angina Pectoris↗
[Therapy of coronary heart disease with nitroglycerin patches. Behavior of anti-ischemic effectiveness in continuous administration and following patch free interval].
Subsequent to the finding of a rapidly attenuated anti-ischemic effect on use of high-dose nitroglycerin patch treatment in patients with coronary artery disease as well as contradictory results obtained with low-dose patch treatment, there are still no reliable guidelines for the use of transdermal nitroglycerin patch therapy. Accordingly, this study was carried out in ten patients with angiographically-documented coronary artery disease, stable exercise-induced angina pectoris and reproducible ST-segment depression, to assess the extent and duration of antianginal and anti-ischemic action of nitroglycerin patch treatment at an intermediate dosage of 15 mg/24 hours after the initial application, after renewed patch application on the second day and after patch application on the third day which had been preceded by a ten-hour patch-free interval in the night. At 2.5 hours after initial application of the nitroglycerin patch there was a 64% reduction in exercise-induced ST-segment depression from 2.6 mm +/- 0.21 (SEM) to 0.93 mm +/- 0.29 (p less than 0.001) (Figures 1 and 2). The exercise capacity to onset of 1 mm ST-segment depression was increased 132% from 191 watt X min +/- 15 (SEM) to 442 watt X min +/- 47 (p less than 0.001), (Figure 3). Eight hours after the initial patch application, exercise-induced ST-segment depression was reduced 37% from 2.6 mm +/- 0.19 to 1.65 mm +/- 0.18 (p less than 0.01); the exercise capacity to onset of 1 mm ST-segment depression was increased 39% from 178 watt X min +/- 18 to 245 watt X min +/- 19 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Topical↗
[Histologically detectable myocarditis in patients with impaired left ventricular function].
In patients with impaired left ventricular function in whom dilated cardiomyopathy is initially suspected after performance of comprehensive diagnostic studies, histologic evidence of myocarditis or status-post myocarditis is being documented with increasing frequency since the systematic use of endomyocardial biopsy has been incorporated into the work-up. This investigation was undertaken to analyze the histologic, clinical, hemodynamic and immunologic findings in these patients to delineate possible relationships between histologically-documented myocarditis and dilated cardiomyopathy. Incidence of histologically-documented myocarditis. In our patient population, 41 of 150 patients with impaired left ventricular function, the etiology of which had been unknown, histologic evidence of myocarditis was documented. In seven of eight in whom active myocarditis was diagnosed at initial biopsy, after a mean follow-up period of two years the histologic findings were consistent with dilated cardiomyopathy. In similar groups of patients comparable incidences of myocarditis have been reported by Parrillo et al. in 19 of 100 (19%) and Fenoglio et al. in 34 of 135 patients (25%). A higher incidence has been reported by Zee-Cheng et al. in 22 of 35 patients (63%). Accordingly, pooled data indicate that the overall incidence of histologically-documented myocarditis was 30% in 528 patients initially suspected to have dilated cardiomyopathy. The variances in the incidence reported by the respective authors may be attributable to differences in the histologic definition of myocarditis, number of biopsies obtained, size of the patient population and the epidemiologically-related incidence of viral disease.(ABSTRACT TRUNCATED AT 250 WORDS)
Autoantibodies↗
[Dilated cardiomyopathy: characterization by clinical and hemodynamic findings].
Dilated cardiomyopathy, a disease of the heart muscle of unknown origin, is characterized by impaired systolic function and dilatation of the left and right ventricles. In the Federal Republic of Germany, there are an estimated 4000 to 5000 new cases reported yearly [40]. Pathologic-anatomic studies have demonstrated that, in addition to an extent of dilatation of all heart chambers dependent on the stage of the disease, up to 60% of those who die can be found to have intracardiac thrombi [37]. Specific histologic changes are absent [34]. Disturbances of the microcirculation, a defect of autonomic innervation and biochemical alterations have been postulated as possible causes [7, 33, 35]. Circulating and bound antibodies against myocardial antigens and pathologic cellular immunoreactions have been reported in association with both myocarditis and dilated cardiomyopathy; this, in turn, has led to the hypothetical assumption of a secondary immunopathogenesis after myocarditis [6, 9, 12, 18, 26, 33]. Clinical and hemodynamic findings encompass a wide spectrum. With a mildly impaired ejection fraction to values between 40 and 54%, in our patients there was an associated enlargment of the end-systolic and end-diastolic ventricular volumes to 60 and 115 ml/m2 (upper normal limits 35 and 95 ml/m2), respectively. Those with increasing degrees of left ventricular function impairment to ejection fractions less than 40%, had additionally pathologic elevation of the filling pressures. In patients with marked impairment of the ejection fraction to values of less than 25%, cardiac output was reduced and systemic and pulmonary vascular resistances elevated.(ABSTRACT TRUNCATED AT 250 WORDS)
Blood Pressure↗
[Early heart failure in cardiomyopathies and heart valve diseases].
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Cardiomyopathies↗
[A new method for the demonstration of the Bordetella bronchiseptica capsule in electron microscopy].
A new and rapid working method is presented for electronmicroscopic preparation of capsules from gram negative bacteria, e.g. Bordetella bronchiseptica and Pasteurella multocida. The advantage of the new technique is the availability of the results within 30 min after starting the preparation. The staining of the capsule by alcian blue has to be done as a first step together with glutaraldehyde fixation, before staining the bacterial cell with phosphotungstic acid. The new staining technic also reveals structural details of the capsule. The described procedure was found to be useful in controlling the development of the bacterial capsule depending on culture media for propagation and maintenance of the above mentioned bacteria.
Alcian Blue↗
[Prevention of the development of tolerance to isosorbide dinitrate in interval therapy].
A number of carefully controlled studies in recent years have unequivocally documented evidence of tolerance development with respect to anti-ischemic effects during longterm treatment with nitrates [1, 3, 4, 5, 7, 8]. To determine to what extent tolerance development can be circumvented through an interval regimen, a study was performed in ten patients with stable angina pectoris and reproducible ST-segment depression according to a randomized, double-blind, cross-over, placebo-controlled protocol. Analysis of the anti-ischemic effect of 20 mg ISDN was carried out after acute administration and during chronic treatment on an interval regimen with the administration of 20 mg ISDN in the morning (at 8 a.m.) and at midday (1 p.m.) (Figure 1). On acute administration, 20 mg ISDN led to a reduction in ST-segment depression from 2.15 to 0.40 mm (p less than 0.01) and during longterm treatment from 2.25 to 0.40 mm (p less than 0.01) (Figure 2, Table 1). After acute administration the plasma concentration of ISDN was 9 ng/ml, 2-ISMN 34 ng/ml and 5-ISMN 149 ng/ml (Figure 5, Table 2). Of the control values during longterm treatment, a detectable level was found only for 5-ISMN with a concentration of 36 ng/ml while that of both 2-ISMN and ISDN was 0 ng/ml. On renewed administration, there was an increase of ISDN to 9 ng/ml, 2-ISMN to 37 ng/ml and 5-ISMN to 208 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)
Angina Pectoris↗